Volume 1 A B Editors-in-Chief
Allan Jamieson The Forensic Institute, Glasgow, UK
Andre Moenssens Forensics and Law Ce...
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Volume 1 A B Editors-in-Chief
Allan Jamieson The Forensic Institute, Glasgow, UK
Andre Moenssens Forensics and Law Center, Columbia City, IN, USA
This edition first published 2009 2009 John Wiley & Sons Ltd Registered office John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, United Kingdom For details of our global editorial offices, for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at www.wiley.com. Bomb-Pulse Dating, pp. 418–422; Radiocarbon Dating, pp. 2231–2233; Dissociative Disorders, pp. 784–792; Footwear and Foot Impressions: Foot Impressions and Linking Foot to Shoe, pp. 1244–1248; Footwear and Foot Impressions: Overview, pp. 1252–1255; Forged and Counterfeit Documents, pp. 1255–1276, are all US Government works in the public domain and not subject to copyright. Accreditation: Laboratory, pp. 1–10, is copyright of The American Society of Crime Laboratory Directors/Laboratory Accreditation Board (ASCLD/LAB) and is used here with their consent. Juvenile Justice: Adolescent Development, pp. 1608–1612, and Juvenile Justice: Transfer to Adult, pp. 1612–1618, are copyright of the John D. and Catherine T. MacArthur Foundation and are used here with their consent. Bloodstain Pattern Interpretation, pp. 97–134, is copyright of the author and is used here with his consent. The right of the authors to be identified as the authors of this work has been asserted in accordance with the Copyright, Designs and Patents Act 1988. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher. Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books. Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought.
Library of Congress Cataloging-in-Publication Data Wiley encyclopedia of forensic science / editors in chief, Allan Jamieson, Andre Moenssens. p. ; cm. Includes bibliographical references and index. ISBN 978-0-470-01826-2 (set : cloth) 1. Forensic sciences–Encyclopedias. I. Jamieson, Allan. II. Moenssens, Andre A. III. Title: Encyclopedia of forensic science. [DNLM: 1. Forensic Medicine–Encyclopedias–English. 2. Forensic Sciences–Encyclopedias–English. W 613 W714 2009] HV8073.W55 2009 363.2503–dc22 2009001881 A catalogue record for this book is available from the British Library. Set in 91/2 / 111/2 pt Times by Laserwords Private Limited, Chennai, India Printed and bound by Grafos S.A., Barcelona, Spain
Editorial Board Editors-in-Chief Allan Jamieson The Forensic Institute Glasgow UK
Andre Moenssens Forensics and Law Center Columbia City, IN USA
Editors BEHAVIORAL SCIENCES
DNA ANALYSIS
Carl Edwards Four Oaks Institute Dover, MA USA
Allan Jamieson The Forensic Institute Glasgow UK
BIOLOGICAL SCIENCES
FIRE
Allan Jamieson The Forensic Institute Glasgow UK
John J. Lentini Scientific Fire Analysis, LLC Big Pine Key, FL USA
CRIMINALISTICS
INVESTIGATION & LAW ENFORCEMENT
Claude Roux University of Technology (UTS) Sydney, New South Wales Australia
Allan M. Scott University of Central Lancashire (UCLAN) Preston UK
DIGITAL EVIDENCE, MULTIMEDIA ENGINEERING
LAW
AND
Zeno Geradts Netherlands Forensic Institute Den Haag The Netherlands
AND
OF
BIOLOGICAL FLUIDS
EXPLOSIVES
Andre Moenssens Forensics and Law Center Columbia City, IN USA
vi
Editorial Board
MEDICINE
TOXICOLOGY
Pekka J. Saukko University of Turku Turku Finland
Olaf H. Drummer Monash University Southbank, Victoria Australia
STATISTICS
TRACE
AND THE
EVALUATION OF EVIDENCE
Christophe Champod Institut de Police Scientifique University of Lausanne Lausanne Switzerland Tacha N. Hicks Institut de Police Scientifique University of Lausanne Lausanne Switzerland
AND
DRUG ANALYSIS
Sheila Willis Forensic Science Laboratory, Department of Justice, Equality and Law Reform Garda Headquarters Dublin Ireland
Contents VOLUME 1 Accreditation: Laboratory Accreditation: Organizational Acid Phosphatase Addictions Adversary Systems of Justice Aggression Aggression: Gender Differences in Airbags Alcohol Alcohol: Analysis Alcohol: Behavioral and Medical Effects Alcohol: Interaction with Other Drugs Alcohol: Use, Abuse, Tolerance, and Dependency Allelic Designation Alterations: Erasures and Obliterations of Documents Amphetamine Amplified Fragment Length Polymorphism Analysis: Computer Network Analysis: Neutron Activation Anthropology Anthropology: Age Determination of Remains Anthropology: Aging the Living Anthropology: Ancestry and Stature Determination Archaeology Arson Investigation: Misconceptions and Mythology Asphyxia Assault: Sexually Motivated Autoerotic Deaths Automated Fingerprint Identification System
1 10 17 18 23 24 36 51 58 81 99 108 120 126 128 134 140 141 150 152 179 188 191 199 207 224 234 243 249
Automatism as a Defense to Crime Autopsy Autoradiograph
253 256 262
Battered Child Syndrome Battered Spouse Syndrome Battered Woman’s Reality Bayesian Networks Behavioral Science Evidence Behavioral Toxicology Benzodiazepines Best Evidence Rule Biological Agents Biological Stains Biological Swabs Biometric Devices Blood Grouping Bloodstain Pattern Interpretation Blunt Force Trauma Bomb Scene Management Bomb-Pulse Dating Botany
263 270 272 276 281 290 293 298 299 314 320 321 338 359 396 411 418 422
VOLUME 2 Cannabis Capacity Assessment Capacity for Independent Living Capacity to Consent to Medical Treatment Capacity to Stand Trial Capacity to Waive Miranda Rights Cardiac and Natural Causes of Sudden Death Case Assessment and Interpretation Ceiling Principle: DNA Chain of Possession of Tangible Evidence
431 437 444 450 456 463 468 483 497 498
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Contents
Chemical, Biological, Radiological, and Nuclear Investigations Chemical Warfare Agents Child Sexual Abuse Child Sexual Abuse Accommodation Children: as Defendants Children: as Witnesses Children: Suggestibility of Civil Commitment Civil Law Systems of Justice Cocaine Cofiler/CofilerPlus Compulsion Compulsion Defense Computer Animation and Simulation Evidence Computers Confessions: Evidentiary Reliability of Confirmation Testing: Toxicology Crime Scene Documentation Crime Scene Investigation Crime Scene Management Crime Scene Photography: US Perspective Crime Victims’ Decision to Report Crime Criminalization of the Mentally Ill Cross-Examination: Impact on Testimony Cross-Examination of Experts Dangerousness: Risk of Databases Dating: Document Daubert v. Merrell Dow Pharmaceuticals Death: Time of Death Penalty and Age Deception: Detection of Deception: Detection of and Brain Imaging Deception: Truth Serum Delusions Demonstrative Evidence Diatoms Differential Extraction Direct Examination of Experts Disaster Mental Health Disaster Victim Identification
500 507 529 537 542 549 553 556 561 562 569 571 576 579 584 588 595 602 614 619 625 643 649 656 662 667 677 684 692 697 717 720 724 728 741 745 748 757 758 760 764
Discovery: Depositions Discovery: Discovery Motions Discovery in the United States: Civil Cases Discovery in the United States: Criminal Cases Discovery of Expert Findings Dissociative Disorders DNA DNA: an Overview DNA: Degraded Samples DNA: Sources of DNA Databases and Evidentiary Issues Documents: Authentication of DQα Drug Analysis Drug Profiling Drug Testing: Urine Drug-Facilitated Sexual Assault Drug-Impaired Driving Duty to Warn
772 774 775 778 781 784 792 800 816 821 831 840 842 844 851 860 868 877 885
Earprints: Interpretation of 891 Education and Accreditation in Forensic Science 897 Elder Abuse: Policy 902 Elder Abuse: Risk 912 Elderly in Court 916 Electrical Engineering 920 Entomology 934 Environmental Science 946 Enzymes 954 Error Rates in Forensic Methods 955 Ethics: Codes of Conduct for Expert Witnesses 957 Evidence: Rules of 963 Evidence Collection and Preservation: Casting 963 Evidence Interpretation: a Logical Approach 968 Evil: Illusion of 977 Examination of Fibers and Textiles 985 Expert Opinion: Appeal v. Trial 998 Expert Opinion: United States 1001 Expert Opinion: United Kingdom, Canada, and Australia 1003 Expert Opinion in Court: a Comparison of Approaches 1004
Contents Expert Opinion in Court: Civil Law Jurisdictions (France, Germany, Italy, and Spain) Expert Witness: Who Is? Expert Witnesses: Selection and Investigation of Credentials Explosions: Scene Investigation Explosion Debris: Laboratory Analysis of Extraction Eyewitness: Suggestibility of Eyewitness Lineups: Identification from Eyewitness Testimony
1007 1012 1013 1019 1028 1060 1065 1072 1075
VOLUME 3 Facial Comparison Facial Reconstruction Falsifiability Theory Federal Rule of Evidence 702 Fibers Fire: Chemistry of Fire: Dynamics and Pattern Production Fire: Scene Investigation Fire and Explosion Investigations: Overview Fire Debris: Laboratory Analysis of Fire Investigator: Standardization, Accreditation, and Certification Fire Modeling and Its Application in Fire Investigation Firearm Discharge Residue: Analysis of Firearm Examination: Ballistics Firearms: Bullet and Cartridge Case Identification Firearms: Identification of Handling of Firearms/Trace Metal Detection Firearms: Overview Firearms: Scene Investigation Firesetting Footwear and Foot Impressions: Comparison and Identification Footwear and Foot Impressions: Databases
1081 1086 1093 1095 1095 1103 1112 1122 1136 1137 1171 1175 1189 1200 1204
1211 1216 1219 1225 1230 1240
Footwear and Foot Impressions: Foot Impressions and Linking Foot to Shoe Footwear and Foot Impressions: Intelligence Footwear and Foot Impressions: Overview Forged and Counterfeit Documents Foundation Testimony Friction Ridge Examination (Fingerprints): Interpretation of Friction Ridge Skin: Comparison and Identification Friction Ridge Skin: Fingerprint Detection and Recovery Techniques Friction Ridge Skin: Interaction between Fingerprint Detection and DNA/Biological Material Friction Ridge Skin: Morphogenesis and Overview Frye v. United States General Acceptance Test for Novel Expert Evidence General Electric v. Joiner Genomics and Behavioral Evidence Geographical Identification by Viral Genotyping Glass Glass Evidence: Bayesian Approach to GSM Analysis and PDAs Guardianships of Adults Gunshot Wounds Hair: Animal Hair: Microscopic Analysis Hair: Toxicology Hallucinations Handwriting and Signatures, Comparison of Handwriting and Signatures, Interpretation of Comparison Results Hardy-Weinberg Equilibrium Head Injury: Neuropsychological Assessment Hearsay Evidence Histology
ix
1244 1248 1252 1255 1276 1277 1282
1292
1318 1322 1331
1333 1334 1335 1342 1348 1351 1360 1371 1380 1403 1415 1427 1432 1436
1451 1458 1459 1465 1468
x
Contents
Homicide: Multiple (Behavior) Homosexual Panic Human Factors: Industrial Incidents Human Remains and Identity Hypnosis and Memory Hypothetical Question
1474 1480 1483 1495 1500 1505
Identification and Individualization Identification of Human Remains Identifiler Image Processing and Analysis In Limine Motions and Hearings Injury: Burns, Scalds, and Chemical Ink Analysis Ink Comparison and Interpretation Insanity: Defense Interpretation: Document Evidence Interpretation: Legal Perspective Interpretation: Low Template DNA Interpretation: Observer Effects Interpreting Expert Opinions: History of Interrogation Interrogative Suggestibility Intersecting Lines: Documents Ipse Dixit Testimony
1508 1511 1518 1520 1528 1529 1541 1546 1552 1557 1561 1566 1575
Judicial Notice of Scientific Principles and Facts Jury Dynamics Jury Instructions on Expert Testimony Juvenile Justice: Adolescent Development Juvenile Justice: Transfer to Adult
1579 1586 1590 1594 1599
1601 1602 1607 1608 1612
Kumho Tire v. Carmichael
1619
Learned Treatises as Evidence Length Measurement Light Bulbs and Filaments: Examination of Low Copy Number DNA Luminol
1623 1624 1632 1639 1645
VOLUME 4 Malingering: Forensic Evaluations Malpractice Actions against Experts
1657 1663
Marks or Impressions of Manufactured Items Mass Grave Investigation Materials Science Matrix: DNA Medical Malpractice Memory: Reconstructive Memory: Repressed Mental Health Courts Mental Retardation Mental Retardation: Death Penalty Mental Status: Examination Microchemistry Microsatellites Microscopy: FTIR Microscopy: High Power Microscopy: Light Microscopes Microscopy: Low Power Microscopy: Scanning Electron Microscopy Mini-STRs Missing Persons and Paternity: DNA Mitigation Testimony Mitochondrial DNA: Interpretation Mitochondrial DNA: Profiling Mixture Interpretation: DNA
1668 1674 1680 1688 1689 1709 1712 1717 1724 1730 1737 1743 1749 1750 1758 1762 1791 1793 1804 1810 1818 1823 1833 1838
Natural Causes of Sudden Death: Noncardiac Neuropsychological Assessment Neuropsychological Assessment: Child Northwest Juvenile Project Nuclear Forensics
1869 1877 1883
Odontology Opioids Oral Fluid Toxicology
1889 1895 1903
Packaging and Transport Paint Paint: Interpretation Palynology Paper Analysis Parental Alienation Parental Rights and Prerogatives Parenting: Assessment of Capacity Particles: Form Peak Height: DNA
1927 1931 1943 1954 1968 1981 1984 1989 2001 2007
1843 1862
Contents Peer Review as Affecting Opinion Evidence Pharmacogenomics Phenotype Photography: Marks, Impressions, and Documents Poisons: Detection of Naturally Occurring Poisons Police Use of Force Policing and Critical Incident Teams Polymorphism: Genetic Postmortem Biochemical Examinations Postmortem Interval: Anthropology Postmortem Toxicology: Artifacts Postmortem Toxicology: Interpretation Postmortem Toxicology: Laboratory Analysis Postpartum Psychosis Posttraumatic Stress Disorder PowerPlex Premenstrual Syndrome Profiles: Psychological and Behavioral Psychological Autopsy Psychological Testing Psychopathology: Terms and Trends Psychopathy Psychopathy Checklists Psychopharmacology Psychopharmacology: Child and Adolescent QiaAmp Quality Systems: Toxicology
2009 2012 2021 2036 2057 2068 2071 2075 2076 2089 2093 2115 2119 2136 2141 2149 2149 2156 2161 2173 2186 2193 2197 2201 2210 2219 2219
VOLUME 5 Radiocarbon Dating Radiology Rape Trauma Syndrome Recollective Accuracy of Traumatic Memories Reconstruction: Accident Reconstruction: Three Dimensional Report Writing for Courts Risk Assessment
2231 2233 2241 2243 2250 2257 2268 2271
Risk Assessment: Patient and Detainee Sampling and Estimation of Quantities Sampling Trace Evidence Scientific Method Compared to Legal Method Seizures: Behavioral Sentencing: Demographic Factors in Serial Homicide Serial Number Restoration: Firearm Sex Determination of Remains Sex Offenders: Treatment of Shaken Baby Syndrome Shooting Distance: Estimation of Short Tandem Repeats Short Tandem Repeats: Interpretation Soil: Forensic Analysis Speaker Recognition Species Determination of Osseous Remains Stalking Statistical Evidence in Court Stockholm Syndrome Substance Abuse Suicide (Behavior) Sweat: Toxicology Syndromes: Psychological Temporary Insanity Therapeutic Jurisprudence Threat Assessment: School Threat Assessment: Workplace Time of Death Determinations Tire Impressions Toolmarks Toxicology: Analysis Toxicology: Forensic Applications of Toxicology: Initial Testing Trace Evidence: Transfer, Persistence, and Value Traffic Fatalities Training and Certification (in Criminalistics) Transfer: DNA Trauma Analysis of Skeletal Remains
xi
2272
2281 2291 2296 2298 2306 2311 2324 2328 2332 2339 2351 2354 2365 2377 2389 2393 2397 2401 2409 2413 2418 2420 2431 2443 2449 2454 2460 2466 2480 2485 2495 2503 2509 2534 2541 2545 2555 2557
xii
Contents
Trauma Causation: Analysis of Automotive Treatment, Mandated: Mental Health Treatment, Right to: Mental Health Treatment, Right to Refuse: Mental Health
2565 2576 2580 2584
Ultimate Issue Evidence by Experts 2589 Use of Knowledge-Based Systems in Forensic Science 2590 Variable Number Tandem Repeats Violence Risk Assessment for Mental Health Professionals Visitation Rights Visual Recognition Systems in Identification
Web Resources Weisgram v. Marley Whole Genome Amplification Wildlife Wood Wounds: Sharp Injury Writing Instruments and Printing Devices
2619 2627 2628 2635 2640 2646 2660
Y-Chromosome Short Tandem Repeats
2677
Glossary Author Index Subject Index
2683 2701 2707
2595 2597 2602 2611
Contributors ABBONDANTE, SERENA F. Australian Federal Police, Weston and Australian Chemical, Biological Radiological and Nuclear Data Centre, Canberra, ACT, Australia ABDEL-MONEM, TARIK University of Nebraska Public Policy Center, Lincoln, NE, USA ABOU-KHALIL, BASSEL Vanderbilt University School of Medicine, Nashville, TN, USA ABRAM, KAREN M. Northwestern University Feinberg School of Medicine, Chicago, IL, USA ADAMS, HOLLY A. Automotive Data Consultants, Centreville, VA, USA AITKEN, COLIN G. G. University of Edinburgh, Edinburgh, UK ALBERINK, IVO Netherlands Forensic Institute, Den Haag, The Netherlands ALEKSANDER, ADAM K. Aleksander & Associates P.A., Boise, ID, USA ALLEN, REBECCA S. Center for Mental Health and Aging, Tuscaloosa, AL, USA ALMOG, JOSEPH The Hebrew University of Jerusalem, Jerusalem, Israel ANDERSON, ROBERT N. RNA Consulting, Inc., Losaltos Hills, CA, USA ANDREWS, PAUL Tyler, TX, USA ANETZBERGER, GEORGIA J. Cleveland State University, Cleveland, OH, USA AUMEER-DONOVAN, SHAHEEN University of Technology, Sydney, New South Wales, Australia BADEN, MICHAEL M. New York State Police, Albany, NY, USA
BADER, SCOTT The Forensic Institute, Glasgow, UK BAKER, DAVID W. The MITRE Corporation, McLean, VA, USA BALDING, DAVID Imperial College, London, UK BALDWIN, DAVID London Laboratory, London, UK BALLANTYNE, JACK University of Central Florida and National Center for Forensic Science, Orlando, FL, USA BARNES, SEAN Binghamton University, Binghamton, NY, USA BARNI, FILIPPO Carabinieri Scientific Investigation Department of Rome, Rome, Italy BENBOW, M. ERIC Michigan State University, East Lansing, MI, USA BERKOWITZ, SHARI R. University of California, Irvine, CA, USA BERNET, WILLIAM Vanderbilt University School of Medicine, Nashville, TN, USA BEYER, JOCHEN Monash University, Southbank and Victorian Institute of Forensic Medicine, Melbourne, Victoria, Australia BICKNELL, DANNA E. United States Secret Service, Washington, DC, USA BLACK, SUE University of Dundee, Dundee, Scotland, UK BLOCK, STEPHANIE University of California, Davis, CA BOHNERT, MICHAEL University of Freiburg, Freiburg, Germany BOTLUK, DIANA Stetson University College of Law, Gulfport, FL, USA BOTTOMS, BETTE L. University of Illinois at Chicago, Chicago, IL, USA
xiv
Contributors
BOWMAN-FOWLER, NICCI University of California, Irvine, CA, USA BRAUN, MICHELLE Wheaton Franciscan Healthcare, Racine, WI, USA BRESLER, SCOTT A. University of Cincinnati, Cincinnati, OH, USA BRICK, JOHN Intoxikon International, Yardley, PA, USA BRIGHT, JO-ANNE Institute of Environmental Science and Research Limited, Auckland, New Zealand BRYANT, VAUGHN M. Texas A&M University, College Station, TX, USA BUCHHOLZ, BRUCE A. Lawrence Livermore National Laboratory, Livermore, CA, USA BUCKLETON, JOHN S. Institute of Environmental Science and Research, Ltd., Auckland, New Zealand BULLING, DENISE University of Nebraska Public Policy Center, Lincoln, NE, USA BURGESS, ANN W. Boston College, Chestnut Hill, MA, USA CANTU, ANTONIO A. Seven Oaks Place, Falls Church, VA, USA CARPENTER, DOUGLAS J. Combustion Science & Engineering, Inc., Columbia, MD, USA CATTANEO, CRISTINA Universit´a degli Studi, Milan, Italy CHAMPOD, CHRISTOPHE Institut de Police Scientifique, University of Lausanne, Lausanne, Switzerland CHENG, WING-CHI Government Laboratory, Hong Kong Special Administrative Region, China CHOI, HYEYOUNG National Institute of Scientific Investigation, Seoul, South Korea CHOI, SANGKIL National Institute of Scientific Investigation, Seoul, South Korea CHRISTENSEN, THOMAS C. San Ramon, CA, USA CHUNG, HEESUN National Institute of Scientific Investigation, Seoul, South Korea
CLEGG, CARL West Virginia University, Morgantown, WV, USA COBLE, MICHAEL D. The Armed Forces DNA Identification Laboratory, Rockville, MD, USA CONNOR, MELISSA Nebraska Wesleyan University, Lincoln, NE, USA CORNELL, DEWEY G. University of Virginia, Charlottesville, VA, USA COSTANZO, MARK Claremont McKenna College, Claremont, CA, USA COSTELLO, JAN Loyola Law School, Los Angeles, CA, USA COURT, DENISE S. Barts and The London School of Medicine and Dentistry, London, UK COWELL, ANTHONY M. University of Lincoln, Lincoln, UK CROSS, DOUGLAS W. Lowick Bridge, Ulverston, UK CURRAN, JAMES M. University of Auckland, Auckland, New Zealand DAVIS, MALCOLM Vashaw Scientific, Inc., Norcross, GA, USA DAY, STEPHEN P. Huntingdon Forensic Science Laboratory, Cambridgeshire, UK DE ANGELIS, DANILO Universit`a degli Studi, Milan, Italy DE BOECK, GERT National Institute of Criminalistics and Criminology, Brussels, Belgium DE LA TORRE, RAFAEL Neuropsychopharmacology Program IMIM-Hospital del Mar PRBB, Barcelona, Spain DEN DUNNEN, M. Amsterdam-Amstelland Police, Amsterdam, The Netherlands DICKSON, STUART Institute of Environmental Science and Research Limited, Porirua, New Zealand DIETZ, PARK Threat Assessment Group, Inc., and Park Dietz & Associates, Inc., Newport Beach and University of California, Los Angeles, CA, USA DOUGLAS, KEVIN S. Simon Fraser University, Burnaby, British Columbia, Canada
Contributors DRUMMER, OLAF H. Monash University, Southbank, Victoria, Australia DUTTON, GERARD Tasmania Police, Hobart, Tasmania, Australia DUVINAGE, NICOLAS Gendarmerie National Forensic Sciences Institute (IRCGN), Rosny-sous-Bios, France DU PREEZ, CHARL University of Technology, Sydney, New South Wales, Australia EASTEAL, PATRICIA University of Canberra, Canberra, ACT, Australia EDELMAN, GERDA Netherlands Forensic Institute, Den Haag, The Netherlands EDELSTEIN, BARRY A. West Virginia University, Morgantown, WV, USA EDWARDS, CARL N. Four Oaks Institute, Dover, MA, USA ELKINGTON, KATE S. Columbia University and New York State Psychiatric Institute, New York, NY, USA ERICKSON, STEVEN K. University of Pennsylvania Law School, Philadelphia, PA, USA ERIKSSON, ANDERS F. Ume˚a University, Ume˚a, Sweden ERVIN, THOMAS The MITRE Corporation, McLean, VA, USA ESSEIVA, PIERRE University of Lausanne, Lausanne, Switzerland EVETT, IAN W. London Laboratory, London, UK FAGAN, JEFFREY Columbia Law School, New York, NY, USA FELGATE, PETER Forensic Science South Australia, Adelaide, South Australia, Australia FIDDIAN, SUSAN Victoria Police Forensic Services Department, McLeod, Victoria, Australia FINCH, INDRA A. Center for Forensic Services – Western State Hospital, Tacoma, WA, USA FINESCHI, VITTORIO University of Foggia, Foggia, Italy FINKENBINE, RYAN West Virginia University, Morgantown, WV, USA
xv
FITTERMAN, ELIZABETH Stetson University College of Law, Gulfport, FL, USA FITZPATRICK, ROBERT W. Centre for Australian Forensic Soil Science/CSIRO Land and Water, Adelaide, South Australia, Australia FLANAGAN, ROBERT J. King’s College Hospital NHS Foundation Trust, London, UK FOUND, BRYAN Latrobe University, Bundoora and Victoria Police Forensic Services Department, Macleod, Victoria, Australia FOWLER, NICCI B. University of California, Irvine, CA, USA FRAZIER, LEEANNE Stetson University College of Law, Gulfport, FL, USA FREMOUW, WILLIAM J. West Virginia University, Morgantown, WV, USA FRUDAKIS, TONY DNAPrint Genomics, Inc., Sarasota, FL, USA FRUMKIN, BRUCE Forensic and Clinical Psychology Associates, South Miami, FL, USA GALLO, FRANK J. Western New England College, Springfield, MA, USA GANIS, GIORGIO Harvard Medical School, Boston, and Atinoulas Martinos Center, Charlestown, and Harvard University, Cambridge, MA, USA GARDNER, ROSS M. Bevel, Gardner and Associates, Inc., Lake City, GA, USA GELLER, JEFFREY L. University of Massachusetts Medical School, Worcester, MA, USA GERADTS, ZENO Netherlands Forensic Institute, Den Haag, The Netherlands GERAERTS, ELKE Harvard University, Cambridge, MA, USA and Maastricht University, Maastricht, The Netherlands GEROSTAMOULOS, DIMITRI Monash University, Southbank, Victoria, Australia GIBELLI, DANIELE Universit´a degli Studi, Milan, Italy GIBLIN, MARY Garda Headquarters, Dublin, Ireland
xvi
Contributors
GILDER, JASON R. Forensic Bioinformatics, Fairborn, OH, USA GILLMAN, VICTORIA C. Australian Federal Police, Weston and Australian Chemical, Biological Radiological and Nuclear Data Centre, Canberra, ACT, Australia GITLOW, STUART Mount Sinai School of Medicine, New York, NY, USA GODDARD, KEN National Fish and Wildlife Forensics Laboratory, Ashland, OR, USA GOODMAN, GAIL S. University of California, Davis, CA, USA GOODWIN, KERRI A. Towson University, Towson, MD, USA GOULD, CHRISTINE E. West Virginia University, Morgantown, WV, USA GRAHAM, ELEANOR A.M. University of Leicester, Leicester, UK GREAVES, CAROLINE BC Mental Health & Addiction Services, Port Coquitlam and Simon Fraser University, Burnaby, British Columbia, Canada GREENBERG, MARTIN S. University of Pittsburgh, Pittsburgh, PA, USA GREENE, EDIE University of Colorado at Colorado Spring, Colorado Spring, CO, USA HACKMAN, LUCINA University of Dundee, Dundee, UK HAMILTON, WARREN D. Rapidtox Pty. Ltd., Brisbane, Queensland, Australia HAMMER, LESLEY State of Alaska Crime Laboratory, Anchorage, AK, USA HANSON, ERIN K. University of Central Florida and National Center for Forensic Science, Orlando, FL, USA HAN, EUNYOUNG National Institute of Scientific Investigation, Seoul, South Korea HARBISON, SALLY-ANN Institute of Environmental Science and Research Ltd., Auckland, New Zealand HART, STEPHEN D. Simon Fraser University, Burnaby, British Columbia, Canada HASEL, LISA E. Iowa State University, Ames, IA, USA
HATTERS-FRIEDMAN, SUSAN University Hospital – Case Medical Center, Cleveland, OH, USA HAYNE, HARLENE University of Otago, Dunedin, New Zealand HAZELWOOD, ROBERT R. Academy Group, Inc., Manassas, VA, USA HENDERSON, CAROL Stetson University College of Law, Gulfport, FL, USA HICKS, TACHA N. Institut de Police Scientifique, University of Lausanne, Lausanne, Switzerland HILL, CHERYL A. West Virginia University, Morgantown, WV, USA HONTS, CHARLES ROBERT Boise State University, Boise, ID, USA HOPEN, THOMAS J. The Bureau of Alcohol, Tobacco, Firearms and Explosives, Atlanta, GA, USA HUNTER, JOHN University of Birmingham, Birmingham, UK IKEGAYA, HIROSHI Kyoto Prefectural University of Medicine, Kyoto, Japan ISENSCHMID, DANIEL S. Wayne County Medical Examiner’s Office, Detroit, MI, USA JACKSON, GRAHAM Advance Forensic Science, and University of Abertay Dundee, Dundee, UK JACKSON, MICHAEL New South Wales Police Force, Sydney, New South Wales, Australia JAMIESON, ALLAN The Forensic Institute, Glasgow, UK JONES, ALAN W. National Board of Forensic Medicine, Link¨oping, Sweden JONES, GRAHAM R. Office of the Chief Medical Examiner, Edmonton, Alberta, Canada JONES, PHILIP J. York, North Yorkshire, UK JUST, REBECCA S. The Armed Forces DNA Identification Laboratory, Rockville, MD, USA KASSIN, SAUL John Jay College of Criminal Justice, New York, NY, USA
Contributors KATSUMATA, YOSHINAO National Research Institute of Police Science, Chiba, Japan KATTERWE, HORST Bundeskriminalamt, Wiesbaden, Germany KAYE, DAVID H. Arizona State University, Tempe, AZ, USA KAYE, NEIL S. Widener University School of Law, Wilmington, DE, USA KEATON, RALPH American Society of Crime Laboratory Directors/ Laboratory Accreditation Board (ASCLD/LAB), Garner, NC, USA ¨ Netherlands Forensic KEEREWEER, ISAAC Institute, The Hague, The Netherlands KEHN, ANDRE University of Wyoming, Laramie, WY, USA KENAN, JOSEPH University of California Los Angeles School of Medicine, Beverly Hills, CA, USA KENNEDY, ROBERT Royal Canadian Mounted Police (Retired), Ottawa, Ontario, Canada KERNBACH-WIGHTON, GERHARD University of Edinburgh, Edinburgh, UK KHANMY-VITAL, AITA University of Lausanne, Lausanne, Switzerland KIM, EUNMI National Institute of Scientific Investigation, Seoul, South Korea KINTZ, PASCAL Laboratoire ChemTox, Illkirch, France KIRKBRIDE, K. PAUL Australian Federal Police, Canberra, ACT, Australia KNOLL, IV, JAMES L. SUNY Upstate Medical University, Syracuse, NY, USA KOEHLER, JONATHAN J. Arizona State University, Tempe, AZ, USA KOPERSKI, J. GEORGE Australian Federal Police, Weston and Australian Chemical, Biological Radiological and Nuclear Data Centre, Canberra, ACT, Australia KOSSLYN, STEPHEN M. Harvard University, Cambridge and Massachusetts General Hospital, Boston, MA, USA KRANE, DAN E. Wright State University, Dayton, OH, USA
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LAMENDOLA, GRETCHEN M. Nova Southeastern University, Fort Lauderdale, FL, USA LANCASTER, SARAH L. Defence Science and Technology Laboratories, Sevenoaks, UK LANGENBURG, GLENN Minnesota Bureau of Criminal Apprehension, St. Paul, MN, USA LAPORTE, GERALD M. United States Secret Service, Washington, DC, USA LAUX, DALE L. Attorney General’s Office, Richfield, OH, USA LEBEAU, MARC A. FBI Laboratory, Quantico, VA, USA LEE, JUSEON National Institute of Scientific Investigation, Seoul, South Korea LEE, LI-WEN G. New York University School of Medicine, New York, NY, USA LEE, SOOYEUN National Institute of Scientific Investigation, Seoul, South Korea LENNARD, CHRIS University of Canberra, Canberra, ACT, Australia LENTINI, JOHN J. Scientific Fire Analysis, LLC, Big Pine Key, FL, USA LENZ, KURT W. Stetson University College of Law, Gulfport, FL, USA LEONG, GREGORY B. University of Washington, Seattle, WA, USA LEO, RICHARD A. University of San Francisco, San Francisco, CA, USA LEWIS, SIMON W. Curtin University of Technology, Perth, Western Australia, Australia LIM, MIAE National Institute of Scientific Investigation, Seoul, South Korea LIPTAI, LAURA L. Biomedical Forensics, Moraga, CA and Orlando, FL, USA LOFTUS, ELIZABETH F. University of California, Irvine, CA, USA LOVELL, ROBERT W. Mercer Island, WA, USA LOVELOCK, TINA J. LGC Forensics, Abingdon, UK
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Contributors
LUONG, SUSAN University of Technology, Sydney, New South Wales, Australia LYNN, STEVEN JAY Binghamton University, Binghamton, NY, USA MAAT, G.J.R. Netherlands Forensic Institute, The Hague and Leiden University Medical Center, Leiden, The Netherlands MACDONELL, HERBERT L. Bloodstain Evidence Institute, Corning, NY, USA MACEO, ALICE V. Las Vegas Metropolitan Police Department Forensic Laboratory, Las Vegas, NV, USA MACVAUGH III, GILBERT S. Mississippi State Hospital, Whitfield, MS, USA MADEA, BURKHARD University of Bonn, Bonn, Germany MAIDEN, NICHOLAS R. South Australia Police, Adelaide, South Australiaa, Australia MALLETT, XANTHE´ University of Dundee, Dundee, UK MARGOT, PIERRE University of Lausanne, Lausanne, Switzerland MARLEEN, LALOUP National Institute of Criminalistics and Criminology, Brussels, Belgium MARSHALL, MAURICE Defence Science and Technology Laboratories, Sevenoaks, UK MARTELL, DANIEL A. UCLA, Los Angeles, CA, USA ` University of MASSONNET, GENEVIEVE Lausanne, Lausanne, Switzerland MASTRUKO, VOJIN Court Expert Witness, Zagreb, Croatia MATTHEWS, ABIGAIL Binghamton University, Binghamton, NY, USA MAZZELLA, W.D. University of Lausanne, Lausanne, Switzerland MCCOY, KATRINA West Virginia University, Morgantown, WV, USA MCCULLOUGH, JOHN Garda HQ, Dublin, Ireland MCDERMOTT, SEAN D. Forensic Science Laboratory, Dublin, Ireland MCKENNA, LOUISE Garda Headquarters, Dublin, Ireland
MCNALLY, RICHARD J. Harvard University, Cambridge, MA, USA MEIJERMAN, L. Netherlands Forensic Institute, The Hague, and Leiden University Medical Center, Leiden, The Netherlands MELOY, J. REID University of California, San Diego, California, USA MELSON, KENNETH E. American Society of Crime Laboratory Directors/ Laboratory Accreditation Board (ASCLD/LAB), Garner, NC, USA MELTON, TERRY Mitotyping Technologies, LLC, State College, LA, USA MERRITT, RICHARD W. Michigan State University, East Lansing, MI, USA MEUWLY, DIDIER Netherlands Forensic Institute, The Hague, The Netherlands MICHEALS, ANASTASIA D. San Jose State University, San Jose, CA, USA MILES, SAMUEL I. Geffen School of Medicine UCLA, Los Angeles and Cedars-Sinai Medical Center, Los Angeles, CA, USA MOENSSENS, ANDRE Forensics and Law Center, Columbia City, IN, USA MOHAMMED, LINTON A. San Diego Sheriff’s Regional Crime Laboratory, San Diego, CA, USA MONNARD, FLORENCE University of Lausanne, Lausanne, Switzerland MORETTI, MARLENE M. Simon Fraser University, Burnaby, British Columbia, Canada MORRISH, BRONWYN C. Australian Federal Police, Weston and Australian Chemical, Biological Radiological and Nuclear Data Centre, Canberra, ACT, Australia MUELLER-JOHNSON, KATRIN University of Cambridge, Cambridge, UK MURPHY, JOHN P. CSIRO Forest Biosciences, Clayton, Victoria, Australia NEHSE, KORNELIA Forensic Science Institute, Berlin, Germany NELE, SAMYN National Institute of Criminalistics and Criminology, Brussels, Belgium
Contributors NELSON, KALLY J. University of California, Irvine, CA, USA NERENBERG, LISA Private Consultant, Redwood City, CA, USA NEUMANN, CEDRIC The Forensic Science Service Ltd, Birmingham, UK and University of Lausanne, Lausanne, Switzerland NEUNER, JOHN K. American Society of Crime Laboratory Directors/ Laboratory Accreditation Board (ASCLD/LAB), Garner, NC, USA NEUSCHATZ, JEFFREY S. University of Alabama in Huntsville, Huntsville, AL, USA NICHOLLS, TONIA L. BC Mental Health & Addiction Services, Port Coquitlam and University of British Columbia, Vancouver, British Columbia, Canada NIKOLOVA, NATALIA L. Simon Fraser University, Burnaby, British Columbia, Canada NORMAN, KEITH W. Australian Federal Police, Weston, ACT, Australia NUNEZ, NARINA L. University of Wyoming, Laramie, WY, USA OJANPERA¨ , ILKKA University of Helsinki, Helsinki, Finland OLLEY, J. GREGORY University of North Carolina, Chapel Hill, NC, USA ¨ STROM ¨ , MATS G. Ume˚ O a University, Ume˚a, Sweden OXLEY, JIMMIE C. University of Rhode Island, Kingston, RI, USA PARK, YONGHOON National Institute of Scientific Investigation, Seoul, South Korea PAYNE-JAMES, JASON Forensic Healthcare Services, Leigh-on-Sea and Royal College of Physicians and Barts & the Royal London Hospitals, London, UK PERRY, SYLVIA University of Illinois at Chicago, Chicago, IL, USA PETERSON, TIAMOYO University of California, Irvine, CA, USA PICHINI, SIMONA Istituto Superiore di Sanit`a, Rome, Italy
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PINALS, DEBRA A. University of California, Sacramento, CA, USA PIPER, AUGUST Seattle, WA, USA POLLAK, STEFAN University of Freiburg, Freiburg, Germany POLLANEN, MICHAEL S. University of Toronto, Toronto, Ontario, Canada PORTA, DAVIDE Universit`a degli Studi, Milan, Italy PORTER, GLENN University of Western Sydney, Penrith South DC, New South Wales, Australia POULSEN, HELEN Institute of Environmental Science and Research Limited, Porirua, New Zealand QUINN, MARY J. San Francisco Probate Court, San Francisco, CA, USA RAES, ELKE Ghent University, Ghent, Belgium RAFF, ADAM N. New York University Medical Center, New York, NY, USA RANDOLPH-QUINNEY, PATRICK University of Dundee, Dundee, UK RAYMOND, JENNIFER J. NSW Police Force, Pemulwuy, New South Wales, Australia RAY, NEELANJAN New York University School of Medicine, New York, NY, USA REED, TOM Widener University School of Law, Wilmington, DE, USA RESNICK, PHILLIP J. Case Western Reserve University Medical School, Cleveland, OH, USA RESOR, MICHELLE R. University of North Carolina at Charlotte, Charlotte, NC, USA RESSLER, ROBERT K. Forensic Behavioral Services, Fredericksburg, VA, USA RIEZZO, IRENE University of Foggia, Foggia, Italy ROBERTSON, JAMES Australian Federal Police, Canberra, ACT, Australia ROFFEY, PAUL E. Australian Federal Police, Weston and University of Canberra, Canberra, ACT, Australia ROMERO, ERIN G. Northwestern University, Chicago, IL, USA
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Contributors
ROUX, CLAUDE University of Technology (UTS), Sydney, New South Wales, Australia ROYDS, DAVID Australian Federal Police, Canberra, Australia RUIFROK, ARNOUT C. C. Netherlands Forensic Institute, The Hague, The Netherlands SALEKIN, KAREN L. University of Alabama, Tuscaloosa, AL, USA SALSAROLA, DOMINIC Universit´a degli Studi, Milan, Italy SAUKKO, PEKKA J. University of Turku, Kiinamyllynkatu, Turku, Finland SAUVAGNAT, FRANCOIS ¸ Universit´e de Rennes-II, Rennes, France SCHIFFER, BEATRICE University of Lausanne, Lausanne, Switzerland SCHNECK, WILLIAM M. Microvision Northwest-Forensic Consulting, Inc. Spokane, WA, USA SCHNEIDER, RICHARD D. The Ontario Court of Justice and University of Toronto, Toronto, Ontario, Canada SCOTT, ALLAN MATHIESON University of Central Lancashire (UCLAN), Preston, UK SCOTT, CHARLES L. University of California, Sacramento, CA, USA SEGOVIA, DAISY A. University of California, Davis, CA, USA SHARFE, GORDON A.I. Wellington Central Police Station, Wellington, New Zealand SHEFCHICK, THOMAS P. Shefchick Engineering, Sunnyvale, CA, USA SHIVER, FARRELL C. Shiver & Nelson Document Investigation Laboratory, Inc., Woodstock, GA, USA SIEGEL, JAY A. Indiana University Purdue University Indianapolis, Indianapolis, IN, USA SILVA, J. ARTURO Private Practice of Forensic Psychiatry, San Jose, CA, USA SINGH, RAJVINDER Punjabi University, Patiala, India SKOPP, GISELA Ruprecht-Karls University, Heidelberg, Germany
SMARTY, SYLVESTER Case Western University/University Hospitals of Cleveland, Cleveland, OH, USA SMITH, ANN C. Columbia City, Indiana, IN, USA SMITH, DELANEY M. Twin Valley Behavioral Healthcare, Columbus, OH, USA SMYTH, LARRY D. Red Toad Road Company, Havre de Grace, MD, USA SORRENTINO, RENEE Institute for Sexual Wellness, Quincy, MA, USA SPIEGEL, DAVID Stanford University School of Medicine, Stanford, CA, USA SQUIER, WANEY John Radcliffe Hospital, Oxford, UK STANKOWSKI, JOY E. Case Western Reserve University, Cleveland, OH, USA STAUFFER, ERIC University of Lausanne, Lausanne, Switzerland STEINBERG, LAURENCE Temple University, Philadelphia, PA, USA STRUB, DIANE S. Simon Fraser University, Burnaby, British Columbia, Canada STUDEBAKER, CHRISTINA ThemeVision LLC, Indianapolis, IN, USA TAKATORI, TAKEHIKO National Research Institute of Police Science, Chiba, Japan TARONI, FRANCO The University of Lausanne, Lausanne, Switzerland TEPLIN, LINDA A. Northwestern University Feinberg School of Medicine, Chicago, IL, USA THAKAR, MUKESH KUMAR Punjabi University, Patiala, India THEAN, A. Netherlands Organisation for Applied Scientific Research (TNO), Delft, The Netherlands THOMAS, TRACY A. West Virginia University, Morgantown, WV, USA THOMPSON, CHRISTOPHER University of California Los Angeles School of Medicine, Los Angeles, CA, USA THOMPSON, WILLIAM C. University of California, Irvine, CA, USA THURMAN, JAMES T. Eastern Kentucky University, Richmond, KY, USA
Contributors TOGLIA, MICHAEL P. University of North Florida, Jacksonville, FL, USA TRAMONTANA, MICHAEL G. Vanderbilt University Medical Center, Nashville, TN, USA TRIDICO, SILVANA R. Australian Federal Police, Canberra, ACT, Australia TULLY, GILLIAN Forensic Science Service, Birmingham, UK TURILLAZZI, EMANUELA University of Foggia, Foggia, Italy TURNER, BARRY University of Lincoln, Lincoln, UK WAALWIJK VAN DOORN, K. Amsterdam-Amstelland Police, Amsterdam, The Netherlands VERSTRAETE, ALAIN G. Ghent University Hospital, Ghent, Belgium VINER, MARK D. Cranfield Forensic Institute, Defence Academy of the United Kingdom, Shrivenham and St Bartholomew’s and the Royal London Hospitals, London, UK VITACCO, MICHAEL J. Mendota Mental Health Institute, Madison, WI, USA VUORI, ERKKI University of Helsinki, Helsinki, Finland VAN
WALKER, JAMES S. Vanderbilt University School of Medicine, Nashville, TN, USA WALSH, SIMON J. Australian Federal Police, Canberra, ACT, Australia WASHBURN, JASON J. Northwestern University Feinberg School of Medicine, Chicago, IL, USA WEINSTOCK, ROBERT University of California, Los Angeles, CA, USA
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WEIR, BRUCE S. University of Washington, Seattle, WA, USA WELLS, GARY L. Iowa State University, Ames, IA, USA WENGER, ERIC Australian Federal Police, Weston and Australian Chemical, Biological Radiological and Nuclear Data Centre, Canberra, ACT, Australia WEST, SARA G. University Hospital Case Medical Center, Cleveland, OH, USA WETTON, JON Forensic Science Service, Birmingham, UK ´ University of WEYERMANN, CELINE Lausanne, Lausanne, Switzerland WHEATE, RHONDA M. The Forensic Institute, Glasgow, UK WHELPTON, ROBIN University of London, London, UK WILSON, CATHERINE M. Simon Fraser University, Burnaby, British Columbia, Canada WONG, STEVEN H.Y. Medical College of Wisconsin and Milwaukee County Medical Examiner’s Office, Milwaukee, WI, USA YANG, SUZANNE University of Pittsburgh School of Medicine, Pittsburgh, PA, USA YORK, CATHERINE The University of Illinois at Chicago, Chicago, IL, USA ZAJAC, RACHEL University of Otago, Dunedin, New Zealand ZEICHNER, ARIE Hebrew University of Jerusalem, Jerusalem, Israel ZOUN, RIKKERT Netherlands Forensic Institute, The Hague, The Netherlands
Foreword Forensic scientists who are attempting to provide guidance that assists investigators and solves crimes are well aware of the capabilities of the various disciplines in which they toil. Even more importantly, they are also cognizant of what their chosen specialty cannot (yet) accomplish. With a carefully nurtured and expanded knowledge base of the strengths and weaknesses of science, experts are often key to solving perplexing and high-profile cases. Their accomplishments on those occasions draw widespread attention from the media but, even more importantly, these experts also labor quietly on a daily basis to solve the more common cases that represent the bulk of their laboratory efforts and analyses. The consumers of forensic science – be they courts, legislative bodies, or regulatory agencies – rely on the solutions and ideas which these dedicated researchers strive to supply. In the past few decades, there have been many new discoveries and advances in scientific disciplines, enabling forensic science specialists to apply an ever increasing depth of expertise in carrying out their tasks. Cases are being solved today using techniques that were unheard of twenty, ten, five, or even one year ago. It seems as if every issue of a scientific or technical journal that is published reports new innovations that are progressing from the experimental to the practical. In that environment, the Wiley Encyclopedia of Forensic Science is no doubt destined to be recognized as the premiere compendium of knowledge. After all, the entries in its volumes have been compiled by recognized, internationally known, and respected experts in every field. There is no denying the popularity of television programs such as CSI, Cold Case, Forensic Files, and others. Indeed, there is perhaps no topic of greater interest in today’s cyber world than the use of forensics to solve crimes. The small (and not-so-small) screen of the home theater also allows people to view a plethora of movies dealing with scientific ways to demystify complex scenarios. Prominent actors are cast in the white coats of laboratory examiners and interact with other participants in an effort to convince us of their prowess. Through television, the movies, and an ever growing number of Internet sites, the public receives an abundance of information about how crime laboratory science assists in solving mysteries. The so-called “CSI effect” influences jurors, and even some judges, who have come to expect real life to mirror what they see on television, the movies, or what they read in other media. Unfortunately, not all of the information purveyed via these mediums comports with reality. Expectations are inflated beyond the possible. Even the most accomplished expert cannot solve cases in one hour or less as their television counterparts suggest they can! Expectations in the legal profession, the courts, those who serve on juries, and the public at large demand that those who deal with the judicial system be familiar and are knowledgeable about what is possible and what is perhaps coming in the future. Experts, and anyone else who seeks knowledge about forensics, must not only be familiar with the well-established foundations of scientific proof, but must also stay reliably informed about new developments in the various forensic science disciplines. Here again, the Wiley Encyclopedia of Forensic Science serves as a complete, accurate, realistic, and up-to-date resource that will sate the knowledge thirst of experts as well as that of consumers of forensic science.
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Foreword
The framework for this five-volume Wiley encyclopedia was designed and compiled by its two Editors-in-Chief, Allan Jamieson of the United Kingdom and Andre Moenssens of the United States, both pre-eminent authorities in forensic science and its practical and legal applications. They are intimately familiar with the formidable strengths of forensic evidence as well as its perhaps less-known weaknesses. In their daunting task to seek a balance reporting on topics from A to Z, all of which straddle different levels of achievement, the Editorsin-Chief were ably assisted by a selection of knowledgeable subject-specialist topic editors and hundreds of contributors from all over the world. The cooperation and efforts of these many leaders in the scientific enterprise ensures that information dispensed in each discipline is reliable, relevant to real-life problems, and useful to a broad audience. There are over 370 articles written by more than 330 contributors. These articles reference the myriad subjects of forensic science and embrace the physical, biological, behavioral, as well as comparative sciences. Laboratory management and case investigative techniques, laboratory support mechanisms, quality control programs, and discussions on the modern trends in interpreting the confidence level accorded test results by reference to statistical likelihood ratios are also dealt with. Concerns about the desired exactness of science, and the inexactness of the law, also required that precedent-setting court decisions and discussions of legal principles that impact on a forensic expert’s performance be explained and analyzed in these volumes. Issues of examiner education, training, and accreditation in various disciplines, as well as the ethical requirements governing scientists’ professional behavior and the problem of expert witness malpractice have not been neglected. For the layperson, the Encyclopedia provides authoritative answers to most questions about specific forensic problems. For the practitioners in specific fields, it reminds them of the basic fundamentals in their own discipline while it also informs them of the totality of knowledge in other fields so as to better understand the system as a whole and its interrelated complexities. References to published data and source materials appended to most articles allow interested persons to study areas of special concern in greater depth. Truly a collection of useful information on most of what is known as “forensic science”, the Encyclopedia provides ready answers for everyone who is either involved or simply interested in forensic science. In assessing how well John Wiley & Sons and all those associated with the production and publication of these volumes have achieved their objectives, there is no doubt the verdict and judgment will be favorable.
The Honorable Haskell M. Pitluck Past President, American Academy of Forensic Science Retired Circuit Judge, State of Illinois April 2009
Preface Forensic science is a broad label. It covers the entire complement of human industry and experience at the point where they interface with legal and legislative processes. This interaction may involve civil as well as criminal concerns and often takes the form of expert testimony offered to answer questions posed by a variety of human institutions. In the exercise of that function, the opinions of experts may vary widely in probative value, weight, and persuasiveness. But forensic science also serves therapeutic and human aspects apart from problem solving, and is often a crucial component in the formulation of policy and the passage of regulatory endeavors destined to insure the health and safety of populations. The advent of DNA profiling has heralded a revolution in forensic science that goes well beyond forensic biology. The techniques and principles used in evaluating forensic scientific evidence are being closely examined at this moment in the light of the work in DNA as an individualization process – considered somewhat as a Holy Grail for forensic science. The ability to develop population databases, based on the easy numerical nature of DNA profiles, enabled the introduction of other approaches to the evaluation of evidence. The scientific rigor of some aspects of this process has posed difficult-to-answer questions for those forensic disciplines that emerged primarily from experience-based endeavors but which, through use, had become accepted in criminal justice systems. The debate as to the response within many of these specialties is ongoing. This state of events has brought us to an era of unprecedented development and debate, as well as a measure of uncertainty, in some forensic science functions. Several disciplines are now broadly divided into “old school” and “new school” practitioners. It is not easy to predict which school will emerge as the dominant thinking in these disciplines, but it is almost certain that the future will see more scientifically robust techniques of evidence evaluation gaining widespread acceptance. Many of the entries in this work may represent the seeds of that future. The existence of these competing schools inevitably creates differences of opinion regarding the science. The constant and varied evolution of science means that the state of the art in one discipline (in instrumentation, analytical accuracy, or evaluation) may be very different from the state of the art in another. Although science may be regarded as international, law is not. Jurisdictional differences also inevitably create differences in the practice of forensic science. We have encouraged authors to be candid, but to represent those differences in their writing, and occasionally different authors will discuss the same or similar topics while offering a slightly different approach. We regard this as healthy and a natural part of the scientific discourse. As such, the debate is encouraged. However, the consequence is that the views expressed within articles are not necessarily the definitive or final word on any topic, nor do they necessarily represent the view of any other author or of the Editors-in-Chief. In bringing together such a large and varied selection of experts in one major work, we were cognizant that imposing a “house style” would be close to impossible. Our limit seemed to be the adoption of American-English spelling and a single reference style. Inevitably, our
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Preface
workload and a variety of deeply ingrained localized or national approaches will have allowed some departures from the standard to slip through the editorial net. We hope that this does not detract from the content. We did not enforce any particular writing style and the varied entries reflect that. One thing that all of our authors had to be aware of was that this is a very unusual major technical reference work in that we aimed to inform an audience that includes people who are not forensic science professionals and who may simply be interested in selected topics discussed in these volumes, such as writers, reporters, educators, but who may have only a sketchy knowledge of the core principles or language of science. The work also purports to inform the legal profession, the judiciary, and paralegals. With these different audiences in mind, we have attempted to maintain sufficient depth to provide a valuable reference source for practitioners and academics as well. Only use will establish the degree to which we have been successful in achieving those disparate aims. The complexity of providing information to a wide potential readership, composed of such a variety of interested parties, placed important choices on the editors in terms of its coverage. No one source can serve all of humanity, and thus the editors sometimes had to make painful judgments on what to include and what to pass over. Sometimes the choices on what to include were dictated in part by the availability of experts willing to share their professional experience with our readers. At other times, choices related simply to the fact that the dividing line between science and pseudoscience required a decision as to whether conclusions reached in a particular field provided sufficient guarantees of trustworthiness and reliability. This in no way can be taken to mean that the lack of appearance here invalidates any particular discipline, nor for that matter that inclusion validates it! Whatever the choice, the editors acted in their best judgment and will remain vigilant so as to select, for later inclusions, those emerging fields currently perhaps on the fringes of forensic science that increase their underlying knowledge-based data and gain a modicum of acceptance in the broader forensic science profession. No work of this nature is perfect. This will not prevent us from striving to improve it online and in subsequent editions. We welcome feedback on any aspect of this work, including topics that, almost certainly, we have missed in our attempts to be all-inclusive. We are only part of a very large and skilled team including our Editorial Board and the team at Wiley. Our heartfelt thanks go to all of them and in advance to you, the reader, for your feedback which will assist us to provide better resources for your future work.
Allan Jamieson and Andre Moenssens April 2009
Abbreviations and Acronyms 1,4-BD 16 PF 2,4-DNT 2,6-DNT 5-HT 5HIAA 5HTOL 6-AM 6-AM
1,4-butanediol 16 Personality Factor 2,4-dinitrotoluene 2,6-dinitrotoluene 5-Hydroxytryptamine 5-Hydroxyindole Acetic Acid 5-hydroxytryptophol 9 -Tetrahydrocannabinol 6-Acetylmorphine
AA AACC AAFS AAIDD
Greatest Angular Apertures American Association of Clinical Chemists American Academy of Forensic Sciences American Association on Intellectual and Developmental Disabilities American Association on Mental Retardation American Association of Physical Anthropology Adult–Adolescent Parenting Inventory Atomic Absorption Spectrophotometry Atomic Absorption Spectroscopy Adaptive Behavior Assessment System – Second Edition American Board of Criminalistics American Board of Forensic Document Examiners American Board of Forensic Entomology American Board of Forensic Medicine American Board of Forensic Odontology American Board of Forensic Psychology American Board of Forensic Toxicology Applied Biosystems ABO Blood Groups American Board of Psychiatry and Neurology American Board of Professional Psychology 2, 2 -azino-di-(3-Ethyl-Benzthiazolinesulfonate) Analysis, Comparison, Evaluation and Verification American College of Forensic Examiners Acetylcholine Acid Phosphatase 1 Association of Chief Police Officers Adenosine Deaminase Accumulated Degree-Days
AAMR AAPA AAPI AAS AAS ABAS-II ABC ABFDE ABFE ABFM ABFO ABFP ABFT ABI ABO ABPN ABPP ABTS ACE-V ACFE ACh ACP1 ACPO ADA ADD
xxviii ADH ADH ADHD ADM ADP AEDs AEME AES AF AFE AFIS AFM AFR AFTE AHG AIDS AIMs AIP AK AKA AKD ALDH ALFPs ALI ALS ALT ALTEs AM AMDIS AMI AMP AmpFLPs AMPS AMS AN ANFO ANN ANSI AP AP APA APA APCI APD APDS APHL API API AP-LS
Abbreviations and Acronyms Accumulated Degree-Hours Alcohol Dehydrogenase Attention Deficit Hyperactive Disorder Alcohol, Drug, and Mental Adenosine Diphosphate Antiepileptic Drugs Anhydroecgonine Methylester Auger Electron Spectroscopy Acid Fuchsin Amniotic Fluid Embolism Automated Fingerprint Identification System Atomic Force Microscopy Association of Forensic Radiographers Association of Firearm and Tool Mark Examiners Antihuman Globulin Acquired Immunodeficiency Syndrome Ancestry Informative Markers Acute Interstitial Pneumonitis Adenylate Kinase Alcoholic Ketoacidosis Alkyl Ketene Dimer Aldehyde Dehydrogenase Amplified Fragment Length Polymorphisms American Law Institute Alternate Light Sources Alanine Aminotransaminases Acute Life-Threatening Events Antemortem Automated Mass Spectral Deconvolution and Identification System Acute Myocardial Infarction Adenosine Monophosphate Amplified Fragment Length Polymorphisms Advanced Mobile Phone System Accelerator Mass Spectrometry Ammonium Nitrate Ammonium Nitrate and Fuel Oil Artificial Neural Network American National Standards Institute Acid Phosphatase Ammonium Perchlorate American Psychological Association American Psychiatric Association Atmospheric Pressure Chemical Ionization Antisocial Personality Disorder Autonomous Pathogen Detection System Association of Public Health Laboratories Application Programming Interface Atmospheric Pressure Ionization American Psychology-Law Society
Abbreviations and Acronyms APPITA APS ARDS ARIs ARVD AS ASA ASA ASCH ASCLD ASCLD/LAB ASD ASM ASME ASQDE ASRIS AST ASTM ATF ATP ATR ATR-FTIR ATSA ATV AUC BAC BAPP BARTS BAWS BCCH BCTMP BE BEECS BFRL BGA BHT BISFA BKV BLEVE BMI BNs BP bp BPIF BPS BrAC BS
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Australian Pulp and Paper Industry Technical Association Adult Protective Services Acute Respiratory Distress Syndrome Actuarial Risk Assessment Instruments Arrhythmogenic Right Ventricular Disease Autonomous System Acetylsalicylic Acid Alkenyl Succinyl Anhydride American Society of Clinical Hypnosis American Society of Crime Laboratory Directors American Society of Crime Laboratory Directors/Laboratory Accreditation Board Acute Stress Disorder American Society of Metals American Society of Mechanical Engineer American Society of Questioned Document Examiners Australian Soil Resources Information System Aspartate Aminotransaminases American Society for Testing and Materials Alcohol, Tobacco, and Firearms Adenosine Triphosphate Attenuated Total Reflection Attenuated Total Reflectance-Fourier Transform Infrared Association for the Treatment of Sexual Abusers Atmospheric Pressure Chemical Ionization Area Under Curve Blood Alcohol Concentration Beta Amyloid Precursor Protein Biological Agent Real-Time Sensor Biological Agent Warning Sensor Broadcast Control Channel Bleached Chemi-Thermomechanical Hardwood Pulps Benzoylecgonine Benign Enlargement of the Extracerebral Spaces Building Fire and Research Laboratory Ball Grid Array Butylated Hydroxytoluene The International Bureau for the Standardization of Man-Made Fibres BK Virus Boiling Liquid and Expanding Vapor Explosion Body Mass Index Bayesian Networks Bandpass Base Pair Bandpass Interference Filters Bricklin Perceptual Scales Breath-Alcohol Concentration Beam Splitter
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Abbreviations and Acronyms
BSA BSDL BSE BSE BTB BTEX BTU BWC BWS
Bovine Sera Albumin Boundary-Scan Description Language Back-Scattered Electrons Black Sheep Effect Sickle Cell Anemia Benzene, Toluene, Ethylbenzene, and Xylene British Thermal Unit Biological and Toxins Weapons Convention Battered Woman Syndrome
CA CA CABs CABL CAC CAC CAD CAD CAF CAFSS CAGE CAI CAI CAM CAN CAP CAPI CAPTA carboxy-THC CAST/MR
Carbonic Anhydrase Cytosine-Adenine Conformity Assessment Bodies Compositional Analysis of Bullet Lead California Association of Criminalistics Child Advocacy Center Computer-Aided Design Coronary Artery Disease Cyanoacrylate Fuming Centre for Australian Forensic Soil Science Computer Aided Glass Evaluation Case Assessment and Interpretation Competence Assessment Instrument for Standing Trial Computer-Aided Modeling Cardiovascular Autonomic Neuropathy College of American Pathologists Child Abuse Potential Inventory Child Abuse Prevention and Treatment Act 11-Nor-9-carboxytetrahydrocannabinol Competence Assessment for Standing Trial for Defendants with Mental Retardation Computed Axial Tomography Cannabidiol Cannabinol Chemical, Biological, Radiological, and Nuclear Common Criteria Biometric Evaluation Methodology Working Group Charge Coupled Device Certified Crime Scene Analyst Certified Crime Scene Investigator Closed Circuit Television Conduct Disorder Cyclodextrin Centers for Disease Control Center for Drug Evaluation and Research Frequency Division Multiple Access Cartridge Discharge Residues Crash Data Recorders Carbohydrate Deficient Transferrin Capillary Electrophoresis
CAT CBD CBN CBRN CCBEMWG CCD CCSA CCSI CCTV CD CD CDC CDER CDMA CDR CDR CDT CE
Abbreviations and Acronyms CEDIA CEIR CESB CF CF CFA CFAST CFC CFD CGS CHD CHF CHINS CI CI CI-MS CIFA CIL CIP CIS CITES CIT CJA CJP CL CMOS CMR-R CMS CMYK CN CNS CO CO-Hb CODIS COHb COPFS COVR CPA CPD CPE CPF CPGR CPI CPIA CPK CPLE CPR CPR CPR
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Cloned Enzyme Donor Immunoassay Central Equipment Identify Register Council of Engineering and Scientific Specialty Boards Compact Flash Corrective Factors Confirmatory Factor Analysis Consolidated Model of Fire Growth and Smoke Transport Chlorofluorocarbon Computational Fluid Dynamics Crow–Glassman Scale Coronary Heart Disease Congestive Heart Failure Children in Need of Supervision Chemical Ionization Cognitive Interview Chemical Ionization Mass Spectrometry Centre for International Forensic Assistance Central Identification Laboratory Commission Internationale Permanente Canadian Information Society The Convention on International Trade in Endangered Species Fauna and Flora Concealed Information Test Criminal Justice Act Capital Jury Project Cathodoluminescence Complementary Metal-Oxide Semiconductor Comprehension of Miranda Rights-Recognition Consecutive Matching Striae Cyan, Magenta, Yellow, and Black Cyanide Central Nervous System Carbon Monoxide Carbon Monoxide Hemoglobin Combined Offender DNA Index System Carboxyhemoglobin Crown Office Procurator Fiscal Service Classification of Violence Risk Cyproterone Acetate Continuing Professional Development Combined Power of Exclusion Cardiac Fibroelastoma Chlorophenolred-β-Galactoside Combined Probability of Inclusion Criminal Procedure and Investigations Act Creatine Phosphokinase Certified Latent-Print Examiner Cardiopulmonary Rescuscitation Chlorophenolred Civil Procedure Rules
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Abbreviations and Acronyms
CPS CPSC CPVT CQT CR CRFP CRT CS CSA CSA CSAAS CSC CSCSA CSD CSE CSF CSFS CSI CSI CSM CT CTAB CTS CV CV CVD CVFI CW CWAs CWC CYP CYP 2B6 CYP 2D6 CYP 3A5 CYP3A CZE
Child Protective Services Consumer Product Safety Commission Catecholaminergic Polymorphic Ventricular Tachycardia Comparison Question Test Conditioned Response Council for Registration of Forensic Practitioners Cathode-Ray Tube Conditioned Stimuli Child Sexual Abuse Crime Scene Analyst Child Sexual Abuse Accommodation Syndrome Crime Scene Coordinator Certified Senior Crime Scene Analyst Circuit Switched Data Crime Scene Examiner Cerebrospinal Fluid Canadian Society of Forensic Science Consensual Sexual Intercourse Crime Scene Investigators Crime Scene Manager Computed Tomography Hexadecyltrimethlyammonium Bromide Collaborative Testing Services Coefficient of Variation Curriculum Vita Cardiovascular Disease Candidate for the Vehicle Fire Investigator Chemical Warfare Chemical Warfare Agents Chemical Weapons Convention Cytochrome P Cytochrome P450 2B6 Cytochrome P450 2D6 Cytochrome P450 3A5 Cytochrome P450 3A Capillary Zone Electrophoresis
D1T2 D2T2 D-AMPS DA DAB DAB DAD DAD DAD DAD DADP DAG DAI
Direct Thermal Transfer Dye Diffusion Thermal Transfer Digital Advanced Mobile Phone System Dopamine Diaminobenzidine DNA Advisory Board Diffuse Alveolar Damage Diode-Array Detector Drowning-Associated Diatoms Photodiode Array Detection Diacetone Diperoxide Directed Acyclic Graph Diffuse Axonal Injury
Abbreviations and Acronyms DART DEA DECT DEM DESNOS DF DFC DFO DFSA DHCP DIC DID DIN DIS-IV DLC DM DM DMA DNA DNS DO DOB DOET DOM DOP DOS DOT DPA DPI DPS DRE DRIFT DRM DSC DSM DSM-III DSM-IV DSM-IV-TR DSPD DTA DTCs DTGS DTO DTT DUID DVI DVT DWI
xxxiii
Direct Analysis in Real Time Drug Enforcement Agency Digital Enhanced Cordless Telecommunication Digital Elevation Model Disorder of Extreme Stress not Otherwise Specified Dedicated File Drug-Facilitated Crime 1,8-diaza-9-fluorenone Drug-Facilitated Sexual Assault Dynamic Host Configuration Protocol Differential Interference Contrast Dissociative Identity Disorder Deutsches Institut F¨ur Normung Diagnostic Interview Schedule, Version IV Diagnostic Link Connector Diabetes Mellitus Dichroic Mirror Dimethoxyamphetamine Deoxyribonucleic Acid Domain Name System Dangerous Offender 4-Bromo-2,5-dimethoxyamphetamine Dimethoxyethylamphetamine 4-Methyl-2,5-dimethoxyamphetamine Degenerate Oligonucleotide Primed Denial-of-Service Department of Transportation Diphenylamine Dots Per Inch Department of Public Safety Drug Recognition Evaluation Diffuse Reflectance Infrared Fourier Transform Deese–Roediger–McDermott Differential Scanning Calorimeter Diagnostic and Statistical Manual of Mental Disorders Diagnostic and Statistical Manual of Mental Disorders, Third Edition Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition Diagnostic and Statistical Manual, Fourth Edition, Text Revision Dangerous Severe Personality Disorder Differential Thermal Analysis Diagnostic Trouble Codes Deuterated Triglycine Sulfate Dithiooxamide Dithiothreitol Driving Under the Influence of Drugs Disaster Victim Identification Deep Venous/Vein Thrombosis Driving While Intoxicated
xxxiv
Abbreviations and Acronyms
EA EA EAAF EAFE EAP EBV EC ECA ECD ECDS ECF ECHR ECLM ECT ED EDD EDDP EDM EDMI EDNAP EDS EDS or EDX EDTA EDX EDXA EEG EER EF EFA EFG EGA EGDN E-HMM EI EI-MS EIA EIA EIC EIP ELISA EME EMG EMIT EMPOP EMS ENAA ENFSI EPA EPG EPI
Enzyme Acceptor European Co-Operation for Accreditation Equipo Argentino De Antropolog´ıa Forense European Association for Forensic Entomology Erythrocyte Acid Phosphatase Epstein Barr Virus Ethyl Centralite Epidemiologic Catchment Area Electron Capture Detector Empirical Criteria for the Determination of Suicide Elemental Chlorine Free European Court of Human Rights European Council of Legal Medicine Electroconvulsive Therapy Enzyme Donor Electrostatic Detection Device 2-Ethylidene-1,5-Dimethyl-3,3-Diphenylpyrrolidine Electrical Discharge Machining Electromyography European DNA Profiling Group Energy-Dispersive Spectrometer Energy-Dispersive X-Ray Ethylene Diamine Tetraacetic Acid Energy Dispersive X-Ray Energy Dispersive X-Ray Analysis Electro-Encephalogram Equal Error Rate Elementary File Exploratory Factor Analysis European Fibres Group Estimated Gestational Age Ethylene Glycol Dinitrate Ergodic Hidden Markov Models Electron Impact Electron Impact Positive Ion Mass Spectrometry Environmental Impact Assessment Enzyme Immunoassay Extracted Ion Chromatogram Extracted Ion Profiles Enzyme Linked Immunosorbent Assay Ecgonine Methyl Ester Electromyography Enzyme Multiplied Immunoassay Technique European DNA Profiling Group MtDNA Population Database Enhanced Messaging Service Epithermal Neutron Activation Analysis European Network of Forensic Science Institutes Environmental Protection Agency Electropherogram Enhanced Product Ion
Abbreviations and Acronyms EPO EPS EQA ERPs ESD EsD ESDA ESEM ESI ESI ESLA ESR EtG ETK EtS EU EUCAP EWG EX
Erythropoetin Extra-Pyramidal Symptoms External Quality Assessment Event-Related Potentials Environmental Secondary Detector Esterase D Electrostatic Detection Apparatus Environmental SEM Electronically Stored Information Electrospray Ionization Electrostatic Lifting Apparatus Environmental Science Research Limited Ethyl Glucuronide Explosive Test Kit Ethyl Sulfate European Union European Collection of Automotive Paint Expert Working Group Exciter Filter
FAAS FABMS FAEE FAME FAR FASE FBI FDA FDE FDR FDS FDS FE FEC FEPAC
Flameless Atomic Absorption Spectroscopy Fast Atom Bombardment Mass Spectrometry Fatty Acid Ethyl Esters Fatty Acid Methyl Esters False Acceptance Rate Forensic Anthropology Society of Europe Federal Bureau of Investigation Food and Drug Administration Forensic Document Examiner Firearm Discharge Residue Fire Dynamics Simulator Fragment Data System Field Emission Forensic Engineering Curriculum Forensic Science Education Programs Accreditation Commission Fast Fourier Transform S-Formylglutathione Hydrolase Forensic Handwriting Examiner Focused Ion Beam Flame Ionization Detector Forensic International Network of Explosive Examiners Forensic Information Retrieval System Fluorescent In Situ Hybridization Filtered Light Examination Fluorescence Lifetime Imaging Family Liaison Officer Forensic Light Source Failure Modes and Effects Analysis Full Metal Jacket
FFT FGH FHE FIB FID FINEX FIRS FISH FLE FLIM FLO FLS FMEA FMJ
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xxxvi
Abbreviations and Acronyms
fMRI FMSF FNAA FOMA FPAC fpc FPD FPIA FPM FQS-I FRE FRI FRR FSAB FSF FSH FSS FSS FSSoc FTA FTD FTIR FTL FTP FUT FWA
Functional Magnetic Resonance Imaging False Memory Syndrome Foundation Fast Neutron Activation Analysis Freedom of Mobile Multimedia Access Forensic Pathology Advisory Commitee Finite Population Correction Flame Photometric Detection Fluorescence Polarization Immunoassay First-Pass Metabolism Forensic Quality Services-International Federal Rules of Evidence Function of Rights in Interrogation False Rejection Rate Forensic Specialties Accreditation Board Forensic Sciences Foundation Follicle-Stimulating Hormone Forensic Science Society Forensic Science Service Ltd Forensic Science Society (UK) Fault Tree Analysis Flame Thermoionic Detector Frustrated Total Internal Reflection Flash Translation Layer File Transfer Protocol Fucosyltransferase Fluorescent Whitening Agent
G6PDH GABA GBL GC GC-ECD GC-FID GC-MS GC-MS/DFPD
Glucose-6-phosphate Dehydrogenase Gamma Amino-Butyric Acid Gamma Butyrolactone Gas Chromatography Gas Chromatography Electron Capture Detector Gas Chromatography Flame Ionization Detector Gas Chromatography-Mass Spectrometry Gas Chromatography-Mass Spectroscopy/Dual Flame Photometric Detection Glascow Coma Scale Glow Discharge–Mass Spectrometry Gastroesophageal Reflux Disease Graphite Furnace Atomic Absorption Spectrophotometry Gamma-Glutamyltransferase Growth Hormone γ -Hydroxybutyrate Geographic Information System Guilty Knowledge Test Glyoxylase I Gaussian Mixture Models Gateway Mobile Switching Center General Neuropsychological Deficit Scale Gonadotropin-Releasing Hormone
GCS GD–MS GERD GFAAS GGT GH GHB GIS GKT GLO GMM GMSC GNDS GnRH
Abbreviations and Acronyms
xxxvii
GPA GPB GPR GPRS GPS GPT GRC GSM gsm GSR GSS GUI GuSCN GUS
Grade Point Average Glycophorin B Ground-Penetrating Radar General Packet Radio Service Global Positioning System Glutamate-Pyruvate Transaminase General Rifling Characteristics Global System for Mobile Grams Per Square Meter Gunshot Residue Gudjonsson Suggestibility Scales Graphical User Interface Guanidinium Thiocyanate General Unknown Screening
Hb HBFP HCM HCN HCR HELIN HERG HF HFC HFE HFE HGN HHV-1 HIC HIV AIDS
Heterozygosity Balance Haematoxylin-Basic Fuchsin-Picric Acid Hypertrophic Cardiomyopathy Hydrogen Cyanide Historical Clinical Risk Higher Education Library Information Network Human Ether-a-go-go-Related Gene Human Factor Hydrofluorocarbon Human Factors Engineering Hydrofluoroether Horizontal Gaze Nystagmus Human Herpes Virus Type 1 Head Injury Criterion Human Immunodeficiency Virus Acquired Immune Deficiency Syndrome Human Leucocyte Antigen Higher Limit of Quantitation Hexamethylene Triperoxide Diamine High-Molecular-Weight Octogen Heavy Petroleum Distillates Highest Posterior Density High Performance Liquid Chromatography High Performance Liquid Chromatography Diode-Array Detector High Performance Liquid Chromatography Mass Spectrometry High Performance Liquid Chromatography with a Pendant Mercury Drop Electrode Detector Human Papillomavirus High-Resolution Gamma Spectrometry Halstead–Reitan Neuropsychological Battery Halstead–Reitan Neuropsychological Test Battery Heat Release Rate Health and Safety Executive
HLA HLoQ HMTD HMW HMX HPD HPD HPLC HPLC-DAD HPLC-MS HPLC/PMDE HPV HRGS HRNB HRNTB HRR HSE
xxxviii
Abbreviations and Acronyms
HTTP HWE
Hypertext Transfer Protocol Hardy–Weinberg Equilibrium
i.d. I/IS IAAC IAAI IABPA IACI IAEA IAFIS IAFS IAI ibd IBG IBIS IBS IC ICC ICC1 ICCID ICD ICDD ICF/DIC
Internal Diameter Insulin or Insulin Secretagogs Inter-American Accreditation Cooperation International Association of Arson Investigators International Association of Bloodstain Pattern Analysts International Association for Craniofacial Identification International Atomic Energy Agency Integrated Automated Fingerprint Identification System International Association of Forensic Scientists International Association for Identification Identical by Descent International Biometrics Group Integrated Ballistics Identification System Identical by State Ion Chromatography International Criminal Court Intraclass Correlation Coefficient Integrated Circuit Card Identifier International Classification of Diseases International Centre for Diffraction Data Intravascular Coagulation and Fibrinolysis/Disseminated Intravascular Coagulation Increased Cycle Number Inductively Coupled Plasma Inductively Coupled Plasma Mass Spectrometry Inductively Coupled Plasma-Optical Emission Spectrometry Inductively Coupled Plasma Atomic Emission Spectroscopy Inductively Coupled Plasma Mass Spectrometry International Criminal Tribunal for Rwanda International Criminal Tribunal for the Former Yugoslavia International Development Agencies Individuals with Disabilities Education Improvement Act Integrated Digital-Enhanced Network Intrusion Detection System International Electrotechnical Commission Improvised Explosive Device Institute of Electrical and Electronic Engineers Interpol European Expert Group on Fingerprint Identification Isoelectric Focusing International Fire Service Training Association International Humanitarian Law International Institute of Forensic Engineering Sciences International Laboratory Accreditation Cooperation International League against Epilepsy Ignitable Liquid Residues Indentation Materializer
ICN ICP ICP-MS ICP-OES ICP/AES ICP/MS ICTR ICTY IDA IDEIA iDEN IDS IEC IED IEEE IEEGFI IEF IFSTA IHL IIFES ILAC ILAE ILR IMED
Abbreviations and Acronyms IMEI/IMSI
xxxix
IMS IMSI IMT-2000 INAA IND IND IND-Zn INFL INH INS IOFOS IP IPEP IQ IQC IR IRA IRC IrDA IRL IRMS IRR IS ISFG ISO ISP ITU ITWG
International Mobile Equipment Identity/International Mobile Equipment Identity Impaired Motorists, Methods of Roadside Testing and Assessment for Licensing Ion Mobility Spectrometry International Mobile Equipment Identity International Mobile Telecommunications-2000 Instrumental Nuclear Activation Analysis 1,2-Indanedione Improvised Nuclear Device Indanedione-Zinc International Nuclear Forensic Laboratories Isoniazid International Neuropsychological Society International Organisation for Forensic Odontostomotology Internet Protocol Improved Primer Extension Preamplification Intelligence Quotient Internal Quality Control Infrared Irish Republican Army Internet Relay Chat Infrared Data Association Infrared Luminescence Isotope Ratio Mass Spectrometry Infrared Reflectance Internal Standard International Society of Forensic Genetics International Standards Organization Internet Service Provider International Telecommunication Union International Technical Working Group
JCAH JFFS2 JINS JPAC JPEG2000 JTAG
Joint Commission on Accreditation of Hospitals Journalized Flash File System Juveniles in Need of Supervision Joint Pow/MIA Accounting Command Joint Photographic Expert Group 2000 Joint Test Action Group
KAAIT KBS KEBQ KIMS KIPS KM KSA
Kaufman Adolescent and Adult Intelligence Test Knowledge-Based System Knowledge of Eyewitness Behavior Questionnaire Kinetic Interaction of Microparticles in Solution Keys to Interactive Parenting Scale Kastle Meyer test Knowledge, Skills, and Abilities
LAB LAC
Laboratory Accreditation Board Location Area Code
IMMORTAL
xl
Abbreviations and Acronyms
LAMMA LAMPA LAN LBA LC LC/ESI/MS LC-MS/MS LC/MS LCN LCP LCV LD LDA LEAA LED LEL LH LHRH LIBS LLE LLoQ LMG LNNB-CR LOC LOD LOQ LP LPC LPCC LPDs LQTS LR LRs LSD LTDNA LTO LVH M-FAST M3G M6G MAC MacCAT-CA MacCAT-T MacSAC-CD MALDI/TOF MAM
Laser Microprobe Mass Analysis Lysergic Acid Methyl Propyl Amide Local Area Network Logical Block Addressing Liquid Chromatography Liquid Chromatography Electrospray Ionization Mass Spectrometry Liquid Chromatography Tandem Mass Spectrometry Liquid Chromatography Mass Spectrometry Low Copy Number Life-Course Persistent Leucocrystal Violet Lethal Dose Linear Discriminant Analysis Law Enforcement Assistance Administration Light-Emitting Diode Lower Explosive Limit Luteinizing Hormone Luteinizing Hormone-Releasing Hormone Laser-Induced Breakdown Spectroscopy Liquid–Liquid Extraction Lower Limit of Quantification Leucomalachite Green Luria–Nebraska Neuropsychological Battery-Children’s Revision Loss of Consciousness Limit of Detection Limit of Quantification Liquefied Petroleum Linear Predictive Coding Linear Prediction Cepstrum Coefficients Light Petroleum Distillates Long QT Syndrome Likelihood Ratio Long Rifles Lysergic Acid Diethylamide Low Template DNA Long-Term Offender Left Ventricular Hypertrophy Miller Forensic Assessment of Symptoms Test Morphine-3-glucuronide Morphine-6-glucuronide Media Access Control MacArthur Competence Assessment Tool-Criminal Adjudication MacArthur Competence and Assessment Tool-Treatment MacArthur Structured Assessment of the Competencies of Criminal Defendants Matrix-Assisted Laser Desorption/Ionization Time-of-Flight Mechanical, Analytical, and Medical
Abbreviations and Acronyms MAM MAO MB MBD MBDB MC-ICP/MS MC1R MCMC MCMI MCQ MCT MCV MDA MDA MDCT MDE MDEA MDMA MDMA MDMA MDMA MDT ME MECA MECC MECE MEOS MERMER MERS met-Hb MFCC MGT MHC MHL MI mIPEP MIR MLE MLP MMC MMDA MMD MMPI-2 MMSD MMSE MND MO MPA
xli
Mono acetyl Morphine Monoamine Oxidase Myocardial Bridging 4-(4-Methoxybenzylamino-7-Nitrobenzofurazan) N -Methyl-Benzodioxazoylbutanamine Multicollector Inductively Coupled Plasma Mass Spectrometry Melanocortin 1 Receptor Monte Carlo Markov Chain Millon Clinical Multiaxial Inventory Multiple-Choice Questions Mercury Cadmium Telluride Mean Corpuscular Volume 3,4-Methylenedioxyamphetamine Multiple Displacement Amplification Multislice Computed Tomography 3,4-Methylenedioxyamphetamine 3,4-Methylenedioxy-N -Amphetamine 3,4 Methylenedioxymethamphetamine Liquid Chromatography Coupled to Mass Spectrometry Methylenedioxymethamphetamine Methylenedioxymeth(yl)amphetamine Multidisciplinary Team Medical Examiner Methodology for Epidemiology of Mental Disorders in Children and Adolescents Micellar Electrokinetic Chromatography Micellar Electrokinetic Capillary Electrophoresis Microsomal Oxidizing System Memory and Encoding Related Multifaceted Electroencephalographic Response Medical Error Reporting System Methemoglobin Mel Frequency Cepstral Coefficients Modified Griess Test Major Histocompatibility Complex Minimal Haplotype Loci Medullary Index Modified Improved Primer Extension Preamplification Mid-Infrared Most Likely Estimate Multilocus Profiling Multi Media Card Methoxymethylenedioxyamphetamine Multimetal Deposition Minnesota Multiphasic Personality Inventory 2 Mass Memory Storage Device Mini Mental State Examination Malingering Neurocognitive Dysfunction Modus Operandi Medroxyprogesterone
xlii
Abbreviations and Acronyms
MPD MPD MPD MPS MP MR MRI MRM mRNA MRS MS MS MSC MSCT MSD MSE MSP mtDNA MTPA (S)-(+)-MTPACl MTT MVD MVN MW
Medium Petroleum Distillate Modified Physical Developer Multiple Personality Disorder Metropolitan Police Service Match Probability Metabolic Ratios Magnetic Resonance Imagery Multiple Reaction Monitoring Messenger Ribonucleic Acid Magnetic Resonance Spectroscopy Mass Selective Mass Spectrometer Mobile Switching Center Multislice Computed Tomography Mass Selective Detector Mental Status Examination Microspectrophotometers Mitochondrial Deoxyribonucleic Acid α-Methoxy-α-(Trifluoromethyl)Phenylacetic Acid (S)-(+)-α-Methoxy-(Trifluoromethyl)Phenylacetyl Chloride Dimethylthiazol 2 yl Diphenyltetrazolium Bromide Multiwavelength Detection Multivariate Normality Molecular Weight
NA NAA NACB NAD NADP NADPH NAE NAFE NAFEA NAFI NAGPRA NAHI NAME NAPQI NAS NAS NATA Native PAGE NBS NC NCA NCANDS NCIDD NCIGC-MS
Numerical Aperture Neutron Activation Analysis National Academy of Clinical Biochemistry Nicotine Adenine Dinucleotide Nicontinamide Adenine Dinucleotide Phosphate Reduced Nicontinamide Adenine Dinucleotide Phosphate Negligent Adverse Event National Academy of Forensic Engineers North American Forensic Entomological Association National Association of Fire Investigators Native American Graves Protection and Repatriation Act Non-accidental Head Injury National Association of Medical Examiners N -Acetyl-p-benzoquinone Imine National Academy of Sciences Network Attached Storage National Association of Testing Authorities Native Gel Electrophoresis National Bureau of Standards Nitrocellulose No Cause Apparent National Child Abuse and Neglect Data System National Criminal Identification DNA Database Negative Chemical Ionisation Gas Chromatograph with Mass Spectral Analyser
Abbreviations and Acronyms
xliii
NCIS NCJRS NCNM NCS NCSI NCSTL NCVS NDIS NDNAD nDNA NE NEISS NEO-PI NEO-PI-R NFA NFI NFIRS NFPA NFSTC NFWFL NG NGOs NGRI NHTSA NIBIN NICHD NIFS NIJ NIR NIST NLQ NMDA NMR NMT NP NPD NPIA NRC NRY NSAID NSTC NTT nuDNA NVFS NY-OCME
National Coroners Information Service National Criminal Justice Reference Service Noncorrosive and Nonmercuric National Comorbidity Survey Nonconsensual Sexual Intercourse National Clearinghouse for Science, Technology and the Law National Crime Victimization Survey National DNA Identification System National DNA Database Nuclear DNA Norepinephrine National Electronic Injury Surveillance System Neo-Personality Inventory Neo-Personality Inventory-Revised National Forensics Association Netherlands Forensic Institute National Fire Incident Reporting System National Fire Protection Association National Forensic Science Technology Center National Fish and Wildlife Forensics Laboratory Nitroglycerine Nongovernmental Organizations Not-Guilty-by-Reason-of-Insanity National Highway Traffic Safety Administration National Integrated Ballistic Information Network National Institute of Child Health and Human Development National Institute of Forensic Science National Institute of Justice Near Infrared National Institute of Standards and Technology Near Letter Quality N -Methyl-D-Aspartic Acid Nuclear Magnetic Resonance Nordic Mobile Telephones Neuropsychological Nitrogen Phosphorus Detector National Policing Improvements Agency National Research Council Nonrecombining Region of the Y Chromosomes Nonsteroidal Anti-Inflammatory Drug National Science and Technology Council Nippon Telegraph and Telephones Nuclear Deoxyribonucleic Acid Nonvolatile File System New York Office of the Chief Medical Examiner
OBAs OCD OCDS OD
Optical Brightening Agents Obsessive Compulsive Disorder Operational Criteria for the Determination of Suicide Overdose
xliv
Abbreviations and Acronyms
OEM OHS&W OLA OOBNs OPC OPCW OPGs ORO OSHA OS OTA OTC OVD
Original Equipment Manufacturer Occupational Health Safety and Wellbeing Oligonucleotide Ligation Assay Object-Oriented Bayesian Networks Organic Photoconductor Organization for the Prohibition of Chemical Weapons Orthopantomographs Oil Red O Occupational Safety and Health Administration Operating Systems Over the Air Over-the-Counter Optical Variable Device
P2P PAC PACE PAE PAI PAP PAR PAS PCA PCB PCB PCC PCDF PCL PCL-R PCL:SV PCP PCP PCPP PCR PCRI PCT PD PDA PDC PDD PDM PDQ PE Pep A PEP PEP-PCR PET PETN PFA PGC–MS
Peer-to-Peer Plasma Alcohol Concentration Police and Evidence Act Preventable Adverse Event Personality Assessment Inventory Prostatic Acid Phosphatase Pseudoautosomal Region Preliminary Alcohol Screening Principal Component Analysis Polychlorinated Biphenyl Printed Circuit Board Pyridinium Chlorochromate Polychlorinated Dibenzofurans Psychopathy Checklist Psychopathy Checklist-Revised Screening Version of the Hare Psychopathy Checklist-Revised Phencyclidine Primary Care Physician Phenyl Cyclopentyl Piperidine Polymerase Chain Reaction Parent–Child Relationship Inventory Procalcitonin Concentration Physical Developer Personal Digital Assistant Personal Digital Cellular Psychophysiological Detection of Deception Psychodynamic Diagnostic Manual Paint Data Query Pulmonary Embolism Peptidase A Primer Extension Preamplification Primer Extension Preamplification Polymerase Chain Reaction Positron Emission Tomography Pentaerythritol Tetranitrate Psychological First Aid Pyrolysis Gas Chromatography–Mass Spectrometry
Abbreviations and Acronyms PGD PGM PHA PHA PHP PHT PID PIN PINS PLM PLMN PLS PM PMA PMDD PMI PML PMR PMS PMS PMT PMT PNE PNES POCT PORT POW ppb PPD PPE ppi PPI PPP pRIA PRNU PSA PSI PSTN PTAH PTE PTFE PTSD PT PUK PVC Py-GC-MS
6-Phosphogluconate Dehydrogenase Phosphoglucomutase Preliminary Hazard Analysis Public Health Agency Phenyl Cyclohexylpyrrolidine Pulmonary Hypertension Photoionization Detector Personal Identifying Number Persons in Need of Supervision Polarized Light Microscope Public Land Mobile Network Partial Least-Squares Postmortem p-Methoxy-Amphetamine Premenstrual Dysphoric Disorder Postmortem Interval Progressive Multifocal Leukoencephalopathy Postmortem Redistribution Phenazine Methosulphate Premenstrual Syndrome Photo Multiplier Tube Premenstrual Tension Pediatric Neurological Exam Psychogenic Nonepileptic Seizures Point-of-Care Testing Perception-of-Relationships Test Prisoners of War Parts Per Billion Postpartum Depression Personal Protective Equipment Pixels Per Inch Proton Pump Inhibitor Postpartum Psychosis Protein Radioimmunoassays Photo Response Nonuniformity Prostate-Specific Antigen Parenting Stress Inventory Public Switched Telephone Network Phosphotungstic Acid-hematoxylin Pulmonary ThromboEmbolism Polytetrafluoroethylene PostTraumatic Stress Disorder Proficiency Testing Pin Unlocking Key Polyvinyl Chloride Pyrolysis Gas Chromatography Mass Spectrometry
QA QC QDE
Quality Assurance Quality Control Questioned Document Examiner
xlv
xlvi
Abbreviations and Acronyms
QM QPN
Quality Management Qualitative Probabilistic Network
RAID RAM RAPID RCMP RC rCRS RDC RDCT RDD RDX RED RF RFC RFID RFLP RFS RFU RFUs RGB RH RI RIA RIM RMNE RMP ROC ROSITA RP RRT RSD RT RT-PCR RTS RUVIS Ry
Redundant Array of Independent Disks Random Access Memory Ruggedized Advanced Pathogen Identification Device Royal Canadian Mounted Police Restructured Clinical Revised Cambridge Reference Sequence Research Diagnostic Criteria Rey Dot Counting Test Radiological Dispersion Device Hexogen Radiological Emission Device Renal Failure Request for Comment Radio Frequency Identification Device Restriction Fragment Length Polymorphism Robust File System Relative Fluorescence Intensity Relative Fluorescent Units Red, Green, and Blue Retinal Hemorrhage Refractive Index Radio-Immunoassay Research in Motion Random Man Not Excluded Random Match Probability Receiver Operating Characteristic Roadside Testing Assessment Readiness Potential Relative Retention Time Relative Standard Deviation Retention Time Real-Time Polymerase Chain Reaction Rape Trauma Syndrome Reflected Ultraviolet Imaging System Ryanodyine Receptor
S/N S/P SAAMI SAC SADS-C SAMHSA SARS SB-5 SBP SBS SCAN
Signal-to-Noise Ratio Saliva-to-Plasma Sporting Arms and Ammunition Manufacturers’ Institute Serum Alcohol Concentration Schedule of Affective Disorders and Schizophrenia-Change Substance Abuse and Mental Health Service Administration Severe Acute Respiratory Syndrome Stanford-Binet Intelligence Scale – Fifth Edition Sellier Bellot, Prague Shaken Baby Syndrome Scandinavian Pulp and Paper Association
Abbreviations and Acronyms SCC SCID SDH SDIS SDS-PAGE SD SD SE SEA SEIR SEM/EDS SEM/EDX SEM/WDS SEM/WDX SEM SF-ICP/MS SFPE SFST SGAs SGM SIB-R SIDS SIM SIM SIM SIMCA SIMS SIMS SIO SIPRI SIRS SLA SLP SLP SLR SMANZFL SMD SMI SMM SMS SMTP SNAP-IV SNP SNRI SOCO SOFT
xlvii
Standards Council of Canada Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, 4th ed.-Text Revision Subdural Hemorrhage State DNA Identification System Sodium Dodecyl Sulphate Polyacrylamide Gel Electrophoresis Secure Digital Standard Deviation Secondary Electron Strategic Environmental Assessment Surface-Enhanced Irregular Reflection Scanning Electron Microanalysis with Energy Dispersive Sensor Scanning Electron Microscopy/Energy Dispersive X-Ray Scanning Electron Microanalysis with Wavelength Dispersive Sensor Scanning Electron Microscopy/Wavelength Dispersive X-Ray Spectroscopy Scanning Election Microscope Sector Field-Inductively Coupled Plasma Mass Spectrometry Society of Fire Protection Engineers Standardized Field Sobriety Test Second Generation Antipsychotics Second-Generation Multiplex Scales of Independent Behavior – Revised Sudden Infant Death Syndrome Selected Ion Monitoring Senior Identification Manager Subscriber Identity Module Soft Independent Modeling of Class Analogy Secondary Ion Mass Spectrometry Structured Inventory of Malingered Symptomatology Senior Investigating Officer Stockholm International Peace Research Institute Structured Interview of Reported Symptoms Symbionese Liberation Army Single Locus Probes Single Locus Profiling Single Lens Reflex Senior Managers of Australian and New Zealand Forensic Laboratories Single-Metal Deposition Severe Mental Illness Stepwise Mutation Model Short Message Service Simple Mail Transfer Protocol Swanson, Nolan, and Pelham Single Nucleotide Polymorphism Serotonin and Norepinephrine Reuptake Inhibitor Scenes of Crime Officer Society of Forensic Toxicologists
xlviii
Abbreviations and Acronyms
SOHO SoHT SOP SP SPECT SPE SPIN SPJ SPM SPME SPR SRT SSD SSM SSM SSO SSRI SSSQ STA STAG START STD STEM STI StPO STR SUDEP SUDNIC
SWGFEX SWGGUN SWGhair SWGIT SWGMAT
Small and Home Office Society of Hair Testing Standard Operating Procedure Shortpass Single Proton Emission Computed Tomography Solid-Phase Extraction Service Planning Instrument Structured Professional Judgment Scanning Probe Microscope Solid Phase Micro Extraction Small Particle Reagent Sodium Rhodizonate Test Scientific Support Department Scientific Support Manager Slipped Strand Mispairing Sequence Specific Oligonucleotide Selective Serotonin Reuptake Inhibitor Street Survival Skills Questionnaire Systematic Toxicology Analysis Statistical Analysis of Glass Short-Term Assessment of Risk and Treatability Sexually Transmitted Diseases Scanning Transmission Microscope Sexually Transmitted Infections Criminal Procedure Code Short Tandem Repeat Sudden Unexplained Death in Epilepsy Sudden Unexpected Death Due to Neoplastic Disease in Infancy and Childhood Support-Vector Machines Sexually Violent Predator Special Weapons and Tactics Scientific Working Group on DNA Analysis Methods Science Working Group on Documents Scientific Working Group for the Analysis of Drugs Scientific Working Group for Friction Ridge Analysis, Study, and Technology Scientific Working Group for Fire and Explosives Science Working Group on Guns Scientific Working Group for Hairs Scientific Working Group IT Scientific Working Group on Materials Analysis
TACS TAPPI TAT TATP TBI TBW TCD
Total Access Communication System Technical Association of the Pulp and Paper Industry Thematic Apperception Test Triacetone Triperoxide Traumatic Brain Injury Total Body Water Thermal Conductivity Detector
SVM SVP SWAT SWGDAM SWEDOC SWGDRUG SWGFAST
Abbreviations and Acronyms TCF TCP TCP TDMA TDx TETRA TDM TDM TdP TDx TEA TEM TEMED TETRA TFPCl TFS4 TGA THC THC-COOH TIAs TIC TIC TIM TIMS TLC TMA TMOT TMJ TMP TMS TNAZ TNT TOF TOF-SIMS TOMM TOR TPMT TPP TSH TSOP TSWG TTI TWGDAM TWGED
xlix
TWGFEX
Totally Chlorine Free Thienyl Cyclohexyl Piperidine Transmission Control Protocol Time Division Multiple Access Fluorescent Polarization Assay Terrestrial Trunked Radio Target Disk Mode Therapeutic Drug Monitoring Torsades Des Pointes Fluorescent Polarization Assay Thermal Energy Analyzer Transmission Electron Microscope Tetramethylethylenediamine Terrestrial Trunked Radio N -(Trifluoroacetyl) Prolyl Chloride Transactional File System Thermogravimetric Analysis 9 -Tetrahydrocannabinol 11-Nor-9-Carboxy-9 -Tetrahydrocannabinol Transient Ischemic Attacks Toxic Industrial Chemical Total Ion Chromatogram Toxic Industrial Material Thermal Ionization Mass Spectrometry Thin Layer Chromatography Trimethoxyamphetamine Trace Metal Detection Test Total Metal Jacket Thermomechanical Pulps Trimethylsilyl 1,3,3-Trinitroazetidine Trinitrotoluene Time-of-Flight Time-of-Flight Secondary Ion Mass Spectrometry Test of Memory Malingering The Onion Routing Thiopurine S-Methyltransferase Thermal Protective Performance Thyroid-Stimulating Hormone Thin Small-Outline Packages Technical Support Working Group Transmit Terminal Identifier Technical Working Group on DNA Analysis and Methods Technical Working Group on Education and Training in Forensic Science Technical Working Group for Fire and Explosive Analysis
UAC UCS UDP
Urine–Alcohol Concentration Unconditioned Stimuli User Datagram Protocol
l
Abbreviations and Acronyms
UEL UGPPA UHP UKAS/NAMAS
UV/Vis
Upper Explosive Limit Uniform Guardianship and Protective Proceedings Act Ultra High Purity United Kingdom Accreditation Service/National Accreditation of Measurements and Sampling United Kingdom National External Quality Assessment Scheme Underwriters Laboratories Ultrarapid Metabolizers Universal Mobile Telecommunication System United Nations United Nations Office on Drug Control Unique Reference Number United States Department of Agriculture United States Supreme Court Ultraviolet Microspectrophotometry Using Visible Light and Ultraviolet Light Ultraviolet/Visible
VA VABS II VCA VDAG VIP VMD VNTR VoIP VoIP/ToIP VQ VRAG VRML VSA VSA VSA VSC
Veterans Administration Vineland Adaptive Behavior Scales II Vacuum Cyanoacrylate Vitamin D Binding Alpha Globulin Validity Indicator Profile Vacuum Metal Deposition Variable Number of Tandem Repeat Voice over Internet Protocol Voice over Internet Protocol/Telephone over Internet Protocol Vector Quantization Violence Risk Appraisal Guide Virtual Reality Modeling Language Video Spectral Analysis Voice Stress Analyzers Volatile Substance Abuse Video Spectral Comparator
WADA WAIS III WAIS-R WAN WAP WAP WDX WGA WHO WIRA WMD WMH-CIDI
World Anti-Doping Agency Wechsler Adult Intelligence Scale, Third Edition Wechsler Adult Intelligence Scale-Revised Wide Area Network Wireless Access Point Wireless Application Protocol Wavelength Dispersive X-Ray Whole Genome Amplification World Health Organization Wool Industries Research Association Weapons of Mass Destruction World Mental Health – Composite International Diagnostic Interview Wechsler Memory Scale
UKNEQAS UL UM UMTS UN UNODC URN USDA USSC UV UV-MSP
WMS
Abbreviations and Acronyms WRB WSQ WTC WWI WWII
World Reference Base Wavelet Scalar Quantization World Trade Center World War I World War II
XBO XRD XRF XSR
Xenon Short Arc Lamp X-Ray Diffraction X-Ray Fluorescence Spectroscopy eXtended Sector Remapper
Y-STRs YAFFS
Y-Chromosome Short Tandem Repeats Yet Another Flash File System
ZD ZPO
Z Direction Zivilprozessordnung(Civil Procedure Code)
li
The International System of Units (SI) There are many different units of measure for most physical parameters such as length, mass, and temperature. The scientific community have agreed on a single system called the SI (Systeme Internationale) as the accepted international system of such units. SI units are either base or derived. Base units are fundamental and not reducible. Table 1 lists the main base units of interest in the discipline of materials science and engineering. Derived units are expressed in terms of the base units, using mathematical signs for multiplication and division. For example, the SI units for density are kilogram per cubic meter (kg/m3 ). For some derived units, special names and symbols exist; for example, N is used to denote the Newton, the unit of force, which is equivalent to 1 kg-m/s2 . Although many use the ‘/’ notation (e.g. m/s) the system uses a superscript or exponent (to the power of) notation where a negative symbol replaces the ‘/’. For example, m/s becomes ms−1 , and m/s2 becomes ms−2 . Table 2 contains a number of important derived units. It is sometimes necessary, or convenient, to form names and symbols that are decimal multiples of SI units. Only one prefix is used when a multiple of an SI unit is formed, which should be in the numerator. These prefixes and their approved symbols are given in Table 3. Symbols for the main units are used in this book, SI or otherwise. Some disciplines retain other nomenclatures by practice or convention, although these are departures from the main scientific recommendations. Table 1
The SI base units
Quantity
SI unit
Length Mass Time Electric current Thermodynamic temperature Amount of substance
meter kilogram second ampere kelvin mole
Symbol m kg s A K mol
liv Table 2
The International System of Units (SI) Some of the SI derived units (including examples of the superscript notation)
Quantity
Name
Area Volume Velocity Density Concentration Force Energy Pressure/Stress Strain Power, radiant flux Viscosity Frequency (a periodic phenomenon) Electric charge Electric potential Capacitance Electric resistance Magnetic flux Magnetic flux density
Formula
Special symbol
square meter cubic meter meter per second kilogram per cubic meter moles per cubic meter newton joule pascal – watt pascal-second hertz
m m3 m/s (ms−1 ) kg/m3 mol/m3 kg·m/s2 (kg·ms−2 ) kg·m2 /s2 , Nm kg/ms2 , N/m2 m/m kg·m2 /s3 , J/s kg/ms 1/s (s−1 )
– – – – – N J Pa – W Pa-s Hz
coulomb volt farad ohm weber tesla
A·s kg·m2 /s2 C s2 C/kg·m2 kg·m2 /sC2 kg·m2 /sC kg/sC, Wb/m2
C V F Wb (T)
Table 3
SI multiple and submultiple prefixes
Factors by which multiplied 12
10 109 106 103 10−2 10−3 10−6 10−9 10−12 (a)
2
Avoided when possible.
Prefix
Symbol
tera giga mega kilo centi(a) milli micro nano pico
T G M k c m µ n p
Guide to Legal Citations What is the Correct Form? There are many systems for citing sources When a publication such as this Encyclopedia is to accommodate technical contributions from authorities across the world, there is benefit in uniformity in the form that source references are printed. Thus, for scientific publications, we decided that the Vancouver style would be adopted. For the most part, that format is followed throughout these volumes. It was more difficult to decide on the format for legal authorities and sources, because there is no single system of citing court cases, statutes, and other law publications. What exists is a conglomeration of conventions that are not always followed by various courts even within the same country. Local custom of reporting legal sources often supersedes what was prescribed as the “official” system in a jurisdiction. Of course, that is only of limited help. In the United Kingdom, for instance, with no less than a dozen different courts that, at one time or another, publish or have published case reports (e.g., Appeal Cases (second and third series), Chancery Division, Criminal Appeal Reports, Queen’s Bench, House of Lords, and other specialty courts), whatever convention exists is not always enlightening when one is confronted with a citation of a court. It is not easy for individuals who are not solicitors, barristers, or trained in law to locate where a particular case report may be found. The confusion is even greater in the United States where there are 50 different states, each printing their case reports in official and/or unofficial reporter systems. In addition, the federal court system publishes cases decided by the United States Supreme Court (in three different reporter systems), by eleven Circuit Courts of Appeal and the District of Columbia (in two different publication forms), and by numerous United States District Court opinions. Then there is also a multitude of reports for specialized courts or federal agencies. To seek to impart uniformity in citation form, editors from the Universities of Harvard, Columbia, Yale, and Pennsylvania Law Reviews have devised what is known as The Bluebook – A Uniform System of Citation. It is referred to as the Bluebook. The latest edition of the tome is the Eighteenth Edition, published in 2007. It comprises 415 pages. Unfortunately, the Bluebook has not imparted uniformity in citation form. First, each of the Bluebook’s editions advocated using conventions that were later partially modified in successive editions. Furthermore, the Bluebook is used essentially by law review journals published by law schools, but courts and other legal writers as well as publishers pay only scant attention to it and report cases in varying ways that they deem rational. Clearly, then, some leeway must be accorded to authors in these volumes in the way they report case law, statutes, and other legal collections, since there is no one accepted way that might be said to be generally accepted as the “correct” format. In the face of these considerations we decided, as a matter of convenience, that legal sources would be cited in the form that was customary in the jurisdiction where the source originated.
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Guide to Legal Citations
It is more important, then, to understand the purpose that references serve. The purpose of a citation is so that the complete opinion of the court or other legal authority can be readily retrieved. Sadly, the convention whereby decisions of courts are cited makes sense only to legally trained individuals or to persons who work within a relatively closed environment.
Basic requirement of an informative citation form An adequate citation of a reported opinion of a court is supposed to contain the following: (i) the name (or “style”) of the case, (ii) the reporter system wherein the opinion has been published, (iii) the court that decided the case, and (iv) the year of decision. This is the preferred order in which court cases are cited in the United States and in many other countries, though the four elements of an informative citation are not always listed in the same order. In the United Kingdom, for instance, the preferred form is to start with (i) the case name, (ii) the year of decision in parentheses, and thereafter (iii) the volume number (if available), (iv) the reporting system, (v) the page, (vi) the deciding court if that information is not otherwise clearly indicated by the reporting system, and (vii) the jurisdiction where the case was decided, if that information is not evident from the context or the citation. It is also preferred that cases be cited from official Law Reports rather than from ancillary sources. The Official Reports consist of the Appeal Courts (A.C.), Queen’s Bench (Q.B.), Chancery (Ch.), Family (Fam.), and Probate (P) Reports. When citing decisions of the House of Lords, the Privy Council, or other sources that may report appeals from more than one jurisdiction, the jurisdiction from which the appeal was taken should be indicated parenthetically. Most forensic scientists may be familiar with the way court opinions are published in their own country, but may not understand where and how foreign legal sources may be found. If, for research purposes, it becomes necessary for them to retrieve a complete court opinion or a statute for which the researcher possesses a citation, help in locating the full text referenced may be obtained from law-trained individuals. Major court systems also maintain libraries staffed by knowledgeable librarians. Legal libraries staffed with helpful librarians are further maintained in most law colleges and by many large legal firms. Because a single uniform system for referencing legal authorities is lacking, some variations may be noted in the citation form used by authors of contributions. With the guidance offered here, the individual who is not legally trained will hopefully be able to decipher the meaning of legal references encountered throughout this Encyclopedia.
Andre Moenssens
Abuse of the Elderly see Elder Abuse: Policy
Accreditation: Criminalistics see Training and Certification (in Criminalistics)
Accreditation: Education see Education and Accreditation in Forensic Science
Accreditation: Laboratory Crime laboratory accreditation has been one of the most powerful forces in improving the efficacy of forensic science services in the twenty-first century. Effective quality assurance programs are the linchpins for good forensic science, reliable techniques
to apply the science, and trustworthy expert opinion testimony [1]. Encouraged by judicial opinions [2], mandated by four state legislatures [3], and implemented by crime laboratory directors [4], accreditation programs have brought needed regulation to a critical segment of our criminal justice system.
Introduction The quality of scientific analyses conducted in crime laboratories varied widely throughout the United States before a program for crime laboratory accreditation was available. There were no generally accepted, published standards and no governmental regulations governing quality assurance in American crime laboratories [5]. A national proficiency testing research project during the mid-1970s [6], conducted by the Forensic Sciences Foundation (FSF) and funded with a grant from the National Institute of Law Enforcement and Criminal Justice Law Enforcement Assistance Administration (LEAA), brought public attention to proficiency problems and other inadequacies in some of America’s crime laboratories [7]. An analysis of the results of the LEAAfunded project revealed “that some crime laboratories were experiencing serious problems in the examination and interpretation of several types of test specimens” [8] (see Error Rates in Forensic Methods; Interpretation: Observer Effects). Some of the concerns cited by critics and commentators about unregulated crime laboratories included the following: (i) lack of written protocols for testing; (ii) lack of proficiency testing; (iii) level of education
2
Accreditation: Laboratory
and competency of examiners; (iv) uninformative nature, and in some cases the nonexistence, of laboratory reports and case files; (v) lack of review of examination results; (vi) experts testifying beyond the scope of their expertise or the science; (vii) questions about the integrity of evidence in the laboratories; (viii) questionable validity and reliability of scientific theories and methodologies used in the laboratories; and (ix) lack of oversight to remediate problems identified in laboratories [9, 10]. Crime laboratory directors and professional organizations [11], as well as legal commentators [12–14], recognized the need for the regulation of crime laboratories and the implementation of universally recognized quality assurance programs [15]. Crime laboratory accreditation programs help implement and oversee quality assurance programs that resolve the types of deficiencies mentioned above and improve the quality of the laboratory and the science performed in the laboratory [16]. That is not to say, however, that the absence of accreditation means a particular crime laboratory does not perform quality work. There are many unaccredited laboratories that have rigorous quality assurance programs ensuring valid and reliable scientific results [17]. Nor does accreditation guarantee that every examiner from an accredited laboratory will always perform up to appropriate standards. Accreditation is a safeguard that helps ensure that the laboratory provides accurate and valid results [18]. Since the LEAA-funded proficiency testing project, several forensic science laboratory accreditation programs have been developed. The American Board of Forensic Toxicology (ABFT) accredits toxicology laboratories, having 24 laboratories accredited under its program [19]. The National Association of Medical Examiners (NAME) established a voluntary accreditation program and has accredited 54 medicolegal death investigative offices [20]. Forensic Quality Services-International (FQS-I) provides accreditation to forensic science testing laboratories in the United States and has accredited 53 crime laboratories and other forensic science laboratories since 2001. It also provides accreditation to Identification Sections and Crime Scene Units within police departments [21]. The National Forensic Science Technology Center (NFSTC) conducts external DNA audits of publicly funded laboratories desiring to receive federal funding and entry into the National DNA Identification System (NDIS). The
NFSTC is funded by a Cooperative Agreement with the National Institute of Justice, Office of Science and Technology [22] (see Databases). By far the oldest, most prolific accreditation program, and the most widely recognized by courts, legislatures and the crime laboratory community, is the American Society of Crime Laboratory Directors/Laboratory Accreditation Board (ASCLD/LAB) [23]. ASCLD/LAB came into existence through the work of the “Committee on Evaluation and Standards,” which was one of the first committees appointed by the ASCLD. The committee was appointed largely because of deficiencies in crime laboratories, which were revealed by the LEAA proficiency testing program. The committee was charged to develop a program which sets standards of operation and a process for evaluation of crime laboratories. ASCLD/LAB received its first accreditation applications in early 1982 and accredited seven Illinois State Police laboratories. By the fall of 1984, ASCLD/LAB had accredited 30 crime laboratories and had achieved a predetermined minimum size to become an independent not-for-profit organization, which was then incorporated in the state of Missouri. Since its inception, ASCLD/LAB has accredited more than 342 public and private crime laboratories at every governmental level, including international laboratories and the major federal law enforcement and military crime laboratories in the United States [24]. As of September 2008, the 342 laboratories holding current ASCLD/LAB accreditation included 178 state laboratories representing 48 states, 109 local government laboratories, 22 federal laboratories, 22 private laboratories, and 11 international (non-United States) laboratories. ASCLD/LAB maintains two programs, ASCLD/LAB-Legacy and ASCLD/LAB-International. The former is the original program under which accreditation is based upon requirements created, adopted and maintained by the ASCLD/LAB Delegate Assembly. The Legacy program is being phased out. The International program, implemented in April 2004, is based on the requirements of the International Organization for Standardization (ISO) and supplemental requirements such as the ASCLD/LAB-Legacy program requirements. In 2007, a separate accreditation program was implemented under the ASCLD/LAB-International program for breath alcohol calibration laboratories. As of September 2008, 69 testing laboratories and one
Accreditation: Laboratory breath alcohol calibration laboratory were accredited under the International program and the remainder under the Legacy program. With more than three-quarters of the publicly funded crime laboratories in the United States accredited by ASCLD/LAB [25], it is significant to the integrity of the criminal justice system that ASCLD/LAB’s accreditation program provides professional regulation and review of a laboratory’s quality assurance program. Accreditation is a part of a laboratory’s quality assurance program which, under ASCLD/LAB’s program, also includes proficiency testing, continuing education, and other programs to help the laboratory achieve excellence and give better overall service to the criminal justice system (see Fire Investigator: Standardization, Accreditation, and Certification; Accreditation: Organizational; Quality Systems: Toxicology). A quality assurance program which meets the ASCLD/LAB standards addresses the criticisms leveled at unregulated laboratories. While the ASCLD/LAB accreditation program is voluntary, some states have mandated accreditation and have chosen ASCLD/LAB as their accrediting authority for multidisciplinary crime laboratories. New York established a Commission on Forensic Science which developed minimum standards and a mandatory program of accreditation for all forensic laboratories within the state [26]. All of the state’s multidisciplinary crime laboratories are now accredited by ASCLD/LAB, while some of the toxicology laboratories are accredited by the ABFT. Likewise, Oklahoma requires that all crime laboratories within the state be accredited by ASCLD/LAB and its toxicology laboratories by ABFT [27]. Legislation passed in the state of Texas in 2003 requires the Texas Department of Public Safety (DPS) to establish a program of accreditation for “forensic examinations” [28]. Missouri requires that after December 31, 2012, any crime laboratory providing reports or testimony to a state court pertaining to a result of the forensic analysis of evidence shall be accredited or provisionally accredited by a laboratory accrediting organization approved by the DPS [29].
The ASCLD/LAB-International Accreditation Program As discussed earlier, the ASCLD/LAB-Legacy program is being phased out of existence, and the
3
ASCLD/LAB-International program is replacing it, using the ISO framework. This transition reflects the future of accreditation programs in the United States by which laboratories and accrediting bodies will be embracing internationally accepted accreditation standards. The ISO has published at least two sets of standards having direct application to the accreditation of laboratories of all types [30]. The first, ISO/IEC 17025: General Requirements for the Competence of Testing and Calibration Laboratories [31] is not specific to crime laboratories, but the standards are, as the name implies, applicable to any organization performing tests and/or calibrations. The second ISO standard of interest [32], ISO/IEC 17011:2004 Conformity assessment – General requirements for accreditation bodies accrediting conformity assessment bodies [33], establishes a system of internationally recognized standards for the accreditation of laboratories [34]. Only in this century has the American forensic science community looked seriously at adopting ISO/IEC 17025 as the foundation of crime laboratory accreditation programs. NFSTC started conducting ISO/IEC 17025 compliant accreditation inspections of forensic laboratories in 2001 [35]. ASCLD/LAB-International was promulgated in December 2003 by the Delegate Assembly, and ISO/IEC 17025 compliant accreditation inspections began in the summer of 2004. Engaging in ISO/IEC 17025 compliant inspections is but one requirement of ISO/IEC 17011 requirements. Compliance with all elements of ISO/IEC 17011 brings an added dimension of quality to crime laboratory accreditation efforts in America. The ultimate purpose of ISO/IEC 17011 is to establish standards for the recognition of competent accrediting bodies. An ISO/IEC 17025 accrediting body may voluntarily comply with the provisions of ISO/IEC 17011 and self-declare compliance, or apply for formal recognition to a body operating a recognition program for accrediting bodies, which in the Americas is the Inter-American Accreditation Cooperation (IAAC) [36]. Regional cooperations like the IAAC exist in most developed regions of the world for the primary purpose of offering recognition to accreditation bodies and facilitating the cooperation of such bodies in those regions. In September 2008, ASCLD/LAB was granted formal recognition by the IAAC for meeting all
4
Accreditation: Laboratory
the applicable ISO and IAAC standards for the operation of a competent accrediting body. After a thorough evaluation by an IAAC international team of evaluators, ASCLD/LAB, and specifically the ASCLD/LAB-International accreditation program for testing laboratories, became the first forensic science accreditation body in the United States to gain international recognition for meeting all applicable ISO and IAAC standards for the operation of a competent accrediting body. ISO standards and concepts in the accreditation of crime laboratories address criticism that previous crime laboratory accreditation programs were designed, adopted, implemented, and overseen solely by the users of each program. Embracing internationally adopted ISO/IEC 17025 standards and opening the accreditation programs to third-party ISO/IEC 17011 scrutiny was the next logical step in the evolution of crime laboratory accreditation in the United States. Perhaps, the greatest strength in ISO compliant programs of accreditation is the increased physical presence in the accredited laboratories. FQS-I operates their program of ISO accreditation on a 2- to 5-year cycle. Depending on the period of accreditation granted, FQS-I will either conduct a full on-site inspection of the laboratory every second year or conduct periodic surveillance visits if the cycle of accreditation is longer than 2 years. The ASCLD/LAB-International program operates on a 5-year cycle of accreditation, but conducts annual on-site surveillance visits in each laboratory. Surveillance visits are abbreviated versions of full assessments. However, there are weaknesses associated with ISO/IEC 17025. The most critical area where the international requirements for accreditation fall woefully short of American programs like ASCLD/LAB-Legacy is proficiency testing requirements. Undoubtedly as a direct result of the LEAA study in the mid-1970s, proficiency testing has become entrenched as a major part of the compliance monitoring phase of crime laboratory accreditation programs in the United States. Even many nonaccredited laboratories participate in internal and external proficiency tests each year. Interestingly, ISO/IEC 17025 is virtually silent on the subject of proficiency testing. To fill this critical gap, ASCLD/LAB-International includes supplemental requirements – like proficiency testing and
specific educational requirements for laboratory analysts (see Expert Witnesses: Selection and Investigation of Credentials). Embracing ISO standards and concepts should not be viewed, however, as a panacea for curing all the current quality issues in America’s crime laboratories. Implementing ISO compliant accreditation programs is but another step in the ongoing process of assuring quality in the forensic sciences and integrity in the criminal justice system. To that end, ASCLD/LAB-International has four objectives which define the purposes and nature of the program. The objectives are • • • •
to improve the quality of laboratory services; to develop and maintain criteria that may be used by a laboratory to assess its level of performance and to strengthen its operation; to provide an independent, impartial, and objective system by which laboratories can benefit from a total operational review; and to offer to the general public and to users of laboratory services a means of identifying those laboratories, which have demonstrated that they meet established standards.
The forensic disciplines for which ASCLD/ LAB-International affords accreditation include controlled substances, toxicology, trace evidence, biology (including DNA), firearms/toolmarks, questioned documents, latent prints, crime scene, and digital & multimedia evidence. ASCLD/LAB-International also offers accreditation to laboratories certifying the calibration of breath alcohol measurement devices. In the area of DNA, the Federal Bureau of Investigation (FBI’s) Quality Assurance Standards for Forensic DNA Testing Laboratories and Convicted Offender DNA Databasing Laboratories are applied during the inspection [37] (see Databases). These quality assurance standards and programs were established pursuant to the DNA Identification Act of 1994 [38]. To receive federal funding for DNA analysis, laboratories must meet these standards. The FBI and ASCLD/LAB have agreed to cooperate in the implementation of these standards in laboratories inspected by ASCLD/LAB. When a laboratory applies for accreditation, ASCLD/LAB requires an assessment of all the recognized disciplines in the laboratory, with the exception of the crime scene discipline. The applicant laboratory director has the option of including crime
Accreditation: Laboratory scene and/or breath alcohol measurement device calibration in the accreditation process. Other than exempting those two disciplines, ASCLD/LAB will not do a partial accreditation of any laboratory. The International program has adopted many accreditation requirements from the well-established standards provided by the Legacy program to supplement ISO/IEC 17025, making the program more relevant and applicable to forensic science testing laboratories. The written format of the supplemental requirements corresponds to the ISO format and contains the basic principles of quality assurance as well as notes to provide clarification or examples. The supplemental requirements are found in the ASCLD/LAB-International Supplemental Requirements for the Accreditation of Forensic Science Testing Laboratories and the ASCLD/LAB-International Supplemental Requirements for the Accreditation of Forensic Science Testing Calibration Laboratories.
The ASCLD/LAB-International Accreditation Process As a part of the accreditation process, an assessment team, composed of a Lead Assessor and Technical Assessors, visits the laboratory or laboratory system and assesses the laboratory against all the applicable accreditation criteria in ISO/IEC 17025 and the Supplemental Requirements document. Assessments are conducted primarily by volunteer assessors from accredited laboratories who have successfully completed the ASCLD/LAB assessor training program and who are trained in the assessment criteria [39]. As a result of the growth in the program, there is now a paid staff employed by ASCLD/LAB, who act as lead assessors, program directors, quality manager, training manager, executive director, and support staff [40]. The assessment team determines whether the laboratory has met each of the accreditation requirements. If it has not, the laboratory receives a “no” as to every nonconforming criterion. “nonconformities” are classified as Level 1 or Level 2. The more serious nonconformity is Level 1, the nature of which directly affects and has a fundamental impact on the work product of the laboratory or the integrity of the evidence. All the other nonconformities are Level 2. Prior to the completion of the on-site assessment, a Summary Assessment Report is prepared by the
5
Lead Assessor and reviewed by an ASCLD/LAB Quality Review Panel to ensure consistency in the application of accreditation requirements and in grading the laboratory. The report is then given to the laboratory director at the summation conference that concludes the assessment visit. In addition, the laboratory director is given a Corrective Action Request for each criterion in which the laboratory was found to be nonconforming. Level 1 nonconformities must be corrected within 180 days and no laboratory will be accredited with an outstanding Level 1 nonconformity. Before the next annual on-site surveillance visit, all Level 2 nonconformities must be corrected or they will be treated as a Level 1 nonconformity. After the summation conference, the Lead Assessor prepares a full assessment report that is again subject to a quality review, which is then given to the laboratory. This is a more formal report that includes all the nonconformities reported during the summation conference. When the Lead Assessor determines that all Level 1 corrective actions have been completed, he or she will prepare a final assessment report to the Board of Directors [41]. The Board then grants or denies accreditation, or may require completion of additional corrective actions [42, 43]. When a laboratory system applies for accreditation, each laboratory within the system will be judged and accredited independently of each other. Accreditation is granted for a period of 5 years, during which the laboratory is expected to remain compliant with the accreditation standards. During the accreditation cycle, compliance with accreditation criteria is monitored on an annual basis by three methods. The first method requires the submission of an Annual Accreditation Audit Report to ASCLD/LAB by each laboratory. If discrepancies with accreditation criteria are revealed, the laboratory is expected to remediate them under the supervision of ASCLD/LAB. If failures appear during the year, the standards require the laboratory to have a procedure in place that must be followed to correct the problems. If there are significant changes in the laboratory during the year, they must also be reported so that ASCLD/LAB can determine whether a special interim assessment is required to assure compliance with the standards. The second method of determining compliance is on-site surveillance visits conducted annually in each accredited laboratory. These miniassessments
6
Accreditation: Laboratory
allow for first-hand, personal observations of the laboratory’s quality assurance program. Core accreditation requirements are assessed, as well as a number of additional requirements selected for the on-site assessment. The annual surveillance visits are conducted much like the full assessment, with a summation conference, and a full and then final surveillance report, with intervening quality reviews. Proficiency testing is the third means of monitoring compliance. ASCLD/LAB has adopted a Proficiency Review Program that outlines the review process for external proficiency test results from approved test providers [44]. For each forensic discipline accredited by ASCLD/LAB, there is a Proficiency Review Committee. These committees review external proficiency test results provided by approved test providers in accordance with the ASCLD/LAB Proficiency Review Program. If a discrepancy is indicated in the report, the committee requests a response from the laboratory as to its investigation of the cause of the discrepancy and the corrective measures that have been taken to correct it. There are three classes of discrepancies. Class I discrepancies are the most serious, the nature and cause of which raise immediate concern regarding the quality of the laboratory’s work product. The Board of Directors has the authority to impose sanctions for discrepancies and the failure to correct them, including probation, suspension, or revocation of the accreditation status. If a failure to comply with the accreditation standards is reported from within the laboratory, from outside the laboratory, or discovered by a special interim assessment or surveillance visit, an investigation will ensue in appropriate cases. The same sanctions described above may be imposed by the Board of Directors on a laboratory that fails to remain compliant. The Board has the authority to send an assessment team into the laboratory at any time to determine compliance with accreditation criteria. In these ways, ASCLD/LAB provides oversight in the remediation of problems in accredited laboratories. For nonaccredited laboratories that experience quality-related problems, ASCLD/LAB has developed an assistance program. At the invitation of the laboratory or the laboratory’s supervising authority, ASCLD/LAB will provide a team of trained assessors to conduct an on-site review of the laboratory’s processes and casework to determine the cause of the deficiencies and errors in examination.
ASCLD/LAB Accreditation Criteria ASCLD/LAB-International accreditation criteria for testing and calibration laboratories cover the following broad categories: laboratory management and operations, personnel qualifications, and physical plant.
Laboratory Management and Operations The laboratory management and operations criteria contain the heart of the accreditation program and include the principles mentioned later. Evidence Control. This series of criteria requires a comprehensive chain of custody to maintain the integrity of the evidence while in the laboratory. Evidence control requires marking evidence for identification purposes, storage under proper seal, and protection from loss, cross-transfer, contamination, and/or deleterious change (see Chain of Possession of Tangible Evidence). Management System. A fully documented management system [45] is required, including a quality manual, in which the laboratory documents the policies and procedures that pertain to quality assurance, including a requirement of compliance by the management and staff. A quality manager must also be appointed who is responsible for the quality system in the laboratory. Internal audits are one of the primary tools used to evaluate, confirm, or verify activities related to quality. Their purpose is to assess compliance with the operational requirements of the entire management system. Periodic audits, along with dayto-day review of scientific reports, provide an effective means for ensuring that quality control activities are being implemented and that each forensic examiner performs in a manner consistent with the quality management system. Procedures that are used in the laboratory must be documented to be demonstrably capable of producing valid results. They must be generally accepted in the scientific field or supported by data gathered and recorded according to the scientific method. New procedures must be scientifically validated before being used. These safeguards, reviewed by the laboratory’s quality manager and by ASCLD/LAB assessors, help assure that valid theories and methodologies are in place for the examination of evidence.
Accreditation: Laboratory The quality aspects of the management system also require that written technical procedures are in place for sample preparation methods, controls, standards, and equipment calibration procedures. These practices are crucial for the reliability of the methodology involved in many scientific tests. These protocols and the protocols established for individual tests in the different forensic disciplines assure that tests are conducted properly and under generally accepted procedures. These protocols not only help to assure validity and reliability but also help to meet the admissibility requirement of the “existence and maintenance of standards controlling the technique’s operation” set forth by the Supreme Court [46] (see Expert Opinion in Court: a Comparison of Approaches; Expert Opinion: United States); Daubert v. Merrell Dow Pharmaceuticals; and Federal Rule of Evidence 702). Laboratory reports must be supported by a comprehensive case record that includes all notes, worksheets, photographs, spectra, printouts, charts, and other data or records used by the examiners to support their conclusions (see Report Writing for Courts). Documentation to support conclusions must be such that in the absence of the examiner, another competent examiner or supervisor could evaluate what was done and interpret the data. Acceptable ways to document the basis for conclusions derived from evidence examination may include a narrative description of the examination process and observations made, photographs, photocopies, diagrams, drawings, and worksheets. This requirement is essential because it allows a technical review. With these requirements in place, it will be much harder for an unscrupulous examiner to hide his or her incompetency, shortcuts, or fraud. Moreover, the complete case record required by ASCLD/LAB allows a more thorough and comprehensive review by defense experts of the tests conducted (see Discovery of Expert Findings). As an additional quality assurance procedure to ensure compliance with testing protocols, technical review by another competent examiner of a percentage of laboratory reports is required (see Peer Review as Affecting Opinion Evidence). In addition, there must be a course of action mandated when discrepancies or nonconforming testing are found. The oversight of the quality of the testing and the reporting is an essential criterion that affords the public confidence that the conclusions issued in reports are accurate and reliable.
7
The courtroom testimony of each examiner is also reviewed annually for several purposes, including determinations that testimony is scientifically consistent with the work documented in the case file. Periodic, random review of testimony discourages examiners from testifying beyond the scope of his or her report and helps discover those that do [47]. Proficiency Testing. Proficiency testing is an integral part of a quality assurance program. It measures the capability of the examiner and the reliability of the analytical results. Such tests help determine where more training is required or where more stringent quality control may benefit. It also demonstrates, in part, the current competence of the laboratory. One test must be administered annually for each discipline in the laboratory and must be provided by an external proficiency test provider. ASCLD/LAB approves providers meeting its requirements. The external review of proficiency test results is a crucial element of the compliance monitoring process. In addition to the external tests required for each discipline, the program requires that each individual in the laboratory participate in at least one proficiency test annually. It should also be noted that the program encourages laboratories to give proficiency tests to each examiner annually in each subdiscipline in which casework is performed. In addition to participating in external proficiency testing, a laboratory should conduct proficiency testing using blind tests prepared internally or externally and submitted as normal casework evidence or by reexamination by another examiner of evidence on which casework was previously completed.
Personnel Qualifications The qualifications of a laboratory’s examiners are of great importance. These criteria establish minimum education, experience requirements, and training. They also require, for most of the forensic disciplines, a minimum of a baccalaureate degree in a natural science or a related field relevant to the scientific discipline in which the examiner is practicing. These criteria have raised the education levels required in many disciplines [48]. While certification of examiners by an appropriate certification organization is not required by ASCLD/LAB, the accreditation standards do require that examiners have the education, experience, and
8
Accreditation: Laboratory
training commensurate with the examinations and testimony they provide [49]. When certification is obtained, it should be by a recognized organization [50]. Initial competency and continued proficiency of examiners is also crucial. Each examiner must pass a competency test prior to assuming casework responsibilities and must successfully pass a proficiency test at least annually.
and a prosecutor. Ralph Keaton, ASCLD/LAB Executive Director, and John K. Neuner, ASCLD/ LAB International Program Manager, contributed to this article, an early version of which appeared in American Bar Association, Criminal Justice Section, Crime Laboratory Accreditation: The Assurance of Quality in the Forensic Sciences, The State of Criminal Justice (August 2003).
References Physical Plant A well-designed and outfitted laboratory can greatly add to its productivity and reliability. These criteria require that appropriate security measures be practiced and address the adequacy and appropriateness of laboratory space. The laboratory’s physical plant should reflect due consideration of space, design, security, health, and safety. A reference guide used by laboratories is the “Forensic Laboratories: Handbook for Facility Planning, Design, Construction, and Moving,” publication NCJ168106, prepared by the US Department of Justice, Office of Justice Programs, National Institute of Justice.
Conclusion While crime laboratory accreditation programs have improved substantially over the last two decades, there is still a lot of work to be done. Report writing, proficiency testing, and ethics training are some of the areas that still need improvement (see Ethics: Codes of Conduct for Expert Witnesses; Report Writing for Courts). Most important, there remain a considerable number of laboratories, both public and private, that have not been accredited by any organization. Forensic sciences now play such an integral role in the criminal justice system [51] that the public and the criminal justice system as a whole demand the implementation of quality assurance programs monitored by outside entities. Accreditation by an internationally recognized program is a safeguard that helps ensure laboratories provide accurate and valid results.
End Notes a.
Kenneth E. Melson is a board member on the American Society of Crime Laboratory Directors/Laboratory Accreditation Board (ASCLD/LAB)
[1]
[2]
[3]
[4]
[5]
[6]
[7]
[8] [9]
The elements which make up a comprehensive quality assurance program are described in National Research Council (1992). Communications on DNA Techniques in Forensic Science. DNA Technology in Forensic Science, p. 98. In Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 594 (1993), the Supreme Court noted that a court ordinarily should consider the existence and maintenance of standards controlling the technique’s operation when determining admissibility of scientific evidence, (citing United States v. Williams, 583 F.2d 1194, 1198 (2nd Cir., 1978) (noting professional organization’s standards governing the technique). Judges are citing the accreditation standards in decisions on admissibility of scientific evidence. See, e.g., Smith v. State, 702 N.E.2d 668, 673 (Ind. 1998). New York, Oklahoma, Texas and Missouri are now the only jurisdictions that require forensic laboratories to be accredited. See N.Y.EXEC. § 995-a (McKinney 1996); OKLA. STAT. tit. 74, § 150.37 (2002); TEX. CODE CRIM. PROC. art. 38.35 (1991), amended by H.B. 2703, 2003 Leg. (Tex. 2003); TEX.GOV.CODE ANN. § 411 (Vernon 1998) amended by H.B. 2703, 2003 Leg. (Tex. 2003); Mo.Rev.Stat. § 650.060 (2008). The American Society of Crime Laboratory Directors voted to begin a voluntary accreditation program for their laboratories in (1981). For a history of accreditation programs in the fields of health care, legal education, and law enforcement and corrections, see Dodd, V.J. (1989). Toward a national system of state court accreditation, Judicature 73, 141. The results of the study were reported in 1978 in Peterson, J.L., Fabricant, E.L., Field, K.S. Thornton, J.I. (1978). Crime Laboratory Proficiency Testing Research Program. Peterson, J.L. & Markham, P.N. (1995). Crime laboratory proficiency testing results, 1978–1991, I: identification and classification of physical evidence, Journal of Forensic Sciences 40, 994–1008. Id. at 994. For examples of problems in crime laboratories, see Giannelli, P.C. (1997). The abuse of scientific evidence in criminal cases: the need for independent crime laboratories, Virginia Journal of Social Policy & the Law 4, 439.
Accreditation: Laboratory [10]
[11]
[12] [13]
[14]
[15]
[16]
[17]
[18] [19] [20] [21] [22] [23] [24] [25]
Maier, T.W. (2003). Inside the DNA Labs, Insight on the News, May 26, (accessed May 2003). Available at www.insightmag.com/news/436794.html. Hansen, L.B. (1992). Stemming the DNA tide: a case for quality control guidelines, Hamline Law Review 211(165), 16. (stating that organizations calling for quality assurance standards include the National Association of Attorneys General, the National District Attorneys Association, and the American Society of Crime Laboratory Directors). Lander, E. (1989). DNA fingerprinting on trial, Nature 339, 501–505. Jonakait, R. (1991). Forensic science: the need for regulation, Harvard Journal of Law & Technology 4, 109–191. Weinstein, J.B. (1998). Science, and the challenge of expert testimony in the courtroom, Oregon Law Review 77, 1005–1011. Bales, S. (2000). Turning the microscope back on forensic scientists, Litigation 26(2), 51–54, (explaining why crime laboratory accreditation is important). A primary recommendation made in the 1997 Office of Inspector General’s report on its investigation of allegations concerning the FBI laboratory was that it obtain accreditation by the American Society of Crime Laboratory Directors/Laboratory Accreditation Board (ASCLD/LAB) as soon as possible. Id. at 54. See U.S. DEPARTMENT OF JUSTICE, OFFICE OF INSPECTOR GENERAL, THE FBI LABORATORY: AN INVESTIGATION INTO LABORATORY PRACTICES AND ALLEGED MISCONDUCT IN EXPLOSIVES-RELATED AND OTHER CASES (April 1997). National Research Council (1992). Cf. Communications on DNA Techniques in Forensic Science, DNA Technology in Forensic Science, p. 107, (suggesting that courts should view the absence of appropriate accreditation as constituting a prima facie case that the laboratory has not complied with generally accepted standards). Bales, S. (2000). Turning the microscope back on forensic scientists, Litigation 26(2), 51–54. As of September (2008). The website for the American Board of Forensic Toxicologists is www.abft.org. As of July (2008). The website for the National Association of Medical Examiners is www.thename.org. As of September (2008). The FQS-I website is www. forquality.org. As of November (2008). The website for the National Forensic Science Technology Center is www.nfstc.org. As of November (2008). The website for ASCLD/LAB is www.ascld-lab.org. As of November (2008). A list of accredited laboratories can be viewed at www.ascld-lab.org. In 2005, 78% of 293 laboratories responding to a Bureau of Justice Statistics’ survey of the 389 publicly funded crime laboratories in the United States were accredited by ASCLD/LAB, with 3% accredited by some other organization. Durose, Census of Publicly Funded Forensic Crime Laboratories, 2005, Bureau of Justice Statistics Bulletin, July 2008. Since 2005,
[26] [27] [28]
[29] [30] [31]
[32]
[33] [34]
[35] [36]
[37] [38] [39]
[40]
[41]
9
ASCLD/LAB has increased the number of publicly funded crime laboratories accredited by one of its two accreditation programs. See N.Y. EXEC. § 995-b (McKinney 1996). See OKLA. STAT.tit. 74, § 150.37 (2002). See TEX. CODE CRIM. PRO. art. 38.35 (1991), amended by H.B. 2703, 2003 Leg. (Tex. 2003); TEX.GOV.CODE ANN. § 411 (Vernon 1998), amended by H.B. 2703, 2003 Leg. (Tex. 2003). Mo.Rev.Stat. § 650.060 (2008). As of November (2008). The website for ISO is www.iso.org. As of November (2008). ISO/IEC 17025: General Requirements for the Competence of Testing and Calibration Laboratories, is available for purchase from the American National Standards Institute (ANSI) at www.ansi.org. IEC stands for the International Electrotechnical Commission. There are more than two ISO standards related to the work and accreditation of crime laboratories. For example, ISO Guide 43 (Parts I & II) addresses, respectively, standards of proficiency testing by interlaboratory comparisons, and the selection and use of proficiency testing schemes by laboratory accreditation bodies. In this context, the term “conformity assessment body” means the laboratory being evaluated for accreditation. As of November (2008). ISO/IEC 17011:2004 Conformity assessment – General requirements for accreditation bodies accrediting conformity assessment bodies is available for purchase at www.ansi.org. NFSTC was the predecessor to FQS-I, and no longer offers full laboratory accreditations. As of November (2008). Additional information about the Inter-American Accreditation Cooperation (IAAC) is available at http://www.iaac.org.mx/. As of November (2008). See www.fbi.gov/hq/lab/fsc/backissu/july2000/codispre. htm, for the standards. 42 U.S.C. § 14131. Using volunteer assessors from accredited laboratories has two distinct advantages. First, these individuals are experts in their field, doing work in the subject matter expertise in the area they are inspecting. Second, participation in the accreditation program gives additional training in quality assurance standards and practices to examiners who work in crime laboratories. Paid staff assessors were added to the program to assure consistency in application of accreditation criteria in the inspection process and the review of inspection reports. The quality manager is responsible for the Proficiency Review Program and the quality of the accreditation program. The Board of Directors is composed of nine voting members, a non-voting ex-officio member representing ASCLD (a separate non-profit organization) and a non-voting Executive Director. Seven of the voting members are elected from among the Delegate Assembly. One elected Board member is a representative of law enforcement and prosecuting attorneys and one is
10
[42]
[43]
[44]
[45]
[46] [47]
Accreditation: Organizational a public member. The Board is elected by the Delegate Assembly, which is composed of the directors of all ASCLD/LAB accredited laboratories and laboratory systems. Contrary to outside criticism suggesting the accreditation program is a trade association administered by a group of golfing buddies, less than ten percent of applicant laboratories under the Legacy program achieved accreditation following the initial inspection. It is expected that the same will apply under the International program. See McDonald, R. (1998). Juries and crime labs: correcting the weak links in the DNA chain, American Journal of Law & Medicine 24, 345–356. Arvizu, J. (2000). Shattering the Myth: Forensic Laboratories, CHAMPION 18, 20–21, 24-May. Despite these early characterizations of ASCLD/LAB, two of the states requiring mandatory accreditation and the United States Department of Justice Office of the Inspector General have all recognized the ASCLD/LAB as an appropriate accreditation body, despite its peer-reviewer structure. The National Research Council in its second study of DNA analysis recommended that laboratories should make every effort to be accredited for DNA work by such organizations as ASCLD/LAB. COMM. ON DNA FORENSIC SCI., NAT’L RESEARCH COUNCIL, THE EVALUATION OF FORENSIC DNA EVIDENCE 4 (1996). The long-standing practice of accrediting bodies like ASCLD/LAB to use senior forensic scientists, with actual experience in a crime laboratory, and who receive specialized inspection training, meets both the letter and intent of peer-reviewer philosophy shared worldwide. See The International Organization of Standardization’s (ISO) ISO/IEC 17011:2004 Conformity assessment – General requirements for accreditation bodies accrediting conformity assessment bodies (assessors (inspectors) must be selected and used based upon their having appropriate technical knowledge and practical experience directly related to the work of the laboratory being inspected); KPI 3: Accrediting Body Staff, Assessors and Experts, in the International Laboratory Accreditation Cooperation’s (ILAC) publication ILAC P7:2003 / Key Performance Indicators (KPIs) (reiterating the necessity for accrediting bodies to use only inspectors who possess the appropriate “technical qualifications and practical experience.”). As of November (2008). The ASCLD/LAB Proficiency Review Program document may be viewed at www.ascld-lab.org. The term “management system” is defined in ISO/IEC 17025:2005 General requirements for the competence of testing and calibration laboratories as “the quality, administrative and technical systems that govern the operations of a laboratory.” Daubert v. Merrell Dow Pharmaceuticals, Inc, 509 U.S. 579, 594 (1993). For an example of a capital murder case where the trial testimony of an expert went beyond the conclusions in the lab report, see Troedel v. Wainwright, 667 F.
Supp. 1456 (S.D. Fla. 1986), aff’d 828 F.2d 670 (11th Cir., 1987). [48] There are many outstanding forensic science programs being offered in colleges and universities. The American Academy of Forensic Sciences formed an accrediting body, called the Forensic Science Education Programs Accreditation Commission (FEPAC), which has as its mission the accreditation of college-level academic programs that lead to a baccalaureate or graduate degree. [49] An indication of the growing recognition of certification is the 2003 amendment to the Oklahoma accreditation statute which exempts latent print identifications performed by latent print examiners certified by the International Association for Identification (IAI) (www.theiai.org) from the requirements of a technical peer review system, a proficiency testing program and accreditation. See OKLA. STAT. tit 74, § 150.37, amended by H.B.1802, 2003 Leg. (OKLA. 2003). For a listing of certification organizations, see Carol Henderson Garcia, Expert Witness Malpractice: A Solution to the Problem of the Negligent Expert Witness, 12 MISS. C.L. REV. 39, 62 (1991). Many of the certification organizations may be found by reviewing the website for the American Academy of Forensic Sciences (AAFS) at www.aafs.org. [50] The American Academy of Forensic Sciences has established an accrediting body, the Forensic Specialties Accreditation Board, to accredit certification organizations. [51] Evidence from an estimated 2.7 million criminal investigations was submitted to the nation’s forensic crime laboratories in 2005. Durose, Census of Publicly Funded Forensic Crime Laboratories, 2005, Bureau of Justice Statistics Bulletin, July 2008.
KENNETH E. MELSON, RALPH KEATON AND JOHN K. NEUNER
Accreditation: Organizational Introduction Accreditation is becoming (see Accreditation: Laboratory; Fire Investigator: Standardization, Accreditation, and Certification) more widely present in criminalistics. According to the most important forensic organizations, such as the European Network of Forensic Science Institutes
Accreditation: Organizational (ENFSI), the American Society of Crime Laboratory Directors (ASCLD), and the Senior Managers of Australian and New Zealand Forensic Laboratories (SMANZFL), the promulgation of accreditation programs is a visible sign of the increasing importance of accreditation in forensic sciences [1, 2]. As an illustration, the ENFSI 2005–2008 strategic plan states that [3] “All ENFSI laboratories need support in complying with best practices and raising the level of quality and science. To achieve this, ENFSI continuously encourages its member institutes to move toward formal quality management and accreditation. Scientific cooperation within expert working groups needs more momentum and a competence assurance system for ENFSI laboratories will be developed.” SMANZFL includes the promotion and enhancement of management and quality practices in their strategic plan (Davey A. Personal communication 2008). There are several reasons for this growing phenomenon. One of them lies in the general tendency for all scientific laboratories to seek accreditation. Forensic DNA laboratories were among the first to follow this development. Simultaneously, the increasing number of private laboratories and customer demand for more accountability also has a great influence. Management systems introduced in the public sector are also undergoing similar changes. Finally, admissibility of scientific evidence is subjected to a constantly increasing scrutiny in the court. Accreditation has been accepted as a means of helping courts to make decisions about the reliability of the evidence provided by a crime laboratory [4]. Contrary to certification (see Training and Certification (in Criminalistics)), which deals with the evaluation of the competency of a forensic scientist, accreditation is concerned with the overall operation of the organization. It is an overview of the managerial and technical requirements of a laboratory in order to comply with a given standard.
Accreditation Accreditation, in its broad meaning, can be defined as [5] “the formal recognition of the technical and organizational competence of an authority to execute a specific service as described in the scope of accreditation. Competence is the key to transparency, confidence, and comparability.” More specifically,
11
laboratory accreditation can be defined as the [4] “formal recognition that a testing laboratory is competent to carry out specific tests or specific types of tests”. It may also include the [4] “recognition of both the technical competence and impartiality of a testing laboratory”. In other words, the entity that wants to be accredited agrees to structure its aims/goals, management system, and technical facilities (i.e., infrastructure, personnel, and methods) so that they meet preestablished agreed criteria (described in a standard). The accrediting body then verifies whether the laboratory seeking accreditation (also referred to as the applicant) fulfills the criteria and complies with the standard. The partnership between the ISO and the IEC has led to the creation of the standard ISO/IEC 17025 general requirements for the competence of testing and calibration laboratories [6]. This standard has been chosen by many forensic/criminalistics laboratories around the world for their accreditation purposes. It describes in a very general but exhaustive manner what is necessary to comply with it. ISO/IEC 17025 includes five chapters covering the entire laboratory operation: scope, normative references, terms and definitions, management requirements, and technical requirements. The first three chapters explain cases in which the standard is applicable and references on which it is based. The management requirements chapter deals primarily with the operation and effectiveness of the quality management system in place in the laboratory. It explains how to describe the system in place, how to detail all stages of the working process, and how to deal with more specific situations. The technical requirements part addresses methodology, test/calibration equipment, and competency of personnel. The combination of management and technical requirements covers the entirety of crime laboratory operations. Because ISO/IEC 17025 is designed for all kinds of testing and calibration laboratories, it does not necessarily consider all of the needs and specificities of a criminalistics laboratory. The application of standards to specific areas may require further explanations through additional documentation called applications or supplementary requirements. These documents are an elaboration of the more general criteria stated in the standards. Supplementary requirements provide an interpretation of the intent of parent standard (ISO/IEC 17025), when applied to specific disciplines
12
Accreditation: Organizational
within forensic sciences. They are usually established with the help of specialists in the field, in the present case criminalists. In the United States, in addition to ISO/IEC 17025 accreditation available through the ASCLD/LAB International program, the ASCLD/LAB Legacy program also accredits crime laboratories. As a matter of fact, more than 90% of US laboratories do not rely on ISO/IEC 17025, but on the ASCLD/LAB Legacy program [7]. In Australia, the National Association of Testing Authorities (NATA) provides a tailored forensic science accreditation program, which comprises ISO 17025 and supplementary requirements for accreditation in the field of forensic science for organizations whose core business is forensic science service provision. In addition, the “forensic module” is available to organizations that hold ISO 17025 accreditation in another field of testing but conduct a limited amount of forensic testing (Davey A. Personal communication, Parsell M. Personal communication 2008). Two other international standards are of interest with regard to accreditation in criminalistics: ISO/IEC 17020 general criteria for the operation of various types of bodies performing inspections and ISO 9001 quality management systems – requirements [8, 9]. ISO 9001 describes the general requirements of a quality management system. Its application is, thus, much broader than is defined by 17025, as it applies not only to laboratories but also to any entity providing services or products. The managerial criteria defined in 17025 are based on the ISO 9001 requirements; however, the main difference between the two standards is that the former also includes criteria on technical requirements and competency. More recently, there have been many discussions regarding the application of ISO/IEC 17020 to criminalistics, more specifically to crime scene investigation [10], although this is not the case in all countries. However, although the application of 17025 for laboratories and 9001 for management systems is not contested, the use of 17020 for crime scene investigation units is still under discussion and has not been widely accepted yet. ENFSI is presently working on a joint project with the European Co-operation for Accreditation (EA) to define which standard, ISO/IEC 17020 or ISO/IEC 17025, is to be used for the different forensic fields [11]. The latest version of the ENFSI’s standards for accreditation document states that [12]
“For activities other than the testing part of the forensic process e.g. work at the scene of crime, ISO/IEC 17020 can be implemented as the standard used to achieve accreditation”. The main goals and requirements for all three international standards (ISO 9001, ISO/IEC 17020, and ISO/IEC 17025) are the same. One of the most important goals is oriented toward customer service. It is crucial to provide a satisfactory service or product, which is recognized as a basic condition by the customer. Another important requirement is documentation. First, documentation of the goals and procedures allows the accredited laboratory to establish a repository of knowledge existing within their laboratory. When training new employees, this comprehensive body of documentation is available and knowledge can be easily passed on. It should, however, be emphasized that this documentation does not replace in-house training but facilitates the whole process. Second, written documentation assists the laboratory to work in a transparent and traceable manner. Ultimately, this helps to establish customers’ confidence. This accountability also renders the customers’ task much easier when choosing between various laboratories to meet their requirements. Third, documentation helps to have an efficient quality management system by keeping a documented chain of custody, a particularly important requirement in criminalistics, and by keeping track of errors. Although a complete management system is more than just the chain of custody and corrective actions, several goals are reached by simply applying a comprehensive documentation policy.
Accreditation Process There are several institutions that are competent to provide accreditations, most of which are national bodies. In the United States, ASCLD/LAB is the most popular. It is also the body chosen by 10 laboratories outside the United States, notably in New Zealand [13]. In Canada, the Standards Council of Canada (SCC) is competent. In Australia, it is the NATA and in the United Kingdom the United Kingdom Accreditation Service/National Accreditation of Measurements and Sampling (UKAS/NAMAS) can provide accreditation. There are three main stages in the accreditation process: preparing for, obtaining, and maintaining
Preparation
Project of getting accreditation
Preparation to accreditation
Informal meeting with accreditation body – evaluation of needs
Revision of internal procedures
Obtention
Formal application for accreditation
On-site inspection by assessment team and identification of nonconformities
Nonconformities remediation
Deliveance of accreditation
Maintenance
Accreditation: Organizational
Internal reviews according to internal guidelines
Issuance of annual accreditation report
Annual external review based on report
Full reaccreditation every 5 years
13
Figure 1 The different steps in the accreditation process. Light gray indicates the steps carried out by the body getting accredited. Dark gray indicates the steps carried out by the accrediting body. The blend of gray indicates the steps involving both the parties
accreditation.a Figure 1 shows the detailed process of accreditation as described hereafter. One of the most important steps in preparing for accreditation is to devise a documented portfolio comprised of the aims/goals, management system, and technical facilities of the laboratory seeking accreditation. This includes the presentation of the laboratory’s internal quality manual, which may already exist in one form or another, but which may need to be adapted to the exact needs of the process. The required documentation can usually be classified into three different levels. The most general level is the quality manual that describes, in general terms, the policies and goals of the work done by the laboratory seeking accreditation. It also describes the structure of the entity and its processes (in a general way) and the basic concepts of the (quality) management system. The second level includes guidelines and standard operating procedures (SOPs). These describe the exact processes used to achieve each task carried out at the laboratory and include information on organizational and technical know–how. Finally, the third level comprises detailed documentation, which may include checklists (or pro formas) to perform specific tasks and/or to maintain instruments as well as other specific documents. Then, the accrediting institution will assign a technical officer who will conduct a preassessment of the laboratory. During this preliminary visit, discussions take place to review the existing measures and procedures in place. These measures and procedures
are then evaluated as to their compliance with the requirements of the standard in question, such as ISO/IEC 17025 for a crime laboratory. Next, the laboratory will review its processes, documentation, and facilities in order to adapt to the standard and meet the accreditation requirements. The time required to carry out this step highly depends on what was already in place at the laboratory. If extensive adaptations must be incorporated, this step may be quite long and tedious. Depending on the accrediting body, an advisory visit may be necessary to address any noncompliances identified during the on-site visit. To obtain accreditation, a formal inspection or assessment of the laboratory by a team of inspectors or assessors must take place. The previously prepared documentation is reviewed in light of the specifications described in the standard. The laboratory is also visited, and the accreditation inspectors scrutinize the operations of the laboratory. All nonconformities are noted and the appropriate corrective actions are discussed. Depending on the accrediting body, there may be two levels of nonconformities [14]. Level 1 nonconformities have a significant impact on the quality of the laboratory product and must be resolved before accreditation is granted. Level 2 nonconformities have a minimal impact and must be corrected prior to the next yearly visit. Some accrediting bodies, such as NATA, require that all conditions identified during the assessment must be satisfactorily addressed before accreditation can be considered.
14
Accreditation: Organizational
Once obtained, accreditation must be maintained. To this effect, internal and external evaluation measures are put into place. Internal measures include the constant update of documentation on techniques, methods, and administration. External measures include annual surveillance visits, the submission of an annual accreditation report to the accrediting body, and results of proficiency tests. Depending on the accrediting body, a full reinspection of the laboratory may take place every five years [15]. NATA’s surveillance program is a little different and includes 18-month surveillance visits and 36-month reassessment visits, with no annual reports required (Parsell M. Personal communication).
Accreditation Applied to Criminalistics Criminalistics laboratories are not the usual testing and calibration laboratories (as covered by ISO/IEC 17025). Therefore, the propositions made in the international standards have to be interpreted according to the specificities of forensic sciences, in general, and criminalistics, in particular. As mentioned earlier, such a supplemental document is an interpretative document of 17025 and is called an application document. One such example is the International Laboratory Accreditation Cooperation (ILAC) Guidelines for forensic science laboratories (ILAC-G19:2002), which provides guidance for laboratories involved in forensic analysis and examination to comply with ISO/IEC 17025 [16] or the NATA supplementary requirements. These documents are structured in the same way as 17025. Its scope is illustrated by providing a specific list of activities that might be undertaken by a forensic laboratory, without being exhaustive. A succinct overview of the different techniques used is also provided. Reference is made to various relevant ISO/IEC guides. Some terms and definitions are also explained: objective test, reference collection, and court statement. Following this, the management requirements are specified. This includes not only the control of records (the aforementioned importance of documentation) but also the mention of negative results. The technical requirements include personnel (competency); accommodation and environmental conditions (e.g., contamination issues); test and calibration methods and method validation (how to carry out validation); equipment (maintenance and calibration); measurement traceability (documentation); sampling (also
depends on competency of staff); handling of test and calibration items (chain of custody and evidence management); assuring the quality of test and calibration results (quality control measures); and reporting the results (preparation of the report and court testimony). Although it is relatively straightforward to adopt ISO 17025 and its application (such as ILACG19:2002 or the NATA supplementary requirements) to fields such as toxicology, DNA analysis, or drug testing, it is much more challenging with disciplines such as handwriting, fingerprints, and other identification areas. One reason for this is the high similarity of activities between analytical forensic sections (DNA, drugs, toxicology, etc.) and regular analytical/pharmaceutical laboratories, since most processes can be described and handled in a standardized manner. Both fields are also largely numerical or quantitative in nature. Although extensive literature and practices exist describing the best way of handling exhibits for fingerprint enhancement, each incoming item has its particularities. Thus, the methodology cannot be applied in a completely standardized manner, although maintaining the integrity of the evidence does not change with the discipline involved – these procedures remain reasonably standard. This means that the description of the work done by the unit or laboratory is a more difficult task. A further consequence of the particular and sometimes random nature of forensic samples is that it might be possible that the technique or method needed is not very commonly used. In turn, this renders it difficult to create or maintain standards for them. Likewise, it might be that a certain technique is only used once a year, which will not be sufficient to demonstrate a regular use and guarantee a routine use by laboratory personnel. This specific issue is covered by ILAC-G19:2002 and the NATA supplementary requirements. The difficulty for the forensic community to adapt to external standards, such as 17025, is not only due to the “degree of subjectivity” of the techniques used but also due to the nature of the work performed, mainly because of the unique and varied character of each item of evidence. As the title of the ILAC application mentions, the guidelines are for forensic science laboratories. The question remains whether or not a crime scene unit falls under the definition of ISO/IEC 17025 (testing and calibrating laboratory). Until now the question has been raised
Accreditation: Organizational but no satisfactory answer has been found. In many countries, the tendency has been to accredit laboratories with ISO/IEC 17025 without considering the crime scene units. This is not true in some countries such as Australia where there has been considerable discussion on this issue and the mindset that “the laboratory” is four walls in a fixed building is seen as narrow and incorrect. As a result, in Australia, Crime Scene Laboratories are accredited to ISO 17025. In Switzerland, the question that has been asked is whether ISO 17020 (designed for inspecting bodies) would be appropriate for crime scene units [10]. Another way is to certify according to ISO 9001, which means that the managerial part, including the documentation, is covered, whereas the technical requirements are still not accredited, but will have to be covered by another form of quality control (internal or other entity than an accreditation body). Creating specific standards for crime scene accreditation remains a possibility [10]. Because of the existence of private or public laboratories and the differences of evidence admissibility in court, accreditation has not undergone the same development in different countries. At the same time, as previously mentioned, the development has also not been the same for the different stages of the criminalistic process. In Europe, the development is reflected by the guidelines established by ENFSI, which state that all their member laboratories [12] “should have achieved or should be taking steps toward ISO/IEC 17025 compliant accreditation for their laboratory testing activities”. According to a recent survey of ENFSI members, one-third of the laboratories are accredited, one-third plan to become accredited by 2009, and one-third do not have a definite timeline or have not undertaken any action yet [17]. Nevertheless, 94% of the laboratories have a quality assurance system in place or are developing one. Furthermore, accreditation as perceived by a laboratory may not agree with the general understanding of accreditation as granted by an international institution or an official national body. Thus, only 20% of the laboratories surveyed are actually accredited according to the above-mentioned international standard ISO/IEC 17025 [17]. In the United States, 294 laboratories are accredited through the ASCLD/LAB Legacy system and 26 through the ASCLD/LAB International system that corresponds to ISO/IEC 17025 [13]. Only 18 of these laboratories are private. In Australia, approximately 85%
15
of the government forensic science service providers (including crimes scene) are accredited to ISO 17025 and the majority of relevant private laboratories either have forensic science accreditation or are accredited with the “Forensic Module” or are moving in that direction (Davey A. Personal communication).
Advantages and Disadvantages Accreditation offers several advantages: transparency, traceability, and accountability. This profits both the provider of a service and its clients. The laboratory will gain a much clearer understanding of what work is done and how it is done. This information is documented so that it is much easier to transmit to new employees who undertake on-thejob training. The client can have a much better view on how his product or service has been performed. It may also be easier for the client to choose which provider has the best offer to meet his needs. Along with this, accreditation leads by its structure to a certain harmonization between laboratories, as the conditions to fulfill are the same and ISO/IEC 17025 gives a common backbone to all laboratories. By rendering comparisons between laboratories possible, the quality of each of them can more easily be evaluated. An expansion on an international market, rather than a national one, is facilitated, as well. Furthermore, international collaboration based on criminalistics may be simplified by the common approach [17]. Among the first disadvantages, most commonly named are the initial cost of implementing all the measures needed and the permanent cost of maintaining accreditation. Sometimes it is also perceived that the extra paperwork and administrative effort needed is disproportionate to the gain resulting in implementing all the measures. A certain loss of flexibility in applying nonvalidated testing or implementing new techniques or methods has also been advanced as a negative point, as each and every change has to be documented according to procedures and accepted for court purposes. The quality of work may also become limited, as a tendency may prevail to comply only with the standards imposed by regulations, instead of using previously higher internal standards. Accreditation can also be used to limit competition with other laboratories by fixing high standards so that not all (private) laboratories can follow them. However, some of these criticisms may disappear when
16
Accreditation: Organizational
it is understood that in reality accreditation sets the “minimum standard only” and not the top standard.
[2] [3]
Conclusion Accreditation, as part of a quality management system, is gaining more and more importance in criminalistics and has been fixed by professional bodies such as ENFSI as one of the goals to be achieved by their members. For criminalistics laboratories, the international standard that seems most appropriate is ISO/IEC 17025 for testing and calibrating laboratories. The specifications of how this standard can be applied to forensic/criminalistics laboratories are found in ILAC-G19:2002 and the NATA supplementary requirements. In the United States, most laboratories are still accredited according to ASCLD/LAB Legacy program. However, ASCLD/LAB also offers an ISO/IEC 17025 accreditation program, which will eventually replace the Legacy program. Future developments are turned toward discussions about how criminalistics/forensic units operating in the field (crime scene units) could comply with these international standards and become accredited. In this regard, the standard ISO/IEC 17020, designed for bodies performing inspections, is being considered by some people. However, one must be cautious about the fact that investigation and inspection are not synonymous.
[4]
[5]
[6]
[7] [8]
[9]
[10]
[11]
[12]
Acknowledgments
[13]
The authors would like to thank Dr Sarah D. Brown for her editorial review of this article. [14]
End Notes
[15]
a.
A more detailed description of the whole process as performed by ASCLD/LAB International is available at http://www.ascld-lab.org/international/ pdf/alpd3013.pdf, last visited 23 November 2007.
References [1]
European Network of Forensic Science Institutes (2007). Welcome to the ENFSI Portal , available at http://www. enfsi.eu.
[16]
[17]
American Society of Crime Laboratory Directors (2007). About ASCLD, available at http://www.ascld.org/about/. ENFSI (2005). Strategic plan 2005–2008–Vision of ENFSI, European Network of Forensic Science Institutes. Smith, F.P. & Kidwell, D.A. (2000). Accreditation of Forensic Science Laboratories, in Encyclopedia of Forensic Sciences, J.A. Siegel, P.J. Saukko & G.C. Knupfer, eds, Academic Press, London, England, pp. 58–64. Swiss Accreditation Service (2007). What is Accreditation? available at, http://www.seco.admin.ch/sas/00026/ index.html?lang=en:. ISO (2005). ISO/IEC 17025:2005 General Requirements for the Competence of Testing and Calibration Laboratories, International Organization for Standardization, Geneva, Switzerland. Stauffer, E., Dolan, J.A. & Newman, R. (2000). Fire Debris Analysis, Elsevier Academic Press, Burlington. ISO (1998). ISO/IEC 17020:1998 General Criteria for the Operation of Various Types of Bodies Performing Inspections, International Organization for Standardization, Geneva, Switzerland. ISO (2000). ISO 9001:2000 Quality Management Systems – Requirements, International Organization for Standardization, Geneva, Switzerland. Swiss Accreditation Service (2005). Guide for the Assessment in the Field of Forensic Evidence Recovery ISO/IEC 17020:1998, State Secretariat for Economic Affairs–Swiss Confederation, Bern, Switzerland. European Co-operation for Accreditation (2007). Standards for Accreditation, available at http://www.europeanaccreditation.org/content/news/cooperation.htm. ENFSI (2007). Standards for Accreditation, European Network of Forensic Science Institutes. American Society of Crime Laboratory Directors/ Laboratory Accreditation Board (2007). Laboratories accredited by ASCLD/LAB, available at http://www. ascld-lab.org/legacy/aslablegacylaboratories.html. ASCLD/LAB (2004). ASCLD/LAB-International Accreditation Program, American Society of Crime Laboratory Directors/Laboratory Accreditation Board, Garner. Caddy, B. & Cobb, P. (2004). Forensic Science, in Crime Scene to Court: The Essentials of Forensic Science, P. White, ed, Royal Society of Chemistry, Cambridge, United Kingdom, pp. 1–20. ILAC (2002). ILAC-G19:2002 Guidelines for Forensic Science Laboratories, International Laboratory Accreditation Cooperation, Rhodes, NSW, Australia. Malkoc, E. & Neuteboom, W. (2006). The Current Status of Forensic Science Laboratory Accreditation in Europe, Forensic Science International 167(2–3), 121–126.
BEATRICE SCHIFFER
AND
ERIC STAUFFER
Acid Phosphatase
Acid Phosphatase Prostatic acid phosphatase (PAP) is an enzyme secreted by the prostate gland and secreted in seminal fluid. Acid phosphatase (AP) is a generic term for a group of isoenzymes, of which PAP is one. AP is not unique to the prostate (although PAP is), being found in other biological fluids such as vaginal secretions. However, AP activity is 50–1000 times greater in human semen than in any other body fluid, and so the test is regarded as a presumptive test for the presence of semen. The only approach to differentiating semen from vaginal secretion is by quantitative analysis or the microscopic inspection for the presence of sperm. In many circumstances, a strong positive reaction for AP indicates that semen is present and that further testing is warranted (e.g., for DNA). There are a number of ways to test for AP. Most, especially those used to identify semen-stained areas, involve a color change. Clothing and swabs are probably the most frequently analyzed items. PAP is found in the vagina following intercourse. Its activity was found to correlate better with the time since intercourse than the presence or absence of sperm. According to Davies and Wilson, and using their test method, a reaction time of less than 30 s was regarded as a “very good indication” of the presence of semen as no vaginal AP reacted within this time. In a series of postmortem examinations using ELISA methods, a level of PAP greater than 100 ng ml−1 was considered positive for sexual intercourse. Importantly, a number of other materials can produce “false positive” reactions with AP (i.e., positive, but not semen). Examples include cauliflower, clover, bindweed, turnips, raisins, and ginger.
17
Moenssens, A.A., Henderson C.E. & Portwood, S.G. (2007). Scientific Evidence in Criminal Cases, 5th Edition, Thomson West, p. 997. Ricci, L.R. & Hoffman, S.A. (1982). Prostatic acid phosphatase and sperm in the post-coital vagina, Annals of Emergency Medicine 11, 530–534.
ALLAN JAMIESON
Action see Compulsion
Actuarial Risk Assessment see Risk Assessment: Patient and Detainee
Actus Reus see Automatism as a Defense to Crime
Acute Stress Disorder see Posttraumatic Stress Disorder
Further Reading
Adaptive Behavior see Mental Retardation
Collins, K.A. & Bennett, A.T. (2001). Persistence of spermatozoa and prostatic acid phosphatase in specimens from deceased individuals during varied postmortem intervals, The American Journal of Forensic Medicine and Pathology 22, 228–232. Davies, A. & Wilson, E. (1974). The persistence of seminal constituents in the human vagina, Forensic Science 3, 45–55.
Adaptive Functioning see Mental Retardation: Death Penalty
18
Addictions
Addictions Definition Addictive diseases are complex primary disease states caused by a combination of genetic, psychosocial, and environmental factors and generally resulting in both physical and behavioral manifestations [1] (see Substance Abuse). Their essential elements are often defined as continued use of a substance or similar maladaptive behavior, such as gambling, despite significant problems resulting from that use or behavior [2]. Extensive scientific research has explored the genetic underpinnings and the environmental contributors [3], the long-term physical findings generally resulting from substance use, and the behavioral differences observed in the addict [4]. For the purposes of this article, psychoactive substances are being used as a prototype addictive agent, but addictive disease also may pertain to other entities, gambling being one which has received diagnostic recognition [2]. Contributions to the literature have also explored other potential addictive agents, including sex, pornography, the Internet [5], videogame [6], and chocolate [7], though whether these represent medical disease states remains a controversial topic. From a physiologic perspective, addiction takes place when a psychoactive drug is taken for a sufficiently long period of time and in sufficient doses to result in either tolerance or withdrawal phenomena. Tolerance is represented by the need for an individual to take more of a given substance to achieve a given effect, or by the decrease in perceived effect over time when a substance is taken in an unchanging dose. Withdrawal is represented by the presence of measurable physiologic change upon cessation of drug intake. Physiologic addiction need not be present for addictive disease to exist. Similarly, the presence of physiologic addiction does not alone imply the presence of addictive disease. Many psychoactive drugs cause measurable tolerance and withdrawal phenomena after only one dose and within a short period of time. A hangover, for example, after a single night of alcohol use, represents a withdrawal state. There are also longer-term effects of even brief exposure; for example, rats fed alcohol for 4 weeks have abnormal responses 6 months later when reexposed
to alcohol [8]. The term addiction, as used by the general medical community, or dependence, as used by the psychiatric community, are rough equivalents that do not apply simply to physiologic addiction but to the well-characterized disease state involving use of substances that cause physiologic addiction. To wit, alcohol is an addictive drug. It causes physiologic addiction in all humans, and indeed in all mammals, who consume the drug. As a result, any individual who drinks alcohol may experience intoxication, and will experience tolerance and withdrawal to an extent consistent with the quantity and duration of alcohol use. Such experiences are neither indicative of the presence of addictive disease, nor are they necessary for such a diagnosis. Gambling is not a physiologically addictive drug, yet it has been accepted within the diagnostic rubric and leads to comparable behavioral consequences in some of those who participate in the activity. Substance use itself can be categorized into several groups, using any number of classification schemes. Terminology has been inconsistent, with substance misuse, abuse, overuse, harmful use, addiction, and dependence all holding different meanings depending upon the individuals using the terms. The fourth edition of The Diagnostic and Statistical Manual of Mental Disorders uses the terms abuse and dependence as referring to condition states with respect to addictive substances. The background as to how these terms were developed and why they differ from generally used terminology has been addressed in the literature [9]. There is agreement that substance use refers to any use of addictive substances, whether such use is by prescription or within constraints of legal codes, or if illegal and of such quantity as to lead to intoxication. Substance use, then, is a quantity-oriented term as it contains all those activities in which substances are used in any quantity other than zero. Addictive disease is not a quantity-oriented term; its presence involves some use during the illness, but neither the quantity nor the frequency of such use is germane to the diagnosis [1, 2]. Addiction within the psychiatric construct [2] can involve alcohol and other sedative agents, amphetamines, cannabis, cocaine, hallucinogens, inhalants, nicotine, opioids, phencyclidine, and steroids. Once an individual has been diagnosed with addictive disease, the diagnosis remains permanently, just as the disease does, so long as the diagnosis was
Addictions retrospectively accurate. Addictive substance use can end as a result of remission, recovery, agonist therapy such as methadone, or a controlled environment such as prison. Where pertinent, such qualifications are added to the diagnosis.
Disease Course Addictive illnesses are primary illnesses in that they are not symptoms of other disease states. It is natural that people try to determine causality as to why they have developed a disease, and many therefore choose to blame their addictive disease upon depression, anxiety, or specific life stressors. Addictive disease, however, has not been shown to arise as a symptom of any other illness. Addictive diseases are involuntary in that afflicted individuals did not choose to have their illness, but this does not imply that those with addictive illness are relieved of the responsibility necessary to recover from their illness [1]. The diseases, without intervention, are often progressive and fatal. Patients often focus their attention upon the addictive substance or behavior, have adverse consequences resulting from the addiction, and deny the relationship between their addictive focus and the negative consequences. In 1990, Block and Shedler published a key longitudinal study which revealed that addictive disease may be present, but for the use of drugs, at a very early stage of life [10]. Psychological differences between frequent drug users and others were noted as being traced to the earliest years of childhood and related to the quality of parenting received. The findings indicated that problem drug use is a symptom, not a cause, of personal and social maladjustment, and that the meaning of drug use can be understood only in the context of personality structure and developmental history. Disease course must therefore examine a complete individual history, not simply document the less important substance use history. More recent studies add the possibility that the problem drug use is not only a symptom of these environmental issues but of specific genetic abnormalities as well; no longitudinal study has yet been conducted, however, to confirm these theories. At some point, the individual with addictive disease will use an addictive substance for the first time. This is intuitively more likely to take place within
19
a society or subculture that encourages such use. Positive subjective experiences during the first use are more likely in those who have addiction [11]. This may be interpreted in one of two ways: either those with addictive illness are more likely to have the disease because they had a positive initial experience, or those with addictive disease have a physiologic abnormality that causes them to have a positive initial experience. Use of the substance increasingly takes on greater importance for the individual afflicted. Efforts at control may be instituted in which the addict attempts to limit his own use, but nevertheless as time passes, important social, occupational, or recreational activities become less important than the addictive behavior itself [2]. Whether through intervention or through selfawareness, addicts often pass through stages of change related to their ongoing behavior. Such stages include precontemplation, contemplation, and preparation, all of which precede any significant alteration of substance use, and are followed by action and maintenance [12, 13], both efforts to obtain and maintain abstinence. Discontinuation of the addictive behavior is a requirement during the action and maintenance phases. Stages may be, and often are, repeated, with relapses common after an initial attempt at abstinence. Cutting back, sometimes referred to as controlled use, is an ineffective treatment approach [14]. Continuation of any addictive behavior places the individual with addictive disease at risk; tobacco use, for example, not only increases the risks of morbidity and mortality due to smoking, but increases the risk of relapse of other substance use as well [15, 16]. Successful long-term recovery may accompany simultaneous long-term abstinence [17] during which no diagnostic signs of the illness remain.
Epidemiology With respect to illness, the term prevalence refers to the percentage of a given population with a given diagnosis at a specific cross-section in time. Widely varying prevalences of addictive disease have been reported, in part because of differing application of definitions. Whether an individual in recovery was counted as one with the diagnosis or not depended upon the study. Some studies separated alcoholism from other drug addictions, again resulting in a
20
Addictions
difficulty in determining even approximate figures. The Epidemiologic Catchment Area (ECA) study indicates a lifetime prevalence of alcohol disorders to be 23.8%, with a one-year prevalence of alcohol disorders to be 11.9% [18]. The National Comorbidity Survey (NCS) showed a lifetime prevalence of alcohol dependence to be 20.1% in men, with a one-year prevalence of 10.7% [19]. In women, the parallel figures were 8.2 and 3.7%. The differential between one-year and lifetime prevalence figures suggests that in these cases, the diagnosis was applied only to cases in which an individual is actively using substances. Clearly, though, these studies indicate how much more prevalent alcoholism is than other substance addiction; the ECA revealed an overall lifetime prevalence of drug abuse and dependence, not including alcohol, at 6.2%. Similarly, the NCS indicated a lifetime prevalence of drug dependence to be 9.2% among men and 5.9% among women. Incidence refers to the risk that any one member of the study population will become afflicted with the disease under study in a specified period of time. In the case of addictive disease, incidence can be difficult to determine, as subjects often have used substances for some time prior to their precisely meeting the definition of illness. Retrospective reviews are therefore problematic. The most dependable findings are those referring to that population at greatest risk: men between 18 and 29 years of age [18].
Treatment Addictive disease treatment is generally quite successful. The Federal Aviation Administration has demonstrated an 85% rate of success for alcoholic pilots attaining and maintaining recovery while being followed closely by physicians during a nine-year study period [20]. Military studies also indicate high rates of recovery over several years of treatment [21]. Similar research of healthcare professionals with substance use disorders has found similarly strong recovery rates [22]. Each of these studies involved ongoing treatment provided primarily by physicians. There have been many studies [23] indicating a far lower rate of success in which subjects generally have the same occupational or financial issues but in which patients are not provided with physician-provided medical care. No studies have
yet been performed to directly compare and contrast outcomes among health care professionals and other clinicians. Initial treatment focuses on the physiologic addiction to achieve a safe withdrawal from substance use. Cessation of the substance use is merely the first step in the treatment of addiction, however, and an ongoing maintenance plan is critical to a successful outcome [24]. Successful medical care generally involves a combination of therapeutic approaches, treatment of any physical and behavioral comorbidities, and the active involvement by the patient in 12-step recovery groups. Pharmacotherapy has proven useful for treatment of opioid [25] and nicotine [26] dependence. Disulfiram (Antabuse) remains the only medication demonstrated to have long-term value in the treatment of alcoholism [27]. Treatment is entirely ambulatory in many cases, but in more severe cases involves inpatient stays at various levels of care, including hospitalization, rehabilitation, partial day programs, and halfway houses.
Relapse Prevention Once patients with addictive disease have stopped their addictive behavior, they now begin to feel the discomfort representative of the disease state – the very discomfort that they gained relief from through the use of substances. Abstinence merely solves the physiologic addiction. Prevention of relapse can be obtained only by addressing the discomfort that is present for a sober addict. There are four common myths regarding relapse [28]: •
The relapse takes place because the patient wants to relapse: It is common for treatment professionals to accuse the patient of a moral lapse leading to relapse, as if the relapse is the desired state for the patient. The patient wants only to feel better. A relapse is the best possible alternative the patient can conceive of if the relapse has taken place. One role for the treating physician is to provide alternative options. Punitive policies such as those held by some programs that administratively discharge a patient following a relapse are inappropriate. Patients who relapse require more care, not less. •
The patient needs to hit bottom before recovery is possible: No empirical data exist to support this.
Addictions •
Relapse means the patient has begun using substances again: Relapse begins long before the patient starts using again. The path to relapse is progressive, with the actual use coming as the final step on the path. Self-help groups often refer to the term dry drunk as meaning that an individual is thinking in the same manner as one who is actively using. •
Once a relapse has taken place, complete loss of control will result: Relapses often consist of a brief episode of use after which the patient suddenly and quickly returns to sobriety. These relapses often follow a period in which the patient has dropped out of treatment or out of self-help groups. The patient then denies any further difficulties until the relapse takes place. Then the individual recognizes that indeed the disease has continued despite the past time of recovery; a return to therapy follows. Such a course is not at all atypical. An individual’s risk of relapse may fall within any of three groups [29]: • Recovery prone Forty percent of addicts attempting recovery fall into this group. Some attain sobriety with no clinical intervention and no attendance at self-help groups. Others seek such assistance and remain sober following this initial intervention. • Transitionally relapse prone Twenty percent of all patients periodically relapse, generally within treatment, but as time passes their relapse episodes become less severe, with shorter durations and greater time periods separating episodes. These patients often enter a long-term sobriety within 3–5 years. • Relapse prone This group of 40% are thought to develop progressive patterns of more severe episodes. Levels of functioning decrease during periods of abstinence. These patients often die of their illness within the first two decades of treatment. This group can be subdivided into those with motivation and those without. The group without is unlikely to present for ongoing treatment. The group with motivation will dutifully try, participating in treatment and self-help, but eventually failing to succeed.
21
Conclusion As with many other diseases, addictive illnesses have a wide spectrum of severities with an accompanying range of related morbidities. Quantity and frequency of substance use, however, are independent of severity [30] and are therefore neither predictive nor useful measures of disease course. Terminology has caused significant difficulties in the field. Alcoholism, the most common addictive disease, has long been a reference to an illness that involves use of any sedative agent that exhibits cross-tolerance with alcohol. Alcohol dependence, the syndrome originally defined in 1976 [31], has come to focus specifically upon alcohol use; other sedatives are included within the “Sedative Dependence” section of DSM-IV. As a result, studies of alcoholism and alcohol dependence differ substantively, resulting in findings for one group that may not apply to the other. There are also many studies involving heavy use of alcohol in which readers might presume incorrectly that findings apply to those with alcoholism. The literature must be analyzed closely and critically to determine whether findings in any one study or group of studies are applicable to any specific individual.
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Morse, R.M. & Flavin, D.K. (1992). The definition of alcoholism, JAMA 268, 1012–1014. American Psychiatric Association (2000). The Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision (DSM IV-R), American Psychiatric Association, Washington, DC. Sher, K.J., Grekin, E.R. & Williams, N.A. (2005). The development of alcohol use disorders, Annual Reviews of Clinical Psychology 1, 493–523. Oscar-Berman, M. & Marinkovic, K. (2007). Alcohol: effects on neurobehavioral functions and the brain, Neuropsychology Review 17(3), 239–257. Meerkerk, G.J., Van Den Eijnden, R.J. & Garretsen, H.F. (2006). Predicting compulsive Internet use: it’s all about sex!, Cyberpsychology and Behavior 9(1), 95–103. Gr¨usser, S.M., Thalemann, R. & Griffiths, M.D. (2007). Excessive computer game playing: evidence for addiction and aggression? Cyberpsychology and Behavior 10(2), 290–292. Bruinsma, K. & Taren, D.L. (1999). Chocolate: food or drug? Journal of the American Dietetic Association 99(10), 1249–1256. Gitlow, S.E., Bentkover, S.H., Dziedzic, S.W. & Khazan, N. (1973). Persistence of abnormal REM sleep
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Addictions response to ethanol as a result of previous ethanol ingestion, Psychopharmacologia 33, 135–140. Saundersa, John.B. & Linda, B. (2007). Cottlerc the development of the diagnostic and statistical manual of mental disorders version V substance use disorders section: establishing the research framework, Current Opinion in Psychiatry 20(3), 208–212. Shedler, J. & Block, J. (1990). Adolescent drug use and psychological health: A longitudinal inquiry, The American Psychologist 45(5), 612–630. Acosta, M.C., Eissenberg, T., Nichter, M., Nichter, M. & Balster, R.L. (2007). Characterizing early cigarette use episodes in novice smokers, Addictive Behaviors. DOI: 10.1016/j.addbeh.2007.09.005. Prochaska, J.O., Norcross, J.C. & DiClemente, C.C. (1994). Changing for Good: a Revolutionary Six-stage Program for Overcoming Bad Habits and Moving Your Life Positively Forward, William Morrow and Co, New York. Ramos, D. & Perkins, D.F. (2006). Goodness of fit assessment of an alcohol intervention program and the underlying theories of change, Journal of the American College Health 55(1), 57–64. Pendery, M.L., Maltzman, I.M. & West, L.J. (1982). Controlled drinking by alcoholics? New findings and a reevaluation of a major affirmative study, Science 217(4555), 169–175. Hser, Y.I., McCarthy, W.J. & Anglin, M.D. (1994). Tobacco use as a distal predictor of mortality among long-term narcotics addicts, Preventive Medicine 23(1), 61–69. Kelly, M., Chick, J., Gribble, R., Gleeson, M., Holton, M., Winstanley, J., McCaughan, G.W. & Haber, P.S. (2006). Predictors of relapse to harmful alcohol after orthotopic liver transplantation, Alcohol Alcohol 41(3), 278–283. Gitlow, S. (2007). Recovery and research: a better paradigm, Journal of Substance Abuse Treatment 33(3), 277–278. Helzer, J.E., Burnam, A. and McEvoy, L.T. (1991). Alcohol abuse and dependence, In Psychiatric Disorders in America: The ECA Study, L.N. Robins & D.A. Regier eds, The Free Press/MacMillan Inc, New York, 81–115. Kessler, R.C., McGonagle, K.A., Zhao, S., Nelson, C.B., Hughes, M., Eshleman, S., Wittchen, H.U. & Kendler, K.S. (1994). Lifetime and 12 month prevalence of DSMIIIR psychiatric disorders in the US, Archives of General Psychiatry 51, 8–19. Russell, J.C. and Davis A.W. (1985). Alcohol Rehabilitation of Airline Pilots. NTIS Technical Report ADA163076. Federal Aviation Administration, Office of Aviation Medicine, Washington, DC. Wright, C., Grodin, D.M. & Harig, P.T. (1990). Occupational outcome after military treatment for alcoholism, Journal of Occupational Medicine 32(1), 24–32. Domino, K.B., Hornbein, T.F., Polissar, N.L., Renner, G., Johnson, J., Alberti, S. & Hankes, L. (2005).
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Risk factors for relapse in health care professionals with substance use disorders, JAMA 293, 1453–1460. Anton, R.F., O’Malley, S.S., Ciraulo, D.A., Cisler, R.A., Couper, D., Donovan, D.M., Gastfriend, D.R., Hosking, J.D., Johnson, B.A., LoCastro, J.S., Longabaugh, R., Mason, B.J., Mattson, M.E., Miller, W.R., Pettinati, H.M., Randall, C.L., Swift, R., Weiss, R.D., Williams, L.D. & Zweben, A. (2006). Combined pharmacotherapies and behavioral interventions for alcohol dependence, JAMA 295, 2003–2017. Mackay, P.W. & Marlatt, G.A. (1990–1991). Maintaining sobriety: stopping is starting, The International Journal of the Addictions 25(9A-10A), 1257–1276. Collins, G.B. & McAllister, M.S. (2007). Buprenorphine maintenance: a new treatment for opioid dependence, Cleveland Clinic Journal of Medicine 74(7), 514–520. Glover, E.D. & Rath, J.M. (2007). Varenicline: progress in smoking cessation treatment, Expert Opinion on Pharmacotherapy 8(11), 1757–1767. Gitlow, S. & Gold, M.S. (2007). The inadequacies of the evidence, Addiction Professional 5, 17–25. Daley, D.C. (1987). Relapse prevention with substance abusers: clinical issues and myths, Social Work 32(2), 138–142. Gorski, T.T. (1986). Relapse prevention planning, a new recovery tool, Alcohol Health and Research World (Fall 1986) 6–11, 63. Gitlow, S.E. (1979). The disease of alcoholism, Cancer Research 39, 2836–2839. Edwards, G. & Gross, M.M. (1976). Alcohol dependence: provisional description of a clinical syndrome, BMJ 1, 1058–1061.
STUART GITLOW
Admissibility: Expert Opinion, USA see Expert Opinion: United States
Admissibility of Expert Opinion Evidence: a Comparison of Approaches see Expert Opinion in Court: a Comparison of Approaches
Adversary Systems of Justice
Admissibility of Expert Opinions Evidence: Civil Law Jurisdictions in France, Germany, Italy, and Spain see Expert Opinion in Court: Civil Law Jurisdictions (France, Germany, Italy, and Spain)
Admissibility of Expert Opinion Evidence in the UK, Canada, and Australia see Expert Opinion: United Kingdom, Canada, and Australia
Admissibility of Expert Opinion Evidence in the United States see Expert Opinion: United States
Admissions of Guilt see Confessions: Evidentiary Reliability of
Adults: Suggestibility of see Eyewitness: Suggestibility of
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Advance Directives see Therapeutic Jurisprudence
Adversary Systems of Justice Legal systems through the world may be classified as belonging in one of two philosophical camps: those that are called adversary systems of jurisprudence and those that are typically referred to as civil law systems (see Civil Law Systems of Justice). Adversary systems of jurisprudence, also referred to as common law systems, are in use in that part of the world where English-speaking rule exists or where the English legal system was the predominant jurisprudential system at one point in time. This includes the United Kingdom, the United States of America, Canada, Australia, New Zealand, and some other countries whose juridical systems were created at a time when the Anglo–Saxon tradition of the common law inspired their development. The adversary system is one that focuses on a factfinding trial, which is a contest between opposing sides in litigation. In this contest, each side seeks to convince the fact finder that their contentions have merit by offering supporting evidence. The fact finder in such a system is, alternatively, the presiding judge if it is a bench trial (nonjury trial), or a jury of the defendant’s peers if a jury trial is permitted under local or constitutional law. In a jury trial, the judge’s role is to preside over the trial, rule on matters of law and on objections interposed by counsel for the litigants, and instruct the jurors on the legal principles they should apply to the facts that they have determined, from the evidence presented, to have occurred. Though there exist many variants in the rules of various jurisdictions, presentation of proof in adversary or common law system countries is subject to an often complex system of rules of evidence. These rules are designed to limit the types of proof that courts will admit. The rules of evidence are designed to assure that the fact finder will base the
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Aggression
outcome of the litigation on mostly appropriately reliable evidence. They also exclude, at times, reliable evidence that, for policy reasons, courts or legislatures have determined to be worthy of special protection and are therefore shielded from disclosure. This would include privileged communications between well-defined classes of individuals, such as communications between doctors, lawyers, clergy, spouses, and parties to civil litigation or defendants in criminal prosecutions.
Age Determination of Documents see Dating: Document
Age Determination of Skeletal Remains see Anthropology: Age Determination of Remains
Related Articles Chain of Possession of Tangible Evidence Civil Law Systems of Justice Expert Opinion in Court: a Comparison of Approaches Hearsay Evidence
Age Determination of the Living see Anthropology: Aging the Living
In Limine Motions and Hearings ANDRE MOENSSENS
Aggression Affirmative Defense see Automatism as a Defense to Crime
AFIS Storage and Retrieval of Fingerprints see Automated Fingerprint Identification System
Age Determination see Anthropology: Age Determination of Remains, Anthropology: Aging the Living
Introduction and Definitions The extreme form of power is All against One, the extreme form of violence is One against All [1], p. 42. The preeminence of aggressiveness in our civilization would already be sufficiently demonstrated by the fact that it is usually confused in everyday morality with the virtue of strength [2], p. 98.
In ordinary language, the concepts of aggression and violence have taken on broad, often metaphorical, meanings. Diseases may be treated aggressively by physicians. A storm may be violent. An aggressive attitude is necessary in training for competitive sports. These common usages suggest the need to define aggression and violence precisely in the setting of legal proceedings and the scientific study of behavior in its social context. Aggression refers to a state of destructive intent, with or without harm. It has been studied in insects and animals [3], with an emphasis on biological and evolutionary factors in behavior [4, 5]. Research on human aggression, in contrast, takes into account the
Aggression additional specificity of social and cultural processes. The impact of civilization on instinctual drives may largely override biological determinants, making human aggression a phenomenon qualitatively distinct from aggression in animals. In its mildest forms, such as irritation or brief moments of anger, human aggression remains within the range of universal, normative experience. According to Bronfenbrenner and Ricciutti, aggression includes “any action, thought or impulse the presumed aim of which is physical or psychological injury either real or symbolic to an individual or his surrogate” (1960, cited in [6]). In this definition, aggression thus reflects an internal state that manifests in a wide spectrum of behaviors. It is characterized by harmful intent, with destructive feelings toward others as well as objects. Aggression may include “[i]nsults and spreading harmful rumors” [7], p. S7. Anger, fear, and irritation are emotional states often associated with aggression, but are not synonymous with it. Frustration may result in anger that does not involve destructive intent of any kind, and may be resolved through verbal expression. As Rothenberg stated in 1971, “Violence and revenge are destructive direct discharges, but they are not expressions of anger per se; they are in part expressions of failed or unattempted communication” [8]. Violence involves physical injury or imminent threat of physical injury to another human being. The Centers for Disease Control (CDC) in the United States conceptualizes violence under the larger public health problem of physical injury, differentiating unintentional injury (accidents) from intentional injury toward self and others [9]. The World Health Organization (WHO) defines violence broadly as “The intentional use of physical force or power, threatened or actual, against oneself, another person, or against a group or community, that either results in or has a high likelihood of resulting in injury, death, psychological harm, maldevelopment or deprivation” [10], p. 5. Although this definition includes violence to oneself and collective violence, researchers have operationalized violence more narrowly as intentional interpersonal acts resulting in injury of another, in order to focus the object of empirical study. The categorization used by the WHO divides interpersonal violence into family and intimate partner violence on the one hand and community violence (between unrelated persons) on the other hand [10], p. 6. The authors of the MacArthur Study of Mental Disorder and Violence defined two types of violent
25
incidents as outcome variables: violence and other aggressive acts, distinguishing violence as “the infliction of injury or the threat of considerable, credible harm” [11], p. 18. The authors of the Historical Clinical Risk-20 (HCR-20), one of the most extensively validated rating instruments for structured clinical judgment of violence risk, define violence as actual or attempted harm to a person, or a threat of harm that is unambiguous [12], p. 24. Acts that would induce fear in most people but that do not actually result in injury, such as nonconsensual attempted physical sexual contact or stalking (see Stalking), are included in this definition. A general guideline according to the HCR-20 is to include as violence any behavior that would be “serious enough to result in criminal or civil sanctions” [12], p. 25 and to exclude from the definition those acts that would not. Verbal insults without overt threat of harm, destruction of property, and harm to animals without intended harm to persons, appropriate self-defense, and sporting injuries are excluded from their definition [12], pp. 25–26. From a historical and sociological perspective, violence broadly encompasses phenomena such as war, genocide, and revolution. Writing from the point of view of a psychiatrist with extensive experience in the correctional system, Gilligan elaborates on the idea that violence serves either to “achieve and maintain justice, or to undo or prevent injustice” [13], p. 12, and that acts of violence can be construed as a reaction to injustice, either real or perceived [13], pp. 18–19. In his formulation of violence as a medical and public health problem, he goes on to extend its definition beyond interpersonal violence to include accidents, which do not involve the specific intent to harm. This latter definition of violence stems from a conceptualization of structural violence as a form of harm that is built into a social system, and for which there is collective responsibility [14]. In this sense, socioeconomic disadvantages such as poverty and large-scale prejudice such as racism are manifestations of structural violence contributing to direct violence, in the sense of preventable deaths [13], p. 192+. The associated problems of war, genocide and torture may become relevant to legal proceedings in international courts of law or in immigration proceedings and merit further discussion, which is beyond the scope of this article. In addition to structural and direct forms of violence, Galtung defined a third major type in 1990, cultural violence, which refers to a system of values that
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Aggression
reinforces or legitimizes both structural and direct violence. In his causal model, structural, cultural, or direct violence can each generate either of the other two types of violence [14]. Although the conceptualization of structural violence is valuable in emphasizing that, with regards to public health outcomes, many events resulting in physical injury are not the result of direct action by individuals with intent to harm others, the empirical study of violence requires differentiation of the phenomena in order to examine them in a meaningful manner. As noted above, for the purposes of research, interpersonal violence is generally distinguished from collective and self-inflicted violence. Different methodologies have been necessary, with reference to the specificities of each type of violence, particularly with attention to the role of human agency and the intent to cause direct harm to another person. This heuristic approach, differentiating multiple types of violence in order to study them separately, has created problems for the generalizability of findings. Even within the restricted field of interpersonal violence, studies have been organized according to the characteristics of specific kinds of violence, resulting in groupings that provide useful information regarding each subtype of violence but which are lacking in the consistency needed for a general or unified theory. An unresolved question is whether interpersonal violence indeed constitutes a coherent whole or whether the word “violence” is used to describe disparate phenomena that have distinct causation and risk, even if the outcome, physical injury, is the same [15]. Recent attempts at synthesis suggest that child abuse, adolescent violence, and domestic violence share common risk factors and that the phenomena are interrelated [16]. Studies of assaultive behavior have proceeded by distinguishing different classes of victims in order to constitute the phenomenon to be characterized, such as child abuse [17], intimate partner abuse [18, 19], violence toward strangers [20], violence among gang members [21], abuse of the elderly [22], victimization of the mentally ill [23–28], targeted violence toward persons in positions of authority (police or politicians [29]), and sexual offenses, where the victims are children [30, 31], adult women [32, 33], or adult men in the context of prison [34, 35]. Another approach has involved the study of violence according to the location where it occurs, for example, at home [36] (domestic or intimate partner violence), at school
[37, 38], in prison [39, 40], in the psychiatric hospital on an inpatient unit [41, 42], or in the workplace [19, 43–45]. Other studies have focused on the identity of the perpetrator by studying violence committed by specialized populations: severely mentally ill patients [11, 46–49], individuals not mentally ill but who meet criteria for psychopathy (see Psychopathy), women (see Aggression: Gender Differences in), children [50], adolescents [51–53], individuals with organic brain disease [54, 55] or low IQ [56, 57], military veterans [58], and substance abusers [59–61]. In addition to the above, features that distinguish types of interpersonal violence include characteristics of the act itself. Violent acts have been distinguished according to whether they are impulsive (driven by an immediate emotional reaction) versus premeditated (planned through thinking in advance) [62, 63]. Studies have also focused on the magnitude and frequency of violent behavior, distinguishing between offenders who engage in acts of serious violence (e.g., characteristics of homicide offenders [64, 65]) and those who repeatedly commit low-magnitude assaults. Homicide refers to the most extreme and irreversible consequence of violence: the loss of life as a result of physical injury by another (see [66]). Although some studies have characterized differences between spousal homicide offenders and perpetrators of lower-magnitude domestic violence [67], the extent to which homicide should be considered a phenomenon fundamentally distinct from assault remains unclear at this time. Further research is needed to determine the frequency with which homicides are the unintended consequence of assaultive behavior.
Behavioral Manifestations Aggression can be viewed in terms of gradations of severity, ranging from the inner state of irritation, hostility, or anger, to physical injury of another person, to death, and can be examined through outward manifestations in behavior. In its mildest forms, aggression may be expressed through passiveaggressive behavior (avoidance, subtly hostile comments, and neglectful behavior that interferes with task completion), which is rarely the basis for legal proceedings, unless poor work performance has led to a fitness for duty evaluation. An individual who is experiencing aggressive feelings may be aware of
Aggression violent fantasies or intense hatred, or he may not have conscious awareness of hostility at all, expressing these feelings instead through maladaptive forgetting of important meetings, complaining, procrastination, or other indirect means.
Escalation Overt behavior indicative of escalating aggression includes verbal expression of anger, which may involve threats that are stated in either explicit or implicit form (veiled threats). Physical gestures, such as finger pointing, shouting, pacing, or intrusiveness are relevant indicators of increasing aggression and hostile intent, along with confusion and irritability [41]. Other behavioral manifestations of escalation include obtaining a weapon, handling or moving a weapon [68], and aggressive gestures toward objects, such as pounding a fist on the table or the destruction of property [41]. Preparatory behaviors indicative of aggressive intent for sexual crimes may not appear overtly hostile, since these crimes are often organized by the perpetrator in a surreptitious fashion, involving seduction and “grooming” of the victim, or secretive observation of the victim’s daily patterns of movement. Acts of violence may also be sudden, impulsive, and without premonitory signs that the individual is moving towards action with harmful intent.
The Act Gilligan [13] and Junginger [69] each argue that analysis of the specific characteristics of the act may reveal a dimension of violence as “symbolic language” that serves as a form of communication. In addition, some acts of violence may serve as an escape from meaning or a failure in symbolization that later on, afterwards, leads others to interpret the act, even though at the time, it was an act that was “senseless” or beyond any intent to communicate a message (see [70, 71]). As previously noted, acts of violence can be analyzed according to whether they are predominantly impulsive (driven by an immediate emotional reaction) or premeditated (involving a purpose known in advance). Many instances of violence may remain unknown to public authorities, particularly in the context of domestic disputes.
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Responses to the Act After the immediate management of the aftermath of violent behavior, which includes medical stabilization of vital functions and treatment of injuries, a variety of reactions can be anticipated concerning each of the involved parties. The perpetrator of violence may or may not experience extreme distress at his own act. If the victim was a loved one who has suffered serious injury or death, or in the context of apprehension by law enforcement, the perpetrator may experience an elevated risk of suicide in the time following the act (see Suicide (Behavior)). The perpetrator may also have memory loss for the act itself [72], either due to failure to register the memory [73], in the context of an altered state of consciousness during and after the act (“red out”) [73, 74], or he may claim amnesia due to malingering (see Malingering: Forensic Evaluations). Perpetrators of violence may experience flashbacks and other symptoms of posttraumatic stress [75]. The presence of posttraumatic stress disorder symptoms (see Posttraumatic Stress Disorder) in perpetrators of serious violence is increasingly recognized among psychiatrists and may be the focus of treatment [76]. Posttraumatic stress disorder has been more extensively recognized in the victims of violence. Ongoing, repeated victimization may result in chronic syndromes described in legal proceedings as battered spouse syndrome (see Battered Spouse Syndrome) or sexual abuse accommodation syndrome (see Child Sexual Abuse Accommodation). Mental health professionals should be alert to the possibility that participation in legal proceedings may itself induce distress in the victim, beyond that arising from the act of violence. Bystanders or others who were not actually present at the time of the violent act may also experience emotional distress in relation to the act.
Sequelae In cases that are prosecuted, one major consequence is punishment of the offender, who may serve time in prison, in jail, or be constrained by home arrest or electronic monitoring. Whether or not the offender is prosecuted, victims and close relations of the victim or the perpetrator may experience anticipatory fear of future violence. The violent incident may have a profound impact on the relationships between the victim and perpetrator and with other family
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Aggression
members, resulting in social isolation. On the other hand, in some communities, participation in an act of violence may be valorized by the group, such as in rites of initiation in gangs or organized crime. In these contexts, violence may serve the symbolic purpose of establishing the perpetrator’s social identity and his or her claim on valued relationships or property. For the victim, enduring physical disability may cause significant impairment and serve as a constant reminder of past trauma.
Sources of Information on Prevalence The most comprehensive prevalence data regarding violent behavior is collected by governmental agencies, though each of these has limitations and they use different definitions of violence. The subjective experience of aggression, hostility, and anger is nearly universal, however, and its prevalence is therefore difficult, if not impossible, to measure. At the international level, the most comprehensive study to date was released by the WHO in 2002 [10]. Although this report demonstrated that the United States has a much higher level of homicide and physical assault when compared with other developed countries, the homicide rate in the United States is substantially lower than in underdeveloped regions, even when deaths due to war are excluded [77]. The CDC in the United States conducted a survey in 1996, the National Violence Against Women Survey, in collaboration with the National Institutes of Justice and the National Center for Injury Prevention and Control, in which 8000 women and 8005 men were interviewed with regards to their fear of and experience of violence [78]. The CDC is currently piloting a new study, the National Intimate Partner and Sexual Violence Survey, to provide national and state estimates of the incidence and prevalence of all forms of intimate partner abuse, sexual violence of all types, and stalking [79]. In addition, the CDC maintains continuous collection of data from 17 states in its National Violent Death Reporting System, which began in 2002 with the aim of combining data from multiple sources in order to provide a comprehensive and detailed picture of the circumstances in which a violent death has occurred, and the relationship of the perpetrator and victim [80]. The Federal Bureau of Investigation (FBI) has maintained crime statistics on homicide, forcible
rape, robbery, and aggravated assault since the introduction of its Uniform Crime Report program in 1929 [81]. From these data, the FBI generates a yearly report called Crime in the United States, compiled from data from over 94% of US jurisdictions, based on monthly reports from state agencies. The US Bureau of Justice Statistics analyses the FBI data and issues yearly and multi-year reports regarding violent crime [82]. Although most homicides and attempted murders do come to the attention of the legal system, crime statistics based on prosecution and convictions are biased in that numerous acts of lower-magnitude violence are reported neither to the criminal justice system nor to medical facilities. The National Crime Victimization Survey (NCVS) is an ongoing data collection project that addresses this bias in law enforcement statistics [83]. Begun in 1973, it underwent a methodological revision that was completed in 1993 in order to improve the wording of questions particularly regarding sexual assault. In its current form, the NCVS collects data on a yearly basis in interviews of a nationally representative sample of approximately 77 200 households, including approximately 134 000 individuals [84]. Many other countries maintain similar databases. Comprehensive statistics regarding mental illness in the perpetrators and victims of violent crime are more difficult for government sources to obtain in a systematic manner. Prevalence information can also be found in articles referenced above under different categories of victims and offenders, though care should be taken to critically examine differences in the sampling methods and definitions of violence.
Causes What a potent obstacle to civilization aggressiveness must be, if the defence against it can cause as much unhappiness as aggressiveness itself! [85] p. 143.
Human aggression and its behavioral expression as violence comprise a complex interweaving of biological, individual, interpersonal, and social or environmental factors, which cannot easily be summarized here (see [86]). The person who engages in an act of violence may have some awareness of aggressive thoughts and feelings, but the determinants of a decision to take violent action, rather than to use other
Aggression strategies for handling aggression, are challenging to identify with precision. Elias describes a societal process of decreased acceptability of aggressiveness and identifies the end of the Middle Ages as a time when new mores and social practices resulted in the “repression” of aggressive behavior through education and internalized values [87]. The incursion of this “civilizing process” on biological drives was the source, according to Freud, of many modern neurotic symptoms [85]. Scientific and policy debate in the 1960s and 1970s led scientists to issue the Seville statement [88], which counters the claim that violence is biologically inherent in the human organism. The empirical study of causation of violence is methodologically complex. Relevant variables associated with violence are numerous and interact with one another [89]. Furthermore, the association of variables with an outcome of violence in a study population does not clearly lead to explanatory power in individual cases: the presence of known risk factors does not prove, in a causal manner, that these risk factors led up to a specific act of violence. Violence is commonly thought of in association with men, though gender differences in aggression have been overestimated and misunderstood (see Aggression: Gender Differences in). Although all age groups are affected by violent victimization and offending, individuals between the ages of 20 and 24 have the highest rates of homicide victimization and offending [66]. The impact of exposure to forced institutional settings, such as present or past imprisonment, is not directly assessed in currently available rating instruments. The biological study of aggression at a molecular level in animals and humans has improved knowledge regarding neurotransmitter systems and the genetic contribution to aggressive behavior [90], though the integration and application of this knowledge to treatment in humans is in a rudimentary but promising state at this time [91, 92]. Risk factors are commonly categorized as static (related to historical elements of the life story that are unlikely to change) and dynamic (modifiable) factors. The HCR-20 [12] includes items such as substance use and major mental illness, which may be assessed according to both static and dynamic components. The use of biographical information and the clinical interview to identify static and dynamic risk factors is an approach that may be called subjective in the
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sense that the risk assessment integrates objectively verifiable data and the individual’s own report of his reaction to the environment in a manner that is specific to the person being evaluated. Subjectivity, however, in regards to the individual’s emotional experience of and attribution of meaning to his past or current life events and situations is not generally measured within validated assessment instruments, even though it is taken into account in the clinical risk assessment interview and plays a significant role in treatment. A recent emphasis on dynamic risk rather than on risk status (based on unchanging past features of the person’s history) has led to the conceptualization and study of risk state as a time-dependent convergence of transient and modifiable risk factors [89]. In their 2005 review, Douglas and Skeem called for theory development and recommended that a theoretical model of the individual’s risk state over time include a model of “relational complexities” of risk factors leading up to violent acts. They also recommended that theory development include an account of strategies for reducing violence in persons at elevated risk [89], pp. 367–368. The formulation of an explanatory theory would require the integration of known risk factors into a model of their interrelation, which may vary widely from individual to individual. Case-specific risk factors and configurations of risk based on the person’s life history are currently not discernible in statistical models using actuarial methods, as these elements emerge only through detailed study of particular cases and may not rise to a level of generalizable patterns within large populations. Qualitative methods have been useful in addressing this gap, by identifying variables of potential relevance to the person’s internal reasoning [93, 94]. Studies outside the field of risk assessment per se point to additional factors that may lead to more accurate prediction as well as to a general theory of causation. Barratt and Slaughter [63] propose a “discipline neutral” model which integrates cognitive, biological, behavioral, and “environmental (physical and social)” concepts of the person. This conception includes the idea that the person is defined in part by his social relations, and a sense of belonging or not belonging to a group. One study has indicated that, under experimental conditions, social rejection or exclusion results in decreased “prosocial” behavior, defined as behavior that privileges
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Aggression
collective values over immediate self-interest [95]. Reminders of “connectedness” or social ties may restore prosocial tendencies and reduce aggressiveness after experimentally induced social exclusion [96]. From several different theoretical perspectives, dehumanization has been studied in relation to violence. In particular, the finding that animal cruelty in childhood may be a predictor of future violence [97], especially when motivated by amusement [98], suggests that treating animals as objects of destruction is an index of the person’s reduced ability to imagine human qualities in other living beings. Bestiality (sexual assault of animals) may represent an inability to socially relate to human beings and a means of obtaining sexual gratification through aggression, coercion, and manipulation of animals as objects [99]. A lack of empathy or reduced capacity to appreciate the mind of another human being [100] suggests a willingness to harm without appreciating the consequences for others. These latter traits are characteristic of individuals with psychopathy (see Psychopathy), which has been strongly associated with an increased risk for violence. Desensitization to and minimization of aggressive behavior, either due to environmental exposure to violence [101] or due to exposure to cultural representations, may be a developmental and dynamic risk factor. Violence in the media includes visual representations of aggression in video games and fictional works as well as in the news and may have an impact analogous to “an environment filled with real violence” [7]. Controversy exists regarding the correlation of violent video games or representations in the media with acts of serious violence [102]. Some studies suggest that there is a process of identification with violent perpetrators when individuals view these scenarios [103]. Although there is solid evidence that viewing violent media produces shortterm increases in aggressive behavior (verbal and physical) in children, adolescents, and young adults [7, 104–106], the long-term effects of violent media are difficult to demonstrate, due to intervening factors in the individual’s life story and environment [102, 106]. On the basis of extensive clinical observation, Gilligan theorizes that interpersonal violence is largely driven by feelings of shame or of being disrespected and he brings known risk factors to converge
upon this common final pathway. He writes, “. . . it is not poverty, racism, sexism, or age-discrimination, as such, that cause violence. It is, rather, that each correlates with violence because each increases the statistical probability that individuals exposed to these social forces will be subjected to intolerable and potentially self-destroying intensities of shame, from which they do not perceive themselves as having any means of rescuing themselves except by violence . . .” [107], p. 66. A relationship between pathologies of narcissism (threatened egotism) to violence has begun to be studied empirically. Whereas previous authors had posited that low self-esteem was correlated with violence, Baumeister et al. [108] reanalyzed the literature in light of the alternative explanatory hypothesis that self-protective behavior in the face of perceived threat is guided by elevated self-esteem. In a subsequent study, Bushman and Baumeister found that the construct of egotism could be differentiated into stable self-esteem and narcissism, the latter condition being unstable and particularly hostile in response to perceived threat [109]. Perceived threat to egotism has also been associated with aggression in psychopathic individuals [110]. Implicit in this theorization of the stimulus for and mechanism of violent action is that past life events, through their effects on the individual’s inner experience, set the stage for interpretation of present experiences, particularly of perceived threat to the individual’s sense of self. Lacan wrote in 1948 that there may be a “persistence in the subject of the shadow of ‘bad internal objects,’ related to some accidental ‘association’ . . . [R]e-evoking certain imaginary personae and reproducing certain situational inferiorities may disconcert the adult’s voluntary functions in the most rigorously predictable way – namely, by their fragmenting impact on the imago involved in the earliest identification” [2], p. 94. Although Lacan’s focus is on persons who remind the perpetrator of past experiences of structural inferiority during infancy, the internal mental mechanism he describes is in principle relevant to past situations, such as the recollection of environments where potential violence was the norm. In this regards, given that perpetrators may be sentenced to prison, it is possible that, beyond learned behavior, exposure to incarceration may contribute, by these means, to an increased future risk for violence.
Aggression
Assessment and Treatment In clinical settings as well as in sentencing or postsentence release hearings, assessment of risk for violence (see e.g., Dangerousness: Risk of) is an essential step in individualized treatment planning (see also Psychopathy; Psychopathy Checklists; Addictions; Substance Abuse and [111]). When violence risk assessment is specifically requested by the court, the examiner often performs both a clinical interview and a standardized assessment using a validated rating scale, since these approaches are complementary. Assessment of risk is an appreciation of likelihood and does not rise to the level of accuracy for prediction per se. It allows clinicians and decision makers in the judicial system to determine what interventions are needed to reduce an individual’s risk for future violence, on a case-by-case basis [112], whether that risk arises from psychiatric or criminological factors (see e.g., Insanity: Defense; Therapeutic Jurisprudence).
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the effective basis for treatment at individual and organizational levels. Institutional and community responses [114], including public information campaigns, have resulted in a decrease in the rate of domestic violence, due to increased reporting and help seeking [115]. One study indicates that employers’ awareness of intimate partner violence and the availability of support in the workplace are predictors of a victim’s continued employment [43]. Although institutional responses such as mandatory arrest may also have a deterrent effect by indicating to the public that violence is not acceptable, prosecution and intervention programs have not consistently demonstrated a reduction in recidivism of offenders [36]. Data collection and the compilation of accurate statistics using combined emergency room and local police sources allow for improved surveillance and planning for prevention strategies [116]. Further study of risk factors and protective factors that serve as a basis for effective prevention programs in widely different but overlapping types of violence may provide indices for a common theorization of aggressive behavior [101].
Prevention Conclusions Power and violence are opposites; where the one rules absolutely, the other is absent. Violence appears where power is in jeopardy, but left to its own course it ends in power’s disappearance . . . Violence can destroy power; it is utterly incapable of creating it [1], p. 56.
Viewed from a public health perspective, prevention may be primary (general measures to prevent the condition from developing), secondary (efforts focused on individuals who are at elevated risk of developing the condition), or tertiary (measures introduced to prevent recurrence in individuals known to have the condition) [107], pp. 20–22+. In the setting of legal proceedings, the latter two types of prevention are of greatest relevance. In 1969, Ilfeld categorized the prevention of violence into treatments of three main types focusing either on the individual or the environment: (i) redirection of aggression through alternate means of expression; (ii) modification of social learning; and (iii) modification of sources of frustration, such as socioeconomic factors [113]. Significant advances have been made in the past decades in understanding
Aggression and its behavioral manifestations encompass a wide range of phenomena that cannot at this time be meaningfully studied as a whole. Reductionist approaches have been useful in defining different types of violence in specialized populations of victims, offenders, and locations. At the present time, a unified theory of causation of violent acts is lacking, even when the field of study is limited to interpersonal violence, at the exclusion of war, torture, genocide, poverty, racism, and other forms of collective or structural violence. In principle, the widely varied forms of violence have in common a choice in favor of destruction, whether this destruction is directly intended or intrinsic to the structure of social institutions. The violent individual’s subjective point of view as a factor in his choice of behavior remains a relevant topic to explore from a clinical or ethnographic perspective, and has implications for a theory of causation. Although the risk for future violence appears to be strongly associated with environmental factors and static features of the individual’s past life experience that are not susceptible to change, the issue of the person’s capacity to choose how to express aggressive
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feelings and his willingness to change past patterns is an important element to consider in future studies of the possible treatment and prevention of violent behavior.
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SUZANNE YANG
Aggression: Gender Differences in Female aggression traditionally has received little attention in the research literature and has been regarded with a certain degree of skepticism by the public and professionals alike. In the past three decades, however, the precipitants and purpose of female aggression and the profiles of girls and women who commit aggressive, violent, and criminal acts have increasingly attracted the attention of researchers, criminal justice, mental health professionals, advocates, and policy makers. The field is beginning to flourish with a small number of longitudinal and large-scale examinations of sex differences and similarities in antisocial behavior and aggression [1–5]. In addition, the importance of examining female aggression separately from male aggression and using that data to inform policies and practice is increasing, and now appears to be well-recognized in developed nations worldwide [6]. This relatively abrupt turnaround reflects increasing numbers of girls and women being charged, arrested, and incarcerated for violent crimes. In addition, research demonstrates that in certain contexts (e.g., romantic relationships and parent–child relationships) and in highly specific populations and settings (e.g., inpatient psychiatric patients) the gender gap in the perpetration of aggressive actions is largely reduced or entirely absent. These circumstances require scholars and practitioners to evaluate the extent to which our understanding of female aggression reflects substantiated research findings versus unsubstantiated generalizations and stereotypes. This article operationalizes aggression and violence (see also Aggression) and reports the prevalence and incidence of aggression among females; documents sex differences and similarities in
aggressive and violent behavior; critically examines the assertion that risk and protective factors are sex-specific, briefly explores clinical implications for prevention and intervention, and closes with reflections on gaps in knowledge and directions for future research.
Prevalence and Incidence of Aggression among Females There is virtually universal agreement that males are more aggressive than females. Across age categories, regardless of the data source (i.e., self-report, family/collateral reports, official records, and victimization surveys), males outnumber females in the perpetration of physical and sexual aggression, violence, and crime. However, methodological advances (e.g., data collection strategies and sources) to studying aggression and more inclusive definitions of aggression have revealed comparable rates across the two genders for some types of aggression and/or in discrete settings and populations. Given the importance of developmental milestones in understanding human behavior, in terms of diagnostic categories (e.g., diagnostic and statistical manual of mental disorders (DSM-IV)-TR, [7]) and with regard to prevention and intervention in the criminal justice system, we present the prevalence and incidence of aggression among females separately for female youth and adult women.
Operationalizing Aggression Although there remains little agreement in the literature regarding how best to operationalize aggressive and violent actions, increasing clarity has been achieved as a result of important studies such as the MacArthur violence risk assessment study [4]. Building on prior definitions [8] and psychometrically advanced measures (Conflict Tactics Scale, [9]), the MacArthur study operationalized “physical aggression” as laying one’s hands on another with the intention to cause physical harm. In contrast, “violence” was defined as actions that result in injury, sexual assaults, or verbal threats of physical aggression with a weapon in hand [4]. “Relational aggression” refers to interpersonal interactions and verbal exchanges intended to harm others through social exclusion and public humiliation [10]. Finally, “verbal aggression” includes threats, ridiculing, name-calling, and
Aggression: Gender Differences in shouting. Although imperfect, with these definitions in mind, we can explore the question: how common is female aggression?
Female Youth Boys perpetrate approximately three times as many violent acts as girls. Girls are also less likely to report carrying a weapon and tend to engage in violent acts at a lower frequency than their male counterparts [3, 11, 12]. Nonetheless, multiple sources of data consistently show increased rates of violence among girls. In the United States, between 1988 and 1998, personrelated offenses increased at more than twice the rate among adolescent females (157%) than among adolescent males (71%; [13]) and between 1993 and 2002, arrests for aggravated assault decreased 29% for boys but increased 7% for girls. Canadian statistics show comparable trends: between 1988 and 1998, the violent crime rate more than doubled for girls (+127%) compared to a smaller increase for boys (+65%; [14]). Furthermore, between 1996 and 2002, when a small decrease was noted in the rate of violent crime committed by boys, a modest increase was observed for girls [15]. Outside North America, the picture is much the same: in the United Kingdom, between 1981 and 1999, there was a 23% decrease in juvenile male offenders and an 8% increase in female offenders, although in 1999 males still outnumbered females by 3 : 1–4 : 1 [16]. Similar trends are evident in epidemiological studies. According to the US Surgeon General’s report [17], between 1993 and 1998, the gap between adolescent girls’ and boys’ self-reported engagement in violent acts shrunk by approximately 50%. Turning to relational aggression, research shows that girls engage in at least equal or higher levels of relational aggression than do boys [18]. Relational aggression can be reliably detected as early as preschool and children who engage in it are more likely to suffer rejection from their peers and are more likely to affiliate with deviant peers who also engage in relational aggression [19, 20]. Rates of relational aggression increase during elementary school for girls but not boys [21], possibly reflecting sex differences in the complexity and psychological relevance of relational contexts. The fact that social aggression can have social “payoffs” for some girls has garnered support from recent studies. For example, Cillessen and Mayeux [22]
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found that young adolescents who were relationally aggressive to others held high social prominence, although they were not well-liked by their peers. This was particularly true for girls. Girls also experience relational aggression as more distressing and harmful than do boys [20].
Adult Women Official criminal data and incarceration rates confirm that within the general population, men are considerably more aggressive than women and come into conflict with the law with much greater frequency. In North America, men vastly outnumber women in correctional settings. Early in 2006, there were 408 women federally incarcerated in Canada [23] compared with 12 263 men. Although the actual number of women admitted to federal institutions increased from 238 to 276 between 2004–2005 and 2005–2006, women constitute a very small proportion (5.8% in 2005–2006) of all federal admissions. The gender disparity in incarceration is most apparent for violent offenses (homicides, sexual offenses, and other violent crimes (men = 96.5%; women = 3.5%). In the United Kingdom, the total prison population is comprised of 6.1% women, 17% of whom were incarcerated for violent offenses [24]. In the United States, a country with one of the highest incarceration rates in the world, females comprised just 7% of the total prison population in 2005 [25]. In other words, males were 14 times more likely than females to be incarcerated, relative to the general population. The gender breakdown for violent offenders, in particular, is slightly higher in the United States relative to Canada and the United Kingdom (4.4% female, 95.6% male). Thus, the picture that emerges from a consideration of official criminal justice data sources clearly demonstrates a vast disparity in criminal offending by gender of perpetrator, that is even greater for when one considers violent offenses. We find that although women are markedly underrepresented in criminal courts and criminal justice settings, female aggression is not uncommon. That is, the gender disparity in aggressive behavior noted in the general population does not appear to be evident among individuals with mental illness [2] nor when one examines aggression that occurs within romantic and familial relationships [26, 27]. Among civil psychiatric patients [28] and forensic psychiatric patients (Nicholls, Brink, Greaves, Lussier, and Verdun-Jones,
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Aggression: Gender Differences in
in press) women match, and sometimes exceed, men in the prevalence and incidence of aggression. Similarly, it has long been recognized that women perpetrate as much as 50% of aggression within familial and intimate relationships (i.e., child abuse, elder abuse, and partner abuse) [29, 30].
Is Female Aggression Increasing? Between 1980 and 2001 the proportion of females incarcerated in the United States nearly doubled (4–7%, respectively) [31]. The US Department of Justice, Bureau of Justice Statistics reported that the number of women under the jurisdiction of State or Federal prison authorities increased 4.5% from year end 2005, reaching 112 498, and the number of men rose 2.7%, totaling 1 458 363 [32]. The increase in female contact with the US criminal justice system is particularly remarkable given that the number of serious violent offenses committed by persons ages 12–17 declined 61% from 1993 to 2005, while those committed by persons older than 17 fell 58% (see [32]). In Canada, the rate of “serious violent crime” committed by adult women increased from 25 to 46 per 100 000 between 1986 and 2005 [6]. Similarly, as noted above, the rate has more than doubled among female youth since 1986, growing from 60 per 100 000 to 132 by 2005 [6]. Despite claims that female offending is rapidly escalating, any increase should be understood in relation to the low base rate of violent crime among women. It is also noteworthy that the rate at which female youth have been charged with serious violent crimes has been on a slow downward trend since 2001. Comparisons between females and males for the same offenses and over the same period of time provide a clearer picture of trends. Between 1986 and 2005, with the exception of a few downturns over the years, the rate at which women were charged with assault level 1 (simple assault) more than doubled (44–93 per 100 000 population). In comparison, the rates among male adults have shifted downward since the early 1990s. Between 1991 and 2005, the charge rate for male adults for serious violent crime dropped 30% (412–290 per 100 000). From 1993 to 2005, the charge rate for assault level one for male adults fell 25% (from 606 to 455 per 100 000 population). These data confirm the narrowing gap between adult females and males charged with violent crime: in 1986, nine men were charged with a violent
offence for every one woman charged. In 2005, this ratio had decreased substantially from five to one. These statistics raise two important questions: what accounts for decreasing male aggression and what contributes to female aggression increasing in both the United States [32] and Canada [6] despite the fact that the rate of violent crime is dropping? It is clear from the accumulation of knowledge to date that the “myth of female passivity” [33] is not borne out of the extant empirical data. Knowledge of these base rates is essential, particularly for informing violence risk assessments and public funding decisions; for instance, but an appreciation of the nature of female aggression, what motivates females to aggress against others, and the consequences of those actions is likely to drive treatment and intervention policy, research, and clinical efforts.
Exploring the Topography of Female Aggression: Sex Differences and Similarities in Aggressive and Violent Behavior Recent research shows a slow but progressive trend in developing research objectives and methodologies to better understand the contexts, functions, targets, and implications of women’s aggression. Moving beyond the question of how often females are aggressive relative to males, research now compares and contrasts the topography in which male and female aggression occurs [34]. An appreciation of the contexts in which aggression occurs and the purposes it serves for females helps us understand, prevent, and reduce the risk of female aggression.
Form and Function Topographical similarities in aggressive acts may serve to mask gender differences, thereby obscuring the underlying motivations and mechanisms involved in females’ use of aggression and exaggerating similarities in the potential risk posed to victims. Trends have been evidenced in research, which reveal both gendered and nongendered forms and functions of aggression. Emerging findings continue to indicate similarities (e.g., perpetration of any assaultive act, instigation, and injury incurred, [35]; nature and
Aggression: Gender Differences in location, Nicholls et al., under review), in addition to a substantial amount of divergence (e.g., use of very severe forms of violence, [35]), between male and female aggression. Form – What is the Nature of Female Aggression?. Self-report surveys and victimization reports generally confirm what we see in the official criminal justice and corrections databases reviewed above; violent crimes remain disproportionately low in women and, that is particularly true of certain forms of interpersonal offending. Data from the United States indicates that, as reported by victims, females account for only 1 out of 7 violent offenders. Further, 1 in 50 offenders committing a violent sex offense (including rape and sexual assault) were women; one in 14 robbers were women; 1 in 9 aggravated assault perpetrators were women; as were approximately 1 in 6 offenders who committed a simple assault [32]. Corresponding Canadian figures for those convicted in 2003–2004 indicate that women accounted for approximately 1 in 99 sexual offenders, 1 in 12 robbers, 1 in 6 offenders committing a major assault, and 1 in 7 who committed a common assault [6]. Charges for murder or manslaughter are rare, regardless of gender (in 1991, 48 charges were laid against women, and 486 against men). Overall, women’s violent criminal charges are primarily for common assault [6]. Fewer are brought about by the commission of robbery, and sexual forms of aggression by women are an exceedingly rare occurrence [36], a pattern that is similar in both Canada and the United States [37, 38]. As with sexual offenders, females engaging in stalking behaviors are relatively rare as compared to their male counterparts (accounting for 15–20% of those who perpetrate stalking offenses, with one in five ultimately attacking the victim; [39]), their occurrence may be a function of stalking as a variant of domestic violence (see [40]). It is important to note that when women are aggressive their assaults occupy the entire continuum of aggression. To clarify, women commit both minor (e.g., verbal aggression) and severe forms of aggression (e.g., kicking, beating, choking, and using weapons), particularly within intimate relationships and against family members (see [41, 42]). In fact, when there is reciprocal aggression (i.e., both partners are abusive) or when only one partner is abusive it is most likely to be the woman who uses severe aggression (see [41, 42]; see [26, 29] for reviews).
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Setting and Targets – Where Does Female Aggression Occur and Who Do Females Aggress Against?. As compared with men’s aggressive acts, women’s expressions of aggression are more likely to occur in the private (e.g., the perpetrator’s home) versus the public (e.g., bars) domain; a finding that holds in data gathered from psychiatric patient samples [35, 43] and is highly consistent with the disproportionate amount of women’s aggression that involves domestic violence, child abuse, and elder abuse. Similar to data from other sources on female aggression, femaleperpetrated homicide data suggests that women are less likely than males to aggress against strangers (3% of victims killed by women vs. 14% killed by men) or casual acquaintances (13% vs. 21%, respectively) than men. The relational aspect of female aggression, however, is perhaps most evident across forms of aggression involving abuse of others who are intimate (or perceived intimate). Differences across gender are readily apparent when considering perpetrator-victim relationship in instances of homicide. In 1994, Statistics Canada reported that 71% of Canadian women charged with homicide were related “domestically” to their victim, whereas this was true among only 24% of their male counterparts. Indeed, in general, the most common target of women’s aggressive acts is the current or previous spouse or common-law partner (30%). Further, in the context of domestic violence, women often report themselves to be either the primary [44] or sole aggressor against their nonviolent partners [42, 45]. Another frequent target is the woman’s child (28% of violent convictions in the United States [6]; 10.4% of females convicted of murder in Canada killed their child/stepchild, [46]). Between 1976 and 1997 in the United States, parents and stepparents killed nearly 11 000 children. Mothers and stepmothers perpetrated about half those child killings [46]. According to the Canadian Centre for Justice Statistics, females (3%) and males (15%) are both unlikely to have more than one victim of a homicide [6]. Child maltreatment studies have long identified mothers perpetrating abuse to a comparable extent as fathers [41, 47]. Sexual abuse as a form of women’s aggression has only recently been examined as perpetrated against adults [48] and in its more prevalent form, against children [49] (for a review see [36]). Consistent with other forms of female aggression, it is also the case that women more often
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than men sexually offend against those to whom they provide care (their own offspring or other related children, children they baby-sit or educate [50]). Function – What Motivates Female Aggression?. An appreciation of why women use aggression and to what extent women’s aggression has similar or unique roots to men’s aggression is an essential means of developing theoretical explanations and informing prevention and intervention strategies. Felson [51] asserted that there are principally three reasons that people perpetrate aggression: (i) to obtain compliance or control the target; (ii) to attain retribution or justice; and (iii) to promote or defend their self-image.a A fourth motive, self-defense is a predominant theme in much of the debate about women’s involvement in intimate abuse. In a comprehensive review of the literature, Graham-Kevan [52] found that, in the context of intimate relationships, there are no consistent sex differences in the use of controlling behaviors. Even in samples selected for high rates of physical aggression, she noted that women sometimes use controlling behaviors with similar frequency men. A consideration of the empirical data suggests that men and women do not differ in their desire to control their partners though they may use different methods to achieve control (for reviews, see [52, 53]). Both men and women experience jealousy, frustration, and disappointment in relationships; thus, efforts to save face are not unique to men and it is not surprising that women are motivated to use aggression for retribution just as are men. Empirical work in the area details both similar and divergent motivations cited by domestically aggressive women themselves. Women often report using aggression against their partners for purposes that are similar to those of men who perpetrate partner violence, that is, a desire to control or punish their partners, to get their attention, as a response to partner emotional abuse, and to express anger [54]. Yet a number of other studies do cite women’s additional motivations of self-defense or retaliation [55, 56], which some feminist scholars argue are not common motivations among males but in fact are frequently cited by men and women [57, 58]. For instance, Follingstad et al. [54] found that women were significantly more likely to report using physical force in retaliation for emotional hurt (55.9% vs. 25.0%; χ 2 = 13.11, p < 0.0001) and men were more likely to report using physical force in
response to being hit first (29.2% vs. 13.6%; χ 2 = 5.61, p < 0.05) whereas men were more likely to report jealousy (41.7%) as a motivator than women (8.5%) (χ 2 = 29.62, p < 0.0001). It is also noteworthy that there was no difference in the likelihood that men and women used aggression to “punish the person for wrong behavior” (12.5 vs. 16.9%). Contrary to widely held conceptions [59], the notion that women are aggressive against partners primarily in self-defense has not withstood empirical scrutiny [54]. Briefly, women are known to initiate physical assaults, aggress against nonabusive partners, and as few as 10–20% of women report using physical aggression to defend themselves (for a discussion, see [26]). In fact, the varied motivational influences reported to account for female aggression against intimate partners and stalking victims tend to relate to dysfunctional expressions of anger, loneliness, and frustration; and to that of power and anger, very similar to their male counterparts [60, 61]. In the particular case of female stalkers, rage at abandonment and perceived betrayal are most often driven by the desire to establish intimacy with their targets [39]. Among Canadian female homicide offenders, the most common motives cited were escalation of an argument (39%) and frustration (22%) [6]. In only 11% of the cases did women cite revenge, jealousy, or resolving accounts as their motive, compared to 27% cited by male homicide offenders [6]. Laboratory research has also offered considerable insight into female aggression, demonstrating the circumstances under which females aggress [33, 62] and challenging traditional conceptions of females. Briefly, studies suggest that many of the same contexts and circumstances that promote male aggression are also found to increase the likelihood that females will aggress (e.g., emotional arousal, rumination). Summary. In sum, women are unlikely to commit certain forms of aggression (e.g., robbery, sexual assault, and physical attacks against strangers) but they are equally represented among perpetrators of physical violence in North American family homes and there is increasing evidence that this finding is consistent in other developed nations [42]. Overall, the general trends concerning the form (i.e., interpersonal/familial based), location (i.e., outside the public domain), and target (e.g., family members) of female aggression are likely contributors to underreporting, lower arrest rates for females perpetrating violence,
Aggression: Gender Differences in and a persistent perception of lower severity. It is important to note here that both men and women view female aggression as less severe than that perpetrated by males. Although it is essential not to lose sight of the fact that women suffer more harm as a result of domestic violence, it may be the expectation of less harm and injury that is fueling increasing rates of female aggression, and thus allows females to justify and minimize the impact of their aggressive behaviors. Moreover, we need to always be mindful of the implications of female aggression (and male aggression) for child witnesses to partner abuse and direct child abuse [63, 64].
Outcomes and Implications – How Serious Is Female Aggression? Aggression is known to have deleterious implications for victims and witnesses that include physical, psychological, emotional, and financial harm (e.g., physical injuries, fear, shame, and posttraumatic stress disorder). Now that there is considerable agreement that the frequency of aggression in women may be on par with men in certain populations (e.g., hospitalized mentally ill patients) or contexts (i.e., within romantic and familial relationships), the debate has shifted to a consideration of whether the consequences of female aggression are on par with the consequences suffered as a result of male aggression. Most scholars agree that female aggression is at least somewhat less likely to result in injury than male aggression. As we have done throughout the manuscript, we focus here on family violence and inpatient aggression, because those are areas of our expertise and there is an abundance of data on the topic. Finally, we end this section by comparing and contrasting the severity of male and female offending as demonstrated by criminal justice statistics on injuries and weapon use. Several studies have found that, compared to men, women sustain more severe injuries as a result of partner abuse [58, 65]. In a meta-analysis of domestic violence research, Archer [66] reported that women were more likely than men to be injured by a partner and men were more likely than women to inflict an injury. Perhaps given physical differences in size and strength it seems to reason that men would be more likely to injure their targets; however, women often even the playing field with weapons or attack their partners when they are defenseless (e.g., sleeping; [26]). On the basis of their review of the literature,
41
Noller and Robillard [67] concluded that several studies show that women commit a larger share of severe violence. Nonetheless, some studies find sex differences in the reaction of victims confronted with male versus female perpetrators [68]: some male victims of female aggression reportedly find the abuse “humorous”b whereas female victims of male aggression do not report such a response [69]. Ultimately, however, it is essential to evaluate harm on a case-by-case basis; it is the extent of exposure to trauma, not gender that predicts the long-term emotional implications of aggression [70, 71]. When evidence of the correspondence between inpatient aggression among male and female psychiatric patients became available, critics argued that the findings failed to address the severity of women’s aggression and the likelihood that women would cause serious injury [35]. Increasingly, however, research is demonstrating that while it is certainly the case that the victim of a male perpetrator faces a greater risk of harm than the victim of a female perpetrator, that discrepancy is small (Nicholls et al., under review). Conversely, in some circumstances female aggression may have more severe consequences than male aggression, at least in part, as a function of the relationship with the victim. For instance, maternal aggression results in severe consequences to children that are unique from the implications of paternal aggression. Maternal aggression may have particularly salient influences because mothers are the primary attachment figure throughout the lifespan and mothers spend more time interacting with their children [64]. It should be noted, however, that there is considerable between-victim variability in this regard, and furthermore, the majority of children from violent homes (35%–45%) do not experience clinically significant outcomes [63]. Finally, there is a likelihood of early parenthood, and a negative implication of maladaptive parenting. These features are not completely unique to females, but are of greater consideration given that most single parent households continue to be headed by women [72]. Criminal justice statistics evaluate the level of injury sustained by victims and the use of weapons as indicators of the seriousness of violent crimes. Statistics show that compared to males, females rarely commit violent crimes, but when they do they are just as likely to injure their victim and to use weapons [6]. Just over half of victims sustained no injury from either female or male perpetrated violence (51 and
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54%, respectively), minor injury requiring no professional medical treatment was less frequent (43 and 38%) and a small minority resulted in major injury requiring professional treatment or death (2 and 4%; [6]). In closing, it is important to be mindful that there is considerable evidence that the gap between the suffering experienced by male and female victims of aggression has historically been exaggerated because of methodological limitations and political agendas [26, 27, 29, 33, 73] further research in this area is required. The field is still relatively new and emerging methodological sophistication (e.g., prospective longitudinal examinations including mental health and physical injury outcomes) enhances our full understanding of the different consequences of male and female aggression [69].
Understanding Female Aggression Are Risk Factors for Aggression Sex-Specific? Considerable discussion in the literature has revolved around the extent to which common or unique risk factors underlie aggression in males and females. Despite sound rationale for the importance of gendersensitivity, few efforts have been made to study empirically whether the predictors and moderators of aggression are sex-specific. Similarly, in the development of risk assessment instruments and other forensic assessment measures (e.g., psychopathy measures) it has been rare for them to incorporate theoretical evidence of sex differences and similarities in the variables of relevance. In addition to an insufficient amount of research, an examination of the extant literature suggests that the findings to date have been equivocal; thus, we examine (i) the extent to which risk factors operate in a similar way, increasing the likelihood of aggression in both males and females; (ii) the differential influence of the same risk factors as a function of gender (i.e., being more influential in one gender than the other); and (iii) gender-specific risk factors (i.e., increasing risk in males or females, but not in both; having the opposite effect, increasing risk for aggression in one and decreasing risk in the other). Many Commonalities. Not surprisingly, many of the factors that leave males vulnerable to committing aggressive behavior also increase the risk of
aggression among females. There is considerable evidence that static risk factors (i.e., unchangeable variables such as a diagnosed serious mental illness, a history of child abuse, etc.) as well as dynamic risk factors (i.e., changeable predictors that are potentially influenced by treatment and interventions, such as substance abuse, anger, impulsivity, and poor social support) are relevant across populations and settings (e.g., mentally disordered and nondisordered offenders; correctional inmates, civil psychiatric patients, and forensic psychiatric patients). Thus, it stands to reason that risk factors known to be relevant to male aggression are potentially relevant to female aggression (see [28, 74–76]). On the rare occasions that scholars have made efforts to develop gender-informed assessment measures from the ground up (e.g., [77]; service planning instrument SPIN) the result has been a remarkable degree of overlap in the variables found in measures previously developed for males. For instance, Blanchette and Taylor [77] examined 176 variables identified as theoretically, empirically, or operationally relevant to security classifications of women in correctional settings. The result was a measure composed of nine variables – all but one of which was common to classification measures developed for men. The authors concluded that despite the attempt to develop a gender-informed measure their results suggest there is little evidence for gender-specific variables; however, they caution that “the order of relevance and weighting of predictive items might differ by gender” (p. 376). Blanchette and Taylor went on to note that evidence of considerable overlap in risk factors for male and female offending is highly consistent with well-established theory [78] and prior research in the field of corrections [79, 80]. Another approach to addressing the question of the extent to which risk factors have a common influence over male and female aggression has been to study the psychometric properties of existing measures constructed based on research with males and test their applicability to populations of females. These efforts have yielded revealing, though generally inconsistent, results. Some studies have found predictive accuracy of existing measures result in similar or better predictive capacity with females [28, 81–84] while other studies have found small or moderate and often insignificant associations with women’s aggression [85–87] (for a review of violence risk assessment with women see [88].
Aggression: Gender Differences in In their longitudinal study of a birth cohort (ages 3–21) Moffitt et al. [3] concluded that the same risk factors predict antisocial behavior in both males and females (also see [1]). Although they did not find any evidence of “replicable sex-specific risk factors” the authors did note that family adversity, compromised intelligence, difficult temperament, and hyperactivity had somewhat stronger effects on males than females. They caution, however, that the sex differences are small and “at best, offer only weak support to the hypothesis that males are more vulnerable than females to risk factors for antisocial behavior” [[3], p. 108]. Given these findings it is important to consider to what extent the same risk factors have a unique bearing on the expression of aggression in males versus females. The Differential Influence of Similar Variables. While there appears to be considerable symmetry in male and female risk markers for violence, evidence also exists for potential differential influences by a number of those shared variables. One particularly noteworthy domain is exposure to elements often present in dysfunctional families of origin. Findings suggest that child abuse and witnessing domestic violence may be more influential in the development of aggression among girls than it is among boys. Differential outcomes are evidenced when the nature of the abuse and the perpetrator gender are taken into consideration as a function of the gender of the victim. For instance, some evidence suggests that childhood maltreatment in the form of sexual abuse may be a risk factor that is especially important in the emergence of girls’ antisocial behavior [89, 90]. Further, experiencing childhood abuse at the hands of ones’ mother has been found to be a powerful predictor of relationship violence [91], as has childhood abuse perpetrated by ones’ father, which appears to explain more of the statistical variance among females than males [64, 92]. There is still reason to expect a greater likelihood of previously victimized women employing violent strategies in their own intimate relationships, as witnessing parental aggression has predicted women’s subsequent use of verbal and physical aggression toward their partner [90]. These findings have been replicated and further refined through more recent research, albeit utilizing a similar sample. Explaining an astounding 51% of the variance in violence, women reported perpetrating more violent acts
43
toward their partners if they had seen their mothers aggress against their fathers [91]. That various gender differences have been evidenced with regard to the impact of witnessing domestic violence, for instance, suggest refinement of the current blanket conceptualization as applied across gender. Evidence from epidemiological studies [93], population-based research [2, 5, 94] and many patient-based studies (see for citations and brief discussions, [28, 93]) call into question the extent to which the gender gap in aggression witnessed in the general population is reflected among individuals with serious mental illness. Mental disorder, a robust predictor of violence, may have a differential association with the likelihood of aggression among females, although the findings to date are equivocal [93]. Swanson et al. [5] assessed the prevalence of self-reported violence over one year in community participants. The authors found that among persons with no mental disorder, violence was much more common among males. The gender difference was substantially reduced among mentally ill individuals. Hodgins [2] reported similar findings through an examination of mental disorder and intellectual disabilities in a Swedish birth cohort. She found that these risk factors had a substantial and differential impact on the risk of crime and violence among females. Specifically, Hodgins [2] reported that women who had a serious mental illness or intellectual handicap were five times more likely to commit a criminal offence than women without those characteristics. Particularly notable for the present discussion, that was twice the increased risk reported for men for the same variables. When specific aspects of mental disorder have been considered, differences are again evident in the expression of violence; for instance, the presence of positive psychotic symptoms has been found to be more prominently associated with physical violence in women than in men [95], although the reason for these differences remains unspecified. Substance abuse as a contributing factor in violence perpetration is more prevalent, and relates more strongly with physical assault in men than in women [95]. Among homicide perpetrators, 71% of males and 65% of females were reportedly under the influence of drugs and/or alcohol during the commission of the offence [6]. Gender differences in substance userelated aggression are further evident when the type of drug is separated in further analysis [96]. Together,
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these findings suggest the differential impact of certain clinical and psychosocial factors on subsequent aggression, and emphasize the need to “drill down” past only the first level of factors under investigation. Socialization and the influence of societal norms and values may have a unique influence on the likelihood of aggression in females as well, protecting females by promoting prosocial behavior, the development of empathy, and an appreciation of caregiving. Conversely, our gender-role socialization of males may actually promote subsequent displays of aggression through rewarding competitiveness and machismo. In general, the influence of protective factors has been overlooked in much of the literature [97, 98] this seems to be no less true of females [82]. Gender-Specific Variables. Reflecting the limited body of evidence to inform this field, it remains unknown to what extent there may be risk variables or protective variables that are unique to the risk of aggression for one gender or the other. For instance, precocious pubertal development and having a mature and/or sexualized physical appearance may present a sex-specific risk for girls entering into aggressive and antisocial behavior [3]. There is also some evidence from the general population and particularly from the sexual offending literature, [36] that antisocial male partners may play an important role in some female aggression. Official criminal statistics offer some support to this hypothesis, demonstrating that women committing violent offenses are more likely to have done so in partnership with a male than are male violent offenders to have committed violent offenses in partnership with a female. Logan’s [36] review of the sexual offending literature reminds us that women do commit serious offenses independently of males and a small but robust proportion of women’s involvement in aggression may reflect the influence of antisocial men (the reverse is likely also true). Though the impact of antisocial peers and negative relationships is hardly unique to females, the role of antisocial male partners, (perhaps particularly older men) may be a unique predictor of adolescent girls’ involvement in aggression. There is some evidence for this in the expression of antisocial and aggressive behaviors emerging later in girls, typically in adolescence, around the time that same-sex socialization gives way to increasing mixed
gender socialization and sexuality. Moreover, criminologists have suggested that being in a romantic relationship with a woman generally inhibits antisocial behaviors in males [99]. Not surprisingly, though, antisocial males and females selectively mate (assortative mating), likely escalating the risk of aggression in both partners, as well as the risk of an intergenerational transmission of aggression to offspring. In what appears to be the most comprehensive examination of empirical data on the etiology of physical violence by male and female dating partners, Medeiros and Straus [57] asserted that most of what has been written about the causes and motives for women’s aggression has been based on writers’ assumptions, in the absence of empirical evidence. Based on their extensive review of the literature Medeiros and Straus [57] found four types of studies they categorized by the type of data reported: (i) seven studies evaluated 25 variables and the statistical relationships between motive and gender; 72% of the relationships analyzed demonstrated no significant gender difference. (ii) The second type of study compared violent men and women on 56 characteristics (e.g., educational attainment, measures of anger, etc.) and demonstrated that in 73% of comparisons no significant difference was found. (iii) The third category also examined violent men and women but did not test significance; therefore, they categorized gender differences that were 20% or more as a gender difference. According to that threshold, they concluded that 43% of variables were similar for men and women (28 variables in six studies). (iv) Finally, the fourth category included studies that examined risk factors for partner assault separately for men and women but did not test for significant differences. In 23 studies, reporting results in relation to 147 risk factors, 60% of variables showed the same relationships for men and women, 39% showed the direction of the relationship to the risk factor was the same for men and women but was significant in one but not the other, and 1% of variables showed opposite relationships in men and women (one positive and significant, the other negative and significant). The authors interpreted these findings to mean that of the risk factors considered there was a similar etiological pattern for men and women for 60% of the risk factors examined, or that 99% of the studies showed the effect of the variable was in the same direction for men and women [57].
Aggression: Gender Differences in Much work remains to parse out the underlying mechanisms by which female aggression emerges. These disparate findings highlight the need for gender-sensitivity when considering female aggression. Although further study is necessary, the research to date seems to suggest that many of the same clinical, psychosocial, and environmental risk factors pertain to males and females, however, there is some evidence that the clinical and psychosocial factors that are associated with increased risk for aggression have a different impact on males and females [3, 95]. As Crick [100] speculated, nonnormative forms of aggression (i.e., overt aggression and physical violence) may reflect maladjustment more than gender normative forms of aggression (i.e., relational aggression and verbal aggression). The as yet unresolved question remains whether gender-specific models of aggression are necessary to explain female, as separate from male, perpetrated aggression. Further methodologically sound exploration into disparities and overlap concerning the roots of female aggression may definitively direct us to adopting extant male models, or alternatively, to considering female aggression as a separate phenomenon.
The Developmental Trajectory Until recently, research on aggression and violence in childhood and adolescence was based on the assumption that aggressive behavior increased from childhood to adolescence, often as a result of exposure to various risk factors. New work on developmental trajectories reveals a different picture: first, aggressive acts such as hitting and biting are sometimes present in over 40% of two-year old boys and almost 35% of girls, and are frequently present in 5% of boys and 1% of girls [101]. After age 2, aggressive behavior tapers off quickly, and by age 11 only 10–15% of boys and girls sometimes engage in aggressive acts and fewer than 5% do so frequently [102]. From age 6 to 16, further desistance is noted for the vast majority of children; however, 4% of boys continue to be aggressive [103]. While girls also show drops in physical aggression with age, girls but not boys increase their use of relational aggression during primary school [21]. Together these findings show that most children learn to inhibit aggression very early in childhood, however a small proportion of boys and girls are not taught or do not learn how to desist,
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and girls in general begin to use greater amounts of relational aggression. The failure to desist in childhood aggression, and to acquire new aggressive behavior early in childhood, is a clear marker for future pathology. Approximately 95% of boys who show severe aggressive behavior early in development (i.e., prior to age 10) continue to show antisocial and aggressive behavior into adolescence and adulthood, thereby lending credence to the distinction between early-onset lifecourse persistent (LCP) versus adolescent limited (AL) conduct disorder [104–106]. Moffitt et al. [3] asserted that the LCP versus AL taxonomy applies equally well to males and females, however the rate of early-onset versus adolescent-onset cases is extremely low among females. For example, only 6 of the approximately 450 females (1.3%) from the Dunedin Longitudinal Study were identified as lifecourse offenders, whereas 78 (17%) were identified as adolescent-onset. Consistent with this finding, the gender gap in rates of conduct disorder is greater in childhood than in adolescence (for reviews see [3, 107, 108]). The fact that adolescent-onset aggression is more common in girls than is childhood-onset has led some to question the validity of this distinction in girls [104, 109]. Silverthorn and Frick [109] proposed that the delayed-onset pattern in girls is comparable to the early-onset pattern in boys in terms of risk markers, stability, and persistence to adulthood. They present findings that show adolescent-onset girls resemble early-onset boys on a range of risk factors [109], and they are more likely to suffer from a multitude of mental health problems in adulthood, including substance dependence, poor physical health, involvement in abusive relationships, antisocial personality disorder, and social welfare dependence [3, 109–111]. However, Moffitt and Caspi [112] proposed that the same model applies to the development of antisocial behavior in girls and boys, and that the delayed onset in girls simply reflects the slower rate of accumulated risk factors for girls. In particular, the higher prevalence of neurocognitive and temperamental risk markers in boys than girls exerts a significant impact on early development and results in boys reaching a threshold of risk for antisocial behavior more quickly than do girls [112]. Yet, whether or not risk factors operate similarly for girls and boys is unclear. Moffitt and Caspi [112] assume a linear and additive model of risk; however, consideration of other
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models is warranted. Some risk factors may have gender-specific impacts, or may interact with other risk factors in a gender-specific way [113]. There is simply too little research to conclude that the risk models developed primarily on boys are accurate in predicting onset and developmental course in girls.
Conclusions: Implications, Gaps in Knowledge, and Future Directions Female aggression remains a topic fraught with controversy and heated debate. Despite widespread consensus of large gender disparities in the amount and consequence of aggression committed by males versus females, we recommend exercising caution in the wholesale acceptance of “well-established” knowledge for which there is little or equivocal empirical evidence. Aggression is complex [114] and no one variable, including gender is a sufficient explanation for why one person is aggressive and another is not [115]. The lens through which society has traditionally examined female aggression has been colored largely by our knowledge of women’s engagement in criminal violence that comes to the attention of the criminal justice system. As we have reviewed here, the picture that emerges from a consideration of arrest and incarceration data clearly confirms a vast disparity in violent criminal offending by males versus females. For this reason, it is not surprising that research calling into question the accuracy of our comfortable classification of females as gentle, nurturing, empathic, caregivers is often received both by the research community and the general population with disbelief and caution and at other times with outrage (see [73]). People who study female aggression have been ostracized and vilified, their efforts to solicit funding and to communicate their research findings have been blocked [73, 116]. Similarly, advocates who work to provide support to victims of female aggression have encountered severe criticism and empty pockets [117]. Readers should be cognizant that sex differences have been exaggerated in the literature as a result of ideology and stereotypes and assumptions have been maintained often due to a lack of empirical evidence to contradict our socially sanctioned assumptions about females [33]. In fact, the extent to which this wisdom holds depends very much on the population and setting, as well as the type of aggression being examined.
As we have suggested, gaining a more thorough understanding of aggression requires a consideration of the multiple manifestations it takes, discriminating between verbal and physical assaults, physical aggression and severe violence, for instance. The extant literature offers compelling evidence that violent females are vastly outnumbered by violent males in the general population but that women contribute to nearly half of the aggression that occurs in inpatient psychiatric settings, intimate and familial relationships; though, they remain somewhat less likely than males to commit harm that results in injury. Violence by females has not been recognized as a public health concern, there is little public education along those lines, funding for research has been purposely directed away from examining the issue (Straus) and the study of relevant variables has been intentionally blocked (e.g., psychopathy, [118]; for a discussion see [84, 119]). As we have demonstrated here, avoiding the difficult questions is not an effective means of achieving increased health and safety. While male aggression is on the decline, female aggression is increasing and that aggression is now known to have widespread, lasting, and substantial implications for victims, perhaps most importantly, children. To move ahead, to effectively reduce aggression in society (i.e., not only among females because female aggression has implications for male aggression and the intergenerational transmission of violence) we must be willing to challenge our most firmly held beliefs about gender, patriarchy, and sexism. As Murray Straus, one of the pioneers in this field has admonished, we have to ask ourselves if we are more committed to maintaining our political perspectives or are we committed to reducing aggression? While always remaining cognizant of many important gender differences, an increasing recognition that female aggression is not uncommon means that we can now can turn our attention away from attempting to credit or discredit research showing gender equity and begin to uncover what contributes to, or conversely prevents, female aggression [29] and why it might be that in certain settings and populations female aggression is uniquely common. Continued contributions to the female aggression knowledge base carry the potential for directly informing development of proactive aggression prevention programs, as well as clinical treatment options to curtail further expressions of violence amongst those most at risk.
Aggression: Gender Differences in
Acknowledgments
[8]
Michael Smith Foundation for Health Research; Social Sciences and Humanities Research Council; Canadian Institutes of Health Research.
[9]
End Notes a.
There are other potential motives of which readers should be mindful, but they are beyond the scope of this article (e.g., excitement, [51]). b. While this finding may offer important insight into gender differences with respect to the fear experienced by female versus male victims of intimate partner abuse several related issues require further study and careful consideration. For instance, it is unknown to what degree reporting reflects male socialization and sex-role expectations (e.g., we do not teach male children to fear their female peers). Further, although men may report less fear than women that offers little evidence that they are actually at less risk. As we noted above, when women commit violent offenses generally and when they are violent to their partners, specifically, there is relatively little difference in the risk of injury to the victim.
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Moffitt, T.E. (1993). AddedAdolescence-limited and life-course-persistent antisocial behavior: a developmental taxonomy, Psychological Review 100(4), 674–701. Tremblay, R.E. (2000). The development of aggressive behaviour during childhood: what have we learned in the past century? International Journal of Behavioral Development 24(2), 129–141. Lahey, B.B., Schwab-Stone, M., Goodman, S.H., Waldman, I.D., Canino, G., Rathouz, P.J., Miller, T.L., Dennis, K.D., Bird, H. & Jensen, P.S. (2000). Age and gender differences in oppositional behavior and conduct problems: a cross-sectional household study of middle childhood and adolescence, Journal of Abnormal Psychology 109(3), 488–503. Zoccolillo, M. (1993). Gender and the development of conduct disorder, Development and Psychopathology 5(1–2), 65–78. Special issue: Toward a developmental perspective on conduct disorder. Silverthorn, P. & Frick, P.J. (1999). Developmental pathways to antisocial behavior: the delayed-onset pathway in girls, Development and Psychopathology 11(1), 101–126. Bardone, A.M., Moffitt, T.E., Caspi, A., Dickson, N. & Silva, P.A. (1996). Adult mental health and social outcomes of adolescent girls with depression and conduct disorder, Development and Psychopathology 8, 811–829. Robins, L.N. (1986). Deviant children grown up, European Child and Adolescent Psychiatry 5(Suppl 1), 44–46. Moffitt, T.E. & Capsi, A. (2001). Childhod predictors differentiate life-course persistent and adolescencelimited antisocial pathways amoung males and females, Development and Psychology 13, 355–375. Moretti, M.M., Odgers, C. & Jackson, M. (2004). Girls and Aggression: Contributing Factors and Intervention Principles, Kluwer-Plenum, New York. Hart, S.D. (1998). The role of psychopathy in assessing risk for violence: conceptual and methodological issues, Legal and Criminological Psychology 3, 121–137. World Health Organization (2002). World Report on Violence and Health: Summary, WHO, Geneva. Straus, M.A. (2008,. February) 30 years of research: Denials and distortions of the evidence and what to do about it. Paper presented at the meeting From Ideology to Inclusion: Evidence-based Policy and Intervention in Domestic Violence Conference, National Family Violence Legislative Resource Centre, Sacramento, California. Pizzey, E. (2008,. February) A history of the domestic violence in the Western world. Paper presented at the meeting From Ideology to Inclusion: Evidencebased Policy and Intervention in Domestic Violence Conference, National Family Violence Legislative Resource Centre, Sacramento, California.
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Laishes, J. (2002). The 2002 mental health strategy for women offenders, Correctional Service of Canada. Retrieved Feb 23, 2008 from http://www.cscscc.gc.ca/text/prgrm/fsw/mhealth/8-eng.shtml. Nicholls, T.L. & Petrila, J. [Guest Editor](2005). Gender and psychopathy: an overview of important issues and introduction to the special issue. Guest editor for this special issue of, Behavioral Sciences and the Law 23(6), 729–741.
Further Reading Denov, M.S. (2003). The myth of innocence: sexual scripts and the recognition of child sexual abuse by female perpetrators, Journal of Sex Research 40, 303–314. Laishes, J. (2002). The 2002 mental health strategy for women offenders. Correctional Service of Canada. Retrieved Feb 23, 2008 from http://www.csc-scc.gc.ca/text/prgrm/fsw/mhealth/ 8-eng.shtml. Monahan, J. (2001a). Major mental disorder and violence: epidemiology and risk assessment, in Clinical Assessment of Dangerousness: Empirical Contributions, G. Pinard & L. Pagani, eds, Cambridge University Press, New York, pp. 89–102. Nicholls, T.L., Brink, J., Greaves, C., Lussier, P. & VerdunJones, S. (in press). Female forensic psychiatric inpatients and aggression: incidence, prevalence, severity, and interventions, International Journal of Law and Psychiatry. Swan, S.C. & Snow, D.L. (2002). A typology of women’s use of violence in intimate relationships, Violence Against Women 8(3), 286–319.
TONIA L. NICHOLLS, CAROLINE GREAVES AND MARLENE M. MORETTI
Aging the Living see Anthropology: Aging the Living
Airbags As with any electronic system, air bag system technology is evolving and being used in more creative ways. Passenger vehicle air bag systems have three main components: the air bag module, the sensors, and the main computer. Within each of these groups,
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Airbags
there are several types of components. Additionally, items such as seatbelt pretensioners and steering column shear capsules factor into the design of the overall passenger safety system. Air bags are passive safety devices. They require no action by the occupants, other than turning on the vehicle, to perform their protective role in the event of an accident. They are designed to work in conjunction with seatbelts. More advanced air bag systems not only work in conjunction with seatbelts, but also use the information regarding whether or not the seatbelt is actually buckled to aid in deployment decisions. This was one of the first types of occupant detection incorporated into air bag systems. Occupant detection is an area of air bag technology that is rapidly evolving. From the simple seatbelt switch to the more complicated seat sensors and cameras, occupant sensing and position discrimination employ some of the newest technologies. But, before the newer systems are discussed, an understanding of the basics of air bag systems must be understood. As stated before, there are three main components to air bag systems: the air bag module, the sensors and the computer. The air bag module is the actual fabric air bag. It is the most visible component. Before it is deployed, the fabric bag is folded in a specific manner and housed behind a molded plastic housing. This housing is designed with a deliberate weak area, called the tear seam, which allows the air bag to
break through the housing when it is deployed. This housing is what the occupant sees in the steering wheel or instrument panel of their vehicle. On the back side, there is an inflator containing the electrical components and chemicals that when ignited by the squib create the gas needed to deploy the air bag. When a deployment decision is made, an electrical current is sent through the wires to the squib causing the ignition of the chemicals and the gas that inflates the air bag. The decision to deploy the air bags is made by the system in the vehicle. Early air bag systems (late 80’s –early 90’s) were called distributed sensor systems. In a distributed system, there are at least two inertia-based switches located outside of the computer box and one inside the computer box. An inertia-based switch is a mechanical switch that closes due to a change in momentum of the vehicle. There is no accelerometer.a To deploy the air bags, one of the external switches and the internal switch had to be closed simultaneously to complete an electrical circuit, sending current to the squib and deploying the air bags simultaneously, as shown in Figure 1. Distributed systems do not contain the amount of crash data that is commonly found in today’s vehicles. Since there is no accelerometer, no acceleration or Delta Vb data can be recorded. The timing of the sensor closures can be recorded along with the status of the seatbelt switch (generally driver only).
Air bag
Air bag
Internal switch (safing/arming) External switches
+ − Battery
Figure 1 A distributed air bag system employs the use of electromechanical sensors. One is on the battery side of the air bag circuit, and one is on the ground side of the air bag circuit. Both must be closed simultaneously to deploy the air bags
Airbags
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Integrated system
Air bag
Air bag
External sensor
External sensor
Accelerometer Microprocessor Internal sensor (safing/arming)
Figure 2 An integrated air bag system uses external sensors connected to the air bag computer in conjunction with the internal accelerometer and internal sensor to make a deployment decision
The next generation of air bag systems began appearing in the early to mid 90’s. These systems employed accelerometers located inside the computer box along with a sophisticated algorithm that analyzed the incoming data to make a deployment decision. The fundamental difference between this integrated system and the distributed system is that the simple completion of an electrical circuit does not deploy the air bags. The air bag computer algorithm must make a deployment decision. The integrated system consists of an accelerometer, an inertia-based switch, and a microprocessor with a deployment algorithm housed inside the computer box. Generally at least one external inertia-based switch is used; however, some integrated systems do not use any external sensors, as shown in Figure 2. With the addition of the accelerometer, more detailed crash data including acceleration and/or Delta V of the crash can be recorded. Successive generations of air bag systems have built upon the basic integrated sensor design. The external sensors have become more sophisticated– some are accelerometers themselves. The algorithms have become more finely tuned. The air bag computer is part of a vehicle-wide network that shares information to help with deployment decisions. Some of the data from the other vehicle computers is saved in the air bag computer crash data files. Seatbelt switches are included in the deployment decision making process, especially when seatbelt
pretensioners are present. Seatbelt pretensioners are pyrotechnic devices that remove the slack from the seatbelt webbing to minimize the forward excursion of the occupant. The air bags are not necessarily deployed simultaneously. And occupant detection systems can override a deployment decision if the air bag may do more harm than good. The amount and type of information recorded by each system is completely dependent on the manufacturer of the vehicle and the manufacturer of the air bag system. Before a discussion on data, directional sensitivity must be addressed. All of the sensors involved in the air bag system are installed in a specific orientation to respond to acceleration pulses coming in certain directions. The sensors associated with frontal air bags are oriented longitudinally on the vehicle. They only respond to acceleration pulses coming from the front to the back of the vehicle. In the same manner, sensors oriented laterally are for side air bag systems. They only respond to acceleration pulse moving right-to-left (passenger side) or left-to-right (driver side). If the acceleration pulse does not occur exactly perpendicular to the front or side of the vehicle (as it rarely does in an actual crash), then the accelerometer is responding to either the lateral or longitudinal component of the crash pulse. As shown in Figure 3, this is called the angle of impact. The farther the angle of impact is from perpendicular, the greater the impact force required to close the sensor, as shown in Figure 4. Issues
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Airbags Directionality Front of vehicle
Cra
Longitudinal (front-to-rear)
sh p ulse
Driver's side
Passenger’s side
Lateral (side-to-side) Rear of vehicle
Figure 3 The direction of the crash pulse is important in determining whether or not the air bags will deploy. The front air bags are deployed based on the severity of the longitudinal component of the crash pulse. Side air bags are deployed based on the severity of the lateral component of the crash pulse
Directionality Crash pulse 1 Long 1 Crash pulse 2 Lat 2
Front of vehicle Lat 1 Longitudinal (front-to-rear)
Long 2
Driver’s side
Passenger’s side
Lateral (side-to-side) Rear of vehicle
Figure 4 Crash Pulse 1 has a larger longitudinal (front-to-rear) component than lateral (side-to-side). Crash Pulse 2 has equal longitudinal and lateral components
regarding the angle of impact are best resolved by accident reconstruction. The second part to making sensors an effective part of the air bag system is their placement. The sensors must be placed so that they correctly respond to different crash pulses. In distributed systems, there
are two types of sensor placement: triangular and inline. A triangular sensor placement used two sensors at the front of the vehicle, left and right. Generally, these sensors are found in the area between the headlight and the outside edge of the radiator. The third sensor is the safing/arming sensor located inside
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Airbags the air bag computer case, which is located near the center of the occupant compartment. The in-line sensor placement used one sensor at the front, center of the vehicle and one sensor behind the firewall in the occupant compartment. The firewall sensor is variously located. The third sensor is the safing/arming sensor, again located inside the air bag computer case. The introduction of integrated systems consolidated all of the sensors into the same casing as the air bag computer through the use of an accelerometer. The use of a centrally located accelerometer only required the development of complex computer algorithms to analyze the acceleration data. Eventually, external sensors were brought back into the air bag system to give additional information to the algorithms and help discriminate whether or not to deploy in crashes that may be borderline or have a very narrow pulse transmission zone, such as poles or trees. A very general rule of thumb for deployment parameters in terms of miles per hour is in a full frontal crash with an impact severity equivalent to hitting a rigid barrier at 8 mph or less the air bags should not deploy. In the same type of crash described above with the impact at 15 mph, the air bags should always deploy. The area between 8 mph and 15 mph is called the gray zone. As air bag systems have become more sophisticated, especially in the area of occupant detection, this general range of deployment parameters can vary widely, going up as high as 20 mph for a properly positioned and seatbelted occupant. Now that all of the parts of the air bag system have been discussed, the basic types of decision tree structures can be presented. These are all meant to be general examples of the progression of air bag technology. Starting with the distributed system, the only requirement for deployment is to have one crash sensor and the safing/arming sensor close simultaneously. This would deploy both frontal air bags simultaneously. There is no input from the air bag computer. This is illustrated in Figure 5. Next, there is an integrated system. In the first generation of integrated systems, the computer algorithm analyzes the accelerometer input and the closure of any external sensors to make a deployment decision, as shown in Figure 6. As the integrated system gains more inputs, the decision process becomes more complicated. The status of seatbelts and the position of
Distributed system flow chart Crash start
Are any external sensors closed?
No
Do not deploy
End
Yes Is the internal sensor closed?
No
Yes Deploy air bags End
Figure 5 This flow chart outlines the base logic behind a distributed air bag system
the front seats can override the air bag deployment command. This is shown in Figure 7. Additionally, in many trucks and SUVs the passenger air bag can be manually turned off by a keyed switch. As the air bag system has become more complicated, the amount of information saved by the air bag computer has increased. The first air bag computers were not intended to record information regarding the deployment event. They were there to monitor the status of the air bag system components and record any diagnostic trouble codes (DTCs or fault codes) that occurred. These DTCs would activate the air bag light in the instrument panel signaling the vehicle should be brought in for service. When being serviced, the technician can access the DTCs through a handheld scan tool to help identify the component causing the air bag light. The first crash-relevant piece of information recorded in the air bag computer was the timing between sensor closures. This time was recorded in milliseconds (1/1000th of a second) and enabled some determination of how quickly the air bags were commanded to deploy. The next piece of data that began to show up consistently was whether or not the driver’s seatbelt was buckled. As air bag systems migrated to integrated systems, the recorded timing data became the time from when the computer recognized the possibility of a non-normal event (wake-up or algorithm enable) to the time the air bags were commanded to deploy. Additionally, since these integrated systems employ an accelerometer, the crash
56
Airbags One possible integrated system flow chart Crash start
Is the internal sensor closed?
No
Do not deploy
End
Yes External sensor inputs
Did the algorithm cross a deployment parameter?
No
Yes Deploy air bags End
Figure 6
This flow chart outlines the base logic behind one possible configuration of an integrated air bag system
One possible integrated system with occupant sensing flow chart Crash start Is the internal sensor closed? Seat belt sensor inputs
External sensor inputs
No
End
Do not deploy
Yes Did the algorithm cross a deployment parameter?
No
Yes Is the crash severe?
No
Is the seat belt buckled?
Deploy air bags End
Yes
Yes
No
Deploy air bags
Deploy pretensioner
End
End
Figure 7 This flow chart outlines the base logic behind one possible configuration of an integrated air bag system that includes occupant sensing
data began to include longitudinal acceleration and/or Delta V. With the advent of side air bags, lateral acceleration and/or Delta V may also be recorded. The final major piece of crash data that may be recorded is pre-crash data. As of the writing of this article, only two manufacturers, GM and Ford, have employed this type of data. In GM’s pre-crash data, four parameters are recorded independently and
continuously in a data storage buffer. When a nonnormal event is detected, the last five data samples of these parameters are saved into the crash data. The four parameters that GM currently records are vehicle speed, engine RPM, throttle percent and brake switch status. In Ford’s pre-crash data, there are many additional data parameters saved for a time interval varying between 26 seconds and over 6 minutes,
Airbags depending on the vehicle in question. However, Ford does not save this data in the actual air bag computer. It is stored in volatile memory in the powertrain control module. This data must be retrieved very carefully to prevent its loss. Additionally, power must not be applied to the vehicle in question or Ford’s pre-crash data will be overwritten with information pertaining to the current, post-accident state of the vehicle. If the vehicle in question has seatbelt pretensioners or any form of occupant position sensing, the status of these parameters may also be recorded, especially if they are part of the deployment decision tree. If one front seat occupant is wearing their seatbelt and that seatbelt has a pretensioners and the other front seat occupant is not wearing their seatbelt, the air bag computer algorithm may make the decision to deploy the pretensioners of the belted occupant and the air bag of the unbelted occupant. Belting and occupant position may also factor into the force with which an air bag is deployed. Some air bag systems have two inflators for their air bags which can be timed to change how fast the air bags are deployed or how long they stay inflated. Once it has been determined that the vehicle in question has the ability to save crash-related data, it can frequently be retrieved. This retrieval process involves the subject vehicle, an interface box, and a laptop computer. There is currently one publicly available interface that allows the user to download the crash data from certain vehicles. If the vehicle in question is not on the list of this public interface system, then the data stored on the air bag computer must be retrieved by the vehicle manufacturer. The amount and type of crash data saved in the air bag computer varies widely by manufacturer. It can also vary within the manufacturer by model and model year. There are also situations, such as power loss during the accident, which can cause the data to not be recorded or to be only partially recorded. The first priority of the air bag computer is to discriminate between a deployment and non-deployment event and deploy the air bags when necessary. The second priority is to record the crash-related data. The data is first stored in a volatile memory called RAM. This type of memory is erased if power is lost. However, the data must be stored in RAM first because, until a deployment decision is made, the computer would not know whether to place the data in the non-deployment or deployment section of the
57
permanent memory. This permanent memory is called EEPROM. Once the data is in EEPROM it cannot be erased due to a power loss. The air bag computer only has a limited amount of backup power which would first be used to deploy the air bags and then record the crash data. Now, manufacturers are just beginning to add crash prevention systems. One type of system employs different types of radar to determine how close the vehicle is getting to the one in front of it. The crash prevention system then predicts whether or not the distance between the vehicles is becoming too small. If it is, the vehicle’s brakes are applied automatically through the cruise control system. This is called adaptive cruise control. The next level of adaptive cruise control will be able to be used at low speeds which will help to prevent minor accidents in bumper-to-bumper traffic. Another facet of crash prevention systems are warnings for lane-departure or side alerts if another vehicle is getting too close. Some manufacturers offer night vision, a head-up display, and even a drowsy driver monitor. As of the writing of this article, not only cost is preventing the widespread use of these technologies, but also the integration of the multiple computers and cameras over the vehicle network needs to be developed that is fast and reliable. As this technology continues to evolve, it will help the air bag system by creating more detailed pre-crash inputs. The following is a list of references for more information on air bag systems and their data: auto.howstuffworks.com/airbag.htm actsinc.org Automotive Coalition for Traffic Safety nhtsa.dot.gov National Highway Traffic Safety Administration iihs.org Insurance Institute for Highway Safety sae.org Society of Automotive Engineers (papers, standards, books, etc.)
End Notes a.
An accelerometer is a device that changes voltage when subjected to a mechanical stress. This change in voltage is measured and calibrated to relate to acceleration values through the use of known pulses.
58
Alcohol
b.
V is the difference between the initial velocity and final velocity. It is not the barrier equivalent velocity or the initial velocity of the vehicle before impact. HOLLY A. ADAMS
Alcohol Introduction Alcohol (ethanol or ethyl alcohol) is the world’s favorite recreational drug, legally available to adults and widely used for pleasure and relaxation without consequence. Indeed, moderate drinking (one to two glasses of wine each day) has a number of beneficial effects on health and is often recommended as a prophylactic treatment to reduce the risk of dying from coronary artery disease and stroke [1]. However, ethanol is also a drug of abuse and chronic drinking eventually leads to dependence and craving for alcohol with serious consequences for the individual and society [2]. Binge drinking and drunkenness have emerged as major public health problems and overconsumption of alcohol is frequently a catalyst and contributing factor in violent crimes such as physical and sexual assault and homicide [3]. This means that alcohol ranks as the foremost psychoactive substance encountered in forensic investigations of unnatural deaths such as suicides, drowning, and especially road-traffic fatalities where 20–40% of crashes are caused by drunken drivers. Forensic investigators need to understand what happens to alcohol in the body and how excessive drinking influences a person’s behavior in a negative way [4]. The ability to perform skilled tasks, to comprehend and communicate and to form intent are questions that often arise in forensic casework and legal proceedings. The need to translate a person’s blood-alcohol concentration (BAC) into the quantity of alcohol consumed is also important and, indeed, ethanol is one of the few drugs for which this calculation is feasible and defensible (see later in this section for details).
During prosecution of drunken drivers, a forensic investigator or expert witness might be asked to perform a backward extrapolation of a person’s BAC from the time of blood sampling to an earlier time, such as the time of driving [5]. This procedure is known as retrograde extrapolation, back-calculation, or back-tracking and is a dubious practice, owing to the many assumptions and unknown factors involved. Alcohol is the foremost psychoactive substance encountered in postmortem toxicology and heavy drinking and drunkenness, either directly or indirectly, are responsible for considerable morbidity and mortality. Whether or not acute alcohol poisoning was the cause of death is not always easy to determine because of wide variation in the sensitivity and reaction of different people to the same dose of alcohol. Interpreting the concentration of a drug measured in blood or other body fluid in relation to the dose administered or the effects produced on the individual is fraught with difficulties. Much depends on the interplay between chemical, pharmaceutical, physiological, psychological, and genetic factors. In the case of ethanol, the situation is simplified thanks to its special physiochemical properties, namely, small molecular size, distribution into the total body water (TBW), and lack of binding to plasma proteins. Table 1 gives a summary of the main physicochemical properties of ethanol. The BAC reached after drinking a known amount of alcohol depends on a host of factors, the most important of which are the quantity consumed and the speed of drinking. Higher doses and more rapid ingestion lead to higher peak BAC (Cmax ) and an earlier Table 1 ethanol
The major physicochemical properties of
Property
Ethanol
CAS number(a) Molecular weight Molecular formulae Chemical formulae Structure Common name Boiling point Melting point Density Water solubility
64–17–5 46.07 C2 H6 O CH3 CH2 OH Primary aliphatic alcohol Beverage or grain alcohol 78.5 ° C −114.1 ° C 0.789 at 20 ° C Mixes completely with water
(a)
Chemical abstract service registry number
Alcohol occurring time to peak (tmax ), and consequently more pronounced effects on the individual concerned. Among pharmacological agents, ethanol is classified as a depressant of the central nervous system even though drinking small quantities tends to elicit a state of excitement and euphoria. However, these feelings arise by suppression of inhibitions in the cerebral cortex and not as a direct stimulant action of the drug [6]. Ethanol is sometimes administered by intravenous infusion, such as 8–10% v/v solutions in physiological saline, as is common practice in some research applications and also in the emergency clinic as an antidote for treatment of methanol poisoning [7]. Absorption of ethanol is rapid when given rectally as an enema, but for all practical purposes alcohol is ingested orally by drinking an alcoholic beverage. Trace amounts of ethanol are produced naturally in the body, either by fermentation of carbohydrates in the gut or during certain minor biochemical reactions of the intermediary metabolism [8]. The concentrations of the so-called endogenous alcohol in blood are normally so low (60 years) and those overweight reach higher BAC for the same dose of ethanol administered compared with a young nonobese individual. Well-known gender differences exist in the distribution space for ethanol because women tend to have less body water per kilogram body weight than men. On the basis of experiments dating back to the 1930s, the average Vd for women was determined as 0.6 l kg−1 compared with 0.7 l kg−1 for men [12]. Note that these values represent the distribution ratio
of alcohol between the body as a whole and the blood compartment. Since the experiments used to determine Vd for ethanol date back to the 1930s, they probably need updating considering the epidemic of obesity in modern society [13]. Table 4 shows the relationship between body mass index (BMI) and clinical manifestations or stages of obesity, which should be considered when choosing the most appropriate distribution factor for use in blood-alcohol calculations. Higher BMI (>30) is associated with lower values of Vd such as 0.4–0.5 l kg−1 rather than 0.6–0.7 l kg−1 [14]. Instead of using the population average Widmark r-factors for men and women, another approach is to calculate a person’s TBW from information available about age, height, and weight (see later in this article). As a general recommendation, an intersubject variation of ±20% should be used in Table 4 Clinical manifestations of obesity in relation to body mass index (BMI), which might impact on the distribution volume of ethanol (Widmark r-factor) Classification Underweight Normal Overweight Obesity class I Obesity class II Obesity class III
BMI (kg m−2 ) 40
62
Alcohol Breath urine sweat 2– 5%
HOOC O
C2H5O Ethanol
HO
1.2 g l−1 or 120 mg/100 ml) such as in many drunken drivers. Alcoholics during detoxification and people that drink continuously over several days or weeks to reach high BAC (>3 g l−1 ). People with a genetic predisposition or in a hypermetabolic state (e.g., after burn trauma or hyperthyroidism).
This calculation assumes a normal nonobese person with a body weight of 70 kg and a Widmark r-factor (distribution volume) of 0.7 l kg−1
70
Alcohol
crime and obtaining a blood sample for toxicological analysis means that some drugs are no longer measurable. The police therefore might want to know what the BAC was at the time of the alleged assault and whether the victim was incapacitated because of too much drink or drugs [26]. In an actual case of drunken driving, a man was arrested by the police and a blood sample was taken for determination of alcohol content. The man was released but sometime afterward he was again observed driving, although on this occasion a blood sample was not available for analysis. Under these circumstances, the police might want to know whether the man was above the legal limit on the second occasion based on the concentration in the first blood sample and information about the rate of alcohol metabolism. Since the metabolism of ethanol occurs at a constant rate per unit time in a large segment of the BAC curve, this makes forward or backward extrapolation feasible under certain circumstances [5, 10, 25]. The first condition necessary is that the postabsorptive phase was reached at the time of driving or when a crash occurred (e.g., 90 min in Figure 3). The second is that the rate of alcohol elimination from the bloodstream is known or a value that does not prejudice the suspect (e.g., 0.1 g l−1 h−1 ) is assumed. Third, a deduction should be made from the average BAC to allow for uncertainty in the analysis and back-extrapolation should then start from this lower value and not the average BAC.
Interpreting Blood-Alcohol Concentrations in Samples Obtained at Autopsy The use and abuse of alcohol in society has meant that drunkenness is a prime factor in many accidents on the roads, at home and in the workplace [3]. Alcohol intoxication is often an underlying factor in violent crime such as homicide, muggings, and sexual assault. Alcohol therefore tops the list of drugs identified in blood specimens taken during routine forensic autopsies and investigations of all out of hospital deaths [27, 28]. During investigations of road-traffic fatalities, a key question is whether the driver was under the influence of alcohol or drugs at the time of the crash. This becomes important when responsibility for the crash is investigated and insurance claims are made.
Likewise, alcohol intoxication and drunkenness are prominent in many other traumatic events including fights, homicides, suicides, and drowning. Knowledge of the BAC in the deceased provides useful information when the cause of death is determined. The methods used to measure alcohol (ethanol) in blood and other body fluids are the same regardless of whether specimens are obtained from the living or the dead [29]. However, great care is needed when the results of postmortem analysis are interpreted and a conclusion is reached about the state of inebriation or drunkenness at the time of death. Unlike drawing blood from a living person, there are a number of artifacts that should be considered in postmortem toxicology [27–29]. However, the situation is simplified because a much wider section of biological specimens are available from a corpse, thus making toxicological results easier to interpret.
Postmortem Aspects The quality and composition of the blood samples obtained at autopsy can vary widely depending on the circumstances surrounding the death and the condition of the body, such as degree of trauma and whether decomposition and putrefaction had commenced [28–30]. The recommended sampling site for blood in postmortem toxicology is a femoral vein after crossclamping. Sampling blood from the heart or pleural cavity is not recommended because of the risk that alcohol might have escaped from the stomach to contaminate the sampling site. Aspiration of stomach contents during the agonal period means that alcohol gets into plural cavity blood via the lungs. After death the body should be handled with care by the crime scene investigators or during transportation and storage at the mortuary to minimize spread of any alcohol. All such factors can lead to redistribution of alcohol from stomach contents if heavy drinking had occurred just prior to death [31]. In bodies autopsied within 24 h of death and when trauma is minimal, the concentration of alcohol in femoral venous blood is the closest one can come to knowing the antemortem concentration. Indeed, there is some evidence that a decrease in concentration occurs after death because metabolizing enzymes retain some activity for a few hours after death as the body cools. If the autopsy and sampling of blood
Alcohol for toxicology is done the same day, then a chemical preservative, such as sodium fluoride, is probably not necessary. For longer delays and when specimens are sent by mail to another laboratory, it is imperative to include sodium or potassium fluoride as a preservative in blood and other biological specimens (1–2% w/v). The fluoride ion functions as an enzyme inhibitor and prevents the synthesis of ethanol by fermentation processes after sampling. However, this does not rule out that ethanol had already been produced before the autopsy was performed [30, 32] (see also Toxicology: Analysis.)
Alternative Body Fluids The results of postmortem blood-alcohol analysis are considerably strengthened if other body fluids are submitted for analysis along with the blood sample (e.g., urine and vitreous humor (VH)). In postmortem work in addition to cardiac or femoral venous blood, urine, VH, and cerebrospinal fluid (CSF) are the most useful specimens for determination of ethanol [33, 34]. These other biofluids, which are ∼100% water, are obtained from the urinary bladder, the eye, and the back of the neck (cisternal fluid), respectively. The concentrations of alcohol depend on water content and also on time after drinking and the status of alcohol absorption and distribution in the body when death occurred. The concentrations of alcohol measured in VH, urine, and CSF are displaced in time compared with the venous BAC. During the absorption stage, the concentrations of alcohol are lower in these alternative fluids compared to the blood, although 1–2 h later when equilibration of ethanol in all body fluids is complete, the VH, urine, and CSF contain a higher concentration, by ∼20%, compared with that of the blood samples. Vitreous fluid from the eye is an important biological specimen in postmortem toxicology for several reasons. First, VH is a relatively clean watery fluid easily obtained with syringe and needle even without conducting a complete autopsy. Second, the remote nature of the eyes compared with the gut means that the spread of bacteria to contaminate the VH is much less likely than the contamination of central or peripheral blood during autolysis [34]. When the corpse has been subjected to severe trauma, a suitable blood sample might not be available and with some reservations the BAC can be estimated indirectly by the
71
analysis of ethanol in the VH or the urine, albeit with considerable uncertainty. When the body has undergone putrefaction, the BAC result is obviously suspect, owing to the risk of microbial formation of ethanol from glucose present in the blood. Under these circumstances, VH gives a more reliable indication of whether the deceased had consumed alcohol and might have been drunk at the time of death. Figure 6 shows a high correlation between the concentrations of ethanol in VH and in femoral blood (r = 0.98) at autopsy. The average VH/BAC ratio of ethanol concentration was 1.19 : 1 (SD = 0.28) and the range was from 0.28 to 2.90 [34]. The distribution ratios for urine/blood, vitreous/blood, and CSF/blood change as a function of time after drinking. Much depends on the position of the alcohol curve and absorption or postabsorptive phase of metabolism at the moment of death [27]. On the ascending limb of the BAC profile, the concentrations of ethanol in urine, VH, and CSF are lower than or about the same as in venous blood. In the postpeak descending limb of the BAC profile, which corresponds to the postabsorptive phase, the concentration of ethanol in urine, VH, and CSR are always higher than that in the blood. Indeed, alcohol might still be measurable in these alternative specimens even though BAC is reported as negative. Table 8 compares the water contents of body fluids and tissues usually available for the analysis of ethanol at autopsy and gives expected ratios of the concentrations of ethanol relative to blood samples. Traumatic injuries and death by blunt force with open wounds and massive blood loss are factors that increase the risk of bacteria entering the body. Under these circumstances fermentation processes might produce ethanol before an autopsy is performed. This risk is heightened at elevated environmental temperatures (summer months) and when a long time elapses before recovery of the body, e.g., after an air disaster or death at sea [28]. Although a fluoride preservative is routinely added to blood specimens taken at autopsy, some alcohol might have been synthesized in body cavities between the time of death and autopsy. After skull trauma, blood is often sampled from a subdural hematoma or a clot in the brain, which furnishes useful information in postmortem toxicology. Because of reduced or nonexistent blood circulation to the clot, any alcohol it contains does not
72
Alcohol 6.0
N = 672 r = 0.98 Residual SD = 0.20 g l−1
Blood-alcohol (g l−1)
5.0 4.0 3.0 2.0 1.0
BAC = −0.06 + 0.81 VH
0.0 0.0
1.0
2.0 3.0 4.0 Vitreous humor alcohol (g l−1)
5.0
6.0
Figure 6 Correlation between the concentrations of ethanol determined in femoral venous blood and vitreous humor samples obtained at autopsy Table 8 Average water contents of whole blood, body fluids, organs, and tissues and the concentration ratios of ethanol relative to whole blood
Specimen Whole blood(b) Plasma/serum Erythrocytes Urine Vitreous humor Cerebrospinal fluid Bile Synovial fluid Liver Brain Skeletal muscle Kidney
Water content (% w/w) 78–81 91–93 68–71 98–99 99–100 98–99 87–97 92–96 80 75 76 79
Ratio of ethanol concentration relative to whole blood(a) 1.0 1.1–1.2 0.8–0.9 1.2–1.4(c) 1.1–1.3 1.1–1.3(d) 0.8–1.0 1.1–1.2 0.6–0.8 0.8–1.0 0.8–0.9 0.6–0.7
(a) The values can differ depending on the concentration of alcohol in the samples and the time after drinking when death occurred (b) Depends on water content and hematocrit of blood sample, which in turn depends on gender and the condition of the body (c) The ratio depends on the stage of alcohol absorption and distribution at time of death (d) Lumbar fluid taken during postabsorptive phase
undergo metabolism. The concentration of ethanol in the sequestered hematoma therefore gives an indication of the person’s BAC some hours earlier, such as
when the trauma occurred. For example, if a person suffers a blow to the head when drunk but survives for many hours before death, considerable amounts of alcohol are eliminated by metabolism (0.15 g l−1 h−1 ). If 10 h elapses before death, then a BAC of 1.5 g l−1 is no longer measurable. However, the concentration measured in the blood clot can furnish useful information about the BAC at an earlier time, such as when the clot was formed. Contamination of the wound with bacteria and the rate of formation of the clot and other factors need to be considered. Any emergency life-saving treatment administered at the crash site, such as intravenous fluids to counteract shock, and massive blood loss are also important to consider. Table 9 lists many of the considerations necessary when results of postmortem alcohol analysis are reported and interpreted.
Biochemical Markers of Alcohol Consumption Considerable research has been done to develop a biochemical marker of acute and chronic alcohol consumption. In this connection, the formation of the nonoxidative metabolites of ethanol, namely, EtG and EtS, has attracted a lot of attention [35, 36]. The presence of these metabolites in body fluids taken at autopsy means that ethanol must have undergone metabolism during life, which supports
Alcohol Table 9
73
Factors to consider when the results of blood-alcohol analysis in postmortem specimens are interpreted
1. Specificity of the analytical method and whether other volatile substances might have interfered with the determination of ethanol. 2. Time between death, recovery of the body, and the postmortem examination. 3. Condition and location of the body: (a) Indoors or outdoors (b) Time of year (c) Temperature and humidity of the environment (d) Extent of traumatic injuries (e) Abdominal trauma, e.g., ruptured stomach (f) Incinerated body (g) Body recovered from water (h) Extent of decomposition/putrefaction, bad smell, maggots, etc 4. Was a preservative (NaF ∼2%) added to all specimens submitted for toxicology? 5. Risk of contamination of specimens with extraneous solvents during emergency service treatment at hospital, the mortuary, or the analytical laboratory. 6. Was the body embalmed and if so what embalming fluids were used and did they contain any alcohols? 7. Compare and contrast the concentrations of ethanol expected in different sampling sites after considering water content of the specimens (blood, urine, and vitreous humor) 8. Should the water content of blood be determined and results of alcohol analysis adjusted to blood-water content of 80% w/w? 9. Variations in alcohol concentration depending on absorption or postabsorptive stage of the blood-alcohol curve when death occurred. 10. How was the body handled at the scene of death and during transport and storage at the mortuary? 11. Any evidence of recent consumption of alcohol before death? 12. Concentration of ethanol in stomach contents, risk of postmortem diffusion, and aspiration of vomit during the agonal period. 13. Changes in ethanol concentration caused by evaporation, dilution, or degradation of ethanol after death.
antemortem consumption of alcohol. If ethanol was present in blood and urine taken at postmortem and EtG and EtS were shown to be negative, then this would raise a warning flag that the ethanol was probably produced after death as a result of microorganisms acting on carbohydrates or other substrates. Even other urinary markers of acute alcohol ingestion such as the metabolites of serotonin and the ratio of 5-hydroxytryptophol (5HTOL) to 5-hydroxyindole acetic acid (5HIAA) are available [36]. Biochemical markers are useful to detect damage to organ and tissue as a consequence of heavy drinking so that treatment can be given before liver cirrhosis and death occurs. This entails measuring the concentration of certain hepatic enzymes such as gamma-glutamyltransferase (GGT), aspartate aminotransaminases, and alanine aminotransaminases (AST and ALT). Concentrations are elevated in serum after a long period of heavy drinking because they leak into the bloodstream when the liver is damaged by the alcohol [37]. Enlarged size of the red blood cells, mean corpuscular volume (MCV), is another widely
used marker of chronic drinking in combination with the enzyme markers [36]. Carbohydrate deficient transferrin (CDT) is another marker of heavy drinking used in clinical medicine but also with forensic applications thanks to good sensitivity and high specificity. Transferrin is a plasma protein synthesized and secreted by the liver that serves to transport iron in the body [36]. After a period of continuous heavy drinking (60–80 g/day over many weeks), glycosylation of the transferrin molecule is altered and this is reflected in the loss of one or more of the carbohydrate moieties, hence the name carbohydrate deficient. The methods used to determine serum CDT are now much improved, e.g., by use of capillary electrophoresis and high performance liquid chromatography (HPLC), and interlaboratory reporting of the results of CDT analysis is now better standardized. CDT is the marker of choice to screen individuals for excessive drinking before the liver is too severely damaged and helps to corroborate results from the use of clinical interviews and questionnaires [35–37]. CDT is considered to be the most specific marker of
74
Alcohol
Table 10 Typical signs and symptoms of alcohol influence in relation to the person’s blood-alcohol concentration (BAC) BAC g l−1 (mg/100 ml)
Signs and symptoms of alcohol influence(a)
0.0–0.2 (0–20) 0.3–0.5 (30–50)
Sobriety, no untoward effects, or outward signs Less inhibited (euphoria), more talkative, impairment of certain cognitive tasks and skills that require divided attention More rowdy and daring, sensory and motor disturbances, slowed reaction time especially in choice situations Lack of coordination, unsteady gait, slurred speech, prolonged reaction to sights and sounds. Obvious drunkenness, aggressive behavior, and ataxia significantly slowed reaction time even when relatively simple tasks are performed; nausea and vomiting in some individuals especially if the BAC increases rapidly to reach these levels Not able to stand upright or walk unaided, incoherent speech, and motor areas of the brain are markedly influenced, thus distorted perception of time and judgment and near comatose state Confusion, stupor, or coma with shallow breathing, risk of respiratory arrest, loss of gag reflex, and risk of inhalation of vomit Profound risk of death from respiratory paralysis and cardiopulmonary arrest
0.5–1.0 (50–100) 1.0–1.5 (100–150) 1.5–2.0 (150–200)
2.0–3.0 (200–300)
3.0–4–0 (300–400) 4.0–5.0 (400–500)
(a) Both subjective and objective measures of alcohol influence are more pronounced on the rising part of the BAC curve close to the Cmax compared with several hours later during the postabsorptive phase. This difference in the effects of ethanol is related to the phenomenon of acute tolerance or the Mellanby effect (see main text for details)
excessive drinking and false-positive test results are rare. CDT has found forensic applications to evaluate drinking habits of convicted drunken drivers before they are allowed to retake a drinking test. Biomarkers find use in many other situations when there is a need to verify that a person is no longer a problem drinker, such as when it comes to rehabilitation of alcoholics and custody of children, etc.
Development of Tolerance to Ethanol It is common knowledge that the effects of drugs differ widely between different individuals despite intake of the same dose under otherwise identical conditions [16]. Regular drinkers can tolerate more alcohol and appear less influenced compared with moderate or nondrinkers with the same BAC. Among other things, this raises the question of whether BAC is really such a reliable indicator of the degree of alcohol influence in any individual case. Table 10 lists various clinical signs and symptoms of alcohol influence as a function of increasing BAC. Much variation can be expected in the individual case, depending on the time after drinking when the observations are made. The degree of impairment after drinking alcohol depends on the speed of drinking, and elapsed time after the end of drinking when tests or observations were made. People feel more impairment on the rising limb of the BAC curve
compared with the declining limb although previous experience with drinking alcohol and habituation are important considerations. The development of tolerance to the effects of alcohol or other drugs and the underlying mechanisms involved are complex topics involving behavioral changes and learning effects [38, 39]. Tolerance implies the ability to lessen the untoward effects of drugs after repeated exposure. To the pharmacologist, tolerance is often illustrated by a shift in the sigmoid dose–response curve to the right so that larger doses of a drug are required to produce the same degree of effect on the individual. Several different kinds of tolerance need to be distinguished and defined in connection with interpretation of BAC in forensic casework. The first and simplest kind of tolerance is referred to as dispositional tolerance, which has to do with altered absorption, distribution, metabolism, or excretion of ethanol during chronic treatment. The rate of absorption of ethanol is closely linked to gastric emptying, which in turn depends on factors such as dose and speed of drinking, fed or fasting state, concentration of ethanol in the beverage, and various hormonal influences [10]. Speed of distribution is determined by blood flow and tissue mass and the proportion of lean-to-fatty tissue in the body. The amounts of ethanol eliminated via breath, sweat, and urine are trivial (2–5%) and are dependent on simple physical
Alcohol
75
phase of the BAC curve compared with the ascending phase [41]. This phenomenon seems to be related to an adaptation of the brain cells and membrane receptors to an alcohol environment within a few hours of exposure to a single intoxicating dose. The exact mechanisms involved are unknown but seem to involve both learning phenomenon and adaptation to the impairment effects of the drug [38, 39]. Acute tolerance to alcohol is sometimes referred to as the Mellanby effect, named after the British pharmacologist (Sir Edward Mellanby), who first observed the phenomenon and published results of his experiments of alcohol intoxication in dogs [41]. Chronic tolerance is a more gradual process resulting in a diminished intoxicating effect after a period of continuous heavy drinking lasting several days or weeks without a period of abstinence. Those with a developed chronic tolerance at first sight will not exhibit overt signs of drunkenness, apart from a strong smell of alcohol on the breath, with BAC of 2–3 g l−1 (0.2–0.3 g%). Table 11 shows the results from a clinical examination and questionnaire administered to a large number of apprehended drunken drivers 2 h or more after they were arrested. The examining physicians were not aware of the person’s BAC and the assessment was based on answers to questions and simple clinical tests of motor and cognitive functioning. The physicians were asked to grade their findings and to conclude whether the people examined were not influenced, slightly influenced, moderately influenced, or heavily under the influence of alcohol. The data in the table demonstrate large discrepancies at one and the same BAC depending on, among other things, differences in training, experience, and enthusiasm on the part of the physician for
diffusion, which in turn is a function of the BAC. These diffusion processes are not markedly altered after a period of continuous heavy drinking. The rate of metabolism of ethanol is accelerated after a period of continuous heavy drinking, although the amounts of ethanol that have to be consumed and the duration of drinking are not well defined. The mechanism seems to involve the CYP2EI enzyme, which acquires an enhanced capacity to oxidize ethanol after chronic administration of substrates, such as ethanol as well as other drugs (e.g., barbiturates). This faster elimination of certain drugs from the body after chronic exposure is referred to as metabolic tolerance. However, studies have shown that after a few days of abstinence from alcohol, the rate of metabolism returns to normal as CYP2E1 enzyme becomes resynthesized. Thus, heavy drinkers or alcoholics do not necessarily show a faster rate of ethanol metabolism after they have remained sober a few days. Some alcoholics might have an abnormally slow rate of metabolism owing to malnutrition and liver damage (cirrhosis) caused by the abuse of alcohol. A well-studied and well-recognized form of tolerance is acute tolerance, which develops during a single exposure to ethanol [40]. The degree of intoxication, both subjective and objective, changes as a function of time after the end of drinking a known amount of ethanol. The signs and symptoms of alcohol influence are less pronounced on the descending limb of the BAC curve about 3–4 h after the end of drinking compared with the ascending limb before reaching Cmax . Acute tolerance to alcohol is therefore characterized by a diminished effect of the drug at the same blood or brain concentration on the descending
Table 11 Relationship between blood-alcohol concentration (BAC), number and percent of individuals judged not, slightly, moderately, or severely influenced by alcohol according to a clinical examination and questionnaire administered by a physician (police surgeon)(a) BAC (g l−1 ) (mg/100 ml)
N
0.0–0.49 (0–49) 0.50–0.99 (50–99) 1.00–1.49 (100–149) 1.50–1.99 (150–199) 2.00–2.49 (200–249) 2.50–2.99 (250–299)
103 223 226 195 104 44
(a)
Not under influence (%)
Slightly under influence (%)
52 (50) 111 (49) 58 (26) 17 (9) 5 (5) 0 (0)
Those examined were suspected for drunken driving in Sweden
47 90 107 65 31 9
(46) (40) (47) (33) (30) (20)
Moderately under influence (%)
Severely under influence (%)
4 (4) 22 (10) 59 (26) 81 (41) 52 (50) 21 (48)
0 (0) 0 (0) 2 (2) 32 (16) 16 (15) 14 (32)
76
Alcohol
this task, and inherent differences in tolerance (acute and chronic) in the people being examined. The type of tolerance that develops after long-term use of alcohol is sometimes referred to as behavioral or functional tolerance because it relates to an altered sensitivity of the brain to the effects of the drug. The underlying mechanism of functional tolerance, which manifests in marked behavioral effects of the drug after repeated exposure, is complex involving environmental, psychological, and genetic factors. The drinking pattern and amounts of alcohol necessary to elicit a chronic tolerance also causes physical dependence. Evidence of this comes from the physiological disturbances after cessation of drinking and when the BAC drops toward a zero concentration. Indeed, the severity of physiological disturbances during alcohol withdrawal can prove life threatening. To alleviate the withdrawal symptoms, patients are treated with drugs, such as barbiturates or benzodiazepines, that exhibit cross-tolerance to ethanol. The corresponding withdrawal stage after acute ingestion of ethanol (a single exposure) corresponds to the well-known hangover syndrome.
How Dangerous is Ethanol? In the field of forensic toxicology, drugs are classified as either licit or illicit and also in terms of their toxicity. Along with nicotine from use of tobacco products and caffeine from consumption of coffee or tea, ethanol is a socially
Relative frequency (%)
35
accepted legal drug. All pharmaceutical products are legal drugs although many such as opiates and benzodiazepines are classified as narcotics and are subject to abuse. The classic illicit drugs are heroin, cannabis, cocaine, ecstasy, lysergic acid diethylamide (LSD), amphetamine, methamphetamine, and gamma-hydroxybutyrate (GHB). When assessing the dangerousness of drugs, there are many factors to consider besides the risk of acute toxicity, such as dependence liability and social and medical harm caused to the individual and the costs to society for treatment and rehabilitation of those addicted to drugs [42]. With regard to acute toxicity, ethanol should be considered a fairly dangerous drug. The BAC associated with mild euphoria (0.4–0.5 g l−1 ) is only 10 times less than the BAC that could cause death (4.0–5.0 g l−1 ), through respiratory paralysis. This gives a ratio of lethal dose to effective dose of 10 : 1, which is a narrow safety margin for a legal drug. Besides acute toxicity, it is also important to consider the potential of a drug to cause physical and psychological dependence and craving. In a large case series of forensic autopsies (N = 693), the concentration of ethanol in femoral venous blood was evaluated when the cause of death was attributed to acute alcohol poisoning [43]. Figure 7 depicts the frequency distribution of BAC in these blood specimens and this shows a good fit to a bellshaped or Gaussian curve. This means that ∼95% of cases are within ±2 SD around the mean. The mean, SD, and median concentration of ethanol in femoral
N = 693, mean = 3.60 g l−1, SD = 0.86 g l−1, median = 3.60 g l−1, 2.5 and 97.5 percentiles = 1.9 and 5.3 g l−1
30
35 30
25
25
20
20
15
15
10
10
5
5
0
0 0.0
1.0
2.0
3.0
4.0
5.0
6.0
7.0
Blood-alcohol concentration (g l−1)
Figure 7 Frequency distribution of the concentration of ethanol in femoral blood in deaths attributed to acute alcohol poisoning (no other drugs present in blood) by the pathologist
Alcohol blood were 3.6 , 0.86, and 3.6 g l−1 , respectively, and therefore 95% of cases are within 1.9 and 5.3 g l−1 (mean ±2SD). Multiple sampling is a golden rule in forensic medicine and toxicology, so besides blood or plasma urine should be also obtained and sent for the analysis of ethanol and other drugs. Figure 8 shows the frequency distribution of urine–alcohol concentration (UAC) in deaths attributed to acute ethanol poisoning and when no other drugs were detected [44]. The mean and median concentrations are noticeably shifted toward higher values compared with BAC (Figure 7) as expected from the difference in water content between blood and urine. The frequency distribution of UAC is also a good fit to a Gaussian curve; mean, median, and 2.5 and 97.5 percentiles of 4.3, 4.3, and 2.4 and 6.1 g l−1 , respectively. The UAC is higher than BAC not only because of the higher water content of ∼100% in urine compared with that of ∼80% in blood, but also because most people die after ethanol is fully equilibrated in all body fluids [44]. The value of the UAC/BAC ratio can give a clue to whether absorptive was ongoing (UAC/BAC values 1.25) at the time of death [33, 44]. The BAC and UAC curves are shifted in time with UAC being less than BAC during the absorption phase and always higher than BAC in the postabsorptive period (Figure 9). This difference in the concentration–time profiles of ethanol in successive urine voids and in blood has implications for
Relative frequency (%)
30
the pharmacokinetic parameters of ethanol in blood and urine. In the experiment depicted in Figure 9, each subject emptied the bladder of residual urine before the start of drinking. Alcohol was served as neat whisky (0.85 g kg−1 ), which was finished in 25 min and consumed on an empty stomach after an overnight fast.
Lethal Dose of Ethanol Deaths caused by uncomplicated alcohol poisoning, that is, through depression of the central nervous system and paralysis of respiration and collapse of circulation generally occur at a BAC between 4 and 5 g l−1 [40, 43]. After drinking massive amounts of alcohol, the individual progresses through various stages of intoxication (see Table 10) before death occurs. If a BAC of 5 g l−1 is considered sufficient to cause death, then the Widmark equation can be used to calculate the amount of ethanol that needs to be consumed to reach this level. Table 12 gives the results of this calculation showing the number of grams of ethanol that are absorbed and distributed in all body fluids in a person with a BAC of 5 g l−1 . The results are illustrated for males and females with body weights ranging from 10 to 100 kg. Besides the mean quantity of ethanol in the body, the 95% range is included based on knowledge about intersubject variation in the distribution volume of ethanol (Widmark’s r-factor). The lethal dose of ethanol is slightly higher for men 3.5 g kg−1 (range 2.8–4.2 g kg−1 ) compared with that
N = 628, mean = 4.26 g l−1, SD = 0.96 g l−1, median = 4.30 g l−1, 2.5 and 97.5 percentiles = 2.4 and 6.0 g l−1
25
77
30 25
20
20
15
15
10
10
5
5 0
0 0.0
1.0
2.0 3.0 4.0 5.0 6.0 7.0 Urine-alcohol concentration (g l−1)
8.0
Figure 8 Frequency distribution of the concentrations of ethanol in bladder urine in deaths attributed to acute alcohol poisoning
78
Alcohol
Ethanol concentration (g l−1)
2.0 Blood Urine 1.5
1.0
0.5
0.0 0
100
200 300 400 500 Time after start of drinking (min)
600
Figure 9 Concentration–time profiles of ethanol in successive urinary voids and in blood samples from healthy volunteers after they drank 0.85 g ethanol per kg body weight on an empty stomach Table 12 The amounts of ethanol absorbed and distributed in all body fluids and tissues and the 95% range considered necessary to cause death by acute alcohol poisoning. Results are shown for both sexes as a function of body weight. In the calculation, a BAC of 5 g l−1 was considered sufficient to cause death by paralysis of respiratory centers in the brain Body weight Males(a) (g ethanol) Females(b) (g ethanol) (kg) Mean (95% range) Mean (95% range) 10 20 30 40 50 60 70 80 90 100
35 70 105 140 175 210 245 280 315 350
(28–41) (56–84) (84–126) (112–168) (134–216) (168–252) (196–294)(c) (224–336) (252–378) (280–420)
30 60 90 120 150 180 210 240 270 300
(24–36) (48–72) (72–108) (96–144) (120–180) (144–216) (168–252) (192–288)(c) (216–324) (240–360)
Average r-factor for males = 0.7 l kg−1 with 95% range ±20% (b) Average r-factor for females = 0.6 l kg−1 with 95% range ±20% (c) A bottle of spirits 40% v/v contains about 240 g ethanol (a)
for women 3.0 g kg−1 (range 2.4–3.6 g kg−1 ). For a man with a body weight of 70 kg, he would need to consume 240 g of ethanol or the amount contained in a whole bottle (750 ml) of liquor (whisky or vodka) to die from acute alcohol poisoning. Heavily intoxicated people are overrepresented among patients admitted to hospital for treatment
of head trauma and brain hemorrhage, which is a common cause of death in alcoholics [3]. Drinking on an empty stomach and neglecting to eat properly is dangerous because of ethanol-induced disturbances in carbohydrate metabolism and risk of developing life-threatening hypoglycemia (low blood sugar). The combined effect of alcohol and other drugs, such as barbiturates or benzodiazepines, has resulted in many adverse drug-related fatalities [7]. Exposure to the cold, such as if a person sleeps outdoors after a night of heavy drinking, has been responsible for many hypothermia-related fatalities because ethanol lowers core body temperature in addition to the low ambient temperature. Inhalation of vomit (aspiration) and asphyxia has killed many drunken people, especially young inexperienced drinkers, who have a nonfunctional gag reflex inactivated owing to gross intoxication and lack of consciousness [29]. A semicomatose person should not be allowed to “sleep it off” unattended and instead should be placed in a semiprone position and inspected regularly until they regain consciousness. A partial obstruction of the trachea during the time a person is in a comatose state after heavy drinking is yet another circumstance that could lead to death by asphyxiation [27–29]. Drinking alcohol too quickly to reach a BAC of 1.5 g l−1 or more often causes nausea and vomiting, especially in novice drinkers. This vomit reflex has saved the lives of many young people by removing unabsorbed alcohol from the stomach contents. However, if a person vomits when already in a state
Alcohol of gross intoxication with depressed gag reflex, there is a grave risk of vomit entering the airways and death being caused by asphyxiation [29]. Many teenagers with little or no previous experience with alcohol consumption have lost their lives in this way. The BAC determined in blood taken at autopsy is often considerably lower than the level that caused incapacitation at some earlier time because of decreases through metabolism at a rate of 0.15 g l−1 per h until the time of death.
Concluding Remarks Overconsumption of alcoholic beverages and drunkenness play a major role in many types of accidents, trauma deaths, suicides, muggings, and other crimes of violence, as evidenced by death certificates and reports from hospital accident and emergency departments worldwide [3, 45]. Moreover, heavy drinking and drunkenness are often the underlying factor in domestic violence, sexual assault, and road-traffic crashes. Accordingly, requests to determine the concentration of ethanol in blood and other body fluids and to interpret the results in relation to degree of impairment and ability to form intent are everyday services obtainable from forensic science and toxicology laboratories [26, 46]. Because a diagnosis of alcohol influence has deep-rooted social, medical, and legal ramifications, great care is needed when the analytical results are interpreted and conclusions reached for use in civil and/or criminal proceedings. Whether a person’s BAC was above or below a threshold limit, such as the legal limit for driving, makes the difference between punishment (fines, loss of driving permit, or incarceration) and acquittal [47]. The qualitative and quantitative determination of ethanol in body fluids is a relatively simple analytical procedure and the use of gas liquid chromatography provides accurate, precise, and specific results [48]. However, correctly interpreting these results requires knowledge about the pharmacokinetics and pharmacodynamics of ethanol as well as intersubject and intrasubject variation, drug-alcohol interactions, and the development of tolerance [11]. When it comes to interpreting the results of ethanol determinations in autopsy specimens, a number of other considerations are necessary, owing to the risk of various postmortem artifacts [27–29].
79
These include the condition and type of specimen, the stability of ethanol in the body after death, diffusion from the gut to other tissue after death, and the possibility of microbial synthesis occurring if the body has undergone decomposition [26–31]. Police investigations, insurance claims, and financial compensation to surviving family members might be jeopardized or invalidated if the deceased was judged to be drunk and incapable at the time of death. An accurate and precise measurement of the BAC is indispensable to reach a conclusion about a person’s state of inebriation at the time of death. (see also Drug-Impaired Driving and Behavioral Toxicology).
References [1]
Klatsky, A.L. (2003). Drink to your health, Scientific American 288, 74–81. [2] Room, R., Babor, T. & Rehm, J. (2005). Alcohol and public health, Lancet 365, 519–530. [3] Cherpitel, C.J. (2007). Alcohol and injuries: a review of international emergency room studies since 1995, Drug and Alcohol Review 26, 201–214. [4] Garriott, J.C. (ed) (2008). Medicolegal Aspects of Alcohol, 5th Edition, Lawyers and Judges Publishing Company, Tuscon, pp. 1–534. [5] Anderson, R.A. (2005). Back-tracking calculations, in Encyclopedia of Forensic and Legal Medicine, J. PayneJames, R.W. Byard, T.S. Corey & C. Henderson, eds, Elsevier, Oxford, pp. 261–270. [6] Meyer J.S. & Quenzer L.F. (2005). Chapter 9 Alcohol, in Psychopharmacology; Drugs, The Brain and Behavior, Sinauer Associates, Sunderland, pp. 215–243. [7] Jones, A.W. (2003). Drug alcohol interactions, in Handbook of Drug Interactions: A Clinical and Forensic Guide, C. Miozayani & L. Raymon, eds, Humana Press, Totowa, pp. 395–462. [8] Logan, B.K. & Jones, A.W. (2000). Endogenous ethanol “autobrewery syndrome” as a drunk driving defense challenge, Medicine Science and the Law 40, 206–215. [9] Brick, J. (2006). Standardization of alcohol calculations in research, Alcoholism Clinical and Experimental Research 30, 1276–1287. [10] Jones, A.W. (2008). Biochemical and physiological research on the disposition and fate of ethanol in the body, in Medicolegal Aspects of Alcohol, 5th Edition, J.C. Garriott, ed, Lawyers and Judges Publishing Company, Tuscon, pp. 47–155. [11] Jones, A.W. & Pounder, D.J. (2007). Update on clinical and forensic analysis of alcohol, in Drug Abuse Handbook, 2nd Edition, S.B. Karch, ed, CRC Press, Boca Raton, pp. 333–376. [12] Widmark, E.M.P. (1981). Principles and Applications of Medicolegal Alcohol Determination, Biomedical Publications, Foster City, pp. 1–163.
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Alcohol Haslam, D.W. & Jones, W.P.T. (2005). Obesity, Lancet 366, 1197–1209. Jones, A.W. (2007). Body mass index and bloodalcohol calculations, Journal of Analytical Toxicology 31, 177–178. Lieber, C.S. (1982). Medical Disorder of Alcoholism, W.B. Saunders publishing Co, Philadelphia. Kalant, H. & Khanna, J.M. (2007). The alcohols, in Principles of Medical Pharmacology, 7th Edition, H. Kalant, D.M. Grant & J. Mitchell, eds, Elsevier, Toronto, pp. 275–288. Lieber, C.S. (2005). Metabolism of alcohol, Clinics in Liver Disease 9, 1–35. Lieber, C.S. (2004). The discovery of the microsomal ethanol oxidizing system and its physiologic and pathologic roles, Drug Metabolism Reviews 36, 511–529. Andreasson, R. & Jones, A.W. (1996). The life and work of Erik MP Widmark, American Journal of Forensic Medicine and Pathology 17, 117–190. Wagner, J.G. (1991). Pharmacokinetics for The Pharmaceutical Scientist, Technomic Publishing Company, Basel. Rowland, M. & Tozer, T.N. (1995). Clinical Pharmacokinetics; Concepts and Applications, 3rd Edition, Williams & Wilkins, Philadelphia. Norberg, A., Jones, A.W., Hahn, R. & Gabrielsson, J. (2003). Role of variability in explaining ethanol kinetics – research and forensic applications, Clinical Pharmacokinetics 42, 1–31. Watson, P.E., Watson, I.D. & Batt, R.D. (1981). Prediction of blood alcohol concentration – updating the Widmark equation, Journal of Studies on Alcohol 42, 547–556. Jones, A.W. & Andersson, L. (1998). Influence of age, gender and blood alcohol concentration on the disappearance rate of alcohol from blood in drinking drivers, Journal of Forensic Sciences 41, 922–928. Ferner, R.E. (1996). Forensic Pharmacology – Medicines, Mayhem and Malpractice, Oxford University Press, Oxford. Drummer, O.A. (2001). The Forensic Pharmacology of Drugs of Abuse, Arnold, London. Jones, A.W. (2000). Alcohol; post-mortem, in Encyclopedia of Forensic Sciences, J.A. Siegel, P.J. Saukko. & G.C. Knupfer, eds, Academic Press, London, pp. 112–126. Kugelberg, F.C. & Jones, A.W. (2007). Interpreting results of ethanol analysis in postmortem specimens: a review of the literature, Forensic Science International 165, 10–29. Pounder, D.J. & Jones, A.W. (2007). Post-mortem alcohol aspects of interpretation, in Drug Abuse Handbook, 2nd Edition, S.B. Karch, ed, CRC Press, Boca Raton, pp. 376–401. Corry, J.E.L. (1978). Possible sources of ethanol ante and post-mortem: its relationship to the biochemistry and microbiology of decomposition, Journal of Applied Bacteriology 44, 1–56.
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Forrest, A.R.W. (1993). Obtaining samples at postmortem examination for toxicological and biochemical analyses, Journal of Clinical Pathology 46, 292–296. O’Neal, C.L. & Poklis, A. (1996). Postmortem production of ethanol and factors that influence interpretation: a critical review, American Journal of Forensic Medicine and Pathology 17, 8–20. Jones, A.W. (2006). Urine as a biological specimen for forensic analysis of alcohol and variability in the urineto-blood relationship, Toxicological Reviews 25, 15–35. Jones, A.W. & Holmgren, P. (2001). Uncertainty in estimating blood alcohol concentration by analysis of vitreous humor, Journal of Clinical Pathology 54, 699–702. Helander, A. & Jones, A.W. (2007). Recent advances in biochemical tests for acute and chronic alcohol consumption, in Drug Abuse Handbook, 2nd Edition, S.B. Karch, ed, CRC Press, Boca Raton, pp. 401–427. Jones, A.W. (2008). Biomarkers of acute and chronic alcohol ingestion, in Medicolegal Aspects of Alcohol, 5th Edition, J.C. Garriott, ed, Lawyers and Judges Publishing Company, Tuscon, pp. 157–203. Rainio, J., Giorgio, F.D., Bortolotti, F. & Tagliaro, F. (2008). Objective post-mortem diagnosis of chronic alcohol abuse – a review of studies on new markers, Legal Medicine 10, 229–235. Kalant, H., LeBlanc, A.E. & Gibbins, R.J. (1971). Tolerance to and dependence on some non-opiate psychotropic drugs, Pharmacological Reviews 23, 135–191. Rigter, H. & Crabbe, J.C. (eds) (1980). Alcohol Tolerance and Dependence, Elsevier Biomedical Press, Amsterdam. Jones, A.W. (2005). Alcohol, acute and chronic use, post-mortem findings, in Encyclopedia of Forensic and Legal Medicine, J. Payne-James, R.W. Byard, T.S. Corey & C. Henderson, eds, Elsevier, Oxford, pp. 39–58. Kalant, H. (1998). Research on tolerance; what can we learn from history, Alcoholism Clinical and Experimental Research 22, 67–75. Jaffe, J.H. (ed) (1995). Encyclopedia of Drugs and Alcohol, Macmillan Library Reference, Simon & Schuster and Prentice Hall International, New York. Jones, A.W. & Holmgren, P. (2003). Comparison of blood-alcohol concentrations in deaths attributed to acute alcohol poisoning and chronic alcoholism, Journal of Forensic Sciences 48, 874–879. Jones, A.W. & Holmgren, P. (2003). Urine/blood ratios of ethanol in deaths attributed to acute alcohol poisoning and chronic alcoholism, Forensic Science International 135, 206–212. Gibbons, B. (1992). Alcohol – the legal drug, National Geographic 181, 3–35. Levine, B.S. (ed) (1999). Principles of Forensic Toxicology, 2nd Edition, American Association of Clinical Chemistry, Washington, DC, pp. 1–394. Walls, H.J. & Brownlie, A.R. (1985). Drink, Drugs and Driving, 2nd Edition, Sweet and Maxwell, London.
Alcohol: Analysis [48]
Jones, A.W. (2000). Medico-legal alcohol determination – Blood or breath alcohol concentration? Forensic Science Review 12, 23–48.
Further Reading Nutt, D., King, L.A., Saulsbury, W. & Blackmore, C. (2007). Development of a rational scale to assess the harm of drugs of potential misuse, Lancet 369, 1047–1053.
ALAN W. JONES
Alcohol: Analysis Introduction In the field of forensic science and legal medicine, investigators are mainly concerned with just one type of alcohol, namely ethyl alcohol or ethanol, which is the pharmacologically active constituent in all alcoholic beverages. However, the word alcohol is a generic term used by chemists to denote a family of organic compounds, the simplest member of which is methanol or methyl alcohol (CH3 OH). Ethanol (CH3 CH2 OH) is the second member in this homologous series of aliphatic alcohols and is known as a primary alcohol, because the hydroxyl bearing carbon atom is attached to one alkyl group. Next comes n-propyl alcohol (CH3 CH2 CH2 OH) along with its structural isomer isopropyl alcohol (CH3 )2 CHOH, the latter is designated as a secondary alcohol because the hydroxyl carbon is bonded to two methyl groups. Structural formulae of the simplest alcohols are given in Table 1. The common feature shared by the entire family of alcohols is that they contain one or more hydroxyl (–OH) functional groups. This property determines Table 1
H
solubility in water and body fluids, ability to form hydrogen bonds with other biomolecules as well as many chemical and biochemical reactions, such as oxidation, reduction, and conjugation. Ethanol is produced on a huge scale by the fermentation of carbohydrates (beverage alcohol) or by the catalytic addition of water to ethylene (nonbeverage usage). Ethanol is considered as a clean fuel and is widely used in industry as a solvent and also occurs in many household products, pharmaceuticals, cosmetics, toiletries, perfumes, etc. Even certain foodstuffs, such as fresh fruits and fruit juices, might contain trace quantities of ethanol or ethyl esters that can undergo hydrolysis in the stomach to form ethanol. Alcoholic beverages are made by fermentation of the sugars contained in a wide variety of naturally occurring raw materials such as potato mashes, barley corn, fruit juices, beet, cane sugar, and molasses. The enzymes in yeast convert one molecule of glucose into two molecules of ethanol and two molecules of carbon dioxide. Depending on the fermentation conditions, such as the source of the yeast and the nature of the starting material, the endproduct might contain up to 15% v/v ethanol. Beers contain 3–5% v/v ethanol and wines generally contain 9–15% v/v. A drink containing higher concentrations of ethanol cannot be produced by fermentation alone, because the yeast enzymes become inactivated. Distillation or fortification of the primary fermentation product is necessary if more concentrated alcoholic drinks (distilled spirits), such as whisky, vodka, gin, and brandy (35–55%v/v) are required. Alcohol is a dependence-producing drug and excessive drinking and drunkenness lead to many negative social, medical, psychological, and economic consequences for the individual and society [1]. Overconsumption of alcohol, binge drinking, and drunkenness constitute major public health issues in today’s society. Intoxicated people are overrepresented at hospital emergency rooms to receive
Chemical structures of the simplest monohydroxy aliphatic alcohols H H
H OH H Methanol CH3OH
H
H H H OH
81
H
CH3
H3C OH
OH
H H
H H H
Ethanol CH3CH2OH
n-propanol CH3CH2CH2OH
H3C Isopropanol (CH3)2CHOH
H3C
OH CH3
t-butanol (CH3)3COH
82
Alcohol: Analysis
treatment for injuries and in deaths caused by drowning, suicide, or road-traffic fatalities. Forensic science and toxicology laboratories worldwide have a long standing interest in the analysis and the interpretation of a person’s blood-alcohol concentration (BAC), which requires considerable knowledge and expertise about methodological, physiological, and pharmacological aspects of ethanol [2, 3]. This article deals with the principles and practice of ethanol determination in biological specimens. The major emphasis is given to the analysis of ethanol in blood and breath, which are the specimens used in forensic casework as evidence for prosecuting drunken drivers [4]. However, the procedures described for handling blood samples can be applied to many other biological liquids such as urine, plasma, serum, and saliva [5, 6]. Indeed, any biofluid or tissue that contains water can serve as a specimen for the analysis of ethanol.
Punishable Alcohol Concentration Limits for Driving Alcohol-related motor vehicle crashes are a major cause of premature death and disability. Many casecontrolled studies have established that the risk of a crash appreciably increases as the driver’s BAC increases above 0.5 g l−1 (50 mg/100 ml or 0.05 g/100 ml). Impaired drivers are overrepresented in crash statistics and 30–40% of those killed on the
roads test positive for alcohol and most victims have BACs above the legal limit for driving. To improve traffic safety and deter drunken driving, governments have enacted punishable limits of alcohol concentration in specimens of blood, breath, or urine above which it is an offense to drive a motor vehicle on the public roads and highways [7, 8]. However, these statutory alcohol limits differ among different countries, which has a lot to do with alcohol control policy and local politics rather than traffic safety research (Table 2). In many publications dealing with forensic aspects of alcohol, confusion arises owing to the different concentration units used to report the results. Examples of the various blood- and breath-concentration units and the countries where they apply are given in Table 3. Also shown is the concentration unit used in clinical and laboratory medicine, namely millimoles per liter (21.7 mmol l−1 = 1.0 g l−1 ). Note also that hospital laboratories commonly determine ethanol in specimens of plasma or serum and not in whole blood. The differences in water content among the different biofluids have important consequences if and when results from hospital clinical laboratories are later used as evidence in legal proceedings, such as impaired driving trials [2]. Ethanol distributes into the water compartment of the body and unlike many other drugs, it does not bind to plasma proteins. The water content of whole blood is ∼80% w/w on average compared with ∼93% w/w for serum or plasma. Because the
Table 2 Threshold concentration limits of alcohol (statutory limits) in blood and breath for operating a motor vehicle in various countries and the blood/breath ratio assumed when setting the corresponding breath-alcohol concentration limit Country/nation(a) Most European nations The Netherlands Norway and Sweden(b) Finland The United States The United Kingdom and Ireland(c) Canada Australia New Zealand (a)
Blood-alcohol concentration
Breath-alcohol concentration
Assumed blood-to-breath ratio
0.50 mg ml−1 (g l−1 ) 0.50 mg ml−1 (g l−1 ) 0.20 mg g−1 (g kg−1 ) 0.50 mg g−1 (g kg−1 ) 0.08 g/100 ml 80 mg/100 ml 0.08 g/100 ml 0.05 g/100 ml 80 mg/100 ml
0.25 mg l−1 220 µg l−1 0.10 mg l−1 0.22 mg l−1 0.08 g/210 l 35 µg/100 ml 0.08 g/210 l 0.05 g/210 l 400 µg l−1
2000 : 1 2300 : 1 2100 : 1 2400 : 1 2100 : 1 2300 : 1 2100 : 1 2100 : 1 2300 : 1
In several countries listed above a lower limit of alcohol concentration operates for novice or provisional drivers (e.g., 0.02 g% in the United States), for drivers under 21 years and 0.04 g% for operators of commercial vehicles (b) Because a BAC of 0.20 mg g−1 is equivalent to 0.21 mg ml−1 , the actual blood/breath ratio operating in Norway and Sweden is close to 2100 : 1 (c) If urine is the specimen donated the threshold concentration of alcohol is 107 mg/100 ml
Alcohol: Analysis
83
Table 3 Concentration units used to report blood-alcohol concentration (BAC) and breath-alcohol concentration (BrAC) for clinical and forensic purposes in different countries Concentration unit for blood alcohol
Concentration unit for breath-alcohol Countries where used
Countries where used
mg g−1 (g kg−1 )
Sweden, Denmark, Norway, Finland, Germany mg ml−1 (g l−1 ) France, Holland, Spain, Belgium mg/100 ml (mg dl−1 ) The United Kingdom, Ireland, Canada, New Zealand g/100 ml (g%) The United States, Australia Hospital clinical chemistry mmol/l(a) laboratories in most countries
mg l−1 µg l−1 µg/100 ml g/210 l ppm(b)
Sweden, Denmark, Norway, Finland, Germany, Spain, other EU countries Holland The United Kingdom, Ireland, New Zealand The United States Environmental health applications
Molecular weight of ethanol is 46.07; thus, a concentration of 21.7 mmol l−1 is equivalent to 1.0 g l−1 (100 mg/100 ml or 0.1 g/100 ml) (b) ppm stands for parts per million where 200 ppm = 0.365 mg ethanol per liter of breath at 34 ° C (a)
distribution of alcohol between plasma and whole blood follows the distribution of water, the mean concentration ratio (plasma/blood) for ethanol is 1.16 : 1 and this can be used as a conversion factor [2]. The actual plasma/blood distribution ratio depends on the factors influencing the water content of the specimens analyzed such as hematocrit value and any medical conditions that influence the volume of red cells (e.g., anemia). Abnormal blood lipids tend to influence the concentration of alcohol in the blood sample. The gender-related differences in hematocrit (men 42–50 ml/100 ml and women 37–47 ml/100 ml) also have a small effect on the plasma/blood distribution ratio of ethanol. If nothing is known about the individual concerned and a request is made to convert the plasma alcohol concentration (PAC) or the serum alcohol concentration (SAC) into the blood alcohol concentration (BAC) the factor used should be chosen to the person’s advantage if the results are intended for use as evidence in a criminal prosecution. BAC = (P AC or SAC)/1.16 (gives the best average estimate)
(1)
BAC = (P AC or SAC)/1.20 (gives a lower limit for most people) (2)
Analytical Methods for the Determination of Ethanol The first analytical methods for the identification and determination of ethanol in human body fluids and
tissues were described approximately 150 years ago [9]. Because of the strong association between a person’s BAC and the impairment of performance of skilled tasks, such as driving, it has become increasingly necessary to interpret the results of analysis in a legal context. The BAC encountered in most forensic casework ranges from 0 to 5 g l−1 (500 mg/100 ml), and a concentration below 0.1 g l−1 is usually reported as negative and no further action or interpretation is necessary. Although the analytical methods used in many forensic toxicology laboratories are capable of measuring much lower concentrations of ethanol below 0.1 g l−1 , this level is appropriate as a practical cutoff concentration for reporting negative results. The limit of quantitation (LOQ) of an analytical method is an important concept in clinical, forensic, and laboratory medicine and this is defined as the lowest concentration of analyte that gives acceptable precision and accuracy under the stated operating conditions of the method. In practice, LOQ is approximately 3.3 times the limit of detection (LOD), which is defined as the lowest concentration of analyte that can be detected. With instrumental methods of analysis, LOD corresponds to a signal to background noise ratio of about 3 : 1. During the development of new analytical methods, a good starting point is to consider the physical, chemical, and structural properties of the substance of interest – the analyte. Ethanol is a low-molecular weight volatile substance (boiling point 79 ° C) with a specific gravity of 0.789 and mixes with water in all proportions. The hydroxyl group is chemically
84
Alcohol: Analysis
reactive and readily undergoes oxidation to an aldehyde group (–CHO) or a carboxylic acid group (–COOH), depending on the reaction conditions such as time and temperature.
Methods Based on Chemical Oxidation The earliest methods suitable for the analysis of alcohol in blood and urine were based on chemical oxidation of the hydroxyl group (–OH), to yield the corresponding aldehyde (–CHO) and then carboxylic acid (–COOH). Various oxidizing agents, such as acidified potassium dichromate or potassium permanganate, were employed. Prior to adding the required chemicals to start the reaction, it was necessary to remove the ethanol from the biological matrix by distillation, desiccation, or aeration or also by the precipitation of blood proteins, e.g., with perchloric acid [10]. The oxidizing reagent was added to the aqueous distillate or filtrate containing ethanol and when necessary the mixture was heated (e.g., to 50 ° C) to speed up the completion of the reaction. The amount of ethanol in the original sample could then be determined by titrimetric analysis or by colorimetry by comparison with known strength standard solutions of ethanol. The basic equation for the oxidation of ethanol with a mixture of potassium dichromate and sulfuric acid is shown below. 2K2 Cr2 O7 + 8H2 SO4 + 3C2 H5 OH −−−→ (yellow color) 2Cr2 (SO4 )3 + 2K2 SO4 + 11H2 O + 3CH3 COOH (green color)
(3)
Methods based on chemical oxidation were rather time consuming and required considerable training to ensure reliable results and not many samples could be completed each working day. Moreover, the oxidation reaction was not specific and other alcohols or acetone if present in the blood samples could not be distinguished from ethanol. Nevertheless, only wet-chemistry oxidation was used between 1900s and 1950s for the quantitative analysis of ethanol in body fluids for legal purposes [8, 9]. When specimens were taken during autopsy, various preliminary chemical tests were necessary to resolve whether other volatile substances might be present that could compromise the reliability of the analytical results.
Methods Based on Enzymatic Oxidation Milder oxidation conditions and improved selectivity of analysis were achieved when enzymatic procedures were developed in the early 1950s. This coincided with the isolation and purification of the liver enzyme responsible for the oxidation of ethanol in vivo, namely alcohol dehydrogenase (ADH). Mammalian ADH was not so suitable for forensic analysis because other aliphatic alcohols (e.g., methanol and isopropanol) were also oxidized and under certain circumstances, these substances might be present in the blood samples. Accordingly, the enzyme derived from yeast was developed commercially and widely used in the enzymatic (ADH) determination of ethanol. Methanol reacted very slowly or not at all under optimum reaction conditions and did not interfere with the determination of ethanol [11]. A major advantage of enzymatic methods over chemical methods was that the procedures could be more easily automated. Indeed, this was becoming increasingly necessary considering the huge increase in forensic casework as drunken driving escalated in the 1950s and 1960s. The oxidation of ethanol to acetaldehyde by ADH is a reversible reaction. Under in vitro conditions, the reaction is facilitated by adjusting pH to 8.8 and adding a reagent (semicarbazide hydrochloride) to trap the acetaldehyde produced. The semicarbazide forms a semicarbazone by reacting with the acetaldehyde to drive the reaction (see below) to the right. During the redox reaction, the coenzyme nicotinamide adenine dinucleotide (NAD+ ) is converted to the reduced form NADH and its formation is monitored by UV spectrometry at a wavelength of 340 nm for quantitative analysis. ADH
CH3 CH2 OH + NAD+ ←−→ CH3 CHO + NADH + H+ CH3 CHO + semicarbazide gives a semicarbazone driving the reaction to completion
(4)
Enzymatic methods gradually replaced the chemical oxidation procedures and became widely used until the emergence of physicochemical methods in the early 1960s. The upsurge of immunoassay methods designed for analysis of drugs of abuse in urine has led to a renaissance for the NAD+ NADH reaction. Highly automated and sophisticated
Alcohol: Analysis instruments are available for the analysis of abused drugs including ethanol by immunoassay. Indeed, some laboratories make a rapid preliminary screening analysis of all specimens by enzymatic methods so as to distinguish negative and positive specimens. Those specimens that tested positive for ethanol are then reanalyzed by more specific methods, such as gas chromatography [12]. Nowadays, the method of choice for bloodalcohol analysis in clinical, forensic, and research applications is gas-liquid chromatography (GC). For the determination of alcohol in samples of breath, dedicated instruments are available that utilize infrared spectrometry or electrochemical oxidation as the analytical principles (see later in this article).
Methods Based on Gas Chromatography The development and implementation of gas liquid partition chromatography in the early 1960s and onwards revolutionized the practice of analytical chemistry at forensic science and toxicology laboratories. The instrument bay in a modern toxicology laboratory is dominated by advanced separation methods involving either gas- or liquid-chromatographic procedures with various detector systems depending on the particular analyte or drug of interest [13].
Basic Principles of Gas Chromatography The principle components of GC are an inert carrier gas (nitrogen or helium), which represents the moving or mobile phase. This is made to flow through a long thin coiled tube (the chromatographic column) containing the liquid stationary phase. The column is kept in an oven held at a precisely controlled temperature, which is a key parameter for the effective separation of the components of a mixture. The liquid stationary phase is coated onto an inert support material to provide a large surface area and to facilitate an intimate contact and mixing of components between the moving gaseous phase and the stationary phase. The components in the sample are vaporized before mixing with the gaseous mobile phase, which transports the substances to be separated through the column. During passage through the column, the components of the mixture partition between the moving gas phase and the liquid stationary phase. Different compounds partition differently depending
85
on their physical and chemical properties and are retained for a shorter or longer time inside the column so that a partial or complete separation occurs. The effluent from the column passes to a detector, which produces a signal proportional to the amount of substance it detects. Different detectors are available for different applications depending on the chemical structure and elemental composition of the target analytes. For compounds with C–C or C–H bonds in the molecules, a flame ionization detector (FID) is widely used. The carrier gas and the substances eluting from the column enter an air-hydrogen burning flame to produce ions and electrons that pass between anode and cathode. The current flowing at a particular voltage between the positive and negative poles is amplified and the signal is monitored as a trace on a recorder known as the chromatogram. The choice of stationary phase is important and when water-soluble alcohols are analyzed hydrophilic phases, such as polyethylene glycols of different average molecular weights, are appropriate. The traditional packed columns, which worked very well for decades and still do, have gradually been replaced by capillary or wide bore columns, which are more expensive and less robust compared with packed columns. The main advantage of gas chromatographic analysis over other methods is that the target analyte (ethanol) is separated from impurities or potential interfering compounds (e.g., acetone) that might be normally present in forensic blood samples. Moreover, both qualitative and quantitative analysis is possible in the same analytical run. The time that elapses after injecting the sample into the column to the appearance of the apex of the peak on the chart recorder or electronic integrator is called the retention time (RT ) and is useful for qualitative analysis. The RT of the unknown substance can be compared with the RT of authentic known standards purchased from a reliable source. The integrated area under the detector response (peak) on the chromatogram is the parameter used for quantitative analysis and is directly proportional to the amount of substance in the sample.
Analytical Details In forensic casework, the specimens of blood or other body fluids should always be analyzed in duplicate and whenever possible, these determinations
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Alcohol: Analysis
should be made by different technicians working independently with different sets of equipments [14]. Importantly, the chromatographic conditions, such as the nature of the stationary phase, should be such that different RTs are obtained for potential interfering substances. The risk that two closely related compounds will have the same RT when analyzed on two different stationary phases is very remote. Alternatively, an increased selectivity can be achieved by the use of two independent analytical methods, such as GC and an enzymatic oxidation procedure, to make the duplicate determinations. Approximately 1–5 µl of the diluted blood specimen is injected directly onto the chromatographic column or into a heated injection port attached to the column where vaporization occurs. Any volatile substances in the sample mix with the mobile phase (carrier gas) and pass through the column, where separation occurs. The effluent from the column is then directed to the detector for quantitative analysis. Blood and other body fluids contain nonvolatile constituents (proteins, fats, etc.), which tend to clog the syringe and injection port of the GC and the column packing material deteriorates after many samples are analyzed. To avoid this problem, investigators developed the headspace sampling technique and this entails the analysis of the vapor phase above the
Concentration in air phase (CA) Concentration in liquid phase (CL)
diluted blood sample. The diluted blood specimen is held in a glass vial, which is kept airtight with a stopper and crimped on aluminum cap and is heated to 50 or 60 ° C to achieve a liquid-vapor equilibration. The use of the headspace method meant that the GC column was not contaminated with nonvolatile substances and several thousands of blood samples could be analyzed without damaging the column and the overall analytical performance. A scheme that illustrates the basic features of headspace GC applied the determination of blood ethanol concentration is shown in Figure 1. A short analysis time and adequate resolution of components in the sample are the key elements in any chromatographic analysis. Ethanol and other low molecular volatiles can be analyzed under isothermal temperature control of the chromatographic oven, which saves much time compared with a temperature program (heating and cooling) being used. For routine applications, the analysis takes about 2–3 min after the injection was made into the GC. By raising the oven temperature or operating with a higher carrier gas flow rate, the RTs can be shortened but often at the expense of an incomplete separation of the components in a mixture. Examples of the RTs (min) for GC analysis of nine different volatile agents analyzed on four different
= Constant Detector response
n -Propanol
Needle Septum
CA
CL
Ethanol
Gas chromatographic separation of volatile components
0 1 2 3 4 5 Headspace vapor in equilibrium with blood
Retention time (min)
Blood sample diluted 11 times with internal standard (n -propanol)
Figure 1 Diagram showing the main features of static headspace gas chromatography where an equilibration is achieved between volatiles in the diluted blood specimen (n-propanol internal standard) and the air phase above the blood. After equilibration is reached (20–30 min), a portion of the air-phase is removed and directed into the gas chromatograph where a separation of the components and a quantitative analysis is made with a flame-ionization detector
Alcohol: Analysis
87
Table 4 Retention times (RT) of ethanol and other low molecular volatile substances analyzed by headspace gas chromatography on four different stationary phases commonly used in forensic toxicology laboratories. RT’s relative to n-propanol as internal standard are shown in brackets Volatile substance Acetaldehyde Acetone n-Butanol Ethanol Methanol Methyl ethyl ketone Isopropanol n-Propanol t-Butanol
Retention time (min) Carbopak C(a) 0.56 1.00 4.68 0.72 0.49 2.45 1.16 1.05 1.90
Retention time (min) Carbopak B(b)
(0.38) (0.68) (3.16) (0.49) (0.33) (1.66) (0.78) (1.00) (1.28)
0.53 0.86 4.11 0.98 0.67 1.49 1.31 1.85 1.68
(0.29) (0.46) (2.22) (0.53) (0.36) (0.81) (0.71) (1.00) (0.91)
Retention time (min) Rtx-BAC1(c) 1.19 2.05 4.63 1.32 1.06 3.08 1.66 2.25 1.98
(0.53) (0.91) (2.06) (0.59) (0.47) (1.37) (0.74) (1.00) (0.88)
Retention time (min) Rtx-BAC2(d) 0.82 1.36 5.28 1.27 0.96 2.49 1.48 2.40 1.65
(0.34) (0.57) (2.20) (0.53) (0.40) (1.04) (0.62) (1.00) (0.69)
Packed glass column (2 m × 0.5 mm i.d.) with 0.2% Carbowax (polyethylene glycol) 1500 Packed glass column (2 m × 0.5 mm i.d.) with 5% Carbowax (polyetheylene glycol) 20 M (c) Capillary column, 30 m × 0.53 mm i.d. (d) Capillary column, 30 m × 0.53 mm i.d. (a)
(b)
columns and stationary phases (two packed and two capillary) under isothermal oven temperature conditions are shown in Table 4. Also listed are the RTs of the n-propanol peak – the internal standard. The overall time of analyzing these nine compounds was only 4–5 min and the longest RT was for n-butanol.
Recommended Procedure for Routine Purposes The basic steps in a well tested and recommended procedure for the quantitative determination of ethanol in blood or urine for legal purposes by GC are outlined below [15]. 1. The tube with the material to be analyzed should be gently inverted for some time to ensure homogeneity of the specimen. This step is important when ethanol is determined in blood samples because the red cells and the plasma fraction tend to separate out on standing. 2. An aliquot (0.1 ml) of the specimen (whole blood, plasma, serum, or urine) is accurately removed from the tube and immediately diluted with an aqueous solution of an internal standard (usually another type of alcohol). This maneuver is best done by the use of specially constructed diluter-dispenser equipment although micropipettes can be also be used. The dilution of the biofluid with aqueous internal standard
should be at least 1 : 5 (6-fold) or 1 : 10 (11-fold). Adequate dilution of the specimen eliminates matrix effects, which is an important consideration when headspace GC analysis is used and determines the choice of the calibration standards. With 6- to 11-fold dilution of blood meant that aqueous ethanol standards can be used to construct a calibrate plot for use in quantitative analysis. Suitable internal standards are aqueous solutions of n-propanol (specimens from living subjects) or t-butanol (in autopsy work) at concentrations of 0.05–0.10 g l−1 . It is important that the substance used as the internal standard is not likely to occur or be produced in the biofluid analyzed. 3. For headspace analysis, the diluted blood specimens are ejected into a glass vial, which is made airtight with a Teflon-coated stopper and crimped on aluminum cap. For analysis of liquid samples the diluted specimens are ejected into a clean dry glass vial and an aliquot (1–5 µl) is injected into the GC using a microsyringe. 4. The peak area ratio of the responses for ethanol and the internal standard are recorded and compared with the corresponding ratios after the analysis of a series of aqueous ethanol solutions with known concentrations as the calibration standards. Alternatively, the ratio of heights of the two peaks on the gas chromatograph can be measured and used for the quantitative analysis.
88
5.
Alcohol: Analysis The plot of peak height or peak area ratio against concentration of ethanol in the standards is used to construct a calibration line for quantitative analysis. A linear relationship exists between the detector response (peak area ratio) and the concentration of ethanol in the sample analyzed over a wide range, such as 0–5 g l−1 (0–500 mg/100 ml) that might be encountered in forensic blood samples. Quality control standards should be included within each analytical run dispersed liberally between the unknown blood samples.
Besides the analysis of unknown blood specimens, each analytical run should include one or more blank specimens (blood without any ethanol) and control standards of known concentration positioned at intervals in the series. Some laboratories might also include a sample containing a mixture of potential interfering substances (e.g., acetaldehyde, methanol, acetone, and isopropanol). The ethanol control standards should be prepared independently from the solutions used as calibrators and the latter should have good traceability to a primary source. A wide range of instruments are available to perform a GC analysis of ethanol in blood and some manufactures produce dedicated instruments for headspace sampling and analysis (e.g., Perkin-Elmer Corporation). Other types of GC instruments are more flexible and can handle liquid injection and are adaptable for headspace analysis [16]. The first GC methods for alcohol analysis involved the use of a packed column, which consisted of a coiled tube made of glass, copper, or stainless steel that was normally 2–3 m long with an inside diameter of a few millimeters. The column contained an inert solid support material impregnated with the stationary liquid phase to facilitate separations and analysis. Currently, most GC analysis in forensic toxicology is done with capillary columns made of fused silica of normally 20–30 m long and with an inside diameter of 0.3–0.5 mm. Figure 2 shows examples of chromatograms obtained from analysis of blood containing methanol, acetone, isopropanol as well as ethanol and the n-propanol internal standard. The blood specimen was analyzed on two different columns and stationary phases thus furnishing different RTs for the volatile components in the mixture. The detector response was normalized to 100% for the most prominent
component in the sample. Note that the chart speed has been purposely increased for clarity, which causes the peaks to be fairly broad compared with if a slower chart speed had been used. Few substances of physiological and forensic interest can be determined with such high accuracy and precision as the BAC. The analytical principles involved and brief practical details of the procedures used for the forensic determination of ethanol in biological specimens spanning the past century are presented in Table 5 in chronological order (see also Confirmation Testing: Toxicology).
Blood Sampling from Living Subjects The quality of the specimen sent for analysis is often a neglected aspect of the overall procedures, which can have negative consequences for the reliability and acceptance of the results for legal purposes. The preanalytical stages include sampling, labeling, transport, and storage prior to arrival at the laboratory [17]. Factors to consider include obtaining informed consent from the subject or suspect, the blood sampling site on the body, the use of a disinfectant to swab the skin, the type of blood-sampling equipment used, whether an evacuated tubes or a syringe and needle. The procedures used to draw blood, the volume and type of container and whether chemical preservatives were added, the mode of transport of specimens, and the storage after arrival are all key elements in the overall reliability of the final results. The chain of custody of the specimens also needs to be well documented to guarantee integrity of laboratory work that might be used as evidence in criminal prosecutions. Table 6 outlines major issues that deserve consideration when blood samples are collected and sent for forensic analysis of alcohol from living subjects. The sampling site for obtaining blood might be a vein, an artery, or a capillary but for all practical purposes the sample is taken from a cubital vein. The blood is conveniently taken using a sterile evacuated glass tube (gray stopper) containing sodium fluoride as a preservative and potassium oxalate as an anticoagulant. The evacuated tubes usually hold a volume of 9–10 ml when full and 100 mg NaF (1% w/v) and 25 mg of potassium oxalate are present as preservatives. Immediately after sampling, the tube of blood should be gently inverted for about 20 s
Alcohol: Analysis
89
100%
n -Propanol
20
Rtx-BAC1
Ethanol
N-propa
10
0.0
0.2
0.4
0.6
0.8
1.0
1.2
100%
1.4
1.6
1.8
2.0
2.2
2.4
40
n -Propanol
Rtx-BAC2
30
2.6
Acetone
Isopropanol
Ethanol
20 N-Propa
10 Etanol
Detector response
Isopropanol
Etanol
Detector response
Acetone
0.0
0.2
0.4
0.6
0.8
1.0
1.2
1.4
1.6
1.8
2.0
2.2
2.4
2.6
Time from injection (min)
Figure 2 Chromatographic traces from analysis of ethanol and other volatiles in a blood sample also containing acetone and isopropanol. On two different stationary phases (Rtx-BAC1 and Rtx-BAC2) thus furnishing different retention times for identification of components
to ensure proper mixing with the preservatives to prevent coagulation. In practice, the volume of the blood in the evacuated tubes might vary from about 1 to 10 ml depending on the care taken with the sampling procedure. Such a variation in volume does not impact adversely on the accuracy or precision of the resulting BAC even when the volume of blood in the tube is abnormally low. The evacuated tubes (5 ml) often used at hospital laboratories for collecting specimens for the analysis of blood-glucose are also suitable for blood-alcohol analysis. These 5 ml tubes normally contain less sodium fluoride and heparin instead of potassium oxalate is present as the anticoagulant. Because the tubes used to sample blood for alcohol analysis are sterile, one might wonder whether an enzyme inhibitor, such as sodium fluoride, is really necessary. However, a claim could be made that microorganisms had entered the blood when the needle penetrated the skin and ethanol, at least in part, was produced by the fermentation of blood-glucose after sampling. Swabbing the skin with a nonalcohol disinfectant or simply cleaning with soap and water is a standard practice before sampling blood. Studies have shown
that even if an alcohol-containing swab had been used by mistake, the risk of contamination of the sample by carryover of ethanol from the skin is negligible. Ethanol can be determined in any body fluid that contains water and methods have been described for the analysis of cerebrospinal fluid, saliva, sweat, and urine by the same GC methods described above for dealing with blood samples.
Specimens Taken at Autopsy The methods described above for the determination of ethanol in blood from living subjects are the same as those used to analyze autopsy specimens [2]. During the postmortem examination a much wider selection of fluids or tissues are available for analytical toxicology. The composition of the autopsy blood samples in terms of fluidity, presence of clots, and degree of putrefaction might differ widely depending on the condition of the body and the circumstances surrounding the death [18]. When the analytical results are interpreted, the water content of the blood
90 Table 5
Alcohol: Analysis Historical developments in the methods used for determination of ethanol in blood and urine samples
Time period
Analytical procedure and brief details of the principles for ethanol determination
1900–1950s
The first analytical methods were based on chemical oxidation of the hydroxyl group in the ethanol molecule. After separation of ethanol from the biological matrix by diffusion, distillation or aeration or protein precipitation, an oxidizing agent such as a mixture of potassium dichromate (K2 Cr2 O7 ) and sulfuric acid (H2 SO4 ) was added. The ethanol is oxidized to acetic acid and the endpoint of the reaction is either determined by volumetric titration or by photometry Oxidation of ethanol by means of enzymes, such as alcohol dehydrogenase (ADH), offered milder conditions and gave a higher analytical selectivity when the enzyme derived from yeast was used. Ethanol was first separated from the biological matrix by precipitation of the blood-proteins with perchloric acid (HClO4 ) and then centrifugation. After adjusting pH of the supernatant to alkaline conditions (e.g., pH 8.8) with buffers that contained the coenzyme (nicotinamide adenine dinucleotide, NAD+ ), the ADH enzyme was added to start the reaction. This redox reaction, which is reversible, was driven to completion by adding semicarbazide hydrochloride, which reacts with the acetaldehyde produced from the oxidation of ethanol. During the reaction, the coenzyme (NAD+ ) is reduced to NADH, which is monitored by absorption of ultra violet light at a wavelength of 340 nm. Enzymatic methods were better suited for automation, e.g., with various autoanalyzer instruments Gas chromatography (GC) is today the method of choice and furnishes both a qualitative identification and a quantitative analysis of ethanol. An aliquot of the blood sample (∼100 µl) is first diluted 1 : 5 or 1 : 10 with an aqueous solution of another alcohol (n-propanol or t-butanol) to serve as the internal standard. About 1–5 µl of the diluted blood is then injected into the heated injection port of the gas chromatograph and vaporized in a stream of nitrogen carrier gas (mobile phase). The volatiles pass through a long thin metal or glass tube (the GC column) containing the stationary liquid phase held on an inert support material. Depending on physicochemical properties and solubility in the liquid phase, the volatiles are held in the column for different times thus achieving separation. A detector, usually a flame ionization detector (FID), is used to measure the effluents when they emerge from the column. The time after injection to appearance of the apex of the peak (retention time) is a characteristic of the substance analyzed and can be used for identification. The area under the peak was related to the amount of analyte. Quantitative analysis required calibration of the detector response with known strength alcohol standards Instead of injecting the diluted blood specimen a modification of the basic GC procedure involved the use of headspace analysis. This entailed sampling a portion of the vapor phase in equilibrium with the blood sample. This offers the advantage that the column packing material is not contaminated by nonvolatile constituents of the biological matrix. As with liquid injection, the blood samples and ethanol standards are first diluted (1 : 5 or 1 : 10) with internal standard and transferred to glass vials made airtight with rubber septa and crimped on aluminum caps. The vials are equilibrated at 50 or 60 ° C and after about 30 min a portion of the vapor phase is removed for GC analysis. Sampling is done with the aid of a gas-tight syringe or by an automated procedure. The original packed GC columns have been gradually replaced by capillary or wide bore columns. The sensitivity of the headspace method can be enhanced and matrix effects can be eliminated by saturating the blood samples and aqueous ethanol standards with salt (NaCl or K2 CO3 ), e.g., 0.5 ml blood + 1 g salt Positive identification of ethanol is accomplished by mass spectrometry with an electron-impact detector producing characteristic ion fragments m/z 31 (base peak for primary alcohols), m/z 46 (molecular ion), and m/z 45 after loss of a proton. The ions m/z 31 and m/z 45 are sufficiently intense to allow quantitative analysis and deuterium-labeled ethanol can serve as internal standard
1950–1970s
1960s
1970s
1980s
deserves consideration, such as when conclusions are reached regarding the antemortem BAC. Some investigators recommend that the water content of autopsy blood samples should be determined in conjunction with the analysis of ethanol. This is easily done by desiccation or freeze drying an aliquot of the specimen so that the BAC can then be adjusted to a
blood-water content of 80% w/w, which applies to fresh blood from living subjects. Table 7 gives a list of the biological specimens recommended for use in connection with forensic analysis of ethanol from living subjects and also in postmortem toxicology. (see also Toxicology: Analysis).
Alcohol: Analysis
91
Table 6 Important considerations (preanalytical factors) in connection with sampling of blood from suspected drunken drivers intended for analysis of ethanol for legal purposes Aspects of blood sampling
Considerations
Qualifications of the person commissioned to draw blood Preparation of the patient or person
Doctor, nurse, laboratory technician, or trained phlebotomist
Blood source and sampling site
Sampling technique
Identification and labeling of the specimen. Collection tubes for blood and preservatives Transport of sample to forensic laboratory Inspection and registration at the laboratory
Storage prior to analysis
Informed consent about the purpose of sampling and information whether the person was sitting, standing, laying down, struggling, conscious/unconscious, or a victim of a traffic crash? Source of the blood sample whether left or right arm cubital vein, artery, fingertip, or earlobe? Any medical treatment given to the person prior to sampling, such as intravenous fluids Type of skin disinfection used if any. Syringe and needle or an evacuated tube – was a tourniquet applied? Volume of blood specimen collected and the time needed for obtaining the sample Record name of suspect, date of birth, time and date of blood draw, and name of the person who took the blood sample Volume of tubes and whether these were made of glass or plastic. What anticoagulant was present and whether an enzyme inhibitor such as sodium fluoride was included and at what concentration Tamperproof packaging, mode of transport to the laboratory (normal postal service or special delivery). Where the specimens were refrigerated during transport. How was chain of custody ensured Date and time of arrival (date stamp). How many tubes of blood were received? What volume of blood in the tubes? Was there obvious hemolysis or clotting, any attempt at manipulation? Were security tapes or seals still intact? Had the tubes been opened Time delay from sampling to analysis, storage of blood in a refrigerator or frozen and known stability of the analytes
Importance of Method Validation Quality assurance and process control are crucial in all kinds of routine analytical laboratory work and especially when results are used in criminal investigations [19]. All analytical methods should Table 7
undergo a rigorous validation and standardization before they can be considered fit for purpose. A careful documentation of the method characteristics including information on accuracy, precision, and the results of external proficiency tests are essential in today’s laboratory environment [19]. The uncertainty
Biological specimens suitable for analysis of ethanol in living subjects and also at autopsy
Living subjects
Dead bodies
Venous blood (10 ml)(a) Capillary blood (fingertip) Plasma/serum Urine fresh void (10 ml)(a) Tear fluid Cerebrospinal fluid (lumber fluid)(c) Saliva Perspiration/sweat Breath (end expired)(a)
Femoral blood (20 ml)(b) Heart blood (if femoral unavailable) Blood clot (subdural hematoma) Urine (50 ml)(b) Vitreous humor (all available both eyes)(b) Cerebrospinal fluid (cisternal fluid)(d) Bile (gall bladder) Synovial fluid (knee joint) Tissue (brain, skeletal muscle, liver)
(a)
Recommended for analysis in people arrested for drunken drivers Recommended for analysis in connection with forensic autopsies (c) From base of spine with the patient in a crouching position (d) From back of neck (lumber sampling not practical) (b)
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in the analytical results also needs to be recognized, reported, and allowed for especially if these are compared with some threshold value, such as the legal alcohol limit for driving [15]. Method validation embraces the process and events by which a newly developed method or laboratory procedure is subjected to a strict testing protocol to establish key performance characteristics including accuracy, precision, specificity, bias, linearity, LOD, and LOQ. Many of the terms used in connection with validation and accreditation of laboratory methods are defined in Table 8. Over the past few decades, more and more attention has been given to laboratory accreditation, which is a formal process by which a laboratory is evaluated for its competence to perform designated analytical tasks or measurements [20]. Aspects of the accreditation process include participation in external proficiency schemes as well as regular onsite inspections by outside experts who examine and evaluate protocols, oversee laboratory facilities, and verify that the staff has appropriate qualifications and training for their task. In today’s climate a forensic science or toxicology laboratory would not survive for long without being accredited for the services it provides including regular inspections and some form of peer recognition. When the results of blood-alcohol analysis are reported to the police authorities, some laboratories consider the uncertainty in analytical results and allow for this in the report. This is done by making a deduction from the mean result of duplicate or replicate determinations. The amount deducted depends on the reliability of the analytical method and the magnitude of random and systematic errors. Because precision tends to decrease as the concentration of ethanol in the blood increases, the amount deducted is greater at high BAC to ensure the same degree of confidence (e.g., 99 or 99.9%) in the final result. After making the deduction, a statement can be made to the court to the effect that the person’s BAC is not less than the value reported with a high degree of confidence such as 99 or 99.9%.
Principles and Application of Breath-Alcohol Analysis It must be a very old observation that some portion of the alcohol a person consumes gets exhaled via the
lungs and can be detected on the breath [9]. Indeed, the smell of alcohol on the breath, together with the person’s general appearance and behavior, often constituted the first indications, albeit primitive, of overindulgence in alcohol. The first scientific studies attempting to measure accurately the concentration of alcohol in a person’s breath were published over 150 years ago [9]. These showed that only a small fraction of the alcohol consumed (2–5%) could be recovered unchanged in the breath and urine collected for several hours afterward. The bulk of the dose of alcohol ingested underwent biochemical oxidation in the liver to provide a rich source of calories (7.1 kcal per gram ethanol). These first studies on breath-alcohol concentration (BrAC) also identified the potential problem caused by the presence of alcohol dissolved in the mucous surfaces of the mouth from a recent drink. This led to a warning (cited below from FE Anstie, The Lancet, Sept. 28, 1867), which still holds true. When a breathalcohol test is made for evidential purposes there is always a mandatory 15–20 min deprivation and observation period after the last drink to avoid the risk of contaminating the sample with alcohol in the mouth [21]. Much caution is necessary, however, in applying this test. It must not be tried during at least the first quarter of an hour after a dose has been taken, for the mouth retains the characteristic smell, even of the most moderate dose, of any of the stronger smelling drinks, for fully this time.
Human breath consists of a mixture of gases being mainly oxygen, nitrogen, carbon dioxide and is saturated with water vapor at body temperature [22]. Additionally, expired air contains trace amounts of other organic volatile compounds (VOCs), which are produced either naturally in the body (endogenous volatiles) or inhaled together with the ambient air breathed. The most abundant VOCs in human breath are ethanol, methanol, acetone, carbon monoxide, methane, and isoprene. The concentrations of these substances are normally extremely low and have no practical relevance to challenge the results when these are used for legal purposes. However, under some circumstances, such as diabetes or other metabolic disorder, or after eating very low carbohydrate diets or if a person consumed denatured alcohol, the concentrations of acetone and isopropanol in breath samples might increase appreciably.
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Table 8 Important characteristics to consider during validation of an analytical method intended for forensic purpose, such as the determination of ethanol in biofluids Characteristic of the analytical method Accuracy
Brief description and/or definition of the characteristic
Accuracy is a measure of the closeness of agreement of analytical results with the true or known concentration of substance in the sample. The true value might be the accepted reference value or a “target” concentration obtained by spiking with a known quantity of analyte Bias Bias is a systematic deviation either constant or proportional to the concentration of the analyte. Bias has to do with correctness of the analytical result and is derived as the difference together with its sign between the known quantity or target value and the result or average of several determinations by the method Precision Precision is the degree of mutual agreement between independent measurements under specified test conditions. This reflects the spread of analytical results when the method is applied repeatedly to aliquots of a homogenous sample. Random errors inherent in the method determine the analytical precision. In mathematical terms precision is computed as the standard deviation of repeated measurements Repeatability This term is used to define within-run analytical precision, same laboratory same operator same equipment – short-term precision Intermediate precision Precision of analysis between-runs in the same laboratory over longer time periods (weeks) by different operators, instruments, reagent batches, and calibrations Reproducibility This term is used to define precision of the analytical method when performed in different laboratories, with different instruments and analysts, such as the standard deviation in external proficiency testing Linearity The ability of an analytical method to give results directly proportional to the concentration of the analyte in the sample within a defined range of values Range The concentration interval between the upper and lower levels of analyte that can be determined with acceptable accuracy and precision. The range usually represents the difference between the lowest and the highest points on the calibration curve Sensitivity This is defined as the difference in analyte concentration corresponding to the small detectable difference in the detector response. It is represented by the slope of the calibration curve. Specificity/selectivity These terms are often used interchangeably and are related to the ability of a particular method to quantify the target analyte in the presence of interfering compounds Recovery Normally expressed as a percentage, recovery refers to the amount of drug removed from the original sample which reaches the end of the analytical procedure. Poor recovery can be compensated for by adding an internal standard to the biofluid before staring the analysis Limit of detection (LOD) LOD is the lowest concentration of analyte in a sample that can be detected but not necessarily quantified Limit of quantitation (LOQ) LOQ is the lowest concentration of an analyte in a sample that can be quantified with acceptable precision and accuracy. LOQ is approximately 3.3 × LOD Robustness Robustness is the capacity of an analytical method to produce accurate and precise results despite small deliberate changes in test conditions and method parameters. In GC analysis of ethanol the addition of an internal standard helps to ensure the method is robust Ruggedness Ruggedness is a measure of the degree of reproducibility of the analytical results when performed under varying tests conditions, such as when work is done by different technicians, instruments, source of reagents, laboratories, or even in different countries Traceability Traceability means that a result of measurement can be traced back, through an unbroken chain of comparisons, to a national or international standard value. The traceability of the ethanol standards used to calibrate the gas chromatography needs to be well documented Uncertainty The word uncertainty means having doubt in something, such as the result of analysis. Analytical uncertainty is defined as a parameter associated with the result of a measurement, which characterizes the spread or dispersion of the results that could reasonably be attributed to the quantity being measured
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The physiological principles that govern the excretion of alcohol in breath and the notion of indirectly estimating the BAC by breath analysis emerged in the 1930s when the concept of a blood/breath distribution ratio was formulated [22]. The first use of BrAC was to estimate the person’s coexisting BAC, because this was accepted as the best objective evidence of drunkenness. The concentration of alcohol in the breath sample analyzed was multiplied by the blood/breath ratio of alcohol (2100 : 1), which allowed reporting the corresponding BAC. Some breath-test instruments, such as the Breathalyzer , was designed and calibrated based on the assumption of a 2100 : 1 factor [22]. BAC = BrAC × 2100
(5)
Experience has shown that use of the above formulae tended to underestimate the true coexisting venous BAC by about 10% [23]. In some applications of breath-alcohol testing, the factor 2300 : 1 is used for calibration, which gives a more unbiased estimate of the venous BAC. However, the above equation is physiologically incorrect because BrAC runs closer to the concentration of ethanol in arterial (A) blood, whereas the sample analyzed for legal purposes is venous (V) blood. The arterial BAC (e.g., blood from a radial artery) is higher than the venous BAC (e.g., from a cubital vein) during the absorption and distribution stages of the BAC curve. The arterial BAC and venous BAC are the same at one time point (60–90 min post drinking), which marks complete equilibration of the ingested dose between the blood and tissue water. After this time, the arterial BAC is less than the venous BAC and remains less for the remainder of time that alcohol is being metabolized. The A–V differences are more pronounced on the rising or absorption phase of the BAC curve and the negative A–V differences on the descending postabsorptive phase is rather small or negligible and can be ignored [2]. In forensic practice it has become common to assume that most drunken drivers are apprehended 1–2 h after the end of drinking when the blood-alcohol curve has entered the postpeak descending phase.
Methods of Analyzing Alcohol in Breath The first methods of breath-alcohol analysis employed chemical oxidation principles as exemplified by the classic Borkenstein Breathalyzer device,
which was widely used for law enforcement purposes, such as for testing drunken drivers in the United States, Canada, and Australia. The oxidizing reagent consisted of a mixture of sulfuric acid and potassium dichromate contained in a glass ampoule through which a known volume of the subject’s breath was passed. Any ethanol present in the breath sample was oxidized to acetic acid with a concomitant reduction of chromium VI (yellow) in dichromate to chromium III (green) and this color change was monitored by photometry after exactly 90 s of reaction. Accordingly the reaction endpoint and the quantitative analysis of ethanol in breath were determined by optical photometry. In the 1970s, physicochemical methods were developed for the analysis of alcohol in samples of breath particularly the use of infrared absorptiometry, which was incorporated in the Intoxilyzer range of instruments [24]. Figure 3 shows the infrared spectrum of ethanol in the gas phase and the major absorption bands corresponding to vibrational frequencies in the ethanol molecule. Those used for quantitative analysis at 3.4 µm (C–H stretch) and 9.5 µm (C–O stretch) are indicated. The quantitative analysis of ethanol utilizes the Lambert–Beer law and monitors the absorption of radiation at 3.4 µm, which corresponds to the carbon–hydrogen stretching in the alkyl groups of ethanol. Under some conditions, acetone might be present in human breath at elevated concentrations and can also absorb IR radiation at 3.4 µm, which suggests a potential interference problem. Accordingly selectivity of the analysis of ethanol was enhanced in later versions of the Intoxilyzer instruments by monitoring IR radiation and more than one wavelength by use of narrow band-path filters set at 3.38 and 3.49 µm so that acetone could be distinguished from ethanol. The latest generation of infrared breath-alcohol instruments incorporate filters to monitor IR radiation also at a wavelength of 9.5 µm, which corresponds to the C–O stretching frequency in the alcohol molecule (see Figure 4). A few instruments (e.g., Intoxilyzer 9000) use both 3.4 and 9.5 µm to give an added analytical selectivity. By contrast, the Alcotest 7110 is a dual detector device with IR absorption at 9.5 µm and electrochemical oxidation (fuel cell) to ensure high selectivity for identification of ethanol. The advantage of IR analysis is that this is a nondestructive analytical method and
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Full infrared spectrum of ethanol
Absorbance (%)
C–H stretch
C–O stretch
H H
H
OH H H
2.5
3.5
4.5
5.5
6.5
7.5
8.5
9.5
10.5 11.5 12.5
Wavelength (µm)
Figure 3 Infrared spectrum of ethanol in the vapor phase showing the absorption bands around 3.4 µm (C–H stretching) and 9.5 µm (C–O stretching) used for quantitative determination in modern evidential breath-ethanol analyzers
if necessary the sample analyzed can be preserved and used for other purposes. The methodologies (analytical principles) incorporated into a wide selection of devices and instruments for breath-alcohol testing over many years are described in Table 9 [24, 25]. In this table, one should distinguish breath analyzers intended for roadside screening analysis with those designed for evidential purposes. The first screening devices were constructed from chemical tubes containing potassium dichromate and sulfuric acid impregnated on a silica gel support material. This mixture of chemicals changed in color from yellow to green if there was alcohol in the suspect’s breath after blowing through the tube and inflating a balloon of fixed volume (∼1 l).
The breath-alcohol screening devices used today by the police for roadside mass testing of motorists are small handheld instruments that incorporate an electrochemical sensor for the analysis of ethanol. Many such instruments are available such as Alcolmeter, Alcotest, AlcoSensor, and LifeLoc, which are sometimes referred to as fuel cell instruments (see Table 9). The ethanol contained in a small portion of the end-exhaled breath (∼1.0 ml) is directed via an inlet tube into a chamber fitted with an electrode (platinum black) and an acidic electrolyte solution, such as phosphoric acid. Oxidation of ethanol at the electrode surface produces acetaldehyde with a simultaneous liberation of electrons. These are captured, amplified, and displayed as a measurable current in direct
Exhalation profile for ethanol
Breath-alcohol (µg l−1)
200 160 End exhalation
120 80 40 0 0
2
4
6
8
10
12
Exhalation time (s)
Figure 4 analyzer
Increase in breath-alcohol concentration during a prolonged exhalation into a modern infrared breath-alcohol
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Table 9 Analytical principles used for determination of ethanol with a wide selection of instruments and devices intended for breath-alcohol analysis Analytical method
Example of breath instruments Brief details of the operating procedure and principles
Chemical oxidation
Drunkometer Alcometer Breathalyzer Alcotest tubes Alcolyzer tubes
Gas chromatography
GC Intoximeter AlcoAnalyzer GC
Infrared spectrometry
Intoximeter DataMaster Intoxilyzer Alcotest Evidenzer
Electrochemical oxidation
AlcoSensor Alcolmeter Alcotest Lifeloc
Metal oxide semiconductor (Taguchi cell)
ALERT J4X
Ethanol in a known volume of breath is analyzed by oxidation with a mixture of potassium dichromate and sulfuric acid, or potassium permanganate or iodine pentoxide. The endpoint of the reaction was either a visual color change (Alcotest and Alcolyzer tubes) or by UV photometry (Breathalyzer) Compact instruments designed for analysis of ethanol in exhaled breath or vapor samples. The gas chromatograph (GC) Intoximeter incorporated a flame ionization detector and the AlcoAnalyzer used a thermal conductivity detector. The need for an external gas supply and frequent recalibration and maintenance meant they these instruments were not very practical for use at police stations Ethanol in the exhaled breath passes through a sample chamber (∼50 ml) and analysis is done by measuring the absorption of infrared radiation according to the Lambert–Beer law. Ethanol molecules absorb radiation at wavelengths of ∼3.4 µm corresponding to the C–H stretching and ∼9.5 µm corresponding to the C–O stretching frequencies. To enhance selectivity for identifying ethanol, the absorption of infrared radiation is done at several different wavelengths Ethanol in a fixed volume of breath (∼1.0 ml) undergoes electrochemical oxidation with the help of a platinum black catalyst and acid electrolyte mounted with electrical connections to form a fuel cell. The molecules of ethanol enter one side of the cell and are oxidized to acetaldehyde thus liberating electrons. The current produced is proportional to the concentration of ethanol in the sample of breath Many small handheld devices incorporate a Taguchi sensor and these are generally inexpensive and mainly intended as self-testers for use by the public. The ALERT J4X incorporated a Taguchi cell and this unit gained approval as a breath-alcohol screening instrument by police forces in Canada. The Taguchi sensor incorporates a tin-oxide (SnO2 ) bead mounted on a ceramic cylinder that measures changes in surface conductivity. The heated bead has a high surface resistance in ambient air but when exposed to combustible gases the surface conductivity increases in proportion to the concentration of substance in the gas phase. The semiconductor is not specific for analysis of ethanol and constituents of cigarette smoke as well as acetone on the breath give a response
proportion to the number of molecules of ethanol reacting at the platinum electrode surface. The output from the fuel cell changes as a function of time after starting the reaction to reach a peak response after about 20 s. The response curve then exponentially falls back to zero. Quantitative analysis is achieved by measuring the peak response or the area under the entire response curve. To speed up the time between tests, the return to a zero signal is achieved
by short circuiting the cell in readiness for the next subject test. One important category of breath-alcohol instruments are those intended and used for evidential testing, that is to generate evidence of sufficient reliability that drunken drivers can be prosecuted. Most evidential breath-alcohol instruments incorporate infrared technology for the detection and analysis of ethanol as discussed above [25]. The test subject
Alcohol: Analysis exhales into the heated breath inlet tube and makes a continuous forced exhalation for as long as possible, usually for at least 6 s. The concentration of ethanol increases as a function of time during a prolonged exhalation, first rapidly and then more slowly as the volume of exhaled breath reaches a maximum forced exhalation (Figure 4). Quality assurance of the breath sample is achieved by means of slope detectors that help to monitor the shape of the breath-alcohol exhalation profile to ensure that it conforms to that expected for normal human breath containing only ethanol [24, 25]. The BrAC at the end of exhalation gives a good indication of the concentration of alcohol residing in the deep lung alveolar air as it leaves the lungs. Instruments used for evidential testing should provide a print-out of the results in real time including identification of the person tested, proof of calibration control of the instrument and the date and time of testing as well as all analytical results. It is good forensic practice to make two independent tests of the person’s breathalcohol concentration about 6 min apart and take the average result [24]. An important aspect of any chemical analysis is the calibration and standardization of the measuring equipment used [19,21]. Calibration refers to the process by which the relationship between the output signal or response of the instrument and the value of the input quantity or concentration is determined. For the purpose of calibration, a series of ethanol standards with known strength are prepared to cover the range of interest. The calibration and control of breath-alcohol instruments is done either by means of a so-called wet-bath simulator device or by use of a compressed dry gas cylinder containing a known content of ethanol mixed with an inert gas such as argon. The wet-bath simulators are the traditional way of calibrating breath analyzers and have the advantage that they resemble the biological specimen (human breath) in composition, that is, being saturated with water vapor at the temperature of exhaled breath (34 ° C). However, the compressed gas standards are more convenient to handle when tests are made away from the laboratory, such as at a police station or in a police vehicle [24]. It seems that compressed dry gas standards are gradually replacing the traditional wetbath simulators for the purpose of calibration control checks of evidential breath-testing instruments. Considerable interest exists in the marketing and sale of breath-testing instruments that are intended
97
primarily for use by the general public as a means of self-testing. These devices are usually small, compact and battery operated, and fairly cheap to buy. However, the results obtained are not always reliable and trustworthy for several reasons. First, a proper control of the way the sample of breath is introduced into the instrument cannot be guaranteed. Second, the alcohol sensors incorporated are usually tin-oxide semiconductors that measure changes in conductivity, which is a nonspecific way to measure ethanol (Table 9). Third, a control of the calibration stability of the instrument is rarely done during long-term usage. Fourth, cigarette smoke, carbon monoxide, exhaust fumes, methane, and other combustible gases react and give a response indistinguishable from ethanol. Accordingly, the use of these self-testers for alcohol should not be encouraged. Another rapidly emerging public safety application of breath-alcohol testing is in connection with ignition interlock devices or socalled alcolocks. These devices are fitted to public transportation vehicles (e.g., buses and trains) and also into many private cars. The aim is to prevent a person who has consumed too much alcohol from being able to start the vehicle and reduce the risk of drunken driving. If alcohol is detected on the person’s breath above a predefined threshold level, the ignition switch is locked and the vehicle will not start. The concentration of ethanol in breath at which the vehicle fails to start is usually set to be fairly low, such as at a BAC of 0.2 g l−1 (20 mg/100 ml) or less, even though the legal limit for driving might be higher (e.g., 0.5 or 0.8 g l−1 ). The overall aim of interlock devices is to improve traffic safety by reducing the risk of alcohol-related crashes. Interlocks are particularly useful as a countermeasure to prevent a previously convicted drunken driver from reoffending. Indeed, some countries make it one of the requirements for relicensing to have an interlock fitted to the vehicle belonging to a previously convicted drunken driver. Most of the currently available interlock devices make use of the electrochemical oxidation reaction to analyze ethanol (Table 9).
Concluding Remarks Knowledge about a person’s BAC or BrAC provides compelling evidence when a conclusion is reached about the effects of alcohol, such as the degree of drunkenness, impairment of cognitive and
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psychomotor functioning, and the ability to form intent. Discussion and debate about culpability is tightly linked to a person’s BAC and this has gained paramount importance in criminal proceedings, such as investigation of alcohol-related crimes including murder, physical and sexual assaults, and drunken driving. This means that the quantitative analysis of alcohol in body fluids is undoubtedly the highest volume investigation performed at most forensic science and toxicology laboratories worldwide [26, 27]. Few substances can be determined in blood and other body fluids with such a high degree of accuracy, precision, and selectivity as the concentration of ethanol [15, 19]. Because the alcohol a person drinks becomes diluted with the total body water, which is ∼50–60% of body weight, the amount of ethanol necessary to cause inebriation and impairment vastly exceed that of all other drugs of abuse. The BACs, typically encountered in legal medicine (0.2–5.0 g l−1 ), are about 1000 times higher than those for most other licit or illicit drugs. The sampling and analysis of alcohol in breath has the advantage that it is noninvasive and the results of the test are obtained immediately afterward [4]. The on-the-spot results of a breath-alcohol test allow immediate decisions to be made, such as allowing a motorist to continue driving, or whether a casualty patient might require emergency surgery e.g., for head trauma or simply be allowed to recover from gross intoxication. Breath-alcohol instruments are being increasingly used in connection with workplace alcohol testing, at probation and rehabilitation centers where people must refrain from drinking and also at school parties and dance venues where alcohol use is forbidden. This review hopefully made it clear that ethanol can be determined in body fluids with a high degree of accuracy, precision, and specificity by a variety of analytical methods [20, 23]. However, the gold standard procedure is the application of GC together with the headspace sampling technique. Such GC methods furnish both a qualitative analysis, based on the comparison of the RT of components in the sample with authentic known substances, and also a quantitative analysis based on detector response (peak height or peak area) displayed on the chromatogram [16]. The GC methods of analysis are easily automated and under optimum conditions, the response for ethanol is adequately resolved from that of other low molecular weight volatiles that might be present in forensic
bloods samples, such as acetaldehyde, methanol, acetone, and isopropanol [15]. Although the methods are the same for dealing with specimens from the living and the dead, the analytical results from autopsy specimens are more difficult to interpret, owing to various postmortem artifacts. This limitation is offset to some extent by the fact that many different biological specimens are available for toxicological analysis during a postmortem examination. Aspects of postmortem alcohol analysis and interpretation have been dealt with in depth in several recent review articles [27, 28]. The recommended specimens for the determination of ethanol in corpses are femoral venous blood from the left or right leg (Table 7) and use of heart blood or from the chest cavity should be avoided. To simplify interpretation of analytical results, pathologists should strive to obtain additional specimens, such as urine from the intact bladder and vitreous fluid from the eyes, for the analysis of ethanol [29]. The consumption of alcoholic beverages is part and parcel of normal social life in most countries and for many individuals, especially among men, moderate drinking often escalates into overconsumption, abuse and dependence. Binge drinking and drunkenness have many negative consequences for the individual and society and results in premature death. Heavy drinking tends to trigger deviant and aggressive behavior, such as family violence and drunken driving. The continued use and abuse of alcohol in society ensure that requests to measure this drug in body fluids and to interpret the results in a legal context will remain the most commonly requested service from forensic science and toxicology laboratories in the distant future.
References [1] [2]
[3]
[4]
Room, R., Babor, T. & Rehm, J. (2005). Alcohol and public health, Lancet 365, 519–530. Jones, A.W. & Pounder, D.J. (2007). Update on clinical and forensic analysis of alcohol Chapter 5.2, in Drug Abuse Handbook, 2nd Edition, S.B. Karch, ed, CRC Press, Boca Raton, pp. 333–376. Hunsaker, D.M. & Hunsaker, J.C. (2005). Blood and body fluid analysis, in Encyclopedia of Forensic and Legal Medicine, J. Payne-James, R.W. Byard, T.S. Corey & C. Henderson, eds, Elsevier, Oxford, pp. 29–38. Jones, A.W. (1988). Enforcement of drink-driving laws by use of per-se legal alcohol limits: blood and/or breath
Alcohol: Behavioral and Medical Effects
[5]
[6] [7]
[8]
[9]
[10]
[11]
[12]
[13]
[14]
[15]
[16]
[17] [18]
[19] [20]
[21]
concentration as evidence of impairment, Alcohol, Drugs and Driving 3, 99–112. Moriya, F. (2005). Forensic sciences – alcohol in body fluids, in Encyclopedia of Analytical Sciences, 2nd Edition, Elsevier Sciences, pp. 368–366. Dubowski, K.M. (1986). Recent developments in alcohol analysis, Alcohol, Drugs and Driving 2, 13–46. Jones, A.W. (2000). Medico-legal alcohol determination – blood or breath alcohol concentration? Forensic Science Review 12, 23–48. Jones, A.W. (1989). Measurement of alcohol in blood and breath for legal purposes, in Human Metabolism of Alcohol, Vol 1, Pharmacokinetics, Medicolegal Aspects, and General Interest, K.E. Crow & R.D. Batt, CRC Press, Boca Raton, Florida, pp. 71–99. Jones, A.W. (1996). Measuring alcohol in blood and breath for forensic purposes – a historical review, Forensic Science Review 8, 13–44. Widmark, E.M.P. (1922). Eine Mikromethode zur Bes¨ timmung von Athylalkohol im Blut, Biochemische Zeitskrift 131, 473–484. Jones, A.W. (1995). Forensic science – determination of alcohol in body fluids, in Encyclopedia of Analytical Sciences, Academic Press, London, Vol. 2, pp. 1585–1594. Kristoffersen, L. & Smith-Kielland, A. (2005). An automated alcohol dehydrogenase method for ethanol quantitation in urine and whole blood, Journal of Analytical Toxicology 29, 387–389. Logan, B.K. (1992). Analysis of alcohol and other volatiles, in Gas Chromatography in Forensic Sciences, Ian Tebbett, ed, Elsevier, North Holland, pp. 87–108. Emerson, V. (2004). Alcohol analysis, in Crime Scene to Court; the Essentials of Forensic Science, 2nd Edition, P.C. White, ed, Royal Society of Chemistry, Cambridge, pp. 350–376. Jones, A.W. & Schuberth, J. (1989). Computer-aided headspace gas chromatography applied to blood-alcohol analysis: importance of online process control, Journal of Forensic Sciences 34, 1116–1127. Tagliaro, F., Lubli, G., Ghielmi, S., Franchi, D. & Marigo, M. (1992). Chromatographic methods for blood alcohol determination, Journal of Chromatography 580, 161–190. Scopp, G. (2004). Preanalytical aspects of postmortem toxicology, Forensic Science International 142, 75–100. Pounder, D.J. & Jones, A.W. (2007). Postmortem alcohol - aspects of interpretation. Chapter 5.3, in Drug Abuse Handbook, 2nd Edition, S.B. Karch, ed, CRC Press, Boca Raton, pp. 376–401. Taylor, J.K. (1987). Quality Assurance of Chemical Measurements, Lewis Publishers, Chelsea, Michigan. Burnett, D. (1996). Understanding Accreditation in Laboratory Medicine, A C B Venture Publications, Association of Clinical Biochemists. Gullberg, R.G. (2000). Methodology and quality assurance in forensic breath alcohol testing, Forensic Science Review 12, 49–68.
[22]
[23]
[24]
[25]
[26]
[27]
[28]
[29]
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Jones, A.W. (1990). Physiological aspects of breath alcohol measurement, Alcohol, Drugs and Driving 6, 1–25. Gullberg, R.G. (2005). Breath alcohol analysis, in Encyclopedia of Forensic and Legal Medicine, J. PayneJames, R.W. Byard, T.S. Corey & C. Henderson, eds, Elsevier, Oxford, pp. 21–29. Gullberg, R.G. (2006). Estimating the measurement uncertainty in forensic breath-alcohol analysis, Accreditation Quality Assurance 11, 562–568. Harding, P. & Zettl, J.R. (2008). Methods for breath analysis, in Medical-Legal Aspects of Alcohol, 5th Edition, J.C. Garriott, ed, Lawyers & Judges Publishing Company, Tuscon, pp. 229–253. Garriott, J.C. (ed) (2008). Garriott’s Medicolegal Aspects of Alcohol, 5th Edition, Lawyers & Judges Publishing Company, Tuscon, pp. 1–534. Carey, K.B. & Hustad, J.T.P. (2005). Methods for determining blood alcohol concentration current and prospective, in Comprehensive Handbook of AlcoholRelated Pathology, Vol 3, V. Preedy & R. Watson, eds, Academic Press, pp. 1429–1444. Kugelberg, F.C. & Jones, A.W. (2007). Interpreting results of ethanol analysis in postmortem specimens, Forensic Science International 165, 10–29. Jones, A.W. & Holmgren, P. (2001). Uncertainty in estimating blood-alcohol concentration by analysis of vitreous humor, Journal of Clinical Pathology 54, 699–702.
Further Reading Dubowski, K.M. (1991). The Technology of Breath-Alcohol Analysis, US Department of Health and Human Services, Public Health Service DHHS Publication No. (ADM), pp. 1–38.
ALAN W. JONES
Alcohol: Behavioral and Medical Effects Introduction Alcohol is one of the oldest drugs known and it affects virtually every organ system in the body. The medical consequences including the economics of medical treatment of alcohol-related disorders are staggering and can have important forensic implications. Alcohol damages the heart and can elevate
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blood pressure, increasing the risk of heart failure and stroke and can impair biochemical regulation of a variety of cellular and metabolic functions that can increase the risk for certain forms of cancer, the risk for accidental injuries and impairs the recovery from those injuries and significantly contribute to the years of life lost. This article reviews the most significant and well-known medical consequences of alcohol in three basic areas of forensic interest: accidental injuries, skeletal fragility, and liver pathologies.
Alcohol and Accidental Injuries Accidental injuries are a direct medical consequence of alcohol intoxication. Laboratory as well as epidemiological field studies conducted over the last few decades clearly establish the fact that alcoholinduced impairment of cognitive and psychomotor functioning while engaging in a variety of behavioral activities increases the risk for injury. Among these, the effects of alcohol on automobile, bicycle, motorcycle, boating, aquatic, and pedestrian injuries, as well as homicide, suicide, and death from fire have been examined.
Impaired Driving Driving while intoxicated is probably the well-studied injurious consequence of drinking of interest and is of importance to forensic examiners. The use of alcohol coupled with increased risk taking and impulsivity, at least among young males [1], and decreased seat belt use [2]. Even at very low blood–alcohol concentrations (BACs), the performance of complex divided attention, a critical factor in a variety of tasks both inside and outside the laboratory, is impaired and the most likely cause of motor vehicle collisions. At BAC above 50 mg/dl that impairment translates into actual highway statistics (in which the intoxicated driver is deemed to be the cause of the accident). At higher BACs (e.g., 150 mg/dl, or more), impairment in proprioception, visual perception, and lengthened simple reaction time are additional significant contributing factors that should be considered into forensic investigations of crashes involving intoxicated drivers, pedestrians, and others. Most people who present with obvious symptoms of intoxication are impaired drivers and at increased risk for a fatal crash. However, the lack of obvious intoxication does not mean
lack of impairment. Most subjects do not appear visibly intoxicated, even though they are intoxicated according to law in regard to motor vehicle operation [3–6]. When most people appear obviously intoxicated, their BAC is probably well in excess of any legal definition of intoxication. Regardless of which functions are affected by alcohol, impaired drivers clearly present a public health risk because of the increased number of accidental injuries due to intoxication. About 16 000 fatalities occur each year related to drunken driving [7] and about 10% of all personal injury accidents and at least 180 000–200 000 property and personal injury crashes, respectively, are caused by alcohol intoxication per year [8]. The risk of injury as well as the responsibility for causing a collision when driving while intoxicated is proportional to the BAC. With the current legal definition of driving while intoxicated in the United States (80 mg/dl), the relative risk for a crash is significantly greater compared with sober drivers. When the interaction among blood alcohol, gender, and single versus multiple vehicle collisions is considered, the relative risk is many times greater than previously believed. For example, the relative risk of a fatal crash in an 18-year-old male with a BAC of 80 mg/dl is about 34 times greater than a sober driver. In comparison, a 40year-old male with the same BAC has a relative risk that is about 11 times greater than a sober control [9, 10]. A more specific breakdown of relative risk based on age, gender, and BAC is presented in Figure 1.
Pedestrian and Fall-down Injuries Earlier studies estimated that about one-third of all fatally injured pedestrians had a BAC of 100 mg/dl or more at the time of their death. More than twothirds of drivers, pedestrians, and bicyclists (see below) killed each year are intoxicated [12]. Driving and pedestrian activity rely on divided attention and visual motor processes. Therefore, it is reasonable to infer that these behaviors share similar alcoholinduced changes in relative risk. However, driving is obviously a more challenging task than walking, but both behaviors require divided attention, vigilance, and other cognitive skills that are sensitive to the impairment produced by alcohol, even at low BACs [13]. In the United States, injuries related to falls are the second leading cause of accidents and account for about 13 000 deaths per year. Most studies suggest
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Figure 1 Alcohol intoxication, behavior, and relative risk for a fatal crash. Line graph shows relative risk (log) as a function of BAC, age, and gender. Data derived from stepwise logistic regression coefficients for relative risk based on single vehicle fatalities [9]. Note that for women age 16–20, a coefficient of 0.03 (range 0.044–0.014) was used. Coefficients are rounded to nearest 10th or whole number [Reproduced from Ref. 11. Taylor & Francis Group, 2008.]
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that alcohol increases the risk for injuries due to falls. Honkanen et al. [14] evaluated intoxicated emergency room patients involved in fall-down injuries and compared them with sober pedestrians who were at the same location of the accident one week later at the same time of the day. The comparison revealed the relative risk or a fall was three times greater for patients with blood–alcohol levels between 50 and 100 mg/dl, 10 times greater for patients with blood alcohol levels between 100 and 150 mg/dl, and 60 times greater for patients with BACs 160 mg/dl, or higher.
Bicycling Also, there are about 200 fatalities and 7000 injuries from alcohol-related bicycle crashes each year. The relative risk of an alcohol-related bicycle crash found that alcohol was involved in 25% of the collision accidents and in 63% of the single accidents involving cyclists aged 15–64 years compared with intoxication in 4% of the nonaccident controls. A relative risk was of the order of 3 overall, and 58 for the collisions related to alcohol use [15]. Moreover, bicyclists who died at the scene were four times as likely as those who died at hospitals to be at or above the legal definition of intoxicated driving. This increased mortality may be due to the effects of alcohol on injury outcome (discussed later in this article). Other studies suggest that fatally injured bicyclists were about twice as likely to be intoxicated as cyclists treated for nonfatal injuries [16].
Fires and Burns In the United States, alcohol intoxication plays a role in the estimated 5000 fatalities and about 1.4 million burn injuries each year [17]. In a review of studies on alcohol and burn injuries published between 1947 and 1986, Howland and Hingson [18] and reported on the percentage of the victims who were intoxicated with alcohol. In the overwhelming majority of the studies published in that period, alcohol exposure was found to be more likely among those who died in fires ignited by cigarettes than from other causes, suggesting that alcohol plays a role in the cause of fires, subsequent burn injuries, and is overly represented in burn victims. In fact, one-third to two-thirds of these victims had blood alcohol levels greater than 100 mg/dl. The authors concluded from
these data that alcohol intoxication is a risk factor for fire deaths [18]. Later studies further revealed that alcohol was a factor in about 22% [19] to 26% [20] of burn injuries. Overall, intoxicated patients have a significantly higher fatality rate in severe burn cases. These data are reviewed elsewhere [21]. Although, impairment from alcohol is a risk factor in a substantial percentage of burn victims, it is not the only factor and may also interact with other factors. For example, Brezel and Kassenbrock [22] examined alcohol and drug abusers, psychiatric patients, and those with neurological dysfunction to determine whether this group had more medical complications, surgical procedures, and longer hospital stays than burn patients without these disorders. Alcohol abuse (defined as six or more cans of beer or the equivalent, per day) was the most common form of impairment, and the authors found that these patients had more complications and required a longer period of hospitalization, alcohol intoxication was only one of the several contributory factors. Both acute and chronic alcohol abuse contribute to burn injuries. In a study of 1074 patients admitted to a medical center burn unit, 40% who were positive for alcohol were more likely to have a greater proportion of bodily burns and greater incidence of smoke inhalation than the controls [23]. Chronic alcoholics also seem to have a higher fatality rate than do patients without a history of chronic alcohol abuse [24]. In a recent review of the incidence and toxicological complications of burn cases, Brick [25] concluded that there is a clear relationship between alcohol or drug intoxication and the risk for thermal injury. It was suggested that the reason alcohol-intoxicated persons were at increased risk for accidental thermal injuries is impaired judgment or psychomotor coordination while engaging in normal fire-starting activities (e.g., cooking). We also noted that psychomotor impairment might be only one part of the problem. Other factors including neuropsychological status while intoxicated may impair various domains of cognitive functioning resulting in a decreased ability to anticipate problems, lowered inhibitions, and increased risk taking. For example, once a fire has started, mental confusion, and failure to recognize risk or danger may lead to an inability to anticipate or respond to danger, particularly at high levels of intoxication.
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Water Sports
Suicide
Alcohol is infinitely miscible in water, at least chemically, but with regard to water sports, alcohol and water do not mix. Nearly half of drowning victims in one study had consumed alcohol and 22% were intoxicated with BACs of 100 mg/dl, or more [26]. More recent studies suggest that alcohol consumption significantly increases the risk for boating fatalities was a factor in up to 21% of reported boating [27]. As alcohol deleteriously impairs balance, motor function, and judgment, intoxicated passengers, as well as vessel operators, are probably at risk for injury [28]. Alcohol intoxication also contributes to and aggravates spinal cord injuries following diving accidents. In this context, Perrine et al. [29] examined the effects of alcohol on the ability to perform shallowwater entry dives under experimental conditions. A progressive and significant impairment of specific aspects of diving performance was detected at blood alcohol levels as low as 40 mg/dl. This study also correlated diving performance with psychomotor performance using the Standardized Field Sobriety Tests (SFSTs). Impaired diving correlated well with impaired SFST performance criteria for the detection of drivers with a blood alcohol level of more than 100 mg/dl [29].
Suicide is the 11th leading cause of death for young people (aged 15–34), and the third leading cause of death in the United States [35]. Suicide is also highly correlated with alcohol intoxication. In a review of suicide attempts, intoxication was present in 40% (range 10–73%) for attempted suicide and 10–69% for completed suicides. The relationship between alcohol use and suicide is not difficult to understand. Acute intoxication reduces inhibitions, narrows attention, impairs the ability to appreciate the consequences of behavior, and may promote depressive thoughts and hopelessness. Chronic alcohol abuse is often complicated by mental illness, including depression [36–38]. Both acute and chronic intoxication, impair cognitive skill, may enhance aggression including self-aggression, or the combination with medications may precipitate pathways mediating this behavior [39]. Although, it is unlikely that people commit or attempt to commit suicide simply because they are intoxicated, premorbid suicidal ideology is more likely to be acted upon while intoxicated. Acute intoxication may be a greater risk factor for suicide than the previous drinking history [40] but the causal mechanism for the interrelationship among alcohol intoxication, alcohol dependence, and suicide is only partially understood [37, 41].
Aircraft Operation Pilots who must divide attention and process information derived from an array of instrumentation and make perceptual and cognitive decisions based on a large amount of information in a multidimensional environment should not drink and fly. It is known that alcohol deleteriously influences the ability of pilots to evaluate their performance [30] and that low levels of alcohol (25–40 mg/dl) impair performance of trained pilots in flight simulators [31, 32]. Although it might appear that both motor vehicle drivers and aircraft pilots are impaired at similar low BACs (e.g., 30–40 mg/dl), there is evidence to suggest that piloting an aircraft is significantly more sensitive to the effects of alcohol. For example, there is some research suggesting that alcohol continues to impair performance on flight simulators many hours after blood alcohol levels have returned to zero [33]. Although some laboratory studies failed to find impairment 12 h after drinking [34], the forensic implications of impairment when alcohol is not in the blood are enormous, need to be evaluated further.
Miscellaneous Injuries People die from many causes including accidental injuries, homicide, and suicide, in which alcohol intoxication is a significant risk factor. Relative to lifetime abstainers and infrequent drinkers, the risk of death from external causes increased logarithmically among infrequent binge drinkers [42] and no evidence of reduced risk of death among light or moderate drinkers. The group at highest risk of death from external causes was drinkers who consumed five or more drinks less than once a month. Within this group of binge drinkers, older subjects (defined as 65-plus years) were at the highest risk. High risk was also observed in younger drinkers (defined as 18–24 years of age), probably because of their lack of tolerance and experience, as middle-aged drinkers (25–64 years of age) who presumably have more experience both as drinkers and drivers, did not show the same increased mortality risk. In summary, infrequent binge drinking increases risk as a function of
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age, possible tolerance, age-related experience, and other variables.
Intoxication and Injury Outcome Alcohol intoxication not only contributes significantly to accidental injuries but may also affect injury outcome, particularly among patients with head injuries. This is highly significant as up to half of the traumatic brain-injured patients have BACs that exceed the legal definition for intoxicated driving at the time of injury [43]. For example, motorcycle riders with head injuries are about twice as likely to have fatal head injuries if they are intoxicated, compared to injury matched, sober riders [44]. Drunk drivers are more likely to be seriously or fatally injured than sober drivers [45] and alcohol-intoxicated accident victims with central nervous system injuries were more than twice as likely to die sooner than anatomically matched controls [46]. Such a belief is not supported by the majority of more current research on this topic [47]. The biochemical cause of the deleterious effect of intoxication in the injury outcome is not proven but there are some intriguing potential mechanisms. For example, it is now believed that the severity of hemorrhagic shock is greater when intoxicated and results in a higher mortality rate compared with the sober controls [48]. Hemorrhagic shock also induces acidosis with marked hypercarbia. In such cases, alcoholinduced acidosis would likely increase morbidity and mortality [48–50] possibly because of the effects of acidosis on ventilatory responses.
Alcohol and the Skeletal System The relationship between alcohol abuse and increased risks for skeletal fractures was observed by the ancient Egyptians [51–53], but the epidemiology and mechanisms of this effect have only recently come under scientific scrutiny. Since alcohol is known to increase risk for injuries that may involve skeletal fractures, generalized skeletal fragility among alcoholics may be an important contributing factor to such injuries.
Alcohol-induced Fractures Epidemiological research on the prevalence of fractures in alcoholic subjects suggests positive
association between alcohol intake and fractures. For example, men hospitalized for alcohol-related problems are four times more likely to have rib fractures than nondrinking patients [54] and up to 14 times more likely to have spinal crush fractures [55, 56]. Two to six drinks per week also increases the risk for fractures in men compared with the same injuries in subjects who consumed less than two drinks per week, and for heavy drinkers, there was almost 10 times the risk of hip fractures as men in the same age group who drank lightly [57]. Weekly alcohol intake was associated with greater risks for osteoporotic fractures in postmenopausal women [58], and women who consumed more than eight drinks per week, the fractures were almost twice as likely as in nondrinkers. Other studies show that the equivalent of two standard drinks per day is associated with a significant increase in hip, wrist, and other fractures [59–61]. However, other investigators have not identified any significant association between alcohol intake and the risks for various fractures in women [62–66]. In addition to the risk of falls and related injuries, alcoholics may also suffer from a generalized skeletal fragility. Low bone density (osteoporosis) is a predictor of fractures [7], and a consequence of excess alcohol use reduced bone density has been confirmed in by many, but not all studies [67–73]. Dietary [68], hormonal [69], metabolic [73], and other factors contribute to this phenomenon (see [11] for a review).
Alcohol-induced Liver Injury Underreporting of alcohol consumption makes the exact prevalence of alcoholic liver disease in the United States difficult to measure, but health statistics suggest that some form of alcoholic liver disease affects more than 2 million drinkers [74]. It is estimated that 900 000 Americans have cirrhosis, and of the 26 000 who die each year, 40–90% have a history of alcohol abuse [74]. It is clear that the development of alcoholic liver disease is due to a combination of factors, most notably, prolonged alcohol consumption. Alcohol abuse is the leading cause of liver-related mortality in the United States. Excessive alcohol consumption leads to three serious types of liver injuries: fatty liver, hepatic inflammation (alcoholic hepattits), and progressive liver scarring (fibrosis or cirrhosis). Chronic heavy drinking can alter the normal metabolism and lead to an accumulation of fat
Alcohol: Behavioral and Medical Effects in the liver. As a result, the liver cells become so infiltrated that the liver itself becomes enlarged and cell damage may occur. However, fatty liver is reversible with abstinence. Continued alcohol abuse may result in hepatitis, a more serious medical condition, characterized by prolific inflammation and tissue damage. Hepatitis is life threatening but there can be significant recovery of function following abstinence. The most serious form of liver damage is cirrhosis, an irreversible disease characterized by scarring and cell death. Impaired liver functioning can also cause primary hepatic encephalopathy. Although this brain disorder precipitated by liver disease is rare, forensic examiners should be aware of it because it is characterized by altered psychomotor, intellectual, and behavioral functioning absent acute intoxication. Chronic, heavy drinking may produce metabolic tolerance and unusually high rates of alcohol elimination. Hepatitis and fibrosis will ultimately impair liver function and produce a reverse metabolic tolerance and impaired oxidation of alcohol. When justified, pharmacokinetic analyses used in making estimates of alcohol consumption or intoxication should account for potential metabolic changes. One question of interest to many people is, “How much alcohol does one need to drink before liver damage occurs”? Epidemiological studies suggest that reliable signs of injury begin after a “threshold” dose of about 600 kg for men and between 150 and 300 kg for women. To place this in perspective, at the high end (for men), this is roughly equivalent to the average consumption of 10–12 drinks a day for 10 years, and at the low end (for women), about three drinks per day. Below these doses, it is difficult but not impossible to reliably detect liver injury [75–78]. The differences in threshold doses between genders cannot be accounted for by anthropometrics or pharmacokinetics. For example, many individuals who consume large amounts of alcohol never develop liver disease and less than onehalf of heavy drinkers develop alcoholic hepatitis or liver fibrosis [75]. This suggests that hereditary and/or environmental factors interact with alcohol to affect the natural history of liver injury [76]. Numerous possible mechanisms may affect the susceptibility of certain people to alcohol-induced liver damage. Nevertheless, alcoholic liver disease is a significant cause of death in the United States and significantly contributes overall ages to 24 (in men) to 28 (in women) years of potential life lost [79, 80].
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Summary and Conclusions As a pharmacological agent, alcohol is a relatively simple compound. The ubiquitous nature of this drug on most, if not all major organ systems is consistent with its simple molecular structure and its widespread use [11]. Of specific interest to forensic issues, alcohol directly affects hepatic and skeletal systems and indirectly affects health and well being when accidental injuries due to intoxication are considered. From the available alcohol research, several conclusions may be drawn regarding the medical consequences of alcohol use. Most notably and across physiological systems, the effects of alcohol are complex and vary as a function of gender, diet, environment, lifestyle, genetics, dose and frequency of alcohol use, use of other drugs, and age. Even so, the majority of studies suggest that, overall, higher doses of alcohol are deleterious to many physiological systems and precipitate a range of psychosocial and biobehavioral problems including shortened lifespan that would be of interest in forensic evaluations.
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mass, and related parameters in alcoholic males, Calcified Tissue International 43, 269–276. Israel, Y., Orrego, H., Holt, S., Macdonald, D.W. & Meema, H.E. (1980). Identification of alcohol abuse: thoracic fractures on routine chest x-rays as indicators of alcoholism, Alcoholism 4, 420–422. Felson, D.T., Kiel, D.P., Anderson, J.J. & Kannel, W.B. (1988). Alcohol consumption and hip fractures: the framingham study, American Journal of Epidemiology 128, 1102–1110. Paganini-Hill, A., Ross, R.K. & Gerkins, V.R. (1981). Menopausal estrogen therapy and hip fractures, Annals of International Medicine 95, 28–31. Tuppurainen, M., Kroger, H., Honkanen, R., Puntial, E., Huopia, J., Saarikoski, S. & Alhave, E. (1995). Risks of perimenopausal fractures: a prospective populationbased study, Acta Obstetricia Gynecologica Scandinavica 74, 624–628. Hernandez-Avila, M., Colditz, G.A., Stampfer, M.J., Rosner, B., Speizer, F.E. & Willett, W.C. (1991). Caffeine, moderate alcohol intake, and risk of fractures of the hip and forearm in middle-aged women, The American Jounal of Clinical Nutrition 54, 157–163. Fujiwara, S., Kasagi, F., Yamada, M. & Kodama, K. (1997). Risk factors for hip fracture in a Japanese cohort, Journal of Bone and Mineral Research : The Official Journal of the American Society for Bone and Mineral Research 12, 998–1004. Cumming, R.G. & Klineberg, R.J. (1994). Case-control study of risk factors for hip fractures in the elderly, American Journal of Epidemiology 139, 493–503. Diaz, M.N., O’Neill, T.W. & Silman, A.J. (1997). The influence of alcohol consumption on the risk of vertebral deformity, Osteoporos International 7, 65–71. Huang, Y.S., Chan, C.Y., Wu, J.C., Pai, C.H., Chao, Y. & Lee, S.D. (1996). Serum levels of interleukin-8 in alcoholic liver disease: relationship with disease stage, biochemical parameters, and survival, Journal of Hepatology 24(4), 377–384. Johnell, O., Gullberg, B., Kanis, J., Allander, E., Elffors, L., Dequeker, J., Dilsen, G., Gennari, C., Lopes, V., Lyritis, G., Mazzuoli, G. Miravet, L., Passeri, M., Perez, C., Rapado A. & Robot C. (1995). Risk factors for hip fracture in European women: the MEDOS study, Journal of Bone and Mineral Research 10, 1802–1815. O’Neill, T.W., Marsden, D., Adams, J.E. & Silman, A.J. (1996). Risk factors, falls, and fracture of the distal forearm in Manchester, UK, Journal of Epidemiology and Community Health 50, 288–292. Holbrook, T.L. & Barrett-Connor, E. (1993). A prospective study of alcohol consumption and bone mineral density, British Medical Journal 306, 1506–1509. Lairinen, K., Karkkainen, M., Lalla, M., Lambergallardt, C., Tunninen, R., Tahtela, R. & Valimaki, M. (1993). Is alcohol an osteoporosis-inducing agent for young and middle-aged women? Metabolism: Clinical and Experimental 42(7), 875–881.
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[69]
Lairinen, K., Valimaki, M. & Keto, P. (1991). Bone mineral density measured by dual-energy X-ray absorptiometry in healthy Finnish women, Calcified Tissue International 48, 224–231. [70] Orwoll, E.S., Bauer, D.C., Vogt, T.M. & Fox, K.M. (1996). Axial bone mass in older women: study of osteoporotic fracture research group, Annals of Internal Medicine 124, 187–196. [71] Peris, P., Guanabens, N., Par´es, A., Pons, F., Del Rio, L., Monegal, A., Suris, X., Caballeria, J., Rodes, J. & Munoz-G´omez, J. (1995). Vertebral fractures and osteopenia in chronic alcoholic patients, Calcified Tissue International 57, 111–114. [72] Blaauw, R., Albertse, E.C., Beneke, T., Lombard, C.J., Laubscher, R. & Hough, F.S. (1994). Risk factors for the development of osteoporosis in a South African population: a prospective analysis, South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde 84, 328–332. [73] Gonzalez-Calvin, J.L., Garcia-Sanchez, A., Bellot, V., Munoz-Torres, M., Raya-Alvarez, E. & SalvatierraRios, D. (1993). Mineral metabolism, osteoblastic function, and bone mass in chronic alcoholism, Alcohol and Alcoholism 28, 571–579. [74] Dufour, M.C., Stinson, F.S. & Caces, M.F. (1993). Trends in cirrhosis morbidity and mortality: United States 1979–1988, Seminars in Liver Disease 13(2), 109–125. [75] Lelbach, W.K. (1975). Cirrhosis in the alcoholic and its relation to the volume of alcohol abuse, Annals of the New York Academy of Sciences 252, 85–105. [76] Marbet, U.A., Bianchi, L., Meury, U. & Stalder, G.A. (1987). Long-term histological evaluation of the natural history and prognostic factors of alcoholic liver disease, Journal of Hepatology 4(3), 364–372. [77] Mezey, E., Kolman, C.I., Diehl, A.M., Mitchell, M.C. & Herlong, H.F. (1988). Alcohol and dietary intake in the development of chronic pancreatitis and liver disease in alcoholism, The American Journal of Clinical Nutrition 48(1), 148–151. [78] Tuyns, A. & Pequignot, G. (1984). Greater risk of ascitic cirrhosis in females in relation to alcohol consumption, International Journal of Epidemiology 13(1), 53–57. [79] Center for Disease Control (2001–2005). Years of Potential Life Lost Report, Average for United States, available at http:apps.nccd.cdc.gov (last accessed 3/18/08). [80] Center for Disease Control (2001–2005). Alcoholattributed Death Report, Average for United States, available at http:apps.nccd.cdc.gov (last accessed 3/18/08).
JOHN BRICK
Alcohol: Elimination see Alcohol: Analysis
Alcohol: Interaction with Other Drugs Introduction The interaction between alcohol (ethanol, unless otherwise specified) and therapeutic medications is often encountered in accident, homicide, and suicide investigations. This review will focus on alcohol–other drug interactions most applicable to forensic evaluations. Reviews of the interaction between alcohol and a broader range of medications on health are available elsewhere [1, 2]. The widespread use of alcohol is coupled with extensive medical consequences and overly represented in accidental or other injuries and criminal actions. For a variety of reasons, including the ability to routinely test for the presence of medications and illicit drugs, the use of alcohol with drugs in accidents and crimes is of increasing forensic interest. The term drug is used here to refer to both licit and illicit drugs, whereas the term medication will refer specifically to therapeutic medications and the term alcohol refers to ethanol, unless otherwise indicated. In the controlled environment of the laboratory the biobehavioral effects of drug interactions are often complex. Outside of the laboratory alcohol–drug interactions are often complicated by real-world variations in dose and drug potency, duration and frequency of use, use of other drugs, and individual characteristics of the user, including physiological factors such as tolerance, metabolic state, diseases, and anthropometrics.
Understanding Alcohol Alcohol is a central nervous system (CNS) depressant, although under some conditions, it is perceived as a stimulant because it increases locomotor activity, loquaciousness, and other behaviors. The biphasic effect of alcohol is probably more related to the
Alcohol: Interaction with Other Drugs decrease in inhibitions produced by this drug rather than actual stimulant effects, at least in humans. Pharmacologically, alcohol acts much more like a CNS depressant or anxiolytic [3, 4]. Suffice it to say, the pharmacology of alcohol is complex and its biobehavioral effects quite broad, since alcohol is capable of altering receptors, ion transport, cell membranes, most cellular mechanisms critical to neurophysiology, and ultimately a range of behaviors. Alcohol also has the ability to alter the pharmacokinetics and pharmacodynamics of other drugs. Changes in bioavailability and efficacy of drugs in the presence of alcohol, or in patients with a history of alcohol dependence, have important implications for diagnoses, treatment, and outcome and should be part of a complete clinical evaluation.
Why Multiple Drug Use? Persons trained in neuropharmacology, toxicology, or medicine are aware of the pernicious effects of some of the more commonly used drugs. The inherent dangers of combining drugs and public service announcements have saturated the media for decades. Yet multiple drug use is still relatively common. Although the biopsychosocial factors of drug use and drug interactions are complex and not fully identified, drug use is usually related to the reinforcing effects of the drug, psychosocial influences, and enhanced performance. Multiple drug use is may be motivated by many factors, including increasing the primary drug effect (e.g., increasing the intensity of the “high” or, when used clinically, increasing the effectiveness of treatment), self-medication to decrease the undesirable side effects of the primary drug (e.g., a depressant may be used to alleviate the edgy feeling after the desired effects of a stimulant wear off), or short supply of the primary or preferred drug (e.g., when the availability of the drug of choice is limited, another drug with similar properties will be substituted). Heroin addicts, for example, may use or combine drugs for many reasons. Among these are sensation seeking (e.g., drug combinations without regard to safety and without any particular rationale other than the desire to become intoxicated), medical management (e.g., in the course of medical treatement, it is not uncommon to prescribe drugs that may interact with therapeutic or nontherapeutic drugs), or they may consume large quantities of alcohol or
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use other depressants to reduce or delay the opioid withdrawal syndrome until additional narcotics can be procured). Physicians must recognize the potential for these interactions (since in addition to a prescription medication, their patients may ingest other drugs, alcohol being the most common) and advise patients accordingly.
Pharmacological Basis of Alcohol–Drug Interactions Drug interactions can produce alterations in physiology and ultimately behavior through changes in pharmacokinetics or changes in pharmacodynamics. Pharmacokinetic mechanisms account for drug interactions when the presence of one drug affects the bioavailability of another drug. Pharmacodynamic interactions account for drug interactions when drugs interact at the receptor level.
Pharmacokinetic Interactions Pharmacokinetics can alter the bioavailability of the drug. If bioavailability increases or decreases the quantity of drug that interacts with receptors or other cellular components, the effect of the drug will in most instances, increase or decrease as well, depending on the dose. Pharmacokinetic interactions can occur through changes in drug absorption, distribution, metabolism, and excretion.
Pharmacodynamic Interactions Pharmacodynamics is the study of the physiological and biochemical effects of drugs and their mechanism of action. Psychoactive drugs alter the functional activity of receptors or endogenous ligands (i.e., neurotransmitters and hormones) in the brain, whereas other drugs may exert similar effects outside the CNS (e.g., cardiac β-receptor antagonists). Changes in the pharmacodynamics or functional activity of neurons that modulate cognitive and psychomotor effects, for example, will alter physiology and behavior. Pharmacodynamic drug interactions can be classified as addictive, synergistic, potentiated, and antagonistic. Additive Effects. Addictive effects occur when the combination of two drugs is equal to the sum of the effect of each drug (e.g., 2 + 2 = 4). For example,
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the CNS depressant effects of many benzodiazepines and alcohol are additive, as are the effects of many barbiturates with alcohol. Synergistic Effects. Synergistic interactions occur when the combination of two drugs produces an effect that is greater than the sum of the effect of each drug (e.g., 2 + 2 = 6). Synergistic interactions produce effects far greater than would be predicted from the sum of effect of either drug. For example, alcohol and carbon tetrachloride, a cleaning fluid, are toxic to the liver. However, the combination of the two produces much more liver damage than would be predicted from the sum of their individual effects. Similarly, in some cases, alcohol synergistically enhances the sedative effect of barbiturates and some effects of opiates. Drug Potentiation. Potentiated drug effects are similar to synergistic effects, but usually describe an increase in the toxic effect of a drug when combined with a nontoxic drug (e.g., 0 + 1 = 2). Histamine (H2 ) antagonists such as cimetidine can be considered to potentiate the toxic effects of alcohol by increasing alcohol bioavailability. Antagonism. An antagonist is a drug that blocks the effect of another drug (e.g., 2 + 2 = 1 or 2 + 2 = 0). Antagonists are very specific. For example, Naloxone has a much higher affinity for opiate receptors than heroin. Administering Naloxone to someone who has overdosed on heroin will produce a rapid reversal of the respiratory depression produced by heroin. Some drugs exhibit dispositional antagonism when the absorption, metabolism, distribution, or excretion of one drug is affected by another drug. For example, ethyl alcohol decreases the metabolism of methanol.
Specific Alcohol–Drug Interactions With a basic understanding of the pharmacological mechanisms by which alcohol–drug interactions may occur, let us examine specific alcohol–drug interactions that may be of forensic interest.
Alcohol and Acetaminophen The over-the-counter (OTC) medication acetaminophen (Tylenol) is one of the most commonly
consumed medications in the United States because of its effective analgesic and antipyretic properties. Acetaminophen is metabolized by the CYP2E1 isozyme to a toxic intermediate, N -acetyl-pbenzoquinone imine (NAPQI). Normally, NAPQ1 is detoxified by the antioxidant glutathione [5], but chronic alcohol use reduces the amount of the glutathione produced in the liver. In other words, the combination of large amounts of acetaminophen reduced glutathione levels from chronic alcohol use increases the bioavailability, and the result is toxic. The resulting hepatotoxicity may progress to the point of fulminant hepatic failure and death. There is no agreement in the medical community as to the amount of alcohol consumed and/or the amount of acetaminophen necessary to cause this toxic effect to occur. Earlier studies indicated that liver damage can occur in alcoholics at therapeutic doses of acetaminophen [6–8], but a more recent study found no increase in liver toxicity among alcoholics given the maximal therapeutic dose (4 g/day) of acetaminophen [9]. They concluded that there was no clinical evidence of increased risk for these patients when acetaminophen is used within recommended doses.
Alcohol and Antibiotics Most medications have some side effects, but when antibiotics used to treat infectious diseases are combined with acute alcohol consumption, some may cause nausea, vomiting, headache, and possibly convulsions. Among these antibiotics are furazolidone, griseofulvin, metronidazole, and the antimalarial quinacrine. Isoniazid and rifampin are used together to treat tuberculosis, a disease especially problematic among the elderly in nursing homes and among homeless alcoholics. In addition, acute alcohol consumption decreases the bioavailability of isoniazid in the bloodstream, whereas chronic alcohol use decreases the bioavailability of rifampin. The pharmacokinetic interaction between alcohol and some antibiotics may reduce their effectiveness [10]. Erythromycin accelerates gastric emptying and may reduce first-pass metabolism of alcohol in the stomach, resulting in increased absorption in the intestines and higher blood alcohol levels. Conversely, many aerobic bacteria in the colon are capable of metabolizing alcohol because they possess alcohol dehydrogenase (ADH) activity. In rats, treatment
Alcohol: Interaction with Other Drugs with ciprofloxacin totally eliminated the colonic metabolism of alcohol, resulting in increased blood alcohol concentrations [11]. Although controversial, patients drinking alcohol while taking metronidazole or ketoconazole may suffer from symptoms similar to those found with disulfiram (Antabuse): abdominal distress, nausea, vomiting, and headache [12]. Similarly, cefoperazone (Cefobid), griseofulvin (Fulvicin, Grisactin), isoniazid (INH), metronidazole (Flagyl), nitrofurantoin (Furadantin, Macrodantin), and sulfamethoxazole (Bactrim, Septra) inhibit aldehyde dehydrogenase and may also produce a disulfiramlike reaction.
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as felbamate, gabapentin, lamotrigine, topiramate, tiagabine, levetiracetam, oxcarbazepine, and zonisamide. Depending on its chronicity of use, alcohol will have totally different pharmacokinetic effects with the older anticonvulsants such as phenobarbital, phenytoin, primidone, ethosuximide, carbamazepine, and valproate. Acute alcohol consumption increases the availability of phenytoin and the risk of drugrelated side effects. Chronic drinking may decrease phenytoin bioavailability, significantly reducing the patient’s protection against seizures, even during a period of abstinence [14, 15].
Alcohol and Antidepressants Alcohol and Anticoagulant Medications Warfarin (Coumadin) reduces the ability of the blood to clot and is commonly used to treat patients with irregular heart rhythms, artificial heart valve, and following open-heart surgery. Warfarin is metabolized by the cytochrome P450 enzyme system in the liver, which is also part of the pathway of alcohol metabolism. Therefore, if a person consumes alcohol, the anticlotting effect of warfarin may be increased above the desired therapeutic effect. This increased bioavailability of warfarin is due to alcoholrelated inhibition of warfarin metabolism by the cytochrome P450 enzyme system [13]. This increase could result in the emergence of potentially lifethreatening hemorrhages. However, in people who drink alcohol regularly, and especially in some alcoholics, the chronic consumption of alcohol will result in induction of the cytochrome P450 enzyme system. The result of this will be an increased rate of metabolism of warfarin, thereby decreasing its bioavailability and interfering with its effectiveness in reducing blood clotting [13]. Such individuals will often need larger doses of warfarin to achieve the desired therapeutic effect, but there is no reported effect of warfarin on alcohol pharmacokinetics or pharmacodynamics.
Alcohol and Anticonvulsants More currently available anticonvulsants in comparison with the classic agents have good absorption, linear kinetics, and minimal potential for interaction with other drugs. The newer anticonvulsants are eliminated through different combinations of liver metabolism and direct renal excretion, such
The literature on the correlation between alcoholism and depression is well established [16] and particularly important in forensic evaluations because alcoholics are often involved in accidents and crimes. Many active alcoholics are prescribed antidepressants leading to a high potential for alcohol–antidepressant interactions. Several classes of antidepressants are available and are defined by how they affect brain neurochemistry. Some antidepressants cause varying degrees of sedating activity but these drugs should not be described as depressants or sedatives. Nevertheless, alcohol increases the sedative and other effects of tricyclic antidepressants such as amitriptyline (Elavil) [17]. In addition, alcohol-induced liver disease further impairs antidepressant metabolism and causes significantly increased levels of active medication in the body [18]. The disposition of imipramine in alcoholic and nonalcoholic patients with depression varied significantly. For example, oral imipramine clearance was more than 2 times greater in alcoholic patients than controls [19] and in recently detoxified men with alcohol dependence, and the elimination half-life for imipramine was more than doubled in alcoholics after intravenous infusion. Plasma concentrations of imipramine were also significantly lower in the alcoholics, suggesting that standard doses of some antidepressants may fail to produce adequate therapeutic changes in alcoholics. For imipramine, the doses may have to be doubled [19]. Popular serotonin reuptake inhibitors (SSRIs) such as fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), and citalopram (Celexa) have the best safety profile of all antidepressants, and no serious interactions seem to occur when these agents are consumed
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with moderate doses of alcohol [20]. In addition, neither fluoxetine nor alcohol alters the pharmacokinetics or psychomotor effects of the other, although alcohol impairs performance of most subjects on psychomotor tests [21, 22]. The use of the monoamine oxidase inhibitors (MAOIs) with alcohol will potentially precipitate a hypertensive crisis and enhance sedation. The mechanism for this reaction has been attributed to increased concentrations of the amino acid tyramine [23], which is a potent hypertensive agent present in many alcoholic beverages (e.g., wines) and foods (e.g., cheeses and bananas). Although most dietary tyramine is destroyed by MAO in the intestines and liver, tyramine will enter the circulation in patients treated with MAOIs and may produce hypertension and, rarely, sudden death [24]. Therefore, alcohol use should be avoided in patients prescribed MAOIs and considered by medical examiners in such cases. Atypical antidepressants generally do not seem to have any problematic interactions with alcohol. However, mirtazapine (Remeron), when combined with alcohol, causes impaired cognition and decreased motor performance [25].
Alcohol and Antidiabetic Medications Oral hypoglycemic agents are commonly prescribed for the treatment of diabetes mellitus in patients not requiring insulin. As previously noted, chlorpropamide (Diabinase), glyburide (Diabeta, Micronase), and tolbutamide (Orinase) inhibit aldehyde dehydrogenase and can cause disulfiramlike reactions following alcohol consumption. Metformin (Glucophage) may increase lactic acid levels in the blood following alcohol ingestion, which could result in acute lactic acidosis with potentially lethal results. Alcohol consumption by patients taking many of these medications could increase the risk of causing lower than normal blood sugar levels owing to impairment of gluconeogenesis during fasting when blood sugar is already low and the body depends on the production of new glucose [18]. Since low blood sugar can cause symptoms of impairment virtually indistinguishable from alcohol intoxication [26], behavioral observations of patients who are diabetic, or diabetics who have consumed alcohol, should be interpreted cautiously.
Alcohol and Antihistamines (H1 -Antagonists) Antihistamines (H1 -antagonists), such as diphenhydramine, are commonly used to treat allergic disorders, and some antihistamines, such as hydroxyzine (Vistaril, Atarax), to treat anxiety. Many antihistamines cause drowsiness, which make them useful to treat insomnia, but are potentially dangerous because they can impair psychomotor and cognitive skills. Alcohol can substantially enhance the sedating effects of these agents and may further impair the ability to drive or operate other types of machinery [27]. Common sedative antihistamines, such as chlorpheniramine and diphenhydramine, significantly impair psychomotor performance and significantly increase the deleterious effects of alcohol on reaction time, coordination, and related psychophysical tests [28–30]. Newer antihistamines such as fexofenadine, loratadine, and cetirizine have been developed to minimize drowsiness and sedation while still providing effective therapeutic value. Nevertheless, these newer medications may still increase risk of hypotension and fall-down injuries among the elderly, particularly when combined with alcohol [18]. The effects of many of the antihistamines with alcohol have not been fully investigated, but it seems more probable than not that the combined use of these drugs will result in increased drowsiness and increased driving risks [31], possibly due to the observation that histamine receptor antagonism can affect alcohol metabolism and change the sensitivity to the hypnotic effects of alcohol [32].
Alcohol and Antipsychotics Many antipsychotics produce sedation and psychomotor impairment. When combined with alcohol, they may increase sedation, impair coordination, and fatally depress respiration. This effect appears to be additive, but the mechanisms of this interaction are uncertain. Antipsychotics, such as chlorpromazine and thioridazine, are more sedating than the high-potency antipsychotics such as haloperidol and fluphenazine and tend to cause more significant CNS depression. For example, chlorpromazine coupled with very low blood alcohol concentrations (∼ 40 mg dl−1 ) impairs skills related to driving and produces subjective complaints of feeling sleepy, lethargic, dull, groggy, and poorly coordinated behavior [33]. Less psychomotor impairment was observed
Alcohol: Interaction with Other Drugs when alcohol was combined with flupenthixol [34, 35] or thioridazine [34–36] but not with haloperidol [34, 35]. Changing doses, steady-state pharmacokinetics, and types of antipsychotic medication make predictions about the acute interactions of these drugs with alcohol difficult. Long-term use of some psychotropic medications may result in extrapyramidal motor system disorders that can be misinterpreted as some form of intoxication. Also, chronic alcohol consumption causes increased metabolism of the antipsychotic medications, resulting in lower blood levels and, ultimately, lesser efficacy of the medication. Since antipsychotic medications are typically used to treat mental illnesses such as schizophrenia, when combined with alcohol, the results may be particularly challenging and unpredictable.
Alcohol and Cannabinoids It is well known by forensic examiners, police, and toxicologists that alcohol and tetrahydrocannabinol (THC) are two of the most widely used and commonly encountered drugs detected in motor vehicle collisions. Tetrahydrocannabinol is the primary psychoactive compound in marijuana and presumed to be the effect-producing drug in studies where marijuana is smoked. The effects of THC on drowsiness, memory, and distortion of space and time are particularly important because of the obvious need for such skills in motor vehicle operation, for example. In one of the earlier interactive studies on the effects of THC and alcohol on driving, Casswell [37] found that (i) alcohol alone increased speed and impaired steering, (ii) THC alone reduced speed and slowed response to instruction, and (iii) alcohol and marijuana tended to increase speed, impair steering, and increase response times to instructions. More recent studies concluded that the effects of THC and alcohol appear to be additive. When THC is combined with low blood alcohol concentrations (BACs) (40 mg dl−1 ), there is evidence of impaired visual search patterns while driving, and reaction times are greater than from either drug alone. The authors point out that the effects of alcohol are greater than those produced by smoking marijuana, noting that the combination is particularly dangerous with regard to motor vehicle operation [38, 39]. Although the majority of more recent studies support the conclusion that alcohol and THC impair driving [40–42], not all investigators found an interaction
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between these drugs. For example, Smiley, Ziedman, and Moskowitz [43] found that after smoking marijuana, drivers became more cautious in overtaking tasks. Alcohol (45 or 75 mg dl−1 ) had a slight effect, but no interaction between alcohol and smoked marijuana was observed. Using a driving simulator, Stein et al. [44] found that after alcohol consumption (100 mg dl−1 ), drivers had more “accidents” and “speeding tickets” and slower and less accurate responses to road signs. Smoking marijuana had “only an occasional effect” and no interaction was observed. The nature of any pharmacodynamic interaction between alcohol and cannabinoids is difficult to explain since the neuropharmacological effects of these drugs are complex and diverse. There is some evidence of a pharmacokinetic interaction between these drugs. Lukas et al. [45] found that smoking marijuana decreases the bioavailability of alcohol, reducing the maximum serum alcohol concentration and delaying the time to peak concentration from 78 mg dl−1 (50 min after drinking) to about 55 mg dl−1 (105 min after drinking). More research on this potential pharmacokinetic interaction is needed, and forensic examiners are cautioned that pharmacokinetic and pharmacodynamic interactions that are measurable at low drug concentrations may be obscured at the higher concentrations, which are more likely to be encountered in forensic evaluations.
Alcohol and Cardiovascular Medications Acute alcohol consumption interacts with some cardiovascular medications (e.g., nitroglycerin, used to treat angina; reserpine, methyldopa (Aldomet), hydralazine (Apresoline), and guanethidine (Ismelin), used to treat hypertension) to cause dizziness or fainting upon standing (orthostatic hypotension). Chronic alcohol consumption decreases the availability of propranolol (Inderal), used to treat high blood pressure, potentially reducing its therapeutic effect. Since alcohol acts as an osmotic diuretic and also causes hypokalemia, patients taking loop diuretics (e.g., furosemide, ethacrynic acid, and bumetanide) or less potent thiazide and various sulfonamide derivatives, are at greater risk for dehydration, hypokalemia and, therefore, risk of seizure. Verapamil, which inhibits the metabolism of the alcohol by the liver, can increase blood alcohol content, whereas alcohol may
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increase the bioavailability of nifedipine by inhibiting its metabolism [46]. The inhibition of aldehyde dehydrogenase by the coronary artery dilator isosorbide dinitrate (Isordil, Dilatrate, and Sorbitrate) and nitroglycerin (NitroBid and Nitrostat) can produce a disulfiram-like reaction (described in the following section) when combined with relatively low amounts of alcohol. Such interactions may complicate drug recognition evaluations (DREs).
Alcohol and Disulfiram Disulfiram (Antabuse) is used to control drinking through aversion therapy, but the combination of drugs has serious and even fatal consequences due to their interactive biochemistry. Alcohol is metabolized by ADH to acetaldehyde, which is metabolized by aldehyde dehydrogenase. Disulfiram inhibits the enzyme aldehyde dehydrogenase, resulting in the accumulation of acetaldehyde. Acetaldehyde is highly toxic and produces many aversive sympathomimetic effects including facial flushing, nausea, vomiting, breathing difficulties, and headache. In extreme cases, respiratory depression, cardiovascular collapse, cardiac arrhythmias, unconsciousness, and convulsions leading to death can occur. In addition to disulfiram, other prescription medications can inhibit aldehyde dehydrogenase and can produce a disulfiram-like reaction in people who consume alcohol while taking them [47]. The following medications may produce severe sympathomimetic reactions when combined with alcohol: the antidiabetic oral medications chlorpropamide (Diabinase), glyburide (Micronase, Diabeta), tolazamide, and tolbutamide; a number of antibiotic medications including cefoperazone (Cefobid), griseofulvin (Fulvicin, Grisactin), INH, metronidazole (Flagyl), nitrofurantoin (Furadantin, Macrodantin), and sulfamethoxazole (Bactrim, Septra); the analgesics phenacetin and phenylbutazone; and the coronary artery dilator medications isosorbide dinitrate (Isordil, Dilatrate, and Sorbitrate) and nitroglycerin (Nitro-Bid and Nitrostat). In patients with certain medical conditions (i.e., those with coronary artery disease), the disulfiram-like reaction could be potentially fatal as a result of cardiovascular effects involved in the pathogenesis of the disulfiram-like reaction (dilation of blood vessels, hypotension, and tachycardia). As it is impossible to predict with
certainty the severity of the disulfiram-like reaction, individuals taking any of these medications should be advised to avoid alcohol, and a thorough review of prescription medications should always be part of any forensic examination if unusual symptoms are present in intoxicated patients.
Alcohol and Histamines (H2 -Antagonists) Alcohol abuse may contribute to gastrointestinal diseases, including gastritis, ulcers, and gastroesophageal reflux disorder (GERD). H2 -antagonists, such as cimetidine (Tagamet), ranitidine (Zantac), and nizatidine (Axid), are commonly used to treat these disorders. As a result, these medications can increase the bioavailability of alcohol. Moreover, gastric ADH may account for a significant percentage of alcohol metabolism [48], at least at low blood alcohol concentrations. In addition, the first-pass metabolism of alcohol is also reduced by cimetidine because of the effect it may have on increasing the rate of gastric emptying, again resulting in increased blood alcohol levels [49]. In many studies, the effect was quite significant – increases of blood alcohol concentrations of about 17–33% by cimetidine and to a much lesser degree by rantidine, if at all [50, 51]. Although these investigators examined this effect through a series of detailed studies and identified dose, drug type, gender, and drinking history to be important variables, the clinical significance of this interaction has been questioned by some researchers [52], and this effect is not universal to all H2 antagonists. For example, Famotidine (Pepcid) appears to have no effect on blood alcohol levels. The use of the H2 -antagonists for the treatment of gastroesophageal reflux disease (GERD) has largely been supplanted by a newer class of agents that reduce gastric acid secretion, the proton pump inhibitors (PPIs) such as omeprazole (Prilosec), lansoprazole (Prevacid), esomeprazole (Nexium), and rabeprazole (Acidphex). The PPIs do not appear to interact significantly with alcohol. Therefore, broad generalizations about alcohol and H2 antagonists should be avoided, and careful examinations of the specific medications and dose should be made in evaluating the role of these new medications in combination with alcohol. In other words, some, but not all, H2 antagonists affect alcohol pharmacokinetics.
Alcohol: Interaction with Other Drugs
Alcohol and Lipid-Reducing Medications Statins, medications used to reduce elevated lipids and cholesterol, are usually metabolized through the cytochrome P450 enzyme system. Atorvastatin (Lipitor), simvastatin (Zocor), and lovastatin (Mevacor, Altocor) are metabolized through the CYP3A4 isoenzyme, which is also involved in the metabolism of alcohol and a number of other medications that bind more strongly to the enzyme than statins. When alcohol or any of these substances block the statin from binding to the CYP3A4 enzyme, the metabolism of the statin is reduced, resulting in increased statin levels and the potential for statin-related toxicity [53–56]. The major toxic reactions include myotoxicity (myalgia, myopathy, and rhabdomyolysis) and hepatotoxicity. Milder cases are often reversible without serious sequelae with substance discontinuation, but severe cases, although rare, may be potentially fatal.
Alcohol and Methanol Alcoholics may drink other forms of alcohol such as methanol when beverage alcohol (ethanol) is not available. Methanol (methyl alcohol) is highly toxic, and consumption of small quantities may result in metabolic acidosis, blindness, and death. Interestingly, the interaction between ethanol and methanol is critical in treating methanol poisoning. Methanol is metabolized by the enzyme ADH to formaldehyde and then to formic acid, a highly toxic compound [57]. Even when relatively small doses of methanol (several ounces) may cause metabolic acidosis, blindness, and cardiovascular instability and death. It is noteworthy that methanol poisoning can be prevented by the administration of ethyl alcohol because ethanol (alcohol) is preferentially metabolized by ADH, thereby decreasing the formation of toxic metabolites from methanol. The decrease in methanol metabolism allows methanol to be excreted unchanged and before toxic metabolites are formed. Patients admitted for acute alcohol intoxication or detoxification should be screened for methanol use so that appropriate prophylactic treatment (e.g., hemodialysis, ADH inhibitors, and ethanol administration) can be initiated.
Alcohol and Non-narcotic Pain Relievers (ASA and NSAIDS) Aspirin (acetylsalicylic acid (ASA)) and nonsteroidal anti-inflammatory drugs (NSAIDs) frequently used
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to treat mild to moderate pain also decrease the activity of gastric ADH. This biochemical damage increases the bioavailability of ingested alcohol and heightens the effects of a given dose of alcohol [50] at least at low blood alcohol concentrations. There are a number of other non-narcotic pain relievers including phenacetin, an acetaminophen precursor (and often found in other drugs including acetaminophen, aspirin, caffeine, codeine, and propoxyphene), and phenylbutazone (Butazolidin), both of which inhibit aldehyde dehydrogenase. Therefore, the use of these drugs with alcohol may result in an aversive disulfiram-like reaction (see previous section on Alcohol–Disulfram interactions).
Alcohol and Opiates The effects of opiate medications such as codeine, morphine preparations, propoxyphene (Darvon), oxycodone preparations (Percocet, Oxycontin), hydromorphone (Dilaudid), hydrocodone (Vicodin, Lortab), meperidine (Demerol), and fentanyl can be enhanced by the depressant effect of alcohol, resulting in decreased motor skills, respiratory problems, drowsiness, and sedation. For example, a single dose of alcohol can increase the bioavailability of propoxyphene, potentially increasing its sedative effect [58]. Opiate medications (i.e., codeine, propoxyphene, and oxycodone) are manufactured as combination products with the non-opiate analgesics (e.g., acetaminophen), which can result in an interaction between alcohol and the acetaminophen, as well as the opiate. The accumulation of toxic breakdown products forms an acetaminophen/alcohol interaction and can be potentially dangerous, resulting in liver damage or failure. Patients who are prescribed any of the opiate/acetaminophen combination preparations should be cautioned about consuming any additional amounts of acetaminophen. Methadone, a synthetic opioid with a relatively long half-life, is used to reduce heroin use in opiatedependent patients. New patients or patients receiving a significant increase in their daily oral dose of methadone may present with symptoms of mild psychomotor and cognitive impairment. However, unlike many other opioids, prolonged methadone use, even at relatively high doses, does not impair cognitive or psychomotor performance [59] including driving [60–62]. However, the combination of alcohol and opiates does increase respiratory depression. It is
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generally advisable not to drink alcohol while taking methadone for a variety of reasons related to recovery, but the interaction between these drugs is limited.
Alcohol and Sedative Hypnotics The depressant effects of barbiturates range from mild sedation to general anesthesia and are similar to alcohol. The interaction between these drugs is additive probably because of both pharmacokinetic and pharmacodynamic mechanisms. Alcohol may also inhibit the hepatic metabolism of barbiturates [63], which would increase their bioavailability and effectiveness. Gamma aminobutyric acid (GABA) interacts with receptors containing recognition sites for anxiolytics and sedative benzodiazepines and barbiturates, which regulate gating of chloride channels. Since alcohol also alters the gating properties of these receptors, a pharmacodynamic interaction between alcohol and these medications exists even though alcohol has little affinity to recognition sites for GABA, benzodiazepines, or barbiturates [3]. Both barbiturates and alcohol derive some pharmacodynamic properties through the GABAA receptor. Barbiturates enhance the binding of GABA to GABAA receptors. Alcohol also shares the ability to increase GABA-mediated synaptic inhibition and chloride ion flux, which explains in part interaction of these drugs. Although other mechanisms are involved in the psychoactive effects of both drugs, the combination of alcohol and barbiturates will result in greater psychomotor and other CNS impairments than either drug alone. Many benzodiazepines and alcohol share similar pharmacokinetic and pharmacodynamic mechanisms, so it is not surprising that the combination of alcohol and benzodiazepines is associated with drug-induced deaths, drug overdoses, and traffic accidents or fatalities [64, 65]. A pharmacokinetic interaction between alcohol and benzodiazepines also exists. For example, there is a decline in the efficiency of the metabolism of the benzodiazepines as a result of increasing age or liver disease. In the elderly, there is a 50% decrease in clearance, with a four- to ninefold increase in halflife, and a two- to four fold increase in the volume of distribution [66]. Alprazolam (Xanax), a benzodiazepine analog, is used in the treatment of anxiety disorders and is currently the most prescribed medication in the
United States. Although there is no synergistic action between this medication and alcohol, an additive interaction has been reported on certain psychomotor and cognitive tasks, such as information processing and memory [67]. The combination of alcohol and alprazolam produces increases in selfreported drowsiness [67], but no significant interaction between alprazolam and alcohol was reported [68] even though each drug produces several effects. Some nonbenzodiazepine anxiolytics, such as buspirone, also do not appear to interact with alcohol to potentiate cognitive or motor performance impairment. Unlike some benzodiazepines, buspirone has been found to have no significant effect on body sway, coordination skills, tracking skills, or nystagmus even when combined with alcohol [69]. This lack of alcohol interactions with some benzodiazepine-like medications should be noted when interpreting DREs performed by police.
Alcohol and Stimulants Although there is some evidence that stimulants decrease fatigue and reaction time while causing an increase in arousal, body temperature, heart rate, blood pressure, and other changes that may decrease some of the depressant effects of alcohol (e.g., sleepiness), the combination of a stimulant and a depressant is often erroneously assumed by laypersons to result in a neutralizing or balancing out of these two opposite effects. The scientific literature indicates the interactions between alcohol and stimulants to be inconsistent and often complex. For example, studies reported no antagonistic effect of dextroamphetamine on the mental and psychomotor impairment produced by alcohol, whereas others have found improved performance compared with controls [70, 71]. Perez-Reyes et al. [71] reported that alcohol (100 mg dl−1 )) significantly increased the bioavailability of high, but not low, doses of dextroamphetamine (25.5 ng ml−1 vs. 15.7 ng ml−1 ). Moreover, amphetamine did not significantly alter peak blood alcohol concentrations, but alcohol significantly increased the bioavailability of dextroamphetamine. Dextroamphetamine attenuated alcoholinduced increases in latency and accuracy while performing an eye–hand–foot reaction time task believed to be related to driving abilities. As the effect was greatest about 4 h after alcohol administration, when blood alcohol concentrations had dropped
Alcohol: Interaction with Other Drugs from a peak of about 100 mg dl−1 to about 60 mg dl−1 , fatigue and dose were probably important factors in the latter finding [71]. The statistical significance of these results probably outweighs their actual value. Although the interactions between alcohol and amphetamines have been studied, the only clear conclusion is that the interaction is complex and task specific, and that there is no simple antagonism between the drugs. There does seem to be an interaction between alcohol and another stimulant, cocaine. One novel consequence of cocaine and alcohol use is that a third compound, cocaethylene, is formed. Cocaethylene (sometimes referred to as ethyl cocaine or cocaine ethyl-ester) is not a natural alkaloid of the coca plant and is not found in pharmaceutical or street cocaine. In fact, cocaine is metabolized to its ethyl configuration only in the presence of ethanol. Cocaine and cocaethylene have similar effects, but the latter extends the euphorogenic and reinforcing effects of the former. In humans, the combination of alcohol and cocaine is greater than the effect of either drug alone, and is associated with an enhanced subjective euphoria, increased heart rate, and increased plasma cocaine concentrations [72, 73]. In humans, insufflation of cocaine before alcohol ingestion does not appear to alter blood alcohol levels or subjective ratings of intoxication of alcohol intoxication. However, when alcohol is administered prior to cocaine insufflation, there is a significant increase in both cocaine plasma levels (possibly due to an inhibition of hepatic cocaine metabolism produced by alcohol) and an augmentation of cocaine’s subjective and heart rate effects [74, 75]. In another study, combining cocaine and alcohol produced a nonsignificant decrease in subjective feelings of drunkenness, an increase in cocaine-induced euphoria, and a significant improvement in alcohol-related changes in psychomotor performance along with a marked increase in heart rate. Subjects who were administered cocaine and alcohol interpreted the effects as “more pleasant” than compared to alcohol alone [76]. Although many drugs are metabolized to form other psychoactive compounds, cocaethylene is the only known example of a third psychoactive drug being formed as a result of administering two other psychoactive drugs of abuse. As cocaine-induced deaths have been observed with a wide range of postmortem cocaine concentrations, often with presence of low blood alcohol levels, the possibility exists that cocaethylene may be partially
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responsible for these deaths [77]. Additional research is clearly required in this area.
Summary and Conclusions With some exceptions, such as the interaction between drugs and specific antagonists to receptors for those drugs, or combinations of drugs of the same class, drug interactions are often difficult to predict with great precision. The interactions between alcohol and therapeutic medications or other drugs are very complex, highly variable events, and dependent upon a number of pharmacodynamic and pharmacokinetic factors. These interactions are further complicated by the potential for alcohol to cause liver pathologies that impact on the therapeutic effectiveness of some medications, even if the patient is sober at the time of the testing. In evaluating drug effects and drug interactions, there are a multitude of factors that can affect outcome including, but not limited to, the anthropometric characteristics of the patient (age, gender, body weight, and height), medication/drug dosage, and the amount and frequency of alcohol consumption. Patients in certain populations (e.g., geriatric) may use multiple medications or be susceptible to age-related physiological effects that could increase the potential for more severe drug interactions. When interpreting empirical research or clinical studies, forensic examinations must be cognizant of the fact that most of these studies involve relatively small alcohol doses for a variety of practical and ethical reasons, and the effects observed at relatively low blood alcohol concentrations may be very different than those in highly intoxicated patients. Similarly, the lack of a significant interaction with low doses of a drug does not guarantee the same results when higher doses are used. As a result, it is very difficult to stipulate a safe dose of alcohol that can be consumed when taking medications. Individuals with little or no tolerance to alcohol or other drugs may be more sensitive to these interactions. In conclusion, the CNS depressant effects of alcohol can be expected to increase the depressant effects of most medications and other drugs with similar CNS effects, but the significance of that interaction will be drug specific, even within some classes of medications. Generalizations about medication or drug effects in combination with alcohol should be avoided, as not alcohol–other drug
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or medication combinations produce pharmacokinetic or pharmacodynamic interactions.
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JOHN BRICK
Alcohol: Metabolism see Alcohol: Analysis
Alcohol: Use, Abuse, Tolerance, and Dependency Alcohol use, abuse, tolerance, and chemical dependence are often factors in the forensic investigation of crimes, accidents, or deaths (accidental or otherwise). Although these terms apply to other drugs, this article
Alcohol: Use, Abuse, Tolerance, and Dependency will focus on and review basic concepts in defining alcohol, its use, abuse, tolerance, and dependence.
What is Alcohol? Most people know what the term alcohol is, but unless specified it can be misleading or inaccurate. In some instances, this may result in a fatal misunderstanding. To an alcohol research scientist, toxicologist, or chemist, three of the most common alcohols are ethyl alcohol (ethanol), methyl alcohol (methanol), and isopropyl alcohol (isopropanol). Each has a similar chemical structure; a hydroxyl group attached to a saturated carbon molecule, each causes intoxication, and each has been represented in forensic cases. The general intoxicating effects of ingesting different alcohols are somewhat similar, but the side effects are quite different. Methanol, also known as wood alcohol, is the most toxic of the three examples given. Relatively small amounts (less than one ounce) may cause retinal damage. Larger quantities (one or more ounces) can be fatal, but toxicity varies greatly [1, 2]. Methanol’s toxicity is the result of its metabolism to formaldehyde, which is metabolized to formic acid, a cellular toxin that is about 6 times more poisonous than methanol itself. Formic acid produces severe metabolic acidosis and tissue hypoxia, and more than 6 to 7 ounces of methanol is lethal for many adults [1, 2]. Methanol intoxication usually occurs by accident, because of lack of knowledge about its harmful effects. For example, mixing methanol in “jungle juice” (a concoction of many different types of liquors and juices), typically served to large groups and popular among college students in the United States, may place the uninformed drinker at significant medical risk. Methanol is also consumed by some alcoholics who, in the absence of beverage alcohol, may consume products containing it, such as antifreeze or dry gas used in automobiles. Initial symptoms of methanol intoxication are somewhat similar to those of beverage alcohol. Unless specifically alerted to possible methanol intoxication, a patient who becomes ill from methanol may be misdiagnosed by untrained or unobservant medical personnel and not receive proper treatment for methanol poisoning. For example, emergency treatment for methanol poisoning, such as ethanol administration, is highly unlikely if the patient is believed to be “drunk”.
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As mentioned, methanol’s toxicity is derived from its metabolism to formaldehyde and formic acid. Methanol is metabolized by the enzyme alcohol dehydrogenase (ADH), which also metabolizes beverage alcohol. Because the affinity of beverage alcohol (ethanol) for ADH is about 10–20 times greater than that of methanol, when beverage alcohol and methanol are present at the same time, the liver preferentially metabolizes beverage alcohol. This allows time for methanol to pass through the excretory system before it is metabolized to harmful metabolites. Therefore, a rapid emergency treatment for methanol poisoning is beverage alcohol. Beverage alcohol, such as whiskey, vodka, rum, etc., is not likely to be administered to an unknown patient who presents symptoms of intoxication in an emergency department. Isopropanol, or common rubbing alcohol, is less toxic than methanol but about twice as toxic as beverage alcohol. Small amounts, as little as several ounces, can also cause permanent damage to the visual system, and 8 ounces is estimated to be lethal [1]. Dose estimates are often based upon postmortem findings. Obviously, it would be highly unethical and illegal to conduct a range of dose–response studies in humans to determine the lethal dose. Actual lethal doses may be lower or higher, depending upon many factors. Some alcoholics may also consume isopropanol intentionally (e.g., some brands of dry gas contain both methanol and isopropanol) or unknowingly, also with potentially harmful or even lethal consequences. However, the alcohol that is the primary subject of this review, and the alcohol consumed as a beverage by most people is ethyl alcohol (ethanol). Ethanol is a relatively odorless chemical formed through a process of fermentation and a drug that affects most organs of the body, including the brain [3, 4]. Ethanol is also lethal but at much higher doses than methanol or isopropanol. The lethal dose (LD50) of acute ethanol is estimated to be a blood alcohol concentration (BAC) of about 400–500 mg/dl, although death may occur at higher or lower concentrations depending upon factors such as tolerance or the presence of other drugs. For example, compared to 6 or 8 ounces of methanol or isopropanol, it would require about 24 ounces of 80 proof liquor (about 16 standard drinks) in a 150-pound male consumed over an hour to reach a BAC that would probably be lethal for about half the population. In this article, unless
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otherwise indicated, the term alcohol will be used to denote ethanol.
Alcohol Use Use in the United States Alcohol use predates recorded history, but for all practical purposes the medical literature documenting the consequences of alcohol abuse goes back less than 200 years. Alcohol consumption and related problems have been well documented. Alcohol-related medical problems account for a disproportionate number of hospital admissions and medical complications [5, 6]. Yet, despite general public awareness about alcoholrelated problems, longitudinal studies suggest that nearly 9% of adults in the United States consume, on average, more than two drinks per day [7]. Among senior high school students (typically 17–18 years old), about 3% use alcohol daily and about half had used alcohol within 30 days of being surveyed. About two-thirds of the adult population in the United States consumes alcohol to varying degrees, and 6% of adolescents (age 12–17) and about 8% of adults meet diagnostic criteria for alcohol abuse or alcohol dependence [8].
Defining Alcohol Use, Abuse, and Dependence Alcohol use can first be defined in terms of how much alcohol was consumed. For example, a standard alcoholic drink is defined as 1.5 ounces of 80 proof liquor (e.g., rum, whiskey, vodka), a 12-ounce beer (about 5.0% v/v), or a 5-ounce glass of wine (12% v/v). Each of these drinks contains the same amount of ethanol. However, drink size can vary considerably in restaurants, bars, or at parties [9–11]. Nevertheless, for reporting purposes, standardization of drinks is useful and recommended in research and in forensic analyses [11]. The term social drinker or light drinker is often used by laypersons and some professionals but these terms may be inaccurate or misleading if not defined correctly. For example, the social use of alcohol is now generally described as a cold beer after a ball game, a glass of wine with meals, or a glass of champagne at festive occasions [12]. Similarly, the terms light, moderate, and heavy drinking are also used to describe drinking habits, but these terms are relative
and may have different meanings when other factors are considered. For example, the US Department of Agriculture Health and Human Services defines moderate drinking as one drink per day or less for women and two or fewer drinks per day for men [13]. However, if someone admits to drinking six or seven drinks per week, that might equate to moderate drinking since it averages about one drink per day, but have an entirely different implication if all six or seven drinks were consumed on Friday nights. Such a pattern of drinking constitutes binge drinking, now defined as four to five drinks within 2 h or a BAC of 80 mg/dl [8]. Whereas one to two drinks per day is considered moderate, heavy drinking is considered by many scientists as the consumption of more five or six drinks a day, but many other factors are considered in making a diagnosis of heavy, or other types of drinking [13, 14], including the impact of drinking on life events [15]. Therefore, the terms light, moderate, and heavy should be interpreted carefully on the basis of individual drinker characteristics or research design. The most recent edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IVTR) [16] defines two types of drinkers: those with alcohol abuse, and those with alcohol dependence. Alcohol abuse is intentional, conscious, and voluntary. Abusers drink too much too often, and make poor choices and decisions regarding their drinking. Their subsequent intoxication often results in injuries to themselves or others, medical consequences and expenses, lost productivity, and family problems. An example of alcohol abuse is drinking and then driving a car, or possibly drinking when pregnant. Most people with alcohol “problems” are alcohol abusers. In contrast to abuse, alcohol dependence is pathological and unintended. Alcoholics lack control over their use of alcohol in lifestyle situations in which abusers would ordinarily stop drinking, even if the desire to do so is strong. For example, a man who drinks a quart of whiskey a day cannot stay employed, has lost his family and friends because of constant drunkenness and is vomiting blood several times a day, and consults with his medical doctor. Even when he is told that alcohol is causing bleeding in his esophagus, the man still cannot stop drinking. Even though there are serious medical consequences to continued drinking, he cannot stop. This is alcohol dependence.
Alcohol: Use, Abuse, Tolerance, and Dependency The new classifications of dependence are confusing to those who remember the old 1950 World Health Organization definition. This latter definition, no longer valid, stated that an addicting drug had three qualities: (i) psychological dependence (equating generally with habituation or “craving”), (ii) tolerance (reduced drug effect so that more drug is needed to produce the original desired effect), and (iii) physical dependence (adaptation of the body to the drug so that one could only function normally when the drug was present. When the drug is discontinued, the previous adaptation of the nervous system no longer functions in the drugfree cellular environment and physical withdrawal symptoms appear). While this definition properly describes dependence on centralnervous-system (CNS) drugs such as heroin and alcohol, the definition falls short of describing dependence on cocaine, a CNS stimulant that has profound emotional withdrawal symptoms, but no significant physical withdrawal. Impaired control, which is at the center of our new definition of addiction, is a characteristic of all drugs that are “addicting”. The new term dependence (addiction) still has both psychological and physical components, but they are different from the old WHO definition. For example, impaired control is an obsessive preoccupation with the use of the drug (psychological) caused primarily by a neurochemical (physical) dysfunction in the brain. Older concepts such as “physical addiction” and “psychological addiction” have no accurate meaning and terms such as alcohol addict or drug addict do not appear in the current edition of DSM-IV. Terms such as addict or addiction are vague and scientifically imprecise and should not be used. Erickson [12] points out that these are pejorative terms (e.g., addict, junkies, and drunks) that detract from the science of alcohol (or drug) dependence as a brain disease [12, 16].
Tolerance and Dependence Tolerance and physical withdrawal are side effects usually associated with moderate to heavy drug consumption, but are not rigid criteria for diagnosing alcohol dependence. In fact, social drinkers and alcohol abusers can demonstrate tolerance. Tolerance is a decrease in the response to a drug as a function of exposure to that drug. The several types of tolerance are discussed below. Although tolerance is still a criterion for alcohol dependence, it cannot
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be inferred that if someone is tolerant they are an alcoholic. Tolerance is merely one of seven maladaptive patterns of use leading to a possible diagnosis of alcohol dependence [17]. Similarly, while anyone who consumes alcohol acquires some form of tolerance (see below), evaluations of alcohol-dependent patients should avoid the error of assuming that all “alcoholics” have a degree of tolerance that precludes any interpretation of their behavior while intoxicated. Although tolerance varies within and between subjects, it rarely confers immunity from most of the intoxicating effects of alcohol that would be of interest in forensic examination (e.g., drinking and driving). However, tolerance (or lack thereof) may be a factor in dramshop or comparative liability cases, where the question of general appearance (not performance on tests) is of legal interest. There are five primary forms of tolerance: acute, chronic, dispositional/metabolic, cross, and nonpharmacological. Acute tolerance was first noted by Mellanby, who observed that in dogs there is greater behavioral impairment when the BAC is rising compared to the same BAC when alcohol is post absorption and declining [18]. A similar effect was observed in humans [19–22], and has since been termed acute tolerance. This phenomenon, which can occur in a single drinking episode, is termed acute tolerance. Chronic tolerance develops in response to chronic or repeated exposure to ethanol and is a resistance to the intoxicating effects of the drug. Chronic tolerance occurs as the nervous system responds to the presence of alcohol and adapts to maintain homeostasis. A history of heavy drinking is likely to confer tolerance and less impairment compared to those in people who are moderate drinkers or abstainers [19, 23]. All drinkers acquire one or more forms of tolerance, but some chronic heavy drinkers become of exceptional tolerance and are able to function (to varying degrees) at BACs that would render less-tolerance drinkers unconscious or dead [23, 24]. Contrary to popular belief, although chronic drinking may reduce obvious symptoms of alcohol intoxication in some drinkers (compared with drinkers having little or no tolerance), it does not confer the same immunity from the impairment of complex tasks, such as driving, particularly at the high BACs often achieved by such drinkers. Dispositional and metabolic tolerance results from differences in ethanol absorption and distribution, whereas metabolic tolerance occurs from more efficient metabolism. The key factor here is tolerance
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occurs because of a change in drug availability to some target tissue. Alcohol is metabolized primarily by enzymes in the liver. For many drugs, including alcohol, repeated administration results in enzyme induction. Under such circumstances, the increased availability of enzyme results in more rapid metabolism of the drug and, therefore, less pharmacological effect. In human alcoholics, the magnitude of metabolic tolerance can vary significantly. For example, most men and women eliminate alcohol at a rate of about 15–20 mg/dl h−1 , but in some chronic heavy drinkers that rate can be significantly higher [25]. When a history of chronic heavy drinking is known or suspected, metabolic tolerance should be considered in pharmacokinetic analyses. In such cases, a range of elimination rates should be used and not a single “average [11]”. Cross-tolerance is present when the use of one drug results in a change in response to a different drug. In other words, the effect of the use of one drug may increase or decrease the response of another drug. Cross-tolerance may be due to changes in CNS sensitivity or metabolic tolerance that occurs when drugs share similar pathways of metabolism. For example, oxidative metabolism catalyzed by cytochrome P-450, reduced nicotinamine–adenine dinucleotide phosphate (NADP), and the microsomal oxidizing system (MEOS) pathways are shared by barbiturates and some minor tranquilizers. In the presence of alcohol, the removal of these drugs can be delayed, resulting in higher than expected drug concentrations [26, 27]. Interactions between ethanol and environmental factors as well as other drugs may also contribute to cross-tolerance [28]. Nonpharmacological or learning-based theories of tolerance demonstrate state-dependent learning, in which a task learned and practiced under a drug state is better performed in the same drug state. The work of Siegel and others has provided additional evidence that learning plays a significant role in the development of tolerance. This research suggests that environmental stimuli preceding drug intake elicit a conditioned compensatory response that attenuates the drug effect. In a classical Pavlovian conditioning paradigm, the conditioned stimuli (CS) consist of the various experimental procedures and environmental stimuli associated with the administration of the drug. The unconditioned stimuli (UCS) are the actual direct pharmacological effects of the drug. The
conditioned response (CR), once formed by repeated administrations of the drug, may then be demonstrated with a placebo by presenting the usual drug administration cues (CS) in the absence of the pharmacological effects of the drug (UCS). Conditioned tolerance has been demonstrated for many different drugs, including ethanol, both in animals [29–31] and in humans [32–34].
Conclusions Alcohol comes in many forms, including ethanol, the form contained in beverages. Alcohol is one of the most widely used and abused drugs in the United States and elsewhere, and is frequently found in toxicology results stemming from investigations of accidental and intentional injuries. Forensic evaluations of cases where alcohol is involved should take into account differences between social alcohol use and alcohol abuse when describing drinker characteristics. Similarly, the biobehavioral consequences of alcohol abuse and dependence should be interpreted in the context of current definitions of abuse and dependence. Multiple forms of tolerance can result from acute or chronic alcohol use. Tolerance is a relative term and should not be considered indicative of alcoholism. Similarly, a diagnosis of alcohol dependence (alcoholism) should not lead to speculation regarding exceptional tolerance unless supported by additional evidence. Finally, tolerance should be considered in pharmacokinetic estimates of alcohol use for example, as well as in describing or predicting behaviors following the consumption of alcohol. By using standardized definitions of what constitute use, abuse, dependence, and understanding the nature of tolerance, forensic examiners can communicate accurately and without bias information relevant to jurors and the court.
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Brick, J. (2008). Medical Consequences of Acute and Chronic Alcohol Abuse, in Handbook of the Medical Consequences of Alcohol and Drug Abuse, J. Brick, ed, The Haworth Medical Press, Binghamton, pp. 9–56. Dufour, M. (1999). What is moderate drinking? Alcohol Research & Health 23, 15–14. National Institute on Alcohol Abuse and Alcoholism, Tenth Special Report to the U.S. Congress on Alcohol and Health (2000). U.S. Department of Health and Human Services, Washington, DC. Dawson, D.A., Grant, B.F., Chou, S.P. & Pickering, R.P. (1995). Subgroup variation in U.S. drinking patterns: results of the 1992 national longitudinal alcohol epidemiologic study, Journal of Substance Abuse (3), 331–344. National Institute on Alcohol Abuse and Alcoholism, US Department of Health and Human Services (2008). Alcohol Alert, Vol.74. Kerr, W.C., Greenfield, T.K., Tujague, J. & Brown, S.E. (2005). A drink is a drink? Variation in the amount of alcohol contained in beer, wine and spirits drinks in the US methodological sample, Alcoholism, Clinical and Experimental Research 29(1), 2015–2021. Case, G.A., Destefano, S. & Logan, B.K. (2000). Tabulation of alcohol content of beer and malt beverages, Journal of Analytical Toxicology 24, 202–210. Brick, J. (2006). Standardization of alcohol calculations in research, Alcoholism Clinical and Experimental Research 30(8), 1276–1287. Erickson, C. (2007). The Science of Addiction: From Neurobiology to Treatment, Norton Press, New York. U.S. Department of Agriculture and U.S. Department of Health and Human Services (1995). Home and Garden Bulletin, No.232, 4th Edition, U.S. Department of Agriculture, Washington DC. Oates, J. & McCoy, O. (1973). Laboratory evaluation of alcohol safety interlock systems Instrument performance at high BALS. Report to the Highway Research Institute, PB224 702/1, National Highway Traffic Safety Administration, Department of Transportation, Washington DC. McLellan, A., Luborsky, L., O’Brien, C. & Woody, G. (1980). An improved diagnostic instrument for substance abuse patients: the addiction severity index, The Journal of Nervous and Mental Disease 168, 26–33. Erickson, C. & Wilcox, R. (2001). Neurobiological causes of addiction, Journal of Social Work Practice in the Addictions 1(3), 7–22. American Psychiatric Association (APA) (2000). Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, American Psychiatric Association, Washington, DC. Mellanby, E. (1919). Alcohol: Its absorption into and disappearance from the blood under different conditions, Special Report Series No 31 HMSO, Medical Research Committee, London. Goldberg, L. (1963). Quantitative studies on alcohol tolerance in man, Acta Physiologica Scandinavica, 5(Suppl 5), 1–126.
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Carpenter, J.A. (1963). Effects of alcohol on some psychological processes, Quarterly Journal of Studies on Alcohol 23, 274–314. Vogel-Sprott, M. (1979). Acute recovery and tolerance to low does of alcohol: differences in cognitive and motor skill performance, Psychopharmacology 61, 287–291. Niaura, R., Nathan, P.E., Frankenstein, W., Shapiro, A. & Brick, J. (1987). Gender differences in acute psychomotor & pharmacokinetic response to alcohol, Addictive Behaviors 12, 345–356. Minion, G.E., Slovis, C.M. & Boutiette, L. (1989). Severe alcohol intoxication: a study of 204 consecutive patients, Clinical Toxicology 27(6), 375–384. Perper, J.A., Twerski, A. & Weinand, J. (1986). Tolerance at High BACs: a study of 110 cases and review of the literature, Journal of Forensic Sciences 31(1), 212–221. Jones, A.W. & Sternebring, B. (1992). Kinetics of ethanol and methanol in alcoholics during detoxification, Alcohol and Alcoholism (Oxford, Oxfordshire) 27, 641–647. Chakraborty, J. (1980). Metabolic Basis of EthanolDrug Interactions, in Psychopharmacology of Alcohol, M. Sandler, ed, Raven Press, New York, pp. 191–198. Lieber, C.S., Pirola, R. (1982). Clinical Relevance of Alcohol-Drug Interactions, in Recent Advances in the Biology of Alcoholism, C.S. Lieber & B. Stimmel, eds, Haworth Press, New York, pp. 41–65. Kalant H., Khanna J.M. (1980). Environmental Neurochemical Interactions, in Ethanol Tolerance in Psychopharmacology of Alcohol, M. Sandler, ed, Raven Press. New York, pp. 107–112. Le, A.D., Poulos, C.X. & Cappell, H. (1979). Conditioned tolerance to the hypothermic effects of ethyl alcohol, Science 206, 1109–1110. Hinson R.E., Siegel S. (1980). The Contribution of Pavlovian Conditioning to Ethanol Tolerance and Dependence, in Alcohol Tolerance, Dependence and Addiction: A Research Handbook, H. Rigter & J. Crabbge, eds, Elsevier/ North-Holland Biomedical Press, Amsterdam, pp. 181–199. Melchior, C. & Tabakoff, B. (1981). Modification of environmentally cued tolerance to ethanol in mice, The Journal of Pharmacology and Experimental Therapeutics 219, 175–180. Dafters, R. & Anderson, G. (1982). Conditioned tolerance to the tachhcardia effect of ethanol in humans, Psychopharmacology 78, 365–367. Newlin, D. (1985). Human conditioned compensatory response to alcohol cues: initial evidence, Alcohol 2, 507–509. Tiffany, S.T. & Baker, T.B. (1986). Tolerance to alcohol: psychological models and their application to alcoholism, Annals of Behavioral Medicine : A Publication of the Society of Behavioral Medicine 8, 7–12.
JOHN BRICK
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Allelic Designation
Algor Mortis see Death: Time of
Allelic Attribution see Allelic Designation
Allelic Designation Introduction Short tandem repeat (STR)-based DNA profiling methodology is effectively at the theoretical limit of detection (LOD) in that typable results can be generated from as little starting material as a single cell [1, 2]. However, one of the most challenging aspects of forensic DNA analysis is the interpretation of lowlevel testing results where it is difficult to reliably distinguish between noise and signal from template DNA that is associated with an evidence sample [3, 4]. This difficulty with minimal samples is often compounded by the consumptive nature of PCR-based DNA testing [5, 6] when material is unavailable for replicate testing. Forensic DNA testing laboratories typically endeavor to minimize the effect of baseline noise and stochastic artifacts by relying upon very conservative minimum peak height thresholds (commonly fixed in the range of 50–200 relative fluorescent units (RFUs)) that are established during the course of their validation processes [7–10]. However, the conservative nature of these commonly employed thresholds can also arbitrarily remove from consideration legitimate signal from trace and secondary contributors to an evidentiary sample – matters of critical importance in many criminal investigations. Any measurement made with a light-detecting instrument, such as a genetic analyzer is subject to at least some level of background noise [11] – defined here as signal not associated with amplified DNA. Instrument-related factors that may contribute to background noise in DNA testing experiments are typically run-specific and include (but are not
necessarily limited to) the age and condition of the polymer and capillary being used, dirty capillary windows, and dirty pump blocks [12]. Background noise may also differ between instruments due to differences in charged couple device (CCD) detectors, laser effectiveness and alignment, and cleanliness and alignment of the optical components [10]. Many amplification-related factors that contribute to background noise (such as analyst skill and stocks of chemicals) are also run-specific and might be reasonably expected to have varying impacts over time.
Limits of Detection and Quantitation Many analytical disciplines aside from forensic DNA profiling have needed to rigorously account for background noise mixed with low levels of signal [13, 14]. It is common for background noise, such as that associated with DNA testing results, not to be constant and for noise levels to be distributed in a Gaussian fashion that can be effectively characterized with a mean and a standard deviation [11, 13–15]. In such circumstances, the LOD is expressed as a statistical confidence limit of noise error, usually 99.7% (i.e., three standard deviations) or LOD = µb + 3σb
(1)
where µb is the average amount of background noise and σb is the standard deviation associated with that value [11, 13–15]. A limit of quantitation (LOQ) represents the threshold beneath which measurements of signal strength cannot be reliably used to determine the relative quantity of detected analyte (e.g., because such measurements may include an appreciable amount of signal arising from background noise). LOQ is commonly expressed as the average background signal plus 10 standard deviations [11, 13–15] or LOQ = µb + 10σb
(2)
Forensic DNA testing laboratories routinely test a positive control, negative control, and reagent blank with every DNA analysis run [7–9]. While these controls are utilized primarily as sentinels for gross failures of the DNA testing processes, such as cross contamination of samples, as well as contamination or inappropriate activity of reagents, they also contain an abundance of subtle but important information about
Allelic Designation the running environment of the DNA testing system – particularly as it pertains to background noise. These ubiquitous controls can be used to establish objective run-specific electropherogram peak height thresholds that need to be exceeded to minimize the possibility that noise will be considered signal arising from a sample being tested [16]. LOD thresholds have been found to be consistently much lower (often by an order of magnitude) than what testing laboratories had previously established as minimum peak height thresholds [16]. Disregarding information associated with electropherogram peaks well above an analytical threshold of detection (and even above an analytical threshold of quantitation) might be considered abundantly conservative in some circumstances, given that DNA testing is a very sensitive process subject to a variety of technical artifacts such as pull-up, voltage spikes, and stutter. However, in this abundance of caution, valid information about the presence of real DNA peaks is being discarded or ignored – especially concerning given that means of reducing or at least identifying most technical artifacts are known or could be developed.
Technical Artifacts – Stutter Among the most commonly observed technical artifacts in PCR-based DNA profiling are signals associated with DNA polymerase “stutter” [17]. Stutter artifacts can be particularly problematic in mixed DNA samples where small peaks situated in stutter positions may be interpreted as either being due to stutter or to amplification product corresponding to an allele from a secondary contributor. Stutter products are amplification products that differ in size from a primary peak (corresponding to the actual genomic template) by integral numbers of the underlying core repeat sequence. They result from slippage of Taq DNA polymerase on template molecules during amplification: either forward (resulting in n − 4 stutter or in n − 8 stutter if two core units are skipped) or backward (resulting in n + 4 stutter) [18]. Numerous organizations including the Scientific Working Group on DNA Analysis Methods (SWGDAM) [9] and the DNA Advisory Board (DAB) [7] have recommended that forensic DNA testing laboratories conduct validation studies to develop cutoffs or thresholds that allow stutter artifacts to be reliably distinguished
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from faithfully amplified genomic DNA. The result has been the publication of numerous validation studies that address the prevalence of n − 4 stutter (i.e., [17]) with relatively consistent observation of stutter artifacts that correspond to 10% or less of the signal strength associated with faithfully amplified templates from the 13 tetranucleotide repeat Combinded DNA Index System (CODIS) loci. Fewer studies on the prevalence of n + 4 stutter have been conducted but a cutoff of 6% is generally considered to be sufficient to remove more than 95% of n + 4 stutter peaks.
Technical Artifacts – Pull-up Amplification products generated during this process are typically labeled with one of three or four different fluorescent dyes to facilitate the examination of several loci simultaneously. Signal associated with one dye color can sometimes give rise to the mistaken perception of signal in a different color in a phenomenon commonly known as pull-up or bleedthrough. Remedies such as shorter injection times or reamplification with smaller amounts of template can usually be invoked to prevent signal strengths from exceeding the 4000 rfu saturation-level threshold. However, situations where these alternatives are not viable (e.g., in mixed samples where the genotype of an unknown secondary contributor is of interest) are commonly encountered in the course of forensic analyses. It is also possible that pull-up artifacts can be associated with primary peaks below saturation thresholds. As a result, significant portions of electropherograms can correspond to regions where legitimate amplification products cannot be reliably distinguished from pull-up artifacts.
Technical Artifacts – Spikes and Blobs “Spikes” are narrow peaks usually attributed to fluctuation in voltage or the presence of minute air bubbles in the capillary. Spikes are usually seen in the same position in all or most of the dye colors used to generate DNA profile electropherograms. “Blobs” are false peaks thought to arise when some colored dye becomes detached from the DNA and gets picked up by the detector. Blobs are usually wider than real peaks and are typically only seen in one color. Spikes and blobs are not reproducible, which means that if
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the sample is run through the genetic analyzer again these artifacts should not reappear in the same place. Hence, the generally accepted way to confirm that a potential spike or blob is an artifact is to rerun the sample. However, analysts often simply rely on their “professional experience” to decide which results are spurious and which are real. This practice can be problematic because no generally accepted objective criteria have yet been established to discriminate between artifacts and real peaks (other than retesting).
[11]
[12]
[13] [14]
[15]
References [1]
[2] [3]
[4]
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[6]
[7]
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[9]
[10]
Findlay, I., Taylor, A., Quirke, P., Frazier, R. & Urquhart, A. (1997). DNA fingerprinting from single cells, Nature 389, 555–556. Oorschot, R.A.V. & Jones, M.K. (1997). DNA fingerprints from fingerprints, Nature 387, 767. Thompson, W.C., Ford, S., Doom, T., Raymer, M. & Krane, D.E. (2003). Evaluating forensic DNA evidence: essential elements of a competent defense review. Part 1, The Champion 27(3), 16–25. Thompson, W.C., Ford, S., Doom, T., Raymer, M. & Krane, D.E. (2003). Evaluating forensic DNA evidence: essential elements of a competent defense review. Part 2, The Champion 27(4), 24–28. Leclair, B., Sgueglia, J.B., Wojtowicz, P.C., Juston, A.C., Fr´egeau, C.J. & Fourney, R.M. (2003). STR DNA typing: increased sensitivity and efficient sample consumption using reduced PCR reaction volumes, Journal of Forensic Sciences 48(5), 1001–1013. Fr´egeau, C.J., Bowen, K.L., Leclair, B., Trudel, I., Bishop, L. & Fourney, R.M. (2003). AmpFLSTR profiler plus short tandem repeat DNA analysis of casework samples, mixture samples, and non-human DNA samples amplified under reduced PCR volume conditions (25 µL), Journal of Forensic Sciences 48(5), 1014–1034. DNA Advisory Board (DAB) (2000). Quality assurance standards for forensic DNA testing laboratories, Forensic Science Communications 2(3), 1–14. Federal Bureau of Investigation (FBI) Laboratory (2005). National DNA Index System (NDIS) Data Acceptance Standards, http://forensics.marshall.edu/NEST/ Nest%20PDFs/Documents/AppendB-NDIS-0505.pdf. Scientific Working Group on DNA Analysis Methods (SWGDAM) (2000). Short tandem repeat (STR) interpretation guidelines, Forensic Science Communications 2(3), 1–14. Moretti, T.R., Baumstark, A.L., Defenbaugh, D.A., Keys, K.M., Brown, A.L. & Budowle, B. (2001). Validation of STR typing by capillary electrophoresis, Journal of Forensic Sciences 46(3), 661–676.
[16]
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Rubinson, K.A. & Rubinson, J.F. (2000). Sample size and major, minor, trace, and ultratrace components, Contemporary Instrumental Analysis, Prentice Hall, Upper Saddle River, pp. 150–158. Applied Biosystems, Inc. (ABI) (2000). Chemistry Reference for the ABI Prism 310 Genetic Analyzer, Applied Biosystems, Foster City. Anderson, N. (1989). Determination of the lower limit of detection [Letter], Clinical Chemistry 35, 2152–2153. Thomsen, V., Schatzlein, D. & Mercuro, D. (2003). Limits of detection in spectroscopy, Spectroscopy 18(12), 112–114. Arinbruster, D.A., Tillman, M.D. & Hubbs, L.M. (1994). Limit of detection (LOD)/limit of quantitation (LOQ): comparison of the empirical and the statistical methods exemplified with GC-MS assays of abused drugs, Clinical Chemistry 40, 1233–1238. Gilder, J.R., Doom, T.E. & Krane, D.E. (2007). Runspecific limits of detection and quantitation for STRbased DNA testing, Journal of Forensic Sciences 52(1), 97–101. Walsh, P.S., Fildes, N.J. & Reynolds, R. (1996). Sequence analysis and characterization of stutter at the tetranucleotide repeat locus vWA, Nucleic Acids Research 43, 854–870. Butler, J.M. (2001). Forensic DNA Typing, Academic Press, San Diego.
Further Reading Fr´egeau, C.J., Aubin, R.A., Elliott, J.C., Gill, S.S. & Fourney, R.M. (1995). Characterization of human lymphoid cell lines GM9947 and GM9948 as intra- and interlaboratory reference standards for DNA typing, Genomics 28, 184–197.
DAN E. KRANE
Alterations: Erasures and Obliterations of Documents Introduction Forensic document examiners (FDEs) are routinely tasked with the examination of a document to determine if there has been an alteration to an entry or erasures, or to decipher an entry that has been obliterated by overwriting. The documents may be as varied
Alterations: Erasures and Obliterations of Documents as a check that has been altered for a different payee and amount, a business contract in which some terms have been changed, or medical records in which the amount of a dosage was changed. The FDE uses techniques that are generally nondestructive, although as a last resort (and with the approval of all parties involved), destructive techniques may be used. Evidence of alteration, obliteration, or erasure is not necessarily pejorative. Changes to documents are often made in the normal course of business and any such evidence found has to be interpreted in the context of the case. If the FDE finds that a document has been subject to alteration, erasure, or obliteration, his next task is usually to restore and decipher what the original entry was. This is accomplished by visual and instrumental means, though in several cases, no success is gained. ASTM International Standard Guide for the Examination of Altered Documents E2331-04 describes procedures that should be followed by FDEs in examinations involving altered documents. The guide includes some very useful definitions [1].
Equipment The FDE uses a variety of instruments and lighting sources in the detection of alterations, obliterations, and erasures. Natural light together with low magnification (X5–X40) is used to examine the obverse and reverse sides of the document. The document is examined with backlighting and with oblique (or side) lighting. The human eye can normally see light wavelengths in the range of 400–700 nm. This is called the visible light range. However, alternative wavelengths that are produced using filters and light sources are quite useful in detecting, deciphering, and restoring questioned entries. These wavelengths are in the ultraviolet (UV) range (200–400 nm) and the infrared (IR) range (700–1000 nm). UV and IR wavelengths are used in combination with a variety of filters to examine how papers and inks fluoresce or luminesce. Specialized instruments have been developed for FDEs and other people who need to look at documents for alterations or security features. Foster & Freeman Ltd. (UK) is a company with offices in the United Kingdom and United States whose video spectral comparator (VSC) range of instruments is used in institutions such as banks to full-service Crime Laboratories. Projectina AG is a Swiss company with a
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similar line of instruments generally known as the DocuCenter or Docubox. These instruments allow the examiner to examine documents quickly with a wide range of wavelengths. It allows for easy documentation of evidentiary information resulting from the examinations. Some enterprising FDEs also build their own instruments and get good results [2]. Fuji introduced a UV/IR camera that allows an examiner to take direct digital photographs of effects seen in the UV and IR wavelengths [3]. Dichroic filters are often used to compare inks. The results complement those obtained with the other instruments [4]. Imaging software such as Adobe Photoshop is used to enhance faded entries and also differentiate between inks [5]. The LAB-Color Mode in Photoshop has shown some promise as an analytical tool for ink comparison [6]. Electrostatic detection devices (EDDs) are used to detect indented impressions in paper. There are several suppliers of such instruments such as the electrostatic detection apparatus (ESDA) manufactured by Foster & Freeman Ltd. and the indentation materializer (IMED) made by Kinderprint. These instruments work on the principle of electrostatics. When entries are handwritten on the top page of a writing pad, impressions of the handwriting are made on the pages below. Indentations have been reported to have been developed as far as eight pages down. Sequencing on impressions and ink strokes may disclose evidence that entries were not written in the time frame as they appear. Research is being conducted using EDDs to detect impressions made by rollers within printers. This may be used to show that a page from a multipage contract was produced by a different printer than that used for the rest of the document [7].
Alterations Alterations can be classified into two types: additive and subtractive (some authors sometimes present a third type: substitution, which in essence is a subtraction followed by an addition). Additive alterations are made by adding content to a document. The content may be as little as a single pen stroke to change a 1 to a 7, for example, or entire paragraphs or pages of writing or printing that changes the context or meaning of a document. In the case of checks in
130
Alterations: Erasures and Obliterations of Documents
which a check writing machine imprinted the amount, the alteration is conducted by simulating the impression of the check writer. This alteration can only “raise” the amount of a check, since the original entry involves perforation of the check stock. Alterations can be quite subtle and a document such as a medical record can be altered by simply changing a decimal point to indicate a different dosage. This alteration would take place on one page amongst possibly hundreds. The FDE has to employ techniques that include overall visual examination, microscopic examination, alternative light sources with various filters, and careful measurement using specially designed rulers or grids. Visual examination on the obverse side of a document may disclose entries that are out of alignment. In handwritten documents, this may be reflected in entries that are cramped into a small space and not in keeping with the remaining handwritten entries on the document. In some instances, an alteration can be shown when line crossings are out of the expected sequence. In handwritten documents, the reverse side of the document is examined with oblique lighting to determine if there is any difference in the degree of embossing made by the pen pressure from the obverse side. Differences may indicate that the document was prepared on different writing surfaces and therefore, possibly, at different times. In typewritten documents, alterations may be detected if different fonts were used. If the alteration was made by addition of text after it was originally typewritten (even using the same typewriter and typing element), the use of special grids can show that the contested text was added later. The increased use of laser and ink-jet printers has made the detection of such additions more difficult. Whereas, in a typewriting case the tolerances would have been one-tenth or one-twelfth of an inch, for a laser printer it is about 1/7200 of an inch. A type of ruler called an E-ruler, which is used in the graphics industry, is the measurement tool for the font size and interlineal spacing. The line spacing and paragraph spacing together with the use of capitalized and bold fonts can make a difference in the measurements and conclusion as to whether an alteration by insertion has been made [8]. Occasionally a crude insertion is seen when different printers are used. Under magnification, it can quickly be determined when this is done.
Toner is a resinous material that sits on the paper and has a slight embossed feel. Ink-jet (for the most part) uses liquid ink that soaks into the paper. There are some ink-jet printers that use solid inks. These were introduced in 1991 by Tektronix. On occasion, a page is substituted into a multipage document such as a will, contract, or medical record, for example. It may be an additional page, or more likely, a page that contains different information than the substituted page. An EDD is essential to these types of cases. Impressions from the pages above the questioned page may not be found on the questioned page as could be expected. Impressions from the questioned page may be found in areas where they should not be. If an impression of a signature and date on a page is found on a page with a later date, this is indicative that the questioned page had been backdated and possibly substituted. If the first page of a document is signed and impressions are found on pages three and four, but not page two, this will raise questions as to the sequence of events in which the document was prepared and signed. Documents produced by two different printers may exhibit differences in the printing media (see Figure 1). Some toners have magnetic properties and some are nonmagnetic. These properties are determined with the aid of a magnetic viewer [9]. Different ink-jet inks may exhibit dissimilarities under IR wavelengths. Dissimilarities in drop size and
(a)
(b)
Figure 1 Two entries on the same contract. The majority of the contract was printed with toner (laser printer) (a). One line was added with an ink-jet printer (b) [Reproduced with permission from Rile & Hicks.]
Alterations: Erasures and Obliterations of Documents distribution of the ink-jet droplets may also indicate different manufacturers [10]. Documents produced with different photocopiers can sometimes be distinguished by different “trash marks” left on the copies. These marks arise from blemishes on the copying platen, from rollers within the machine, from the drum and charging devices or cleaners [11]. Copies made from the platen and from the automatic document feeder on the same machine may also display different trash marks since the copying mechanism is different for both processes [12]. Different color copiers and certain high-end color laser printers also produce characteristics that allow copies or prints to be identified to a particular machine [13–15]. Thus page substitution can be proved if a different machine is used. In multipage documents, marks left by items such as staples and paper clips can be of significant evidentiary value to proving page substitution. The number of staples and staple-holes through each page should be the same. Holes that are unaccounted for or not present when they should be, place doubt on the integrity of the page and the document as a whole. Similarly, paper clips or other binding devices and their impressions are useful in exploring the history of how a document was produced. Additions can be produced by a single ink stroke. A difference in the width of the pen lines could indicate that a different writing instrument was used for the addition. IR reflectance and IR luminescence are very powerful tools in detecting different inks (see Figure 2). It is important to note that the IR techniques cannot conclude that inks are the same. The technique
(a)
(b)
Figure 2 Infrared luminescence showing a check “raised” from 8000 to 80 000. (a) Visible entry on check and (b) entry viewed with infrared luminescence [Reproduced with permission from Foster & Freeman.]
131
can only differentiate different inks. Some different inks from different pens will have similar formulations and will give similar results under IR. Further information can be found in Ink Analysis. Raman spectroscopy, thin-layer chromatography, gas chromatography, and liquid chromatography are other techniques that can be used for further ink differentiation. However, the majority of these techniques will involve some destructive testing and are best performed by specialized ink chemists (see Ink Analysis). The latter specialists can apply ink dating techniques, which may prove that a questioned entry was written at a later date or is contemporaneous with the nonquestioned entries [16, 17]. Security documents normally have specialized antialteration features some of which are incorporated during the manufacture of the paper stock and others during printing [18]. In questions of alteration, the FDE has to be very careful when presented with a photocopy for examination. It is fairly easy to use readily available imaging software to conduct “cut and paste” alterations. The original document is scanned and the image is then manipulated by electronically cutting or adding various portions of text or images [19, 20]. The changed document is then printed and offered as a genuine document. Signatures are probably the most popular choice for an alteration by addition to make a document appear to be genuine. If the original signature is found, it can be proved that it was used as the model for the “cut and pasted’ document.
Erasures There are two types of erasures: mechanical and chemical. A mechanical erasure is one in which the entry is rubbed off using an abrasive substance. Erasure of penciled entries is perhaps the most common form of mechanical erasure. Ordinary black pencil has a marking core containing principally a mixture of graphite and clay. In writing, flakes of graphite form the black stroke. They rub off the point and adhere to the paper surface wedged between the paper fibers. The graphite cannot and does not penetrate the paper fiber as does ink [21]. The hardness of a pencil is a contributory factor in the ease of erasing its line. A soft black pencil leaves an intense black line with little pressure while a hard pencil leaves a lighter trace.
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Alterations: Erasures and Obliterations of Documents
Examination of pencil erasures is time consuming and can involve use of oblique lighting and EDDs. IR reflectance is useful since graphite is opaque to IR and so the pencil traces appear darker. This makes the faint entry easier to read. It is often necessary to photograph the erased area with lighting from each side at a time. These photographs can then be electronically “stitched” to make a composite picture, which shows the entire erased area lighted from all sides. It is a useful technique both for decipherment and court display [22]. Mechanical erasure involves an abrasive rubbing over the paper surface. This results in the paper fibers being disturbed. This is easily seen with oblique light. The use of lycopode spores has also been shown to detect erasures [23]. However, this together with other powder and chemical means should be used as a last resort [21]. Excessive rubbing may wear away the fibers such that the paper in the area of the erasure becomes almost translucent. Backlighting quickly reveals this effect. UV light is also used to detect these erasures as there will be a difference in the reflection between the erased portion and the smooth paper. It should be noted that different erasers also have different effects on the paper. A soft art gum eraser will leave much less trace of an erasure than a typical rubber eraser. Chemical erasures are normally used to remove ink lines or commercial printing. Typical solvents include bleach, acetone, brake fluid, and other cocktails of chemicals. Quite often, the use of the solvent is detectable by sniffing the document. Some documents have printing that is affected by the use of solvents and this effect will generally be seen very easily. UV light is probably the best means of detecting the stain left by a chemical used for an erasure. In some check-washing cases, there is no patent evidence that the check has been washed [24]. Comparison with other checks from the same check book may show some faintness of color in the washed check. Some security documents have printing that reacts to bleaching agents. This will make the erasure attempt patent. Examination with IR wavelengths may show some traces of the eradicated entries. In many erasures, it is virtually impossible to decipher the original entries. It is sometimes possible to recover some of the entries by examining the embossing on the back of the document caused by
the tip of the pen. It is important to note that when photocopies are examined, evidence of an erasure on the original may not have been reproduced on the copy.
Obliterations An obliterated entry is obvious to the reader of a document. It may be done in desperation or at leisure at the time of writing. The former is more likely to result in a decipherment of the original entry since a different pen may be used. Examinations with infrared reflectance (IRR) and infrared luminescence (IRL) are often successful in filtering the obliterating ink to reveal the original (see Figure 3). If the same or similar inks are used, then these techniques may not work. In this case, the FDE can examine the obliterated entry with high magnification and using an enlarged copy, go over the lines that comprise the obliteration. Whatever remains may constitute part or all of the
7 Tuesday (341-24)
(a) 7
Tuesday
(341-24)
(b)
Figure 3 Decipherment of an obliterated entry. (a) Obliterated entry in a diary and (b) original entry deciphered using IRR [Reproduced with permission from Foster & Freeman.]
Alterations: Erasures and Obliterations of Documents original entry. This requires some interpretation on the part of the examiner and the result may not be definitive. A common form of obliteration is conducted with the use of the ubiquitous correction fluid. Sometimes, the obliteration is a cursory pass of the brush with the fluid. In other instances, the entry gets a severe pasting, which results in a thick coat of correction fluid. Examination with backlighting in the first instance is usually sufficient to reveal the obliterated entry. IR radiation and filters can be used to induce luminescence in the ink entry. This luminescence can be observed through the correction fluid. In circumstances where the correction fluid is exceptionally thick, substances such as petroleum ether or a xylene substitute can be used to remove some of the correction fluid [25]. A combination of techniques is generally required to reveal all or a portion of the obliterated entry. In an examination of a photocopy, the FDE has to look for any evidence of obliterations. If a person carefully uses correction fluid, it may be impossible to tell on a photocopy. Some telltale signs are missing parts of lines or characters in the area of the obliteration. However, the FDE should not confuse normal dropouts caused by the photocopying process as evidence of obliteration.
[8]
[9]
[10]
[11]
[12]
[13]
[14]
[15]
[16]
References [1] [2]
[3] [4]
[5] [6]
[7]
ASTM International Standard Guide for Examination of Altered Documents E 2331-04. (2004). Drexler, S. & Smith, G. (2002). Ink differentiation for the fiscally challenged, Journal of the American Society of Questioned Document Examiners 5, 20–27. Richards, G. (1999). Beyond visible light, Evidence Technology Magazine 5, 32–35. Richards, G. (2003). Dichroic filters: their use in questioned document examination, Journal of the American Society of Questioned Document Examiners 6, 91–96. Herbertson, G. (2002). Document Examination on the Computer, Wideline Publishing, Berkeley, CA. Hammond, D. (2007). Validation of LAB-Color mode as a non-destructive method to differentiate blue ball pint pen ink. Paper Presented at the 65th Annual General Meeting of the American Society of Questioned Document Examiners, Boulder, CO. LaPorte, G. (2004). The use of an electrostatic detection device to identify individual and class characteristics on documents produced by printers and copiers – a preliminary study, Journal of Forensic Sciences 49, 610–620.
[17]
[18]
[19]
[20]
[21] [22]
[23]
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Kelly, J. & Lindblom, B. (eds) (2006). Scientific Examination of Questioned Documents, 2nd Edition, Taylor and Francis, Boca Raton, FL, pp. 159–175. Welch, J. (1985). Magnetic aspects of printing, photocopies and bank cards, Journal of the Forensic Society 25, 343–347. La Porte, G. (2004). Modern approaches to the forensic analysis of ink jet printing – physical and chemical examinations, Journal of the American Society of Questioned Document Examiners 7, 22–36. Kelly, J. (1983). Classification and Identification of Modern Office Copiers, The American Board of Forensic Document Examiners, Inc., Houston, TX. Frost, B. & Bell, J. (2007). The role of the slit glass in a photocopy system and its effect on photocopied documents. Paper presented at the 65th Annual General Meeting of the American Society of Questioned Document Examiners, Boulder, CO. Tweedy, J. (2001). Class characteristics of counterfeit protection system codes of color laser copiers, Journal of the American Society of Questioned Document Examiners 4, 53–66. Li, C.K., Chen, W.C., Cheng, Y.S. & Leung, S.C. (2004). The differentiation of color laser printers, Journal of the American Society of Questioned Document Examiners 7, 105–109. Li, C.K. & Leung, S.C. (1998). The identification of colour photocopies: a case study, Journal of the American Society of Questioned Document Examiners 1, 8–11. Aginsky, V. (2006). Using TLC and GC-MS to determine whether inks came from the same manufacturing batch, Journal of the American Society of Questioned Document Examiners 9, 19–27. Roux, C., Novotny, M., Evans, I. & Lennard, C. (1999). A study to investigate the evidential value of blue and black ballpoint inks in Australia, Forensic Science International 101, 167–176. Ware, C. (2003). A new check security feature: Thermochromic ink, Journal of the American Society of Questioned Document Examiners 6, 34–37. Hicks, F. (1995). Computer imaging for questioned document examiners: the benefits, Journal of Forensic Sciences 40, 1045–1051. Hicks, F. (1995). Computer imaging for questioned document examiners: the potential for abuse, Journal of Forensic Sciences 40, 1052–1054. Hilton, O. (1991). Detecting and Deciphering Erased Pencil Writing, Charles C. Thomas, Springfield, IL. Mohammed, L. & Williams, D. (2006). Using Adobe Photomerge to prepare demonstration charts. Poster presentation at the American Academy of Forensic Sciences Conference, Seattle, WA. Ellen, D. (2006). Scientific Examination of Documents: Methods and Techniques, 3rd Edition, Taylor and Francis, Boca Raton, FL. p. 185.
134 [24]
[25]
Amphetamine Kelly, J. & Lindblom, B. (eds) (2006). Scientific Examination of Questioned Documents, 2nd Edition, Taylor and Francis, Boca Raton, FL. p. 320. Kelly, J. & Lindblom, B. (eds) (2006). ibid. p. 332.
Amok: Running see Homicide: Multiple (Behavior)
LINTON A. MOHAMMED
Amphetamine Alterations in Documents: Detection of see Alterations: Erasures and Obliterations of Documents
Alternative Specimens: Hair see Hair: Toxicology
Alternative Specimens: Oral Fluid see Oral Fluid Toxicology
Alternative Specimens: Sweat see Sweat: Toxicology
American Law Institute Standard of Insanity see Insanity: Defense
Introduction The amphetamines represent a family of drugs that stimulate the central nervous system (CNS) and other parts of the body to produce euphoria and increased vigor and alertness. They are related chemically to the naturally occurring substance, ephedrine, which is found in Ephedra species. Related stimulants are also found in khat (Catha edulis grown in the horn of Africa and the Middle East, containing cathinone and other alkaloids), and mescaline. Mescaline is the active alkaloid in the peyote cactus (Lophophora williamsii ) from Northern Mexico and Southern USA and other cactus species growing in subtropical and temperate areas of South America. Pharmacologically, the amphetamines are all related to the hormone adrenaline (epinephrine) and the neurotransmitter noradrenaline (norepinephrine). Figure 1 illustrates the similarities of the naturally occurring stimulants ephedrine, cathinone, and mescaline as well as the hormones adrenaline and noradrenaline with amphetamine. Some amphetamines are available legally, i.e., amphetamine for use in narcolepsy and attention deficit hyperactivity syndrome (ADHD); however, the majority of these drugs that are used in the community are from illegal sources. The amphetamines are produced in clandestine laboratories either from simple chemical precursors or from legally available drugs such as ephedrine and pseudoephedrine. The synthesis of designer drugs containing methylendioxy moiety is usually done using safrole (extracted from sassafras oils) as precursor.
Types of Amphetamines
Amnesia see Dissociative Disorders
Amphetamine, or sometimes known as dexamphetamine, is the prototype drug in this class of drugs. Modifications on the benzene ring and nitrogen
Amphetamine OH
135
O H N
NH2
NH2
O O O
Ephedrine
Cathinone
OH
Mescaline
OH H N
HO
HO OH
OH
Epinephrine
Figure 1
NH2
NH2
Norepinephrine
Amphetamine
Chemical structures of selected stimulants and hormones
H N
NH2
H N
O O
Amphetamine
NH2
O O
Methamphetamine H N
O O
MDA
H N
O O
MDEA NH2
O
MBDB
NH2
O
O PMA
MDMA
DOM
O Br
NH2 O DOB
Figure 2 Chemical structures of selected stimulants. DOM, 4-methyl-2,5-dimethoxyamphetamine; DOB, 4-bromo-2,5dimethoxy amphetamine; MDA, 3,4-methylenedioxyamphetamine; MDMA, 3,4-methylenedioxymethamphetamine; MDE, 3,4-methylenedioxyethylamphetamine; MBDB, N-methyl-benzodioxazoylbutanamine; PMA, 4-methoxyamphetamine
end have led to numerous “designer” stimulant drugs. The most common is methamphetamine (methylamphetamine or “speed”), which is the N-methylated form of amphetamine. Ring substitution with methylendioxy moiety leads to analogs including 3,4-methylenedioxy-methamphetamine (MDMA or ecstasy), 3,4-methylenedioxyamphetamine (MDA), 3,4-methylenedioxyamphetamine (MDE, or “eve”), or N -methyl-benzodioxazoylbutanamine (MBDB).
Ring substitution with lipophilic groups (like methoxy groups) leads to analogs including 4-methoxyamphetamine (PMA), 4-methyl-2,5-dimethoxyamphetamine (DOM), or 4-bromo-2,5-dimethoxyamphetamine (DOB). Figure 2 illustrates the similarity in the chemical structures of few selected stimulants related to amphetamine. Drugs with the dextro configuration (D) are more active than those with the levo (L) configuration.
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Amphetamine
For example, L-methamphetamine is less active than D-methamphetamine and is used as a decongestant in some countries (as L-desoxyephedrine), while the D-isomer is the abused form of the drug.
required in higher doses compared to other forms and this in turn has a greater risk of harm and prospects of developing serious addiction [3].
Pharmacology and Disposition Abuse of Amphetamines Amphetamines are arguably one of the most abused drugs. Amphetamine is the predominate member of this class abused in Western Europe while methamphetamine is the predominate member in Eastern Europe, Asia, Australia, and North America. MDMA and related designer amphetamines are common in the night clubs worldwide due to their ability to promote empathy and a sense of well being. Ecstasy tablets are primarily composed of MDMA but can also contain other stimulants such as methamphetamine. The United Nations Office on Drug Control (UNODC) estimates that approximately 34 million people consume amphetamines annually with 8 million consuming ecstasy [1]. The prevalence of use varies substantially from region to region and between types of amphetamines. However, the proportion of the population using the drug that is over 15 years of age generally ranges from about 1–4% with much higher numbers in younger males. Amphetamines tablets come in several different forms, sizes, colors, and shapes [2]. Apart from the different appearances of the tablets, amphetamines can be used in different forms, as hydrochloride salt or as free base. The form used illustrates the common street names and the common way of intake of the drug. For example, methamphetamine used as hydrochloride salt is usually injected or taken orally and is known as speed or ice. When methamphetamine is used as a free base, it is often smoked and is known as base or crystal meth. These products can be manufactured locally or imported through a criminal network. Low purity forms (powders and tablets) of methamphetamine are usually administered by snorting or injecting, and can be mixed with other drugs such as ketamine. A gluggy, pasty, or oily form is often brown or yellow due to the presence of iodine and other organic impurities, and crystal meth or ice is high purity, crystalline methamphetamine that comes in the form of large translucent/white crystals that are usually smoked or injected. Free base methamphetamine is
Mechanism of Action and Effects Amphetamines interact with noradrenaline- (norepinephrine-) and dopamine-containing nerves to either replace the monoamine neurotransmitter in the nerve ending and act as a false transmitter, or to facilitate the release of neurotransmitters from nerve endings. Mood and behavior can be affected by some amphetamines (e.g., MDMA) due to the release of serotonin at nerve endings in the brain. The sudden “rush” or “high” experienced with intravenous injections, or smoking, is caused by the sudden release of noradrenaline and related monoamines from nerve endings [4]. Amphetamines stimulate the heart and cause irregular rhythm. Increases in heart rate also occur. Amphetamines produce CNS effects such as movement disorders (locomotor activity) and can produce a stereotyped behavior. This behavior will manifest itself as repeated movement or agitation, unusual facial expressions or grimacing, pacing, grooming, etc. Overt aggression and a feeling of increased strength is also a frequent serious side effect of amphetamine use, particularly with repeated use. Amphetamines can reduce fatigue but this is shortlived as tolerance sets in with repeated use leading to hypersomnolence. This is a serious risk factor in longdistance truck drivers using amphetamines to ward off the effects of long driving hours. Chronic use of amphetamines can produce psychotic conditions, which is often associated with violent and irrational behavior.
Potency and Duration of Action As one would expect, the various amphetamines have different potencies to cause an effect, and consequently each amphetamine is associated with a different range of common doses. These are tabulated in Table 1. Chronic abuse invariably involves higher doses than initiation doses in na¨ıve users. Depending on the dose and the type of amphetamine, the effects can last for at least onehalf day and up to more than two days when higher
Amphetamine Table 1
137
Common doses for selected stimulants
Drug Amphetamine Cathinone Ephedrine Methamphetamine MDMA MDA MDE PMA
Dose range (mg)
(a)
5–60 50 or more to 240 5 or more 50–150 50–250 50–250 50–100
Duration of action (b) Half to one day Several hours Half day Up to two days Half to one day Half to one day Half to one day Half to one day
Common blood concentrations (mg l−1 )(c) 75% African admixture determined using the 176-AIM panel is most likely to have an M (eumelanin content) value above 40 and an individual with less than 50% African ancestry is most likely to have an M value less than 40. With larger databases, we could provide not only an expected M value by
Phenotype 90
2027
Percent African ancestry v. melanin index in Puerto Ricans 70.0 African American African Caribbean European American
70
60.0 Melanin index
Melanin index, M
80
60 50 40 30
40.0 30.0
y = 0.1857x + 30.912 R 2 = 0.5521 P < 0.0001
20.0 10.0
20
0.0
10 10 0
90
80
70
60
50
40
30
20
10
0 0
(a)
50.0
10
20
30
(b)
40
50
60
70
80
90
100
Percent African ancestry
Percent African ancestry
Figure 5 Regression of eumelanin value (M) from skin measurement on African individual genomic ancestry estimates in a population of (a) African Americans, European Americans, and Afro-Caribbean samples, obtained using a 30-AIM panel [12] and (b) Puerto Ricans, obtained using the 176-AIM panel described in the text [3, 10]. Each spot represents the point estimate of African admixture for an individual. Higher M values correspond to darker skin colors (higher concentration of eumelanin per unit skin area)
Sample size Correlation coefficient, r
695 0.2826
Significance level
P < 0.0001 0.2127 – 0.3496
95% confidence interval for, r
4.0 3.5
Color
3.0 2.5 2.0 1.5 1.0 0
20
40
60
80
100
EU
Figure 6 Regression of iris eumelanin scores from digital photographs on European individual genomic ancestry estimates in a population predominantly of self-described “Caucasians”. Each spot represents a point estimate of European admixture for an individual. Higher color scores correspond to lighter colors (less eumelanin)
taking an average but we could also quantify the reliability of this value with confidence intervals. A correlation has also been demonstrated between iris color and European ancestry [13]; we can see from Figure 6 that while individuals with high “European”
admixture have light (color > 2.2) and darker iris color (color < 2.2), individuals with substantial nonEuropean admixture (20% or greater) almost always have darker iris colors. Thus, a crime-scene DNA sample determined to have been deposited by an
2028
Phenotype
individual with 40% East Asian and 60% European admixture, or 50% African and 50% European admixture can be inferred to have an iris color on the darker end of the range observed in the human population. With larger databases, we could even quantify the likelihood that this type of conclusion is wrong. For example, if we see that the conclusion is true for 999 of 1000 individuals, we could estimate that the conclusion is correct with 99.9% certainty and that only 1 in 1000 such conclusions would be wrong. As of this article, the indirect method can only be used for these two phenotypes but through the construction and use of admixture databases, we may soon learn of others. For example, if we construct an admixture database of individuals, which included the self-described “ethnicity” and a digital photograph for each entry, and then query the database with a particular admixture profile (± a reasonable range), we might get a return of several entries like that shown in Figure 7. From these returns, we could discern whether the individuals are more likely to refer to themselves as belonging to one particular population than another, and how reliable such an inference can be expected to be. Using software biometric tools, we might learn that the average distance between the eyes (for example) is significantly different from that
of a random collection of individuals, or a group of individuals with a different type of admixture profile. Some investigators may be able to use collections of digital photographs corresponding to an admixture profile to mentally compile a composite sketch, though the future promises to provide software for identifying all of the phenotypes statistically characteristic of the profile (compared to randomly specified samples) as well as the ranges of trait values, we can expect algorithms to construct an in silico “rendering” of the suspect similar to that provided by a human eyewitness. A very important point that needs to be highlighted is that if our admixture methods are insensitive or inaccurate, if there are problems with the population model or parental representatives we have built our test on, or if there are glitches with the database software, there will be error. However, assuming that the size of the database is adequate, this error is expected to result in an increase rather than a decrease in entropy of the system [3]. The increase in entropy leads to a loss of information and an inability to recognize correlations in regression analyses (false negatives) rather than an ability to recognize false correlations (false positives). For example, an admixture assay based on only a few AIMs covering only
1. BDE_0022 Estimate (%)
Ancestry
54
European
37
Sub-Saharan African
9
East Asian
0
Native American Country of origin
Self United States
Mother
Father
MGM
Canada
Kenya
Canada
PGM
PGF
Canada Kenya
MGF
Kenya
Ethnic identity Self
Mother
Father
MGM
MGF
PGM
PGF
East Black White White Black Black Canadian African/Cannadian (Kenya) (Canada) (Canada) (Kenya) (Kenya)
Figure 7 Example of an admixture database entry. Entries in this particular database (www.dnawitness.net) included a digital photograph taken under standardized conditions, country of origin, that of their mother, father, and their maternal grandmother (MGM) and paternal grandmother (PGM) as well as maternal grandfather (MGF) and paternal grandfather (PGF). Similarly, the self-reported “ethnic identity” is provided by each subject. The laboratory that administers this database took the photograph and determined the admixture profile with respect to a global four-population model using the 176-AIM panel discussed in the text. The database had 4700 entries as of August 2007
Phenotype one chromosome would produce a large standard error in admixture estimates and the imprecise estimates may be so scattered about their true values in a regression plot that the relationship between trait value and ancestry is concealed (e.g., in Figure 5b, imagine the spots so far scattered above and below the line at low as well as high African admixture values that the sum of squared distance to a line indicating no correlation is similar to that for one indicating a good correlation). False positives can only obtain if false positive correlations are produced between phenotypes and elements of ancestry, which equates to the creation of false pattern, but random error that we would expect from a poorly performing assay would, by definition, obfuscate pattern and increase the entropy. It is possible to create false pattern from an assay that produces estimates with biased error, but with admixture/phenotype databases even these tend to result in a decrease rather than an increase in entropy. For example, consider an assay that has a tendency to erroneously estimate low levels of African admixture for South Asians (but not for other “European” populations such as Middle Eastern or Continental Europeans). It might seem that this error could lead to the mistaken conclusion that low levels of African admixture for individuals of primarily European ancestry is correlated with very dark skin color, even though most Continental Europeans with low levels of African admixture exhibit lighter skin colors (e.g., Figure 5). However, note that all of the Europeans would be present in the database, and using the high European/low African profile to query the database would result in a jumble of various light and dark skin color phenotypes rather than the shade that would be observed, were the error not present. Thus, we have an increase in entropy over which we would expect without the error, leading to an inability to make an accurate inference and false negative (type I) error rather than the creation of a false positive. Nonetheless, admixture panels that produce biased estimates are easily identified if they are properly validated and characterized [3]. A properly constructed and validated admixture panel should exhibit single-digit percentage accuracy (total error from statistical imprecision and bias combined). The laboratory of the author operates such a validated admixture/phenotype database (n = 4700 samples as of August 2007) and has used it in several homicide cases, but as we discuss later, so far only to indirectly infer skin color and iris color. Finding other
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phenotypes for which the indirect method will be useful in the future and the development of more advanced data mining and composite sketch software tools will require significantly greater investment.
Direct Method Though they can be correlated with phenotypes, ancestry and markers of ancestry do not cause phenotypes – genes do. In contrast with the indirect method, the direct method relies on measurements of the actual genes underlying the phenotype of interest. Though far more satisfying in a theoretical sense, since we expect to be able to do a better job of predicting trait value (more accuracy and tighter confidence intervals), the direct method is rarely practicable because it requires an understanding of the dominant aspects of the genetic architecture of a phenotype, and acquiring this understanding is a very expensive and time-consuming endeavor. To date, research on the genetic basis for only human iris color and one aspect of hair color has been productive enough to enable direct phenotyping from DNA. The objective with the direct method is to define polymorphisms associated strongly enough with the phenotype that they are predictive for that phenotype with good sensitivity and specificity. Note that hundreds of good gene/phenotype associations have been described in the literature over the past decade or so (mostly for clinical phenotypes), but few of them are sufficiently strong or detailed enough within each gene to enable “genetic classification”. Given the complexity of human phenotypes, useful polymorphisms are likely to be found for phenotypes where expression is controlled by one to a few genes at most, and will almost always be useful in the context of diplotypes (diploid pairs of haplotypes, where a haplotype is a chromosomal string of SNP alleles). Which diplotypes are associated with which trait values would be best determined through an empirical process of database construction and query, as with the indirect method, except we query with diplotypes rather than admixture profiles.
Iris Color The best example of an effective direct system for inferring a human phenotype is human iris color. Linkage screens and association scans have shown
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Phenotype 1
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Figure 8 Examples of iris color inference enabled with the 33 marker/iris color database described in the text. Iris color is inferred using the average color exhibited by samples in the database with matching diplotypes and an interval is provided around this point estimate using the range of colors exhibited or a default range, whichever is larger. This inferred range is then used to query the database and all of the irides falling within the range are presented. This typically produces tens or hundreds of irides of similar overall color from a distance (determined by eumelanin content) though of different pattern, depending on the color and database size. Shown here are returns for 27 test subjects. Six representatives of the inferred iris color score range are provided for each of the 27 test irides below the line and the actual color of the test iris is shown above the line
that variable human iris color in humans is primarily determined by polymorphism in the Oculocutaneous Albinism 2 (OCA2) gene [13–15]. OCA2 was first discovered by researchers studying the human albino phenotype as a locus with mutations that affected iris melanin production but not skin melanin production (as well as other mutations that affect both). Recently, [13] built upon earlier reports [14–17] to identify 33 OCA2 SNPs associated with digitally quantified iris color independent from their ancestry information. As it is with many phenotypes (e.g., Figure 5), ancestry was itself correlated with the phenotype (Figure 6) and correcting the associations with respect to population structure was crucial for demonstrating that they were bona fide (that is, that the association was with iris color, not an element of population structure that is itself correlated with iris color; [3]). Though each of the 33 SNPs were marginally (independently) associated with iris color, none were very useful on their own as iris color classification features. However, when assembled into diplotypes, the alleles for these 33 SNPs were highly predictive for the overall eumelanin content of the iris; among 1100 diplotypes from individuals of European descent, there existed 96% concordance of iris colors among those samples with the same diplotypes [3, 13]. To predict the iris color of a given sample, this team thus built a database of phenotyped diplotypes, and then queried the database much as we do with the indirect method of phenotyping – though, in this case, with test diplotypes rather than admixture profiles. The return for this query provides an average iris color and range of iris colors as a point estimate and range
of inferred color for the test diplotype. The results were satisfying; a validation sample provided a 96% accuracy rate (the inferred or predicted iris color for the unknown iris fell within the predicted range 96% of the time; Figure 8) and demonstrated that the method was capable of pinpointing the overall eumelanin content of the iris and often the particular shade, though not the pattern of iris pigmentation [13]. Particularly interesting from this work on iris color is what it teaches us to expect for other phenotypes. The predictive power of these SNPs required a consideration within the context of diplotypes. Not only were SNPs unable to provide predictive power on their own, haplotypes were equally insufficient and even diplotypes composed using smaller numbers of SNPs than these 33 (such as hap-tag SNPs) were insufficient to achieve good prediction results [13]. This illustrates the apparent historical and mechanistic complexity of even this relatively simple (predominantly single-gene) phenotype. A by-product of this complexity is the need for a massive database in order to handle most test samples; with so many SNPs part of the equation, the number of diplotypes in the human population is very large and the chances that a test sample from a crime scene would have a match in the database at its current size (n = 1100, Summer, 2007) is about 10%. Nonetheless, the inferences for these 10% are highly accurate and based on this utility, the iris color diplotype database system has been developed as a forensic service by DNAPrint genomics under the trade name Retinome (DNAPrint genomics is the laboratory within which the author conducted much of the work
Phenotype described here and throughout this article). So far the method has been applied to several homicide cases; however, due to the currently small size of the database, many detectives desiring to use Retinome have been unable to do so because their crime-scene samples did not have a match in the database. For this method of predicting iris color to have more of a broad impact on the investigative process, the size of the database will have to be increased substantially. In spite of its limitations, the Retinome system was the first system for the direct inference of a complex human phenotype. Since its introduction on the lecture circuit in 2004, other OCA2 systems involving additional single nucleotide polymorphisms (SNPs) were described [23], and eventually, a single SNP was discovered in 2008 [24–26] that was so powerfully associated with the light/dark iris color dichotomy that it was posited to represent no less than a founder mutation – an evolutionarily instrumental mutation that not only explains but also represents the historical genesis of the crude light versus dark dichotomy extant throughout the world today. The strength of the association (nearly perfect, with respect to the dichotomy), functional studies with cultured melanocytes, the universality of the association (the C allele associated with lighter colors in individuals from around the world), and the location of the SNP in an important regulatory region of the OCA2 gene all combined to suggest that this hypothesis is indeed true. Although the SNP is only useful for crude predictions (lighter versus darker colors), the founder status of the mutation meant that prediction was suddenly possible for all samples – not merely a small fraction. Indeed, it is likely that some of the previously described SNPs were useful as components of a predictive tool through linkage with this founder mutation. However, others are likely to represent important pieces of the final solution for predicting precise colors and shades with economy and practicality. For example, one of the 33 Retinome SNPs (rs1800407) was demonstrated to be a penetrance modifier of the newly discovered founder mutation, and a minimalist set of OCA2 polymorphisms for the “ultimate” in forensics utility (precise color, perhaps pattern as well, for all crime-scene samples) will likely require a composite diplotype system involving the founder mutation and some number of the previously described SNPs in [3] and [23]. This “ultimate” system has not yet been developed, though integration of the founder mutation with those of the Retinome
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system in a newly available forensic service called Retinome 2.0 (DNAPrint genomics, Inc., Sarasota, Florida) represents a step toward this goal.
Hair Color Hair color cannot yet be comprehensively predicted from pigmentation gene genotypes. The iris color polymorphisms just described are not associated with human hair color and association and linkage scans have so far been relatively fruitless in identifying other useful associations ([3]; Zhu G. and Martin N., Queensland Institute of Medical Research, Brisbane AU, personal communication, and T. Frudakis unpublished results). This may be due to the fact that unlike the crudest aspect of iris color – the quantity of eumelanin in the iris – the genetic basis for hair color is a function of significant locus heterogeneity and complex historical origin. However, it appears that red color may be an exception. Valverde et al., [27] was the first to identify MC1R associations with pheomelanogenic red hair color (RHC), and subsequently, several other authors have extended these results to identify what are today called the RHC phenotype alleles (all SNPs, Box et al., [28]; Duffy et al., [29]; Smith et al., [30]; Palmer et al., [31]; Box et al., [32]; Bastiaens et al., [33]; Bastiaens et al., [34]; Kennedy et al., [35]; Flanagan et al., [36] and reviewed by Sturm, [37]). The associations are sufficiently strong to enable good predictive power – with odds ratios ranging from 2.3 to over 100 (reviewed in Sturm, 2002; [3]). The United Kingdom’s forensic science service (FSS) has condensed the major MC1R redhair polymorphisms into a 12-marker test that is sold to the forensics community. This test is generally only useful in cases of homozygosity; individuals who are homozygous for any of these mutations, or heterozygous for any two separate mutations (called compound heterozygotes) are accurately predicted to be redheaded (accuracy = 96%, from a test with n = 48 subjects) and those without a mutation (homozygous wild type) are almost always not redheaded (accuracy = 100%, from a test with n = 35 subjects; [18]). Approximately 84% of redheads are detectable by these criteria. Predictive ability is lower in the case of simple heterozygotes (only one mutation present, in the heterozygous state), which is by definition the state in which most of these RHC SNP alleles are expected to be found, in which case 88% are not redheaded while 12% are redheaded (n = 33). Indeed,
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we might expect that each of these mutations will have varying influences on the phenotype depending on the MC1R context within which it is found, and application of diplotype databases as described for iris color may be helpful in teasing more predictive power.
Other Phenotypes Databases are not yet available for the direct inference of skin color, but this may change soon. [12] and Bonilla et al., [38] used a process called admixture mapping to identify variants in the OCA2, MATP, ASIP, and TYR pigmentation genes associated with skin color in a manner that is independent from their ancestry information content. None of these appear to be strong enough to enable accurate prediction, but [19] convincingly described additional variants of the SLC24A5 gene that underlie additional variable skin pigmentation in humans (as well as other vertebrates). Diplotypes involving SNPs in these five genes may be sufficient for accurate inference of skin color within the context of the database systems we have been discussing, though such as database has not yet been constructed. Promising markers for human stature have also been identified in the RUNX2 gene [20] and RANK gene [21], but its unclear whether these two genes are sufficient for predicting this phenotype (especially since environment is likely to play such a role) and RUNX2/RANK variant databases for this phenotype have also not yet been constructed. Ethical/Procedural Issues and Case Studies. Were the STR profile for each of the world’s human inhabitants deposited into an international forensic DNA database, there would be no need to infer phenotype from crime-scene DNA since we would always be able to achieve a database match. Owing to ethical and procedural concerns, this is unlikely to come to pass in the foreseeable future. The ethical issues surrounding the inference of phenotype are extensively covered in [3], but for our purposes here, we can simply note that there is not a fundamental difference between learning about phenotype from human eyewitnesses versus DNA, except when DNA is available, it is more likely to provide reliable and falsifiable information. At some point, ethicists that decry the use of DNA for predicting phenotype as part of the investigative process will have to choose between the rights of DNA donors to remain
anonymous and uncharacterized and the rights of future victims of these donors not to be future victims. Phenotype profiles may cause the inclusion of innocent individuals into suspect pools, which would cause inconvenience to these individuals but not increase the likelihood of a false conviction (their CODIS profile must still match that of the crime-scene sample, the probability of which is not reasonably a function of whether or not they are tested using the current state-of-the-art CODIS assays, and is irrespective of their phenotype). It could be argued that many such individuals would or should become suspects for other reasons – such as a life of crime, proximity to the crime scene and/or relation to the victim – and that information about phenotype merely hones attention to a subset of these individuals. Indeed, many investigators consider these other reasons adequate priors (bases) on their own for defining who is and is not of interest in an investigation and honing attention to a subset of them with DNA-based phenotype information could reduce unnecessary inconvenience for many not fitting the phenotype “profile”. Notwithstanding, weighted against the death of innocent victims that could be caused by not applying intelligence provided by DNA-based methods, inconvenience caused to innocent individuals subsequently proven not to match the CODIS profile of a given crime-scene sample pales toward insignificant in comparison. Indeed, we seem to have made the decision to use physical information to shape investigations already – as it pertains to human eyewitness testimony; even with all of its pitfalls, its subjectivity, and poor performance rate, eyewitness testimony currently represents one of the most important cornerstones of the investigative process. The use of DNA-based methods promise only to improve this performance using DNA as an additional and/or alternative source for information, at least for cases where DNA is available. Even so, ethicists have complained that DNA-based phenotyping methods are akin to “racial profiling”, but the difference between using physical information gleaned from a crime-scene specimen and “racial profiling” is the application of falsifiable science rather than prejudice. For example, focusing on an individual based on information extracted from a crime scene is an exercise based on evidence and data and the conclusions are falsifiable by other laboratories. In contrast, focusing on an individual based on a belief
Phenotype that individuals of “group X” are more likely to be criminals – lacking specific data derived from a crime scene – is based more on prejudice and subjectivity than the scientific method and generally speaking, such correlations are not adequately powerful in a predictive sense to constitute meaningful priors when determining the likelihood of an individual’s involvement in a crime. The methods described in this article have been applied to numerous criminal investigations. The first application of the indirect method was for the Louisiana Multiagency Homicide Task Force Investigation (Louisiana Serial Killer Case) in the spring of 2003 [3, 22]. Investigators had adequate DNA from various rape/murder scenes throughout the state, but without a CODIS match, they were forced to target their investigation based on two eyewitness accounts that subsequently proved irrelevant to the case. Over a year passed with the task force looking for a “Caucasian” male (not only with standard investigative practices but also with DNA sampling dragnets) until a 73-AIM version of the DNAPrint 176-AIM genomic ancestry panel described in this article (which was also sold under the trade name DNAWITNESS as version 2.0) was applied and indicated that the donor was an individual of primarily African ancestry (85%) with a small amount of Indigenous American admixture (15%). In this particular case, the lack of European admixture was used to infer a relatively dark skin shade with respect to the average African-American in the United States (Figure 5a). The investigation was refocused with this data and within a couple of months, the newly refocused investigation lead to an ex-con in the area fitting this profile whose CODIS STR profile was subsequently matched to the crime scene. Were it not for the application of the phenotyping methods, the investigation would have continued on its misdirected path, and others would likely have been raped and murdered [22]. Another murder case in Napa California was initially focused on Hispanic suspects based on an eyewitness account. Napa detectives applied the 176AIM panel discussed in this article and obtained a continental admixture result that was found from DNAPrint genomics’ DNAWITNESS 2.5 database to be consistent with individuals of Continental European as well as Middle Eastern descent – not Hispanic. They then applied the DNAPrint Eurasian panel of 320 AIMs and the RETINOME iris color
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panel described earlier in this article and learned from database searches that the individual was most likely of Northern European ancestry and of light-colored irides. The investigation was focused appropriately, and the perpetrator of the crime in this particular case (who was of Northern European descent with blue eyes) was eventually identified and linked to the crime scene via the CODIS profile. As with human eyewitness data, DNA-based phenotype information does not always result in quick arrests of course, and of the hundred or so investigations that have employed the methods described herein, the majority remain open. However, even for these cases, investigators have saved money and time that would have been spent investigating individuals with phenotypes very different from the crime-scene DNA donor. To advance the field, the SNP and AIM associations and databases currently available need to be amplified so that an inference for every sample can be obtained, and more research is needed so that additional phenotypes can be considered. In the near future, this may be an uphill battle, at least in the United States. For example, many US grant-funding agencies have not embraced much of the work described in this article – particularly those associated with indirect methods of phenotype inference and it seems most likely that the task of expanding this field will likely to be left to private enterprise or public laboratories outside the United States. Indeed, the work described in this article was funded with private capital, and though commercial demand for the products has not so far economically justified the investment, the work has at least provided some public service and could prove just as useful for other more commercially lucrative areas of research such as in drug development (where constructing a portrait of an ideal patient for a given drug could have a significant impact on the likelihood of clinical trial success). The institutional resistance in the United States toward the type of work discussed in this article is interesting and deserves some thought here. Some argue that the US justice system is not built for efficiency and is biased toward the interests of the accused. If true, this may explain why US budgets for solving crimes are often limited such that US investigators have difficulty funding basic CODIS processing of their crime-scene samples (which should always be done first since identity testing provides probative, not merely presumptive results). For example, backlogs of a year or more
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and anecdotal reports of rape kits stacked to the ceiling awaiting funding for CODIS processing are not uncommon in the United States. For agencies experiencing such backlogs, budget allocation for phenotyping is likely to remain de-prioritized and until phenotyping methods have had more time to penetrate the field through continued demonstration of utility. Until the problems underlying the CODIS backlogs have been solved, the application of DNAbased phenotyping methods is likely to continue on a case-by-case basis, with emphasis on high-profile cases that investigators are under unusual pressure to quickly solve (such as serial homicide cases).
[7]
[8]
[9]
[10]
[11]
Acknowledgments I would like to thank all of the volunteers who provided their informed consent to be part of our forensic databases here at DNAPrint genomics, Inc.
End Notes
[12]
[13]
a.
Though, since all loci carry some ancestry information, calculations on the statistical certainty of such a match requires the use of appropriate population databases since they are based on allele frequencies that vary subtly from population to population.
[14]
[15]
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polymorphisms and risk of melanoma: Is the association explained solely by pigmentation phenotype?, American Journal of Human Genetics 66(1), 176–186. Box, N., Duffy, D., Irving, R., Russell, A., Chen, W., Griffyths, L. et al., (2001). Melanocortin-1 receptor genotype is a risk factor for basal and squamous cell carcinoma, The Journal of Investigative Dermatology 116, 224–229. Bastiaens, M., ter Huurne, J., Kielich, C., Gruis, N., Westendorp, R., Vermeer, B. et al., (2001a). The melanocortin-1-receptor gene is the major freckle gene, Human Molecular Genetics 10(16), 1701–1708. Bastiaens, M., ter Huurne, J., Kielich, C., Gruis, N., Wetendorp, R., Vermeer, B. et al., (2001b). Melanocortin-1 receptor gene variants determine the risk of nonmelanoma skin cancer independently of fair skin and red hair, American Journal Human Genetics 68(4), 884–894. Kennedy, C., ter Huurne, J., Berkhout, M., Gruis, N., Bastiaens, M., Bergman, W. et al., (2001). Melanocortin 1 receptor (MC1R) gene variants are associated with an increased risk for cutaneous melanoma which is largely independent of skin type and hair color, The Journal of Investigative Dermatology 117(2), 294–300. Flanagan, N., Healy, E., Ray, A., Philips, S., Todd, C., Jackson, I. (2000). Pleitotropic effects of the melanocortin 1 receptor (MC1R) gene on human pigmentation, Human Molecular Genetics 9, 2531–2537. Sturm, R. (2002). Skin colour and skin cancer – MC1R, the genetic link, Melanoma Research 12(5), 405–416. Bonilla, C. Parra, E., Pfaff, C., Dios, S., Marshall, J., Hamman, R. et al., (2004). Admixture in the Hispanics of the San Luis Valley, Colorado and its implications for complex trait gene mapping Annals of Human Genetics 68, 139–153.
TONY FRUDAKIS
Phosphatase: Acid see Acid Phosphatase
Photography: Length Measurement see Length Measurement
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Photography: Marks, Impressions, and Documents
Photography: Marks, Impressions, and Documents Introduction Photography plays a pivotal role in criminalistics by providing several key functions including nondestructive methods of detection, recording, preservation, and enhancement of physical evidence. Standard operating procedures for most forms of physical evidence require the evidence to be photographed either at the crime scene or in the forensic laboratory. In many cases involving crime scene investigation, the photographs of physical evidence obtained at the scene become the only form in which that evidence exists. The preservation of perishable forms of physical evidence places a higher emphasis on photographic methods to retain the evidence long after the scene has changed or the physical evidence has perished. Some forms of crime scene photographs also under go a process of comparative analysis made directly from the photographic source. Evidence such as bloodstain patterns, footwear impressions, fingermarks, toolmarks, and tire impressions all require a forensic examination made directly from the images. These photographs become the primary source [1] of the forensic analysis, and the value of the physical evidence is a function of the quality and accuracy of the photographic evidence. The application of photography certainly covers a broad range of activities and some specific taxonomy needs to be developed when attempting to model photography’s purpose in the forensic sciences [2]. This section discusses the central technical aspects of photography when used in criminalistics. Information regarding basic camera operation or techniques for simplistic recording of items found at a crime scene are not provided in this section. It will, however, examine the aspects of photographing evidence that utilize photographs in the analysis of evidence by forensic criminalists. Aspects including accurate recording methods, specialized techniques, and optical enhancement of evidence are discussed. Currently, photography can be divided into two separate forms: silver halide (film) photography and
digital photography. Both the forms of photography are currently practiced in the forensic science domain and are considered the same in this section. The lightsensitive recording mechanisms are the most obvious differences between each technology; however, camera operation remains relatively the same (with some exceptions). Digital imaging is a different concept that involves using digitized images on a computer platform and a distinction is made between digital photography and digital imaging. Digital photography is the practice of photography using a digital camera, while digital imaging is the processing or alteration of digital images using image editing software programs or the digitization of a photograph using peripheral computer equipment such as a scanner. The practice of digital photography and digital imaging are naturally implicit. The application of image editing software (i.e., Adobe Photoshop ) is also an integral element within the overall digital photography workflow. It is important to recognize, however, that the improvement capacity of images using image editing software does not substitute for consistent quality photography techniques at the capture stage. This section presents information regarding the optical enhancement of evidence in three separate components: (i) maintaining the image integrity, (ii) optical enhancement, and (iii) digital imaging enhancement.
Image Integrity The debate regarding the legitimatization of digital images in law enforcement and forensic science has been an exhaustive process by several law enforcement working parties, committees, and organizations over the years [3–5]. Legal organizations have generally accepted the new technology and have adopted their own forms of operating procedures when using digital photography. Like all modes of physical evidence, continuity of the evidence is a critical component of the management of the evidence integrity. Photography should be not different to any other mode of evidence and sound procedural policy regarding forensic photography practices should be developed and maintained throughout all the forensic organizations. It is, however, not the function of this section to discuss those procedures.
Photography: Marks, Impressions, and Documents Image integrity also refers to the ability of the image to represent the aspects of the photographic evidence accurately, reliably, and truthfully. The integrity of the photography evidence is a paramount consideration in criminalistics. The following attributes are considered in relation to image integrity for the photography of physical evidence that requires analysis directly from those photographs. More simplistic applications of photography to record the subjects in situ may not require such strict technical parameters.
Dimensional Integrity The reproduction of three-dimensional subjects into accurate two-dimensional photographs is fraught with difficulty by the very nature of this dimensional transition. The need for accurate dimensional representation is, however, a consideration when examining evidence such as fingermarks, footwear impressions, toolmarks, and bloodstain pattern evidence. Conveniently, these evidence forms are mostly represented as two-dimensional (or very close to it) and photography can reproduce a fair representation
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in this dimensional exchange (two-dimensions into two-dimensions). Accurate reproduction in this situation is not, however, automatic and requires some technical considerations to exclude the aspects of image distortion. Figure 1 shows four photographs taken of the same subject, a wire frame. It demonstrates how different the same object may be represented in a photograph and the importance of accurate photography. The image in Figure 1(a) has correctly maintained the subject’s dimensional integrity, while those in Figure 1(b–d) show keystoning or optical distortion. Forensic photographs that are used in comparative analysis must maintain the integrity of the subject’s dimensional aspects. Images that do not represent the subject’s dimensions and shape accurately are considered to be distorted. Image distortion is caused by several visual conditions including: (i) the camera viewpoint in relation to the subject (perspective distortion), (ii) the optical characteristics of the lens (curvilinear distortion), (iii) the dimensional stability of the recording material (film), and (iv) incorrect resizing of images in digital imaging software.
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Figure 1 Four photographs of the same object displaying different representations of image dimensional integrity: (a) correctly photographed displaying good image dimensional integrity; (b) image displaying perspective distortion or keystoning; (c) image displaying barrel distortion; and (d) image displaying pincushion distortion
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Photography: Marks, Impressions, and Documents
Figure 2 Camera position in relation to the subject. The lens axis is perpendicular to the subject and film planes while the film plane and subject planes are parallel
There are two essential requirements for the successful photography of physical evidence while maintaining the dimensional integrity of the evidence: (i) position the camera correctly to avoid perspective distortion (keystoning) and (ii) always use a distortion-free lens (Hard return). The camera viewpoint must be directly over the subject, which means the lens axis is perpendicular to the subject plane and the camera focal plane and subject plane are parallel [6]. Figure 2 illustrates the camera position in relation to the subject to avoid introducing perspective distortion while maintaining the integrity of the subject’s dimensional aspects. Several lens designs suffer from an optic aberration called curvilinear distortion [7], which will also corrupt the integrity of the image dimensional qualities. Curvilinear distortion is often described by the visual result that appears in the image and is referred to as either barrel distortion or pincushion distortion [8, 9] (see Figure 1). These effects are indicative of their descriptions and are caused by variations of image magnification across the field [1]. Curvilinear distortion can be minimized by using a symmetrical or quasi-symmetrical lens design. Lenses that are significantly asymmetrical in design, such as
telephoto and retrofocus lenses, tend to suffer appreciably from curvilinear distortion [8]. Zoom lens are also prone to distortion aberration and generally display pincushion distortion at longer focal lengths and barrel distortion at shorter focal lengths [8, 10]. Lens designs that are distortion free are called orthoscopic lenses [8, 11]. A critical aspect of photographing physical evidence and maintaining the dimensional integrity of the evidence is to select a lens that is free from curvilinear distortion. Macro lenses are designed for photography at shorter working distances than infinity (∞) or for a magnification range of 0.1–1.0 times [12]. They are also either symmetrical or quasi-symmetrical in design and are considered as highly corrected for curvilinear distortion aberration. All photography of physical evidence that requires a high standard of image dimensional integrity should be taken with a macro lens and never with a telephoto, wide angle retrofocus, or zoom lens. This aspect of forensic photography quality is imperative for evidence such as fingermark impressions, footwear impressions, physical fit evidence, toolmark evidence, and other forms of evidence requiring the examination of photographs. This aspect is naturally not as important for general recording of evidence such as in situ images at crime scenes. Zoom lenses are very useful for general crime scene photography but not for more critical forensic photography. Some digital imaging software provides the facility to correct lens distortion. Even though lens distortion may be corrected using digital imaging software such as Adobe Photoshop [13, 14], digital correction of this image artifact should only be applied when it is absolutely necessary and should not replace the standard photography practices that avoid lens distortion. Prevention is better than the cure and it is certainly more preferable to avoid curvilinear distortion by using a lens that is considered as distortion free or orthoscopic in the first instance.
Representation of Scale The incorporation of linear scales into physical evidence photographs is an essential practice when recording evidence. There are various linear scales available for different types of evidence. Linear scales are used as a reference to the size of the subjects photograph and this reference is used to enlarge the photographs to predetermined magnifications for
Photography: Marks, Impressions, and Documents comparative analysis examination (1 : 1 for footwear impressions, 5 : 1 for fingerprint impressions, etc.). Linear scales are also used to calibrate the scale of digital images when using image analysis applications. Calibration is achieved when the amount of pixels are counted across a known length present in the image. Each pixel then represents a lineal value and several mathematical functions may be applied to the image. Important considerations when incorporating linear scales include the following: (i) use an appropriate sized scale for the type of evidence photographed, (ii) make sure the scale does not hide the features of the evidence, and (iii) the position of the linear scale must be parallel to the subject and at the same height. Some linear scales also incorporate circular references to detect any perspective distortion that may have resulted from poor photography technique. Digital correction of perspective distortion may also be conducted using Photoshop and using the circular references as a standard. Table 1
Image Quality The quality of the image is naturally an important aspect of recording evidence that will undergo further examination and analysis. Image quality for forensic purposes may be defined by several parameters including image sharpness or resolution, detail or clarity, image contrast, color fidelity and dynamic range, and dimensional integrity. Table 1 provides a list of those parameters and also describes what influences these considerations of image quality. The maintenance of image quality needs to be carefully considered and embedded into the forensic practitioners working practice. Image quality forms a critical basis for forensic photography and is an essential requirement before further optical and digital enhancement techniques may be applied. Digital enhancement is not a correction for poorly executed forensic photography. Evidence enhancement techniques build on the foundation of sound image quality and permit further visualization and the application of forensic evidence.
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Evidence Enhancement The most common rationale to enhance physical evidence is to improve the visibility of the evidence. Contrast between the evidence and background can become problematic when evidence is found on items that are of similar color or tonal value. Increasing the difference of brightness values between the evidence and the background provides an increase of contrast. Evidence deposited onto material with complex patterns can also lower the visibility of the evidence and cause problems with interpretation of the evidence. An optical enhancement example is found in the two crime-scene photographs (Figure 3). The photograph in Figure 3(a) is a bloodstained footwear impression made on a black ceramic tile found at a crime scene. This image displays very little visibility and contrast between the bloodstain impression and the black tile background. Figure 3(b) is the same footwear impression that has undergone chemical and optical enhancement to increase the contrast and improve the visibility of the evidence. The bloodstain footwear impression was first treated
with a blood reagent called Hungarian Red and photographed using a monochromatic light source of 530 nm. A Wratten 25 barrier filter was attached to the camera lens. Evidence enhancement may be achieved by using the following methods: • • • •
chemical treatment (development or staining); optical enhancement; specialized lighting techniques; and digital imaging enhancement.
Enhancement may be conducted using a single method or a combination of methods as demonstrated in Figure 3(b). Chemical treatment to enhance or develop physical evidence is a practice that is well established in forensic science. The treatment may independently increase contrast due to chemical staining or it may combine physically with the deposited material and alter the spectral qualities of the material. Optical or photographic enhancement involves various techniques utilizing the optical properties of the evidence material and its relationship to the radiation source and spectral sensitivity
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Figure 3 (a) Footwear impression in blood on a black ceramic tile. (b) Same impression treated with Hungarian Red and photographed with a 530 nm monochromatic light source and a Wratten 25 barrier filter on the lens
Photography: Marks, Impressions, and Documents of the capture device. Digital imaging enhancement also utilizes digital imaging editing software such as Adobe Photoshop . Optical and digital imaging enhancement are discussed in the next section.
Optical Enhancement Chemical treatment of physical evidence (i.e., blood or fingermarks) will either stain the material to increase the contrast or make the material react to a light source of specific spectral output. Details regarding the various chemical treatments are discussed elsewhere in this section, however, the reaction of chemically treated specimens to certain wavelengths of light provides the basis of optical enhancement. Optical enhancement of physical evidence provides the visualization of latent evidence or provides improved visibility by increasing the contrast between the evidence and its background. There are three essential elements that form the foundation for optical enhancement of physical evidence. These elements include: (i) the specific spectral distribution of the light source illuminating the specimen, (ii) the specimen’s response when illuminated by the light source, and (iii) the spectral sensitivity of the capture device (film or digital sensor). Each component requires careful consideration when performing optical enhancement of physical evidence.
Spectral Distribution of Light Sources The approximate spectral sensitivity range of human vision is between 400 and 700 nm, with higher sensitivity within certain ranges depending on the level of illumination. When light enters the eye and forms an image on the retina, nerve cells called photoreceptors [15] convert the light energy into a signal that is translated by the mind. There are two types of photoreceptors within the retina called rods and cones and these receptors react to different levels of illumination. Malacara [16] suggests there are approximately 100 million rods and 5 million cones. The cone receptors are used for bright light conditions and have a sensitivity peak at 555 nm, while the rod receptors provide vision in low light (night vision) and have a sensitivity peak at 505 nm [16–18]. Most digital cameras capture color by using a color filter array positioned over the camera’s sensor.
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This array consists of a mosaic of red, green, and blue (RGB) filters known as a Bayer filter. The Bayer filter has twice the number of green filters as red or blue to produce color images that relate to the spectral sensitivity of vision [19]. The spectral output of a light source is called its spectral distribution and may be measured using a spectrophotometer. Optical enhancement techniques use various different light sources including natural sources such as direct sunlight and open shade, and artificial light sources such as incandescent tungsten, tungsten halogen, electronic flash, xenon arc lamps, and others. White light containing a mixture of several colors is considered as a polychromatic light source. Polychromatic light is suitable for most general photography applications and essential for color photography. However, optical enhancement techniques often require a light source with a narrow spectrum or monochromatic light sources [20]. Monochromatic light sources are produced by filtering polychromatic light through an optical filter or filters. Lasers are another source of monochromatic light [21]. Specialized forensic lighting equipment such as the Rofin Polilight provides monochromatic light for a range of forensic applications including optical enhancement. These units use a high-intensity xeon light source with inbuilt interference filters to produce monochromatic light with bandwidth of ≈40 nm for most settings. The inbuilt interference filters are also tunable by adjusting the angle of the filter in relation to the transmitting light through the filter. A tuning rate of 30 nm may be achieved with a 45° tilt and the shift is always downtuned toward a shorter wavelength. Figure 4 provides details of the spectral distribution of the Polilight on the 590-nm setting. The monochromatic nature of the light output can be seen by the narrow shape of the spectrum.
Spectral Response of Specimen Optical enhancement operates on the premise that specimens record in a particular way when they are irradiated by specific wavelengths from a monochromatic light source or transmitted through an optical filter over the camera lens. Optical filtering of the illuminating light to produce a monochromatic source isolates the response from the specimen. These effects can be achieved with polychromatic light sources; however, due to the broad nature of polychromatic
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Photography: Marks, Impressions, and Documents Spectral distribution – polilight 590 nm 90 Relative intensity (%)
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Monochromatic spectra from a Polilight forensic light source (setting 590 nm)
lighting, the effects are not seen or are masked by the other wavelengths. Optical filters placed over the camera lens can also alter the properties of light transmitting through the optical system. Optical filters produce specific spectral responses from the specimen. The application of optical filters on the camera lens allows optical enhancement to be conducted in standard white light conditions, unlike using monochromatic light sources, which will need to be conducted in a darkened room. However, the monochromatic forensic light sources available today provide a narrower spectrum that is difficult to achieve when using a single optical filter over the lens. Optical enhancement may produce four different conditions or responses from the specimen when illuminated by monochromatic lighting: •
the specimen may absorb the light and darker; • the specimen may reflect the light and lighter; • the specimen may transmit the light and transparent; and • the specimen may luminesce and fluorescent.
become become become become
These responses to certain wavelengths of monochromatic light may be referred to as modes of optical enhancement lighting. These modes may be described as (i) absorption mode, (ii) reflection mode, (iii) transmission mode, and (iv) photoluminescence mode. The purpose of optical
enhancement is to make the specimen visible or introduce greater visibility by enhancing the contrast between the specimen and background. When monochromatic light sources are used in the optical enhancement of evidence, natural color rendition of the specimen is not possible due to the specific spectral range of the light used. Strong color casts are produced when using monochromatic light with color photography and this effect should be avoided because it often appears like a photographic error. Digital images photographed in color should be converted to a grayscale image or the color desaturated to – 100%. Absorption and Reflection Modes. Absorption and reflection modes are chromatic effects that provide an increase of contrast between the specimen and its background. These modes operate on the principle of selective absorption or selective reflection of a colored specimen when illuminated with a specific monochromatic light source (or transmitted via an optical filter). When a monochromatic light source illuminates a color specimen, the specimen will either darken or become lighter in tone depending on the relationship between the color of the light source and the color of the specimen. Absorption mode is a method of increasing the contrast between the specimen and the background by darkening the tonal value of the specimen or background. Absorption occurs when a colored specimen is illuminated by a monochromatic light that is an opposite color to that of the specimen [20]. The specimen darkens due to its selective absorption properties
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Figure 5 (a) Color image of a fingermark made in cyan-colored paint on a red background. (b) Absorption mode on a red background. (c) Reflective mode on a red background. (d) Grayscale image without enhancement. (e) Absorption mode on white background. (f) Reflective mode on black background
and this mode is most commonly used to increase the contrast. Reflection mode is also a method of increasing the contrast, however, it lightens the specimen or background by selective reflection. Refection is also a chromatic condition and requires a colored specimen and a monochromatic light source of similar color to the specimen. Figure 5 is a photograph of a fingermark made in cyan colored paint found on a red document. Figure 5(a) is the color image using standard white light (electronic flash), while Figure 5(d) is the same image converted to a grayscale image. Figure 5(b) uses a red monochromatic light (650 nm central bandwidth) and darkens the fingermark due to the absorption of the red illumination. Figure 5(c) uses a blue monochromatic light (450 nm central bandwidth) and lightens the fingermark’s tonal value. This series of images also demonstrates an ideal situation for absorption and reflective modes. The color of the background is opposite to that of the specimens. Although this ideal condition is rarely observed in reality, the examples provide an optimum result for this technique. The general rule for selecting the color of the monochromatic light source for absorption or reflection mode is based on the selective absorption and selective reflection properties of the specimen [20]. It suggests that the color of the light source lightens its own color and darkens its opposing color. Figure 8(a) represents two models of color synthesis
that are regularly used in photography and digital imaging. The two models are “additive” and “subtractive” color synthesis. Additive color synthesis uses primary colors such as red (R), green (G), and blue (B). In an ideal condition, if equal quantities of red, green, and blue light are added together, their combination will produce white light [8]. Hence, RGB primary colors are considered as additive and each color ideally represents one-third of the white light (visual) spectrum. The reproduction of color using the three components of red, green, and blue is called trichromacy and relates to the function of color vision known as the Young and Helmholtz theory [8, 15–17]. The subtractive color synthesis model is based on the subtraction of opposing primary colors (called complementary) from white light. Therefore, if green is taken out of white light, the resultant color will be magenta. Magenta light is considered as without the green component of white light due to its subtraction. Primary colors may be subtracted from the white light by using the subtractive color synthesis model comprising of the complementary colors, e.g., cyan (C), magenta (M), and yellow (Y). When an ideal complementary filter (cyan, magenta, or yellow) is placed over a white light source, one-third of the spectrum is subtracted (red, green, or blue) while two-thirds is transmitted. Therefore, subtractive color synthesis is a combination of the two remaining primary colors and makes up two-thirds of the
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Photography: Marks, Impressions, and Documents Cyan (minus red) Relative density
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Figure 6 A representation of spectral output from ideal conditions for additive and subtractive color synthesis. The graphs on the left illustrate that each primary color (RGB) produces approximately one-third of the visual spectrum. However, the subtractive model comprising of CMY colors produce two-thirds of the white light spectrum
visual spectrum. Figure 6 illustrates the relationship between additive and subtractive color synthesis models. Each color in the additive color model (RGB) represents one-third of the visual spectrum, while each color in the subtractive model (CMY) make up to two-thirds of the white light. Additive and subtractive models of color synthesis are also the basis of color film technology and digital imaging color modes [22, 23]. If you examine an image on a color negative film (minus the integral layer which is the amber base color of the film base) you will see that the color image is represented in its negative colors. That is, the reds will
be cyan, greens will be magenta, and blues will be yellow. This effect can also be seen if you invert a color digital image. Figure 7 provides an insight into how these two modes of color synthesis are used in photography. The colors rendered in the inverted or negative image clearly show the relationship between additive and subtractive colors in photography. Digital imaging also uses the same color modeling with RGB color and CMYK color modes. The “K” is an additional channel and represents black. RGB color is the standard for most digital photography applications, while CMYK is a color space often
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Photography: Marks, Impressions, and Documents Inches
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Figure 7 Positive and negative color images displaying the relationship between additive and subtract color synthesis in photography
used for photography used in graphic reproduction (reproduction of images in print media). Figure 8(a) further displays the relationship between additive and subtractive color models and provides a guide for the selection of monochromatic light for absorption or reflective modes. Each triangle represents a color synthesis model, RGB or additive and CMY (without the K) or subtractive, to produce a color wheel or more appropriately a color star. Colors on the opposing points of the star (e.g., red and cyan) represent opposite colors, while the colors positioned on points next to the additive primary colors are their composites. The opposing colors will provide optimum absorption for specimens and selective monochromatic light sources or optical filters and will darken the specimen. The two adjacent colors next to each opposing color will also darken the specimen. This diagram forms the basis for absorption mode and the specimens opposing color should be selected as the color of the monochrome light source or optical filter. While absorption mode is usually more effective to enhance contrast than reflective mode, selecting the same color monochrome light source as the color of the specimen will lighten the tonal value of the specimen. Color wheels as
illustrated in Figure 8(a) are for photographic applications and are calculated based on the additive and subtractive models of color synthesis of light [22]. Color wheels that are designed for pigments and used in painting and graphic design are not the same and are not suited for optical enhancement or photography. The color of the background is also a factor to consider when increasing the contrast using absorption and reflective modes. Neutral backgrounds such as white, gray, or black will display little change when illuminated by monochromatic light due to the achromatic (without color) character of these tones. However, if the background is colored, then the same absorption or reflection principles will occur to the background as it does to the specimen. Backgrounds, which are the opposite color to the specimen, have the potential to produce the highest degree of contrast when applying absorption or reflective modes. White backgrounds also work well with absorption mode because the specimen can be darkened against a light background. Black backgrounds work best with reflective mode by making the specimen lighter to enhance contrast. Figure 5(e) demonstrates the results of absorption mode with a white background, while
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Photography: Marks, Impressions, and Documents G Y
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Figure 8 (a) Additive and subtractive color synthesis models demonstrating color opposites; (b) Additive and subtractive color synthesis models demonstrating the tonal changes when using monochromatic light sources. The object colors positioned above the horizontal line will record in a lighter tonal value, while the object colors indicated below the line will record darker in tone due to the absorption of the light
Figure 5(f) illustrates the effect of reflection mode on a black background. As previously mentioned, absorption and reflective modes may also be achieved by using optical filters placed on the camera’s lens and photographed using standard white light. This technique has a long history with black and white film photography. Optical filters, known as contrast filters, provide a similar effect as monochromatic lighting, except that the effect is influenced and controlled by the transmission properties of the optical filter with white light [24–26]. Filter factors must also be applied to the camera exposure to compensate for the loss of light caused by the absorption of light by the filter. The application of photographic filters may also be achieved digitally with Adobe Photoshop . Digital imaging enhancement is discussed in the following section. Transmission Mode. While an increase of contrast is the objective for absorption and reflective modes of optical enhancement, transmission mode has a different function. The function of transmission mode is to reveal evidence that may be obscured or not visible [27]. It uses the transmission properties of selective wavelengths of light incorporation with the spectral characteristics of the specimen and
the spectral sensitivity of the recording medium. This enhancement mode allows the specific wavelengths of light to transmit through thin specimens of specific spectral qualities and renders the specimen transparent [6, 26–29]. When the specimen becomes transparent, items beneath the specimen can become visible. An example is shown in Figure 9 where the obliterated writing on a document has become visible due to the transparent properties of the ink covering the text. Photoluminescence Mode. When specimens possessing certain properties are illuminated by specific wavelengths of monochromatic light, they may absorb the excitation light and then reemit light of a different wavelength. This effect is know as luminescence [29, 30]. There are two different results caused by luminescence: (i) fluorescence that emits light at a longer wavelength while the excitation source is illuminating the specimen and (ii) phosphorescence that emits light and continues to do so for a period of time after the excitation source ceases to illuminate the specimen [29, 31, 32]. The material painted onto watch dials that illuminate in the dark is an example of phosphorescence.
Photography: Marks, Impressions, and Documents
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Figure 9 Transmission mode. The ink obliterating the text has become transparent and allowing the visualization of the text beneath the ink
There are also other forms of luminescence such as bioluminescence that is found in several organisms (e.g., glowworms) and chemiluminescence that is caused by a chemical reaction (e.g., luminol) [29]. Bioluminescence and chemiluminescence are caused without the presence of an excitation light source. Lennard and Stoilovic [31] suggest that luminescence caused by the absorption of light is called photoluminescence and this type of luminescence is often used in optical enhancement. Bioluminescence, chemiluminescence, and photoluminescence effects can all be photographed; however, due to the low level of light emission, these procedures must be conducted in a darkened environment [29]. Photoluminescence mode enables the specimen to fluoresce and the emitted light from the specimen can be recorded by a camera. Recording specimens using this type of luminescence is also called fluorescence photography [29, 32, 33]. This mode requires consideration of all aspects of the optical enhancement triangle including (i) the specific spectral output of the excitation light source, (ii) a photoluminescent response (fluorescence) from the specimen, and (iii) the spectral sensitivity of the recording device (film or digital sensor). The selection of the specific excitation spectra will depend on the photoluminescent properties of the specimen material. Forensic evidence specimens such as seminal fluid, saliva, and urine fluoresce
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naturally when illuminated with certain excitation light sources [30, 33]. This naturally occurring phenomena is referred as autofluorescence [1, 29] and optical enhancement may be achieved without chemical treatment in these cases and is nondestructive. Other forms of evidence that do not naturally fluoresce (like blood) may be induced to fluoresce by chemical treatment with a fluorochrome [29]. This process is called the secondary fluorescence [1, 29] and treatments such as Rhodamine 6G, Indanedione, Diazofluorenone (DFO), and Hungarian Red are some of the common reagents used in posttreatment for photoluminescence mode [34]. Photoluminescence mode is often an alternative to other optical enhancement methods when the background does not suit the absorption or reflective modes. An example may be found in blood evidence. Absorption mode is generally the preferred method for blood evidence using a monochromatic light source at 415 nm, the maximum absorption of dried blood [33]. However, if the blood evidence is deposited onto a dark background, absorption mode will not provide an increase of contrast. Instead, it will darken the blood against a dark background, resulting in very little contrast. Figure 3(b) provides an example of photoluminescence mode for blood evidence. Excitation ranges for photoluminescence mode vary depending on the autofluorescent characteristics of the specimen or the reagent used for posttreatment secondary fluorescent photography. Most forensic applications use spectral ranges in the lower order including ultraviolet (UV), violet, blue, and green region wavelengths. The resultant emitting light from photoluminescence mode is always longer in wavelength than the excitation source used. Therefore, most photoluminescence applications provide an emission light within the visual spectrum (400–700 nm). Some document examination applications are the exception where infrared luminescence methods produce an emission source further into the invisible spectrum. This method is generally outside the standard photography range and is conducted using specialized instrumentation called a video spectral comparator (VSC). The emission light source produced by the photoluminescence is usually quite weak in brightness value and as previously mentioned requires photography in a darkened environment. Barrier filters are also applied to the camera lens to improve the contrast
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Photography: Marks, Impressions, and Documents Camera Monochromatic light source
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Figure 10 Photoluminescence mode displaying the application of a monochromatic light source, a specimen that fluoresces and a barrier filter over the camera lens
between the specimen and background. The rule for applying barrier filters for photoluminescence mode is to use a filter of the same color as the emission source. This provides maximum transmission of the fluorescence and will also darken any opposing background reflected light. For example, when a blue-colored light source is used to produce an orange-colored fluorescence, an orange barrier filter transmits the orange colored emission and darkens the reflected blue light of the background. Photoluminescence mode requires the following parameters: (i) an excitation source suitable for the specimen material, (ii) a specimen that provides fluorescence (naturally or induced), (iii) a barrier filter to improve contrast, and (iv) the appropriate spectral sensitivity of the recording device (usually within the visual spectrum). Figure 10 illustrates the requirements of photoluminescence mode. Figure 11 is a fingerprint dusted with a green fluorescent fingerprint powder and photographed using a 540 nm excitation source. Figure 3(b) is a bloody footwear impression treated with Hungarian Red reagent excited by 530 nm excitation source from a Polilight and a Wratten 25 (red) barrier filter on the camera lens.
Spectral Sensitivity of Capture Device The spectral sensitivity of the recording mechanism (digital sensor or film) is the spectral range that the
Figure 11 Fingermark using photoluminescence mode
Photography: Marks, Impressions, and Documents device or material is able to record. Spectral sensitivity is an essential consideration when conducting optical enhancement methods. The recording device must be capable of recording in the spectrum used in the enhancement method. The spectral sensitivity of film may be examined using wedge spectrograms. Wedge spectrograms are graphs that plot the spectral response of the film. These graphs are produced by exposing film to a dispersed light that has passed through a diffraction grating and then a neutral density wedge, which is placed on the film’s surface. Tripack color films have a spectral sensitivity range within the visual spectrum (400–700 nm). These films are not sensitive in the infrared region and an UV absorption layer is situated before any of the RGB sensitivity layers which prohibits any recording in the UV region. Generally, color films are not used in optical enhancement techniques. They produce a color cast when using monochromatic lighting or using a colored optical filter and are not sensitive outside the visual spectrum. Film emulsion is the suspension of silver halides in gelatin to form a light sensitive emulsion. It is naturally sensitive only to UV and blue wavelengths and early film remained only sensitivity in these regions. In 1873, Vogel discovered that film emulsions can be made sensitive to blue and green spectra by adding a dye to the emulsion [8]. This process of dye sensitization was later refined and emulsions spectral sensitivity were extended into the red and infrared spectra. Black and white films are regularly used in optical enhancement and are still available in various spectral sensitivities. There are five classes of black and white films with different spectral sensitivity ranges. These classes are as follows: •
blue sensitive – only sensitive to UV and blue wavelengths; • orthochromatic – sensitive through to the green region; • panchromatic – sensitive through to red or covering the visual spectrum up to ≈650 nm; • extended red sensitivity – extends further into the red spectrum up to ≈750 nm; and • infrared – sensitive into the infrared region up to ≈900 nm. For a more detailed examination of the film’s spectral sensitivity, consult wedge spectrograms for
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each film type. Film manufactures readily publish this information with the product description. The spectral sensitivity of digital cameras is more difficult to obtain from most of the camera manufacturers. There are generally three different types of digital sensors, also called semiconductors, used in digital cameras: • • •
charged coupled device (CCD); complementary metal oxide (CMOS); and Foveon.
semiconductor
Single-shot digital cameras using CCD or CMOS sensors use a Bayer filter, which is a mosaic of RGB filters placed over the pixels. Foveon sensors, however, use a system of three different layers of semiconductors stacked together to form a multilayer sensor. These sensors design replicates that of the tripack color film, which consists of three different color sensitive layers (RGB). Each layer is suspended in a silicon wafer and the longer wavelengths are able to penetrate through the previous layer/s [35]. The advantage of Foveon sensors is that they do not require demosaicing interpolation like systems using a Bayer filter and the physical size of the sensor is not divided by each color channel (therefore, increasing sensor resolution). Digital sensors have spectral sensitivity characteristics like all the light sensitive devices. CCD and CMOS sensor’s spectral sensitivity works very differently to that of silver halide film. While film is naturally sensitive to UV and blue light and is made sensitive to other spectral regions using dye sensitization, digital sensors are more sensitive to the infrared (IR) region with very little sensitivity in the blue and UV spectral regions. The lower sensitivity in the blue region is the cause of higher noise levels found in the blue channel. Digital sensors are monochromatic and color is produced by processing of the image using trichromacy (combination of RGB). To improve chromatic aberration effects on the optics, most digital cameras also place an infrared blocking (absorbing) filter over the sensor to limit the spectral sensitivity to the visual spectrum. The spectral sensitivity of digital cameras is therefore a combination of (i) the spectral response of the monochromatic semiconductor, (ii) the absorption properties of the IR blocking filter, and (iii) the transmission properties of the Bayer filter.
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Various digital cameras are available for forensic photography. Excluding the standard low-end consumer compact digital cameras, cameras suitable for forensic photography include: standard digital singlelens reflex (SLR) (pro and proconsumer models), digital SLR cameras with the IR blocking filter removed (modified for infrared photography) and scientificbased monochrome digital cameras. These scientific types of digital cameras provide various ranges of spectral sensitivity and generally publish the response data. Standard SLR camera manufacturers rarely publish the spectral sensitivity data and are generally only considered for applications within the visual spectrum (400–700 nm), although some cameras will perform slightly outside this range.
Specialized Lighting Techniques Photography readily exploits light and its interaction with the surfaces of objects. The term lighting is used in photography as a way of describing the “visual effect” that results when this interaction of surfaces and light energy manifests. Some lighting techniques provide aesthetic elements to a photograph, while some others may enhance aspects of the physical evidence. Lighting may provide a visual representation of shape, line, form, subject texture, detail, aerial perspective, and many more visual aspects [35]. The topic of photographic lighting is an expansive consideration and cannot be fully justified in this section of the text. However, four specialized lighting techniques used for the enhancement of physical evidence are discussed in this section, which are as follows: • • • •
axial illumination; near-axial illumination; diffuse reflection method; and oblique lighting.
Axial Illumination Axial illumination is the light that illuminates the specimen from the camera’s optical axis [36]. This form of lighting produces no shadow visible by the camera and is a form of shadowless lighting. Owing to its directionality, it may be used successfully to photograph specimens in cavities when getting light into small crevices is difficult. Axial illumination is used to detect topographical variances found on flat metal surfaces including coins or medals. It is also
a technique that may also be used to photograph untreated fingermarks found on metal or reflective surfaces. Axial illumination is a similar technique as epiillumination used in photomicroscopy [18, 36]. This form of illumination is produced by using a collimated (parallel) light source directed onto a thin semitransparent (semisilvered) mirror beam splitter positioned at a 45° to the lens axis [36, 37]. Thin semitransparent mirrors are more suitable than plane glass because the mirror surface increases the illumination efficiency and reduces the double-image effect, which is more visible on plane glass beam splitters. A slight double image results due to the separation between the two surfaces of the beam splitter (front and back). Thicker beam splitters produce a greater shift between each image that makes this artifact more obvious. Other ambient light must also be carefully controlled to avoid extraneous light reflecting off the beam splitter’s reflective surfaces. In particular, reflected light transmitting through the beam splitter and illuminating other objects within the room can produce a reflection on the near side of the beam splitter and cause a reflection of the object within the image space. A light absorber such as black velvet cloth should be used to absorb this light (see Figure 12). Figure 12 illustrates the components of axial illumination.
Near-Axial Illumination Near-axial lighting produces a similar lighting effect as axial illumination. The light source is positioned close to the lens axis [36] producing a light quality that is void of form, texture, and shadow. The intent of near-axial lighting is to illuminate an object or scene evenly. Several portable light sources, including portable flash, may be used to produce this form of illumination. Ring light attachments (see Figure 13) attach to the camera lens and can also produce a diffuse near-axial illumination [36].
Diffuse Reflection Method When light reflects off a surface, the properties of the surface will affect the type of reflection produced. There are two types of reflected light possible: diffuse reflection and direct reflection [8, 17, 38]. Direct reflection (also referred to as specular reflection) results from light reflected off polished surfaces.
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Camera
Lens hood
Semi transparent mirror (beam splitter)
Black absorber Collimated light source
Figure 12 Axial illumination lighting diagram
Figure 13 A ring flash attachment on a digital SLR camera used for near-axial illumination
Direct reflection follows the first law of reflection which states that the angle of incidence equals the angle of reflection (i = r) [8, 12, 17, 22].
Diffuse reflection is the scattering of reflected light caused by a matt surface. The uneven nature of matt surfaces reflect the incident light in different directions by maintaining the first law of refection (i = r). The effect produces reflected light in multiple directions causing a diffuse effect (see Figure 14b). Diffuse reflection may also be considered as partly diffuse or totally diffuse [22]. Totally diffuse reflected light is perfectly diffuse meaning the spread of reflected light forms evenly across the entire surface. Totally diffuse reflections obey Lambert’s law and the surface is considered to be a Lambertian surface [8, 12, 22]. Diffuse reflection lighting method exploits the outcomes of both direct and diffuse reflection. Figure 15 is a photograph of an untreated (undeveloped) fingermark on a highly polished flat surface, which is a computer hard drive. This subject produces two different surfaces: the highly polished surface of the hard drive and the matt surface of the fatty deposit of the fingermark. When incident light is applied to both surfaces simultaneously, a direct reflection will be produced off the hard drive and a diffuse reflection from the fingermark. The relationship between the position of the camera lens, the position of the incident light source, and the position of the specimen are all critical aspects of this technique. Their positions are also interrelated and careful consideration is essential. The camera should be positioned perpendicular (90° )
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Direct reflection
Direct reflection
(a)
Diffuse reflection method
Camera Incident ray
Polished surface
Direct reflection not recorded by camera Diffuse reflection
Diffuse reflection
Diffuse reflection
Direct reflection
Incident ray (b)
Matt surface
Diffuse reflection recorded by camera
Incident ray
(c)
Figure 14 (a) Direct reflection from a polished surface (i = r), (b) diffused reflection from a matt surface, and (c) lighting, illustrating diffuse reflection method seen in Figure 15
to the subject plane. The incident light source is positioned at ≈45° angle from the specimen, which will also result in a ≈45° angle from the lens axis (see Figure 14c). The visualization of the fingermark is achieved due to the differences between the reflected light values from the diffuse light reflected from the fingermark and the direct light from the polished surface. Owing to the law of reflection (i = r), ≈100% of the direct reflection will reflect away from the camera lens and not record in the camera. This will result in the polished surface having no light entering the camera and producing a dark toned surfaced in the photograph. The diffuse reflection emanating from the fatty deposit of the fingermark will direct some reflected light into the camera lens and record in the photograph. The result is illustrated in Figure 15 whereby the fingermark records a light tone against a dark background. Diffuse reflection method is a simple and effective method of recording fingermarks on polished surfaces without having to treat or develop the mark.
Oblique Lighting Figure 15 Untreated fingerprint found on a highly polished computer hard drive and photographed using diffuse reflection method
Oblique lighting (also referred to as side lighting) is one of the most valuable lighting techniques used
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Digital Imaging Enhancement
(a)
(b)
Figure 16 (a) Photograph depicting the heel of a shoe using near-axial illumination (ring flash). (b) Same shoe using oblique lighting. Schallamach patterning becomes more visible with oblique lighting
when photographing mark evidence. Oblique lighting may provide a significant increase in detail and provide the visualization of individual identification characteristics that may be crucial to the examination. Oblique lighting is achieved by positioning the light source at an oblique or low angle to the specimen. The lighting direction runs across the surface of the specimen and essentially increases the local contrast or variations of highlight and shadow on the surface of the specimen. This effect increases the topographic detail and provides further visual information to examine. Figure 16 provides an example of the differences between oblique and near-axial illumination. The Schallamach patterning found on the heel of a shoe is greatly emphasized by oblique or side lighting. Figure 16(a) was photographed using a near-axial portable flash, while Figure 16(b) uses oblique lighting. Oblique lighting has increased the local contrast on the surface of the heel making the Schallamach pattern more visible.
Digital enhancement of physical evidence is the application of computer software to make adjustments to digital images of evidence. Digital enhancement provides several similarities to the techniques used in digital photography and optical enhancement. The most significant advantage digital imaging has provided forensic science is its ability to make fine adjustments to image parameters such as contrast, color, sharpness, image noise, and many other adjustments. Items in images can also be quantified by counting, measuring, and making mathematical calculations using image analysis applications. The advantages of digital imaging for forensic science are expansive. This section examines two common practices of digital enhancement using such controls as contrast and the chromatic modification of specimens. Digital enhancement of physical evidence should not be considered as a process of correcting poorly executed digital photography. Digital enhancement of evidence requires the input of quality digital photography and the enhancement techniques provide further tools for the forensic scientist. Concepts of quality include sharpness, image dimensional integrity, lighting, exposure, and dynamic range. Digital images record brightness linearly unlike film which responds to light nonlinearly [39]. Film’s nonlinear response to light may be seen in the “S”shaped characteristic curves that plot their exposure and density parameters. Obtaining quality digital images with a higher dynamic range is preferable when performing digital enhancement. Essentially, the more inherent information the digital image contains, the more control image enhancement offers. Best practice suggests digital images should be captured (camera or scanner) using a 16 bit (or a 14 bit for some cameras) and RAW images are better processed using Photoshop processing appliances such as Camera Raw than in-camera processed JPEGs. Compression applications such as the JPEG captured and processed in-camera at an 8 bit offers significant less information and enhancement control. Digital enhancement processing in Photoshop should also be carried out using the 16 bit per channel for improved results [13, 19]. There is a significant difference in pixel depth between 8 and 16 bit per channel modes. The 8 bit per channel provides 256 variations per channel that results in approximately 16 million possibilities for RGB files. While the
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16 bit per channel images contain 65 536 variations for each channel and results in billions of color and tonal representation possibilities.
powder. To avoid specular reflections, the fingermark was the photograph using brightfield illumination that combined a small sheet of white Perspex situated behind the fingermark and a portable flash positioned behind the mark was used as the illumination source. The original image displayed high levels of detail but with low contrast and the contrast was enhanced using the “curves” adjustment. The inserts situated in each image provide details of the before and after curve adjustments. The first graph shows a straight line (curve) diagonally across the graph which represents the linear nature of digital images. The gradient of the curve influences the degree of image contrast. The greater the gradient (more steeper the curve) the less variation there is between certain sections of the shadow and highlight regions resulting in more image contrast. Lowering the gradient (flatter curve) reduces the contrast. The second insert found in Figure 17 shows an increase in the gradient of the curve that has resulted in the increase of contrast. The shadow and highlight regions were also “clipped” slightly which also added to the contrast improvement. Contrast enhancement adjustments using “curves” may be conducted in each channel separately or as an alpha channel indicated as “RGB”.
Contrast Adjustment Digital imaging can provide adjustments to image contrast with significantly more control and ease than more traditional film-based technology. Visualization of evidence is predominately made possible by the contrast between the evidence and its background. Fingermark evidence is a good example and is most reliant on contrast between the friction ridge detail and the substrate background. Like optical enhancement, digital imaging enhancement using contrast adjustments in Photoshop is an effective method of improving the detail and visualization of evidence. There are various methods in Adobe Photoshop that allow contrast adjustment. The most suitable method is using the “curves” function located in the “Image > Adjustments > Curves” menu. In Photoshop versions greater than CS3 the exposure histogram is also embedded into the curve graph. Figure 17 is an example of how curves may adjust to the contrast of the specimen. The image is of a fingermark on a glass window and developed in black
(a)
(b)
Figure 17 Before and after fingermarks when contrast is enhanced using Photoshop curves
Photography: Marks, Impressions, and Documents
Chromatic and Tonal Modification Adjustments to the spectral response of color may also be modified in digital imaging software in a similar way to optical enhancement techniques. When working with Adobe Photoshop there are always several different methods to obtain the same or similar result. Changing the chromatic aspects of specimens can also be achieved using several Photoshop functions; however, the “Black & White” adjustment is most likely the simplest. The “Black & White” adjustment automatically converts the image to a monochrome image while maintaining the file in RGB mode, so that modification of the colors, now tones, can be adjusted. As previously explained, when using optical enhancement techniques using monochromatic lighting or colored optical filters over the camera, the image should be converted to a monochrome image to avoid color casts. The “Black & White” function can be found on Photoshop versions higher than the CS3 and work on the principles of black and white contrast filters (see optical enhancement). It may be found on the Photoshop menu “Image > Adjustment > Black&White”. Like contrast filters used on the camera with monochrome film, the “Black & White” function alters the brightness of tonal values by altering the spectral reflective and absorption properties. Logically, the digital imaging application is altering the spectral response artificially by adjusting the brightness values of each color and its resultant tonal value in monochrome (unlike optical enhancement). The “Black & White” function provides individual
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darkening or lightening of the following colors; red, green, blue, cyan, magenta, and yellow. These are the colors previously mentioned in the additive and subtractive models. There are three options when operating this function: (i) the custom option which uses slider bars to modify the tonal value of each color, (ii) use preset filters in the drop-down box, and (iii) develop your own presets. The custom function offers more control over the tonal values of each color and is considered more suitable for evidence enhancement. The image must be in RGB mode to operate “Black & White” and it does not operate in grayscale or CMYK modes. As previously mentioned, working with 16 bit per channel images provides a distinctive advantage for this method due the more subtle changes possible between tonal adjustments. Figure 18 provides and example of how the “Black & White” adjustments function can enhance evidence by selective contrast variations of tones due to their original color. The blue ink of the stamp was lightened by moving the blue slider bar to the right to increase its brightness value. The red ink of the handwriting was darkened slightly by moving the red slider bar left or lowering the brightness value of the red color. The result is a remarkable difference in contrast difference between the blue and red inks and the blue stamp has almost disappeared. The signature can now be examined without the interference of the overlaying blue stamp. The Black & White function is also useful for removing colored backgrounds that interfere with developed fingermarks. Figure 19 is a ninhydrin
Figure 18 The handwriting on the bank check was written in red ink. The blue stamp has obliterated components of the signature and check amount. The Black & White adjustment has lightened the blue stamp and darkened the writing slightly to increase the contrast between the two inks (stamp and pen)
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(a)
(b)
Figure 19 (a) Color photograph of a ninhydrin developed fingermark; (b) The same fingermark with the blue lines and blue area of the document removed and the ninhydrin fingermark darkened
developed fingermark on a document with strong blue lines and blocked sections of blue. The blue lines and blue background were removed using the “Black & White” filter application and the magenta color of the ninhydrin print darkened to enhance the contrast between the fingermark and the background. This process takes approximately 20–30 s to complete once the image is loaded into Photoshop , making it a highly efficient method of evidence enhancement.
[6] [7] [8]
[9] [10] [11]
References [1]
[2] [3]
[4]
[5]
Porter, G. (2004). Specialised photography and imaging, in The Practice of Crime Scene Investigation, J. Horswell, ed, CRC Press, pp. 139–159. Porter, G. (2007). Visual culture in forensic science, Australian Journal of Forensic Sciences 39(2), 81–91. House of Lords, Select Committee on Science and Technology (1998). Digital Images as Evidence: Evidence, The Stationary Office, London. House of Lords, Select Committee on Science and Technology (1998). Digital Images as Evidence: Report, The Stationary Office, London. SMANZFL (2004). Australasian Guidelines for Digital Imaging Processes, Version 2, National Institute of Forensic Science.
[12] [13]
[14]
[15] [16] [17] [18]
Robinson, E.M. (2007). Crime Scene Photography, Academic Press. Langford, M. (1998). Advanced Photography, 6th Edition, Focal Press. Jacobson, R.E., Ray, S.F., Attridge, G.G. & Axford, N.R. (2000). The Manual of Photography: Photographic and Digital Imaging, 9th Edition, Focal Press. Taylor, J.T. (2005). The Optics of Photography and Photographic Lenses, Elibron Classics. Canon, E.F. (2003). Lens Works III: The Eyes of EOS, Canon. Ray, S.F. (1995). Applied Photographic Optics, 2nd Edition, Focal Press. Ray, S.F. (1992). The Photographic Lens, 2nd Edition, Focal Press. Reis, G. (2007). Photoshop CS3 for Forensic Professionals: A Complete Digital Imaging Course for Investigators, Sybex. Baron, C. (2007). Adobe Photoshop Forensics: Sleuths, Truths and Fauxtography, Thompson Course Technology. Fraser, B., Murphy, C. & Bunting, F. (2005). Real World Color Management, 2nd Edition, Peachpit Press. Malacara, D. (2001). Color Vision and Colorimetry: Theory and Applications, Spie Press. Overheim, R.D. & Wagner, D.L. (1982). Light and Color, John Wiley & Sons. Morton, R.A. (ed) (1984). Photography for the Scientist, Academic Press.
Poisons: Detection of Naturally Occurring Poisons [19] [20]
[21] [22] [23] [24]
[25] [26] [27]
[28] [29] [30]
[31]
[32] [33]
[34]
[35] [36] [37] [38]
[39]
Fraser, B. (2007). Real World Imaging Sharpening With Adobe Photoshop CS2, Peachpit Press. Champod, C., Lennard, C., Margot, P. & Stoilovic, M. (2004). Fingerprints and Other Ridge Skin Impressions, CRC Press. Lee, H.C. & Gaensslen, R.E. (eds) (1991). Advances in Fingerprint Technology, CRC Press. Saxby, G. (2002). The Science of Imaging: An Introduction, Institute of Physics Publishing. Mitchell, E.N. (1984). Photographic Science, Wiley & Sons. Langford, M., Fox, A. & Smith, R.S. (2007). Langford’s Basic Photography: The Guide for Serious Photographers, 8th Edition, Focal Press. Kodak (1990). Kodak Photographic Filters Handbook, Eastman Kodak Company. Kodak (1976). Using Photography to Preserve Evidence, Eastman Kodak Company, Pub. M-2. McKechnie, M.L., Porter, G. & Langlois, N. (2008). The detection of latent residue tattoo ink pigments in skin using invisible radiation photography, Australian Journal of Forensic Sciences 40(1), 65–72. Kodak (1980). Applied Infrared Photography, Eastman Kodak Company, Pub. M-28. Kodak (1968). Ultraviolet and Fluorescence Photography, Eastman Kodak Company, Pub. M-27. Vanderberg, N. & van Oorschot, R.A.G. (2006). The use of Polilight in the detection of seminal fluid, saliva and bloodstain and comparison with conventional chemical-based screening tests, Journal of Forensic Science 521(2), 361–370. Lennard, C. & Stoilovic, M. (2004). Application of forensic light sources at the crime scene, in The Practice of Crime Scene Investigation, J. Horswell, ed, CRC Press, pp. 97–123. Pountney, H. (1971). Police Photography, Elsevier Publishing. Stoilovic, M. (1991). Detection of semen and blood stains using polilight as a light source, Forensic Science International 51, 289–296. Lennard, C. (2007). Fingerprint detection: current capabilities, Australian Journal of Forensic Sciences 39(2), 55–71. Peres, M.R. (ed) (2007). The Focal Encyclopedia of Photography, 4th Edition, Focal Press. Ray, S.F. (1999). Scientific Photography and Applied Imaging, Focal Press. Weiss, S.L. (2009). Forensic Photography: The Importance of Accuracy, Pearson Prentice Hall. Hunter, F., Biver, S. & Fuqua, P. (2007). Light Science and Magic: An Introduction to Photographic Lighting, 3rd Edition, Focal Press. Russ, J.C. (2001). Forensic Uses of Digital Imaging, CRC Press.
GLENN PORTER
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Photography: Scene see Crime Scene Photography: US Perspective
Physical Injury see Aggression
Plants see Botany
Plethysmography see Sex Offenders: Treatment of
PMI see Human Remains and Identity
Poisons: Detection of Naturally Occurring Poisons Introduction A large number of plants produce compounds that may cause serious illness, injury, or even death. Some plants contain toxic compounds in all parts, whereas other plants are poisonous in some parts and edible in others. Examples include potatoes and tomatoes, which contain toxic alkaloids in the green parts of the plant, but these alkaloids are not present in the ripe potato tuber and tomato fruits. A comprehensive list of toxic plants is not possible because of the large number of poisonous substances. Although many plants contain toxic substances, only a few species cause poisonings in humans. The actual
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number of cases of plant poisoning is hard to determine. Even the numbers of fatal poisoning by plants is not always very obvious. Severe or even deadly poisonings with plants are relatively rare; the frequencies and the plants involved are regionally different. A published report of the Poison Information Centre in Chile showed that only 0.43% of the medical consultations from January 1998 to June 2000 were with respect to intoxications with plants or mushrooms [1]. Compared to Chile, the Poison Information Centre of northern Germany reported in 2005 that 12% of medical consultations were related to the use and misuse of plants or plant products. Most of these consultations were due to accidental ingestion of the plant material or the misuse of herbal drugs of abuse [2]. Severe and fatal poisonings by plant materials are very rare. The Poison Information Center, Mainz, Germany, has recorded 31 severe and fatal poisonings caused by plants from January 1995 to July 2007 [3]. The majority of these cases (55%) were caused by an abuse of plant material; only five cases (16%) were a suicide attempt. A total of 5 of the 31 severe poisonings were recorded as fatal. A study analyzing the self-poisoning fatalities in rural Sri Lanka from March 2002 to March 2003 has shown that 44 of 198 people died from ingestion of the plant oleander [4]. The higher number of plant poisonings in Sri Lanka compared with other countries may also reflect the availability of drugs or poisons used in suicide attempts. In Australia, the National Coroners Information Service (NCIS) recorded that 9 persons of 131 400 recorded deaths had died from plant or mushroom poisoning in the period between July 2000 and July 2007 [5]. In general, severe or fatal plant poisonings are not very common and are limited to a small number of poisonous plant species.
Manner of Poisoning with Plants Unintentional Ingestion of Plants and Plant Material Unintentional ingestion of plant material not only occurs in children, especially younger ones, but also in adults. It is obvious that the reason for accidental ingestion in different age groups is completely different. Whereas children discover their environment
by trying bits of plants that appear attractive to them, adults ingest them accidentally [6]. For children, the attractive parts of plants are mostly fruits and seeds with colorful seed coats. Examples include the fruits of deadly nightshade, which look similar to cherries, and the red seed coats of the yew. In the case of yew, the seed coats are very sweet and are not poisonous, but the seeds inside are very poisonous. Children can also be attracted by fruits that are similar to edible plants. A good example is the fruit of laburnum, which looks like peas or beans. For adults, the reason for an unintentional ingestion of plant material is usually a mix-up. Poisoning occurs as a result of ingestion of poisonous plant due to confusion. The affected persons are usually looking for alternative sources of food or self-medication with herbal drugs. A common example is the collection of meadow saffron instead of wild garlic. Also the mixup of mushrooms is very common. Many case reports have shown that the deadliest mushroom is the death cap, which looks similar to edible champignons [7]. Accidental ingestion of plant material is also possible by taking herbal medication that has been either incorrectly prepared or in which the wrong plant material has been used. A common problem is the use of aconitum in traditional Chinese medicine, which can be toxic when prepared incorrectly.
Intended Ingestion of Plant Material Besides unintentional ingestion of plant materials, plants have always been, and are still, used in homicides and suicide attempts. Historical records show that plant materials have caused the death of many famous personalities. An example is the death of Socrates, which was caused by the application of the plant hemlock [8]. But even today, poisonous plants are used from time to time in homicide cases. However, the suicidal ingestion of natural poisons is more common. In developed countries, drug- or poison-related suicide attempts are mostly in connection with prescriptive drugs. However, case reports describe the use of very poisonous plants like deadly nightshade, aconite, and yew in suicides. These patients are often well educated and know about the toxicity of the plants they use. As an example, one patient was growing aconite in his garden, harvested the root of the plant, and prepared an extract, which he ingested and injected. He had
Poisons: Detection of Naturally Occurring Poisons studied literature about the toxicity of this plant and had even shown the literature to an emergency physician [3]. In rural parts of developing countries, suicidal ingestion of plants is far more common due to a lack of availability of prescription drugs [4].
Ingestion of Plant Material Due to an Abuse The use of plants and plant material for psychoactive effects has been known and recorded for millenniums. The knowledge of the psychoactive effects and the toxic side effects were extensively observed by shamans and other users and has been passed down from generation to generation. In recent years, the use of herbal drugs for their psychoactive properties has become increasingly popular among illicit drug users. The reasons for this increase are diverse. Some of the herbal drugs are not scheduled, and are generally easily accessible, and are sometimes considered to be safe since they are natural. The assumption of less toxicity is simply not true. Plants often contain pharmacologically highly active compounds. In addition, using hallucinogenic poisonous plants carries the danger of an overdose. The amount of active ingredients in the plant is strongly dependent on geographical and climate conditions. A consumption of two leaves in spring might be hallucinogenic, whereas the consumption of two leaves in autumn may be fatal [6]. Overdoses due to an abuse of plant materials are often described for plants like deadly nightshade [9], datura [10], and kath [11]. Even a nonoverdose situation might cause dangerous behavior. It is well known that the anticholinergic syndrome triggered by atropine or scopolamine causes hallucinations and dry, hot skin. The drug users therefore try to cool down by jumping into water, risking a death by drowning. Hallucinations can also sometimes cause self-inflected injuries. The NCIS (Australia) recorded two cases of death due to self-induced stab wounds under the influence of magic mushrooms [5].
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Table 1 List of common names of poisonous plants and their associated botanical names Common English name Aconite Angel’s Trumpet Autumn crocus Belladonna Castor bean Castor oil plant Deadly nightshade Death cap Devine cactus Dwale European yew Golden chain tree Hemlock Jimson weed Kath Kava Laburnum Laurier rose Magic mushroom Meadow saffron Mescal button Miraa Monkshood Naked lady Oleander Peyote Poison hemlock Quat Thornapple Wolf’s Bane Yaqona Yew
Botanical name Aconitum napellus Datura stramonium Colchicum autumnale Atropa belladonna Ricinus communis Ricinus communis Atropa belladonna Amanita phalloides Lophophora wiliamsii Atropa belladonna Taxus baccata Laburnum anagyroides Conium maculatum Datura stramonium Catha edulis Piper methysticum Laburnum anagyroides Nerium oleander Psilocybe mexicana Colchicum autumnale Lophophora wiliamsii Catha edulis Aconitum napellus Colchicum autumnale Nerium oleander Lophophora wiliamsii Conium maculatum Catha edulis Datura stramonium Aconitum napellus Piper methysticum Taxus baccata
used. The scientific names have the advantage that only one name exists for each plant, whereas the commonly used names may not be unique and can be used for more than one plant. Table 1 translates the most commonly used English names of the plants into their scientific names. In the following sections, selected plants and fungi, which are often involved in plantrelated poisonings, are described in monographs. The monographs are listed in alphabetical order of the scientific names of the plants. Figure 1 provides representative photographs of some poisonous plants.
Description of Selected Plants and Fungi Aconitum Napellus In the following sections toxicologically important plants and some fungi are described in detail. To avoid confusion, scientific names of the plants are
The herbaceous perennial plant Aconitum napellus (Figure 1), known as aconite or monkshood, grows to
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Figure 1
Poisons: Detection of Naturally Occurring Poisons
Flower and leaves of Aconitum napellus
a height of 1 m, and is native to western and central Europe. The English name “monkshood” is derived from a part of the dark blue flower of A. napellus that has the shape of a cylindrical helmet. The toxicity of A. napellus is mentioned in Greek mythology, where it is described as the first poisonous plant. In fact, aconite is the most poisonous plant in central Europe due to its alkaloid-like aconitine. All species of the gender Aconitum are highly toxic and have been used for many centuries as arrow poison or common poison in homicides. Roots, leaves, flowers, and seeds are all exceedingly poisonous to man and livestock. The main active alkaloid in plants from the genus Aconitum is aconitine [6]. An accidental poisoning due to a mix-up with other nutrient plants is quite unlikely owing to the lack of similarity. Also, children are not attracted by the plant very often. However, aconite is a source of many fatal poisonings described in case reports [12]. The most common causes of a poisoning with plant material of the genus Aconitum are either a suicide attempt or an incorrect preparation of the plant in traditional Chinese medicine. Aconite is used in the traditional Chinese medicine [13], and can be freely purchased from herbal shops around the world. An incorrect preparation, or a wrong dosage of the plant material, may produce a fatal dose of the toxic alkaloid.
Amanita Phalloides Amanita phalloides is a deadly poisonous mushroom, commonly known as death cap. This mushroom
appears after periods of rain from late summer to the end of autumn. Death cap originates from Europe, but can be found worldwide. The fungal fruiting body of A. phalloides has a convex yellowish or greenish cap, usually 5–15 cm across. The stem is up to 20cm long. The flesh of the fruiting body is white. With similarities to champignons, parasol mushrooms, and paddy straw mushrooms, this fungus can be confused with other fungi. The toxicity of A. phalloides has been extensively studied since the largest number of deadly mushroom poisonings are caused by this species. All parts contain amatoxins and phallotoxins, and the toxin most responsible for the deadly effects is alpha-amanitin [14]. The peptide alpha-amanitin is a very stable compound and even prolonged cooking or maceration with salt does not decrease the toxicity. The toxin acts by inhibition of RNA polymerase II and therefore blocks protein synthesis. The lethal dose of amanitin is only 0.1 mg kg−1 , which means that a medium-sized mushroom can cause the death of a human. Death caps have been reported to have a pleasant taste, and a mix-up cannot be recognized by the taste. The symptoms of a poisoning with A. phalloides are initially gastrointestinal in nature. Colicky abdominal pain, vomiting, and watery diarrhea characteristically start approximately 8 h after ingestion. These symptoms resolve in a period of two or three days, giving the false sign of a remission. After a few days, a hepatic and renal failure causes symptoms like jaundice, delirium, seizures, and coma. Death occurs usually 6–16 days after ingestion of the mushroom. The treatment of a poisoning with death cap includes gastric lavage, activated charcoal, the correction of metabolic acidosis, and an intravenous antidote treatment with silibinin. Silibinin is extracted from blessed milk thistle (Silibum marianum) and is supposed to prevent the uptake of amatoxins into liver cells. In some cases, liver transplants have been necessary.
Atropa Belladonna The perennial plant Atropa belladonna (Figure 2) is commonly known as deadly nightshade. Other common names such as dwale, death’s herb, or witch berry give an impression of its toxicity and use in the middle age. The toxicity and pharmacological effects of the plant are part of the etymology of the botanical name. The genus Atropa is named after the goddess
Poisons: Detection of Naturally Occurring Poisons
Figure 2
Berry and leaves of Atropa belladonna
Atropos, who is known in Greek mythology to cut the life thread. The species name belladonna is Italian for beautiful lady and originates from its historical use of the berry juice by women to dilate their pupils [6]. All parts of A. belladonna contain toxic tropane alkaloids. Even though the root contains that highest alkaloid concentration, the most dangerous parts, in terms of accidental intoxication, are the berries because of their attractive look and sweet taste. Besides accidental ingestion, poisonings are reported after an abuse of A. belladonna due to the hallucinogenic properties of the tropane alkaloids. The main alkaloids present in A. belladonna are l-hyoscyamine and l-scopolamine. Even though only l-hyoscyamine is present in the plant, l-hyoscyamine is converted to a racemic mixture of 50% lhyoscyamine and d-hyoscyamine. This conversion is either as a result of extraction or release after ingestion. This racemic mixture is called atropine. Atropine acts pharmacologically via blocking acetylcholine receptors of the muscarine subtype. The blockage of these receptors causes symptoms like tachycardia, dilated pupils, decreased gastrointestinal motility, dry hot skin, and dry mouth due to a decreased sweat and saliva production. Apart from these peripheral effects, atropine also affects the central nervous system and causes agitation, disorientation, and hallucinations [15].
Catha Edulis The evergreen shrub Catha edulis, which is native to tropical East Africa and the Arabian Peninsula,
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is known as khat or qat. In these countries, the use of khat for therapeutic and recreational purpose has been an integral part of the local culture for centuries. In the second part of the twentieth century, the consumption changed to an uncontrolled abuse and spread throughout other continents. For example, more than 2300 kg of khat was confiscated at Frankfurt Airport (Germany) in 1998 [16]. This new aspect of khat consumption has raised increased concern in international organizations. In 1980, the World Health Organization classified khat as a drug of abuse that is able to produce dependence. The main psychoactive alkaloids of khat are cathinone and its metabolite cathine, also known as norpseudoephedrine. Cathinone was found to have a pharmacological profile closely resembling that of amphetamine. Cathinone acts as a central nervous system stimulant and shows sympathomimetic effects by releasing catecholamines from presynaptic storage sites. Experiments have shown that cathine acts like cathinone, but is less effective. Both substances are controlled substances in many countries due to khat abuse.
Colchicum Autumnale Colchicum autumnale is a perennial plant that grows from corms. The most common English names are autumn crocus, naked lady, and meadow saffron. These names represent the similarity of the flower to crocuses. However, this similarity is limited to the appearance of the flowers. In contrast to most other plants, the plant flowers in autumn, long after the leaves have died back, and therefore the English name naked lady. The fertilized fruits emerge from the ground with the new leaves appearing the following spring [6]. Colchicine is the main active alkaloid of Colchicum. It is present in all parts of the plant, but particularly in the corm, seeds, and flowers. Colchicine inhibits the function of microtubules and therefore acts as a cytotoxic. It also reduces the activity of leukocytes and lymphocytes. This mechanism of action is suspected to be the reason for its success in the treatment of gout. The plant has been used to treat gout for more than 2000 years. Although colchicine has many side effects, it is still recommended as a treatment for acute gout [17].
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Figure 4 Flower, leaves, and unripe fruit of Datura strammonium Figure 3 Habitus of Conium maculatum [Image by Thomas Schoepke – http://www.plant-pictures.com]
Conium Maculatum The 1.5–2-m tall biennial plant Conium maculatum (Figure 3) is known as hemlock or poison hemlock. The smooth green stem of hemlock is characteristically spotted with purple on the lower half. The leaves are finely divided and the white flowers are small and clustered in umbels. The plant is similar to fennel, parsley, or wild carrot. The root of hemlock, white and fleshy, is often unbranched and shows a similarity to parsnip. The toxicity of hemlock has been known in Greece since 399 BC, as the symptoms of the lethal poisoning of Socrates were described by his pupil Plato. In the middle ages, the medicinal use of hemlock was very limited due to its known high toxicity [8]. Conium maculatum is native to Europe but has been introduced and grows as a weed in Asia, North America, and Australia. All parts of the plant are poisonous. The highest concentrations of the toxic alkaloids are found in unripe seeds, but concentrations vary significantly depending on temperature, moisture, and the season. The main toxic alkaloids of hemlock are coniine and γ -coniceine. The exact mechanism of action of these toxic alkaloids is not known. The primary action is on the central nervous system with symptoms similar to nicotine poisoning. The most common symptoms of hemlock poisoning are problems in movement, dilation of pupils, slow and weak pulse, heavy salivation, and nausea. After a severe poisoning, coma and death from respiratory failure are possible [18].
Datura Stramonium The annual plant Datura stramonium (Figure 4), which is often found in nutrient-rich soils, grows to a height of up to 1 m. This plant of the nightshade family is commonly known as thornapple, Jimsonweed, or Angel’s Trumpet. The large flowers of Datura are white, erect, and tubular. The tubular shape and its psychoactivity are related to the name Angel’s Trumpet. The name thornapple is related to the fruits, which are spiky large green capsules containing numerous black seeds. The plant is distributed generally throughout temperate and subtropical regions. The Brugmansia species are similar to Datura in botanical appearance and are often cultivated in pots as house plants [6]. All parts of Datura and Brugmansia are toxic and contain tropane alkaloids. As already described for A. belladonna, the main alkaloids are l-hyoscyamine and l-scopolamine. Owing to the presence of these alkaloids, these plants are often abused for their hallucinogenic properties. This increasing misuse has forced a prohibition by law in Florida against planting Angel’s Trumpets. The symptoms of a poisoning as well as the treatment are similar to those described for A. belladonna.
Laburnum Anagyroides Laburnum anagyroides (Figure 5), also known as laburnum, grows as a shrub or a small tree. The plant has yellow flowers in pendulous racemes, and therefore it is known in German as “Goldregen”, which is often translated as golden rain acacia.
Poisons: Detection of Naturally Occurring Poisons
Figure 5 Flower of Laburnum anagyroides [Image by Thomas Schoepke – http://www.plant-pictures.com]
Because the plant is attractive and frost tolerant, laburnum is very popular as ornaments in parks and gardens. The fruits are silky hairy pods; the unripe pods are similar to bean or pea pods. The seeds are similar to small beans [6]. All parts of laburnum are toxic and contain quinolizidine alkaloids. The main toxic alkaloid is cytisine, with the highest concentration detected in the ripe seeds and seed pods. Knowing about the toxicity, laburnum has been used in traditional medicine by American Indians, who have consumed the seeds for their emetic effects during rites and magical practices. During the Second World War, the leaves of laburnum were used as a tobacco substitute due to its similar effects. Studies have also shown that cytisine is effective as an aid to smoking cessation [19]. Cytisine binds with a high affinity to nicotinergic acetylcholine receptors. Like nicotine, cytisine acts as a blocking agent on the central nervous system via an overstimulation of these receptors. Owing to the mechanism of action, the symptoms of a poisoning are similar to a nicotine overdose. The central-stimulating effects can cause delirium and convulsions [19]. Death is possible through a respiratory paralysis or failure of the circulatory system. The treatment of a poisoning with laburnum is symptom orientated, with no specific antidote available [6].
Lophophora Williamsii The small spineless cactus Lophophora williamsii is commonly known as peyote. This cactus grows
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extremely slowly and flowers sporadically. It takes in the wild up to 30 years to reach the size of a golf ball and to produce the first flowers. The small pink fruits of peyote are sweet tasting and delicate. The cactus is native to southern United States and Mexico, but is cultivated all over the world. A recent study has shown prehistoric use of peyote by native North Americans. A radiocarbon study dated dried cacti, so-called mescal buttons, to the time interval 3780–3660 BC. Because in these dated buttons psychotropic alkaloids were present, it was concluded that they were used for their psychoactive effects [20]. The main reason for the psychoactive effects of peyote is due to the presence of the phenethylamine alkaloid mescaline. The effects of peyote and mescaline in humans are well studied. Native peyote cults used the cactus because it produces rich visual hallucinations. These effects were also used in psychiatric studies as a chemically induced model of mental illness. The mechanism of action is similar to that of lysergic acid diethylamide (LSD) or psilocin. These substances act as partial agonists at 5-hydroxytryptamine (5-HT) receptors. Although the acute toxicity of peyote or mescaline is not as high as other herbal alkaloids, fatalities have been described. Owing to the strong hallucinations, fights among drug abusers or self-harm situations are not uncommon.
Nerium Oleander The evergreen shrub Nerium oleander (Figure 6), simply known as oleander is native to northern parts of Africa and the Mediterranean region. The scientific name is deduced from their preference to grow near water; Nero is the Greek word for water. The leaves of oleander are thick and leathery, dark green and narrow lanceolate, and up to 20-cm long. The leaves grow typically in pairs or whirls of three. The flowers of oleander are white, pink, or yellow, are up to 5 cm in diameter, and grow in clusters. Even though the flowers of N. oleander can be slightly yellow, the so-called yellow oleander is Thevetia peruviana. Both oleander and yellow oleander can easily be grown in warm subtropical regions and are extensively used in parks and roadsides worldwide [6]. Both plants are highly toxic and contain cardiac glycosides of the cardenolide type in all parts. The highest glycoside concentrations were detected in the
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Figure 6
Poisons: Detection of Naturally Occurring Poisons
Flower and leaves of Nerium oleander
seeds of oleander, and the main glycoside present in these plants is oleandrin. Oleandrin acts like other cardiac (cardiac) glycosides of the cardenolide type by inhibition of the sodium potassium exchange, which causes an increased calcium level in heart cells, which increases contractions of heart muscle cells. An overdose of the cardiac glycosides causes dysrhythmia and a possible heart block. The first scientific study showing the therapeutic usefulness of cardiac glycosides was published in 1785 by Withering [21]. The therapeutic range of the cardiac glycosides is narrow. Many fatal and severe poisonings have been reported after ingestion of oleander or other plants containing cardiac glycosides, such as Digitalis purpurea (foxglove), Adonis vernalis (pheasant’s eye), or Convallaria majalis (lily of the valley). The typical symptoms of an overdose with cardiac glycosides are dizziness and vomiting, followed by cardiac arrhythmias [6]. The treatment of an overdose is dependent on the severity of the poisoning. For treatment of severe poisonings, an antibody-based antidote has been developed to specifically remove the glycosides. In case of poisoning with plants or self-prepared extracts, this antidote is unfortunately poorly effective. The antidote removes therapeutically applied pure glycosides, but it is likely that some cardioactive glycosides are not removed [6].
Piper Methysticum The common English name for the western pacific plant Piper methysticum is kava. Other names for the plant are ‘awa’, used in Hawaii, or ‘yaqona’, common in Fiji. Kava is an evergreen bush growing up
to 3 min height, with heart-shaped leaves up to 20 cm in length. The plant is closely related to black pepper (Piper nigra) and also has a spicy taste. Kava is psychoactive, indicated by the scientific species name methysticum, which is Greek for intoxicating. Kava is consumed on many western pacific islands and Australia [6]. Traditionally Kava is prepared by grinding or chewing the rhizome, which is mixed with water or coconut milk. The effects after consumption of kava are talkative and euphoric behavior, anxiolytic effects, sense of well-being, clear thinking, and relaxed muscles. The plant contains a mix of kavalactones and kavapyrones. Extracts of the plant were introduced into modern medicine as a mild anxiolytic. After the report of some deaths due to its medicinal use, kava medicines were banned. Kava-containing medicine causes acute liver failure [22]. The traditional use of kava by Pacific Islanders and by some aboriginal communities is not believed to be associated with liver damage. A recent study has shown that kava feeding in rats does not cause liver damage [23]. Further investigations are necessary to demonstrate the long-term safety of kava preparations.
Psilocybe Species The small brown mushroom genus Psilocybe sp is best known for their psychoactive properties and are therefore called “magic mushrooms”. The fruiting bodies of the magic mushrooms are small to medium in size and typically show a brown coloration. Hallucinogenic species of Psilocybe can be found in temperate regions throughout the world [24]. The psychoactive species contain as active ingredients psilocin and psilocybin. These compounds are structurally related to serotonin, a neurotransmitter in the central nervous system. Psilocin and psilocybin cause effects like the synthetic drug of abuse LSD. The effects of intoxication with magic mushrooms are mainly hallucination; the acute toxicity of the compounds is low. However, the consumption of these compounds is dangerous. Severe hallucinations can cause self-inflected injuries. Deaths due to selfinduced stabbings following consumption of magic mushrooms have been recorded [5]. Two patients died from the wounds after they had stabbed themselves in the chest while under the influence of magic mushrooms.
Poisons: Detection of Naturally Occurring Poisons
Figure 7
Leaves of Ricinus communis
Figure 8
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Fruit and leaves of Taxus baccata
Ricinus Communis
Taxus Baccata
Ricinus communis (Figure 7), the castor oil plant, is cultivated all over the globe for oil production. The annual bushy shrub is believed to have its origin in tropical Africa, but grows nowadays worldwide. The plant with glossy palmately divided leaves is often used for ornamental purposes in gardens. The fruit of R. communis is a soft, spiny capsule with three almost oval seeds, which are the so-called castor beans. The attractive seeds have a hazelnut-like taste and contain 45–55% of fatty oil. The seeds also contain up to 25% protein. The protein fraction contains the highly toxic lectin ricin, which is poisonous via ingestion, inhalation, or injection. Ricin acts via an inhibition of protein synthesis. As a lectin, it binds to glycoproteins, facilitating the entry of the toxin into the cytosol [25]. After ingestion of ricin, the symptoms are nausea and diarrhea. In severe poisonings, liver and renal dysfunction, and possibly death, occurs. After inhalation, coughing and dyspnea can occur. These symptoms can progress to respiratory distress and death. The injection of ricin causes symptoms of general weakness and myalgias. Death is possible due to hypotension and multiorgan failure. Ricin poisoning is possible by accidental or suicidal eating of the seeds. After oral ingestion of the seeds, the toxicity depends on how well the seeds are chewed. Some factors make the castor beans dangerous, such as their attractive appearance and the stability of ricin toward proteolytic enzymes. The treatment of a poisoning with ricin is recommended to be symptomatic. No specific antidote for ricin poisoning is available [25].
The conifer Taxus baccata (Figure 8) is widely known as yew, and is often considered to be the oldest plant in Europe. The age of some yew trees is estimated to be 5000 years. The plant is a small to medium-sized tree, which grows relatively slowly. The leaves of this conifer are dark green and lanceolate, with a length of up to 4 cm. The plant has very characteristic single seed cones surrounded by a bright red colored berrylike structure, called an aril. All parts of the plant are highly toxic, except the arils. This enables the cones (including the arils) to be eaten by birds, but the seeds remain undamaged in the bird’s droppings. The plant contains pseudoalkaloids of the taxane type. The main compound responsible for the toxicity of the European yew (T. baccata) is taxine B [6]. Some taxane-type pseudoalkaloids are also important in the treatment of cancer. In recent years, Taxol , which contains paclitaxel, has become of particular interest in the treatment of ovarian, breast, and non-small-cell lung cancer. Paclitaxel has been isolated from the Pacific yew, Taxus brevifolia. Because of the extensive use of Taxol and the fact that more than 1000 trees are needed to obtain 1 kg of paclitaxel, pharmaceutical companies have found an alternative source of the drug. A precursor of paclitaxel is isolated from cultivated European yew plants, and paclitaxel is synthesized using this precursor. The mechanism of action of taxanes is an inhibition of cell division by stabilization of the microtubuli. Therefore, these substances have cytotoxic effects. In the case of an overdose with yew plants, the symptoms are nausea, dizziness, abdominal pain,
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shallow breathing, and tachycardia. Death can occur as a result of respiratory paralysis, with the heart in diastolic arrest. The treatment of a poisoning with yew is symptomatic, with no specific antidote available [6].
Analytical Methods Because of the diversity of the toxic compounds in plants and mushrooms, a general laboratory screening procedure is not possible. Therefore, various specific methods for detection have been developed. Table 2 summarizes the major active compounds and the most
Table 2 List of botanical names, the corresponding main toxic compounds, and the common detection of these compounds in biological fluids
Scientific name Aconitum napellus Amanita phalloides Atropa belladonna Catha edulis Colchicum autumnale Conium maculatum Datura stramonium Laburnum anagyroides Lophophora wiliamsii Nerium oleander Piper methysticum Psilocybe mexicana Ricinus communis Taxus baccata
Main toxic compound(s)
Common detection in biological fluids
Aconitine
HPLC, LC-MS
Amanitine
Immunoassay, LC-MS GC-MS, LC-MS
Hyoscyamine, scopolamine Cathinone Colchicine
GC-MS, LC-MS HPLC, LC-MS
Coniine
GC-MS, LC-MS
Hyoscyamine, scopolamine Cytisine
GC-MS, LC-MS
Mescaline
GC-MS, LC-MS
Oleandrine
Immunoassay, LC-MS HPLC
Kavaine
LC-MS
Psilocin, psilocybin Ricin
GC-MS
Taxine B
LC-MS
Immunoassay
common detection methods of the plants described in this article. Methods for detection of naturally occurring toxic compounds include high-performance liquid chromatography (HPLC), liquid chromatography mass spectrometry (LC-MS), gas chromatography mass spectrometry (GC-MS), and various immunoassay techniques. The use of HPLC is common for detection of compounds like aconitine, colchicines, and the ingredients of kava. Kavalactones and kavapyrones are commonly used for the detection of aconitine and colchicine. The modern and more sensitive LCMS techniques have been applied to many naturally occurring substances, especially if low concentrations have to be detected. The use of GC-MS techniques is applicable if the substances are thermostable and provides a powerful tool for detection of alkaloids like atropine, cathinone, and mescaline. While GCMS techniques are useful, LC-MS techniques are preferred for the detection of low concentrations in blood. The use of immunoassay techniques is possible for some poisonous compounds of herbal origin. It has been shown that the cardiac glycosides of oleander can be detected using an immunoassay technique for cardiac glycosides. This technique is not able to differentiate between the cardiac glycosides. A differentiation is possible using HPLC techniques. Also the detection of ricin is commonly performed using immunoassay techniques, such as radioimmunoassay (RIA) and enzyme-linked immunosorbent assay (ELISA). Owing to the physicochemical properties of the protein ricin, chromatographic techniques are more challenging and cannot at the present time be easily confirmed by conventional chromatographic techniques due to its large molecular size. Detection methods using immunoassay techniques were also developed for the proof of death cap poisoning. Amanitin can be detected in urine up to 24 h after ingestion by the use of immunoassay techniques. A postmortem detection of the toxic substances is often challenging. Determination of these is often likely in urine, but for some compounds like colchicine bile is the most useful specimen for postmortem analysis. Some toxins like amanitin are unlikely to be detected in postmortem specimen because death occurs many days after ingestion.
Poisons: Detection of Naturally Occurring Poisons Some substances like psilocin and psilocybin are chemically unstable; hence concentrations need to be interpreted carefully. See Toxicology: Initial Testing for further information on general drug detection techniques.
[9]
[10]
Summary and Conclusions Fatal plant and mushroom poisonings are relatively rare. The diversity of poisonous compounds and their widespread occurrence in plants and fungi makes a comprehensive list of dangerous flora impossible. Besides, the majority of fatal cases are limited to a small number of plants and mushrooms. These poisonings can occur either after unintentional or intended ingestion or after abuse for their hallucinogenic effects. While plants and fungi can be dangerous to humans, fatal cases are avoidable. However, the analytical detection of a poisoning from an unknown plant or fungus can be a challenge for toxicologists.
[11]
[12]
[13]
[14]
[15]
[16]
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Manriquez, O., Varas, J., Rios, J.C., Concha, F. & Paris, E. (2002). Analysis of 156 cases of plant intoxication received in the Toxicologic Information Center at Catholic University of Chile, Veterinary and Human Toxicology 44(1), 31–32. Poison Information Centre Goettingen (2005). Harmonized Annual Report 2005 . Ritter-Weilemann, I. (1995–2007). Annual Reports, Poison Information Centre, Mainz. Eddleston, M., Gunnell, D., Karunaratne, A., de Silva, D., Sheriff, M.H. & Buckley, N.A. (2005). Epidemiology of intentional self-poisoning in rural Sri Lanka, The British Journal of Psychiatry 187, 583–584. Australian National Coroners Information System (NCIS), search conducted in July 2007. www.ncis. org.au. Frohne, D. (2005). Poisonous Plants: A Handbook for Doctors, Pharmacists, Toxicologists, Biologists and Veterinarians/Dietrich Frohne and Hans Jrgen Pfnder, 2nd Edition, Manson Publishing, London. Trim, G.M., Lepp, H., Hall, M.J., McKeown, R.V., McCaughan, G.W., Duggin, G.G. & Le Couteur, D.G. (1999). Poisoning by Amanita phalloides (“deathcap”) mushrooms in the Australian Capital Territory, The Medical Journal of Australia 171(5), 247–249. Daugherty, C.G. (1995). The death of Socrates and the toxicology of hemlock, Journal of Medical Biography 3(3), 178–182.
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Jaspersen-Schib, R., Theus, L., Guirguis-Oeschger, M., Gossweiler, B. & Meier-Abt, P.J. (1996). Serious plant poisonings in Switzerland 1966–1994. Case analysis from the Swiss Toxicology Information Center, Schweizerische Medizinische Wochenschrift 126(25), 1085–1098. Boumba, V.A., Mitselou, A. & Vougiouklakis, T. (2004). Fatal poisoning from ingestion of Datura stramonium seeds, Veterinary and Human Toxicology 46(2), 81–82. Giannini, A.J. & Castellani, S. (1982). A manic-like psychosis due to khat (Catha edulis Forsk.), Journal of Toxicology. Clinical Toxicology 19(5), 455–459. Elliott, S.P. (2002). A case of fatal poisoning with the aconite plant: quantitative analysis in biological fluid, Science and Justice 42(2), 111–115. Chan, T.Y., Chan, J.C., Tomlinson, B. & Critchley, J.A. (1993). Chinese herbal medicines revisited: a Hong Kong perspective, Lancet 342(8886–8887), 1532–1534. Wieland, T. (1967). The toxic peptides of Amanita phalloides, Fortschritte der Chemie Organischer Naturstoffe 25, 214–250. Rang, H.P. (1987). Pharmacology, 2nd Edition, H.P. Rang & M.M. Dale, eds, Churchill Livingstone, Edinburgh, pp. 547–567. Toennes, S.W., Harder, S., Schramm, M., Niess, C. & Kauert, G.F. (2003). Pharmacokinetics of cathinone, cathine and norephedrine after the chewing of khat leaves, British Journal of Clinical Pharmacology 56(1), 125–130. (2006). Gout: finally, diagnosis and treatment guidelines. A European task force offers the first recommendations on dealing with this painful arthritic condition, Health News, 12(10), 10–11. Drummer, O.H., Roberts, A.N., Bedford, P.J., Crump, K.L. & Phelan, M.H. (1995). Three deaths from hemlock poisoning, The Medical Journal of Australia 162(11), 592–593. Tutka, P. & Zatonski, W. (2006). Cytisine for the treatment of nicotine addiction: from a molecule to therapeutic efficacy, Pharmacological Reports 58(6), 777–798. El-Seedi, H.R., De Smet, P.A., Beck, O., Possnert, G. & Bruhn, J.G. (2005). Prehistoric peyote use: alkaloid analysis and radiocarbon dating of archaeological specimens of Lophophora from Texas, Journal of Ethnopharmacology 101(1–3), 238–242. Wade, O.L. (1986). Digoxin 1785–1985. I. Two hundred years of digitalis, Journal of Clinical and Hospital Pharmacy 11(1), 3–9. (2002). Kava kava may cause irreversible liver damage, South African Medical Journal 92(12), 961. DiSilvestro, R.A., Zhang, W. & DiSilvestro, D.J. (2007). Kava feeding in rats does not cause liver injury nor enhance galactosamine-induced hepatitis, Food and Chemical Toxicology 45(7), 1293–1300. Musshoff, F., Madea, B. & Beike, J. (2000). Hallucinogenic mushrooms on the German market – simple
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Police Use of Force
instructions for examination and identification, Forensic Science International 113(1–3), 389–395. Audi, J., Belson, M., Patel, M., Schier, J. & Osterloh, J. (2005). Ricin poisoning: a comprehensive review, Journal of the American Medical Association 294(18), 2342–2351.
JOCHEN BEYER
Poisons: Natural see Poisons: Detection of Naturally Occurring Poisons Police Interviews and Interrogations see Confessions: Evidentiary Reliability of
Police Use of Force Traditionally, the hallmarks of policing involve officers responding to criminal and noncriminal calls for police service, detecting and preventing criminal activity, investigating past crimes, and enforcing laws. To carry out these activities, the police have institutional authority to use force. Such authority, power, or legal right comes from rules of law, which recognize that the police must sometimes use coercive action against law-violating citizens to accomplish legal objectives. Because police agency records and published statistics such as the annual figures reported by the Bureau of Justice Statistics consistently show that some citizens are willing to violate the law, use of force by the police remains a central part of their occupation (see also Policing and Critical Incident Teams). When the police use force, they have the discretionary power to choose from a range of possible responses available in a given law enforcement activity. Responses can include the police using their presence or show of authority to using deadly force to deal with law-breaking behaviors by citizens. Whenever the police invoke their legal right to use force
against citizens, there are court decisions regarding legal standards for making the right force choice. Courts in the United States, where the use of force by police is subject to constitutional restraints, generally apply three major legal decisions that clarify standards surrounding the appropriateness of police use of force: West v. Atkins [1], Graham v. Connor [2], and Tennessee v. Garner [3]. Under the umbrella of West v. Atkins, the police must act under color of law to be liable for use-of-force actions against citizens that amount to violations of police authority. The police must make objectively reasonable use-of-force choices under the Graham rules, which include a balancing test, subjective, objective, hindsight, and totality of circumstances tests. If the police decide to use deadly force against law-violators, then the Garner rules highlight three conditions in which deadly force may be reasonable: deadly force is necessary, suspects are dangerous, and the police are able to warn suspects.
Standards Governing Acting Under Color of Law Before courts consider allegations that the police used wrongful or excessive force against citizens, they make legal determinations on whether the police were acting in their official capacity; that is, whether the police used force while “acting under color of law” whereby they exercised a power or right granted by law [1]. Generally, the use of force by the police against law-violating citizens is a law enforcement activity normally carried out under color of law. Not all uses of force by the police, however, amount to acts under color of law. The question of official conduct is not always clear especially during off-duty hours, during acts of self-defense that happen in personal circumstances [4], or during acts of force that occur in secondary employment settings such as security venues. When making color of law determinations in these situations, courts weigh heavily the nature of the officer’s behavior [5]. They have considered behaviors such as flashing of a badge [6], wearing a police uniform [7], identifying themselves as police officers [4], driving a marked police vehicle [6], or brandishing a department issued weapon [8], in concert with force as acts under color of law. Courts may also consider off-duty police acts within their jurisdiction and on which they file
Police Use of Force official police reports as behaviors that constitute acting under color of law [9]. Although sometimes the question of official conduct is ambiguous, courts have employed a threeprong test in color of law determinations: public function test, state compulsion test, and nexus test [10, 11]. For example, under the public function test, the court would consider whether an officer’s use of force was a state action normally reserved for the police and usually performed by them during their official duties, or a personal action [12]. Making investigatory stops, arrests, or performing searches are uses of force that the police usually carry out under color of law [8, 13]. Under the state compulsion test, the court would determine whether the state or government compelled the officer to use force to enforce a government interest such as arresting a citizen who commits a crime of domestic violence. The central question is whether the use of force was an action required by law or police department policy [7]. Finally, the nexus test would involve the court’s consideration of whether the officer’s use of force involved conduct closely linked to or associated with the state [14]. For example, the action of an off-duty officer who grabs and arrests a citizen who commits a larceny may constitute state action because there is a sufficiently close nexus between the officer’s conduct and the state’s regulation of arrest powers. While courts have employed the police function, state compulsion, and nexus tests in making legal decisions about police uses of force that fall under color of law, they have not used them in a formulaic fashion. Instead, they have considered the totality of circumstances surrounding each particular use of force case when employing them. To hold the police liable for wrongful uses of force that amount to constitutional violations, courts must first find whether they were clothed with official authority.
Standards Governing Objective Reasonableness Whenever the police use force while acting under color of law, they must ensure that their use-offorce tactics do not violate the constitutional rights of citizens. Police uses of force against free citizens mostly occur in the course of an arrest, investigatory stop, or other seizure. The Fourth Amendment and its “reasonableness” standard is the precise
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constitutional right that provides free citizens protection against unreasonable seizures or excessive force by the police. In Graham v. Connor [2], the court established five substantive tests for judging the reasonableness of police use of deadly or nondeadly force against citizens: balancing test, subjective test, objective test, hindsight test, and totality of circumstances test. Using the balancing test, courts weigh the rights of free citizens under the Fourth Amendment against the interests of the government to take action against them. For example, an officer has a legal interest to stop or seize a motorist who travels through a stop sign without stopping. Yet, the motorist has a right to travel freely along the highway without police interference if the officer cannot substantiate a legal interest to carry out the traffic stop. Where the police establish a legal interest to take action against citizens, the Fourth Amendment recognizes that the interest carries with it the need to use some degree of physical coercion or threat [15]. Built into the application of the balancing test is a principle of proportionality: Is the officer’s act of force in the correct relationship to the citizen’s violation of law? For example, a suspect disobeys an officer’s verbal commands during an arrest. This form of behavior is less severe than is the suspect shooting at the officer. Both suspect behaviors require some degree of force by the officer to handle them and complete the arrest, but at obviously different levels. Therefore, courts balance the amount of force the police use against the amount of force they need to use in a particular situation [16]. When employing the objective test, courts consider whether another well-trained officer under the same set of circumstances would observe and conclude that the use of force by the police was reasonable. It requires a retrospective investigation and opinion by the well-trained officer (or expert) who has special knowledge of issues surrounding police use of force. Both carrying out the investigation and giving an opinion involve seeing through the lens of the officer on scene: what the officer’s observations were; what the officer’s observations meant; what the officer’s experience and situational knowledge were; and what the officer’s realty was. The expert weighs heavily the citizen’s behavior because it has a large degree of power in influencing the officer’s choice of force [17]. In the light of the particular circumstances, the expert conveys to the court whether he or she
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believes that the officer’s choice of force was within the range of objectively reasonable options available because there is no precise formula for determining a single or best force option. Under Graham, the subjective test discounts the personal motivations of the police because they have no value in the court’s application of the Fourth Amendment’s reasonableness standard. For example, an officer’s evil intentions do not raise a Fourth Amendment claim of excessive force when his or her use of force was objectively reasonable. Alternatively, the officer’s good intentions do not make an objectively unreasonable use of force constitutional. Using the hindsight test, courts would not consider every grab or push by the police even if they later seem unnecessary as violations of the Fourth Amendment’s protection against unreasonable seizures. Courts make allowances for errors by the police who must at times make split-second decisions about using force in situations that are tense and uncertain, and that evolve rapidly. What gives rise to constitutional violations are more than police acts that amount to mere mistakes. For example, having probable cause to arrest a person but arresting the wrong person, or having a warrant to search a house but carrying it out at the wrong house would not in every case violate the Fourth Amendment’s reasonableness standard. The hindsight test takes into account police mistakes and uses the at-the-moment perception of another well-trained officer on scene as the basis for a reasonableness inquiry and not the after-the-fact perception of others. The last Graham test – totality of circumstances – involves evaluating the circumstances of a use of force event. Because the Fourth Amendment’s reasonableness standard is not capable of an exact definition, its application requires attention to the totality of circumstances. The central question is whether the totality of circumstances justifies a particular use of force by the police. Circumstances that the police know before and when they use force are relevant in courts’ determinations of reasonableness [18]. In Graham, the court suggests careful attention to the severity of the crime; whether the suspect poses an immediate threat to the police or others nearby, the suspect attempts to escape police custody, or the suspect fights against arrest. On the face of these circumstances, deciding to use deadly force to shoot a suspect of a felony crime who resists the police and attempts to escape arrest might seem permissible.
The calculus of reasonableness in deadly force cases, however, requires some attention to the Garner [3] rules because Graham v. Connor is a nondeadly force case.
Standards Governing Deadly Force The only US Supreme Court decision that deals directly with the use of deadly force by the police is Tennessee v. Garner [3]. Under the Garner rules, police may use weapons or other use-of-force tactics that amount to deadly force to prevent the escape and make the arrest of fleeing felons under three conditions. First, the police have probable cause to believe that a suspect poses a threat of significant physical harm to them or others: the danger condition. The immediacy of the threat and the dangerousness of it are the cornerstones of this condition. The dangerousness element suggests that suspects who threaten the police or others with weapons “or” suspects who commit crimes where they cause or threaten to cause significant physical harm are dangerous because of their violent or potential violent behavior. Under Garner, the “or” aspect of dangerousness suggests that the possession of a weapon or the threat to use one is not necessary to satisfy dangerousness. Courts, however, have considered suspects armed with guns, knives, or flashlights, and suspects who have used a vehicle as a weapon against an officer or have attempted to seize an officer’s weapon as dangerous [19–24]. They have recognized murder, bank robbery, and armed robbery as felony crimes that demonstrate dangerous behaviors that justify the use of deadly force [25–27]. The immediacy element of a suspect’s physical threat to the police or others suggests that the period during which the threat occurs and the threat actually happens is important. Unfortunately, not all courts measure this period the same. Some may apply an “imminent” yardstick whereby significant physical harm is about to happen such as a suspect pointing a handgun at an officer [28]. Others may use more than a yardstick whereby they consider the “unpredictability” of a dangerous suspect, which is not easily foreseeable and measurable [29]. Nevertheless, courts carefully examine the totality of circumstances in all cases when making determinations about immediacy. Second, the police may only use deadly force against a dangerous suspect when necessary: the
Policing and Critical Incident Teams necessary condition. Unless the suspect satisfies the danger condition, deadly force is unnecessary. What is necessary or needed, however, may invite hindsight arguments. For example, in Plakas v. Drinski [30], Plakas ran at an officer and tried to use a fireplace poker to kill him. The officer shot and killed Plakas. In this case, the plaintiff argued that the officer had nondeadly force options available and that the officer did not try them. The officer could have used a spray or a police dog to disarm Plakas; deadly force was unnecessary. At both the district and federal court levels, the courts ruled in this case that the officer’s force was reasonable. The Fourth Amendment’s reasonableness standard does not require police to use less intrusive uses of force. Federal courts have rejected necessary arguments that the police could have used nondeadly force options when deadly force ones were reasonable [31]. Third, the police must warn – where feasible – a suspect of their intention to use deadly force: the warning condition. Unless the suspect satisfies the danger condition, both a warning and deadly force are unnecessary. The use of deadly force may also be unnecessary if a dangerous suspect submits to an arrest after a warning. Whether the police make decisions to use deadly or nondeadly force options to seize free citizens, their choices must fall within the range of objectively reasonable options available in particular situations. The Fourth Amendment’s reasonableness standard is the appropriate test in claims that the police used excessive force in the course of an arrest, an investigatory stop, or other seizures. However, not every police abuse of force occurs under these conditions. An officer who uses excessive force against a prisoner would violate either the Fourteenth Amendment’s due process clause or the Eighth Amendment’s prohibition against cruel and unusual punishment. It is important then to identify the specific constitutional right that is the precise textual source of an officer’s use-of-force conduct [2].
[6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17]
[18] [19] [20] [21] [22] [23] [24] [25] [26] [27] [28] [29] [30] [31]
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Neuens v. City of Columbus, 303 F.3d 667 (6th Cir., 2002). Roe v. Humke, 128 F.3d 1213, 1216 (8th Cir., 1997). Abraham v. Raso, 183 F.3d 279, 287 (3d Cir., 1999). Kappeler, V.E. (2006). Critical Issues in Police Civil Liability, Waveland Press, Illinois. Ellison v. Garbarino, 48 F.3d 192, 195 (6th Cir., 1995). Wolotsky v. Huhn, 960 F.2d 1331 (6th Cir., 1992). Bonsignore v. City of New York, 683 F.2d (2nd Cir., 1982). Pickrel v. City of Springfield, 45 F.3d 1115 (7th Cir., 1995). Cooper v. Parrish, 203 F.3d 937, 952 (6th Cir., 2000). Terry v. Ohio, 392 U.S. 1 (1968). Flores v. City of Palacios, 381 F.3d 391 (5th Cir., 2004). Adams, K. (1999). What we know about police use of force, in Use of Force by Police: Overview of National and Local Data, J. Travis, J.M. Chaiken & R.J. Kaminski, eds, U.S. Department of Justice, National Institute of Justice and Bureau of Justice Statistics, Washington, DC. pp. 1–14. Palmquist v. Selvik, 111 F.3d 1332 (7th Cir., 1997). Butler v. City of Detroit, 386 N.W.2d 645 (Mich. App. 1985). Ealy v. City of Detroit, 375 N.W.2d 435 (Mich. App. 1985). Haineze v. Allison, 216 F.3d 1081 (5th Cir., 2000). Nelson v. County of Wright, 162 F.3d 986 (5th Cir., 1988). Pittman v. Nelms I.I.I., 87 F.3d 116 (4th Cir., 1996). Rhiner v. City of Clive, 373 N.W.2d 466 (Iowa, 1985). Ford v. Childress, 650 F.Supp. 110 (D.C. Ill. 1986). Ryder v. City of Topeka, 814 F.2d 1412 (10th Cir., 1987). Trejo v. Wattles, 654 F.Supp. 1143 (D. Colo. 1987). Boyd v. Baeppler, 215 F.3d 594 (6th Cir., 2000). Hegarty v. Somerset County, 53 F.3d 1367 (1st Cir., 1995). Plakas v. Drinski, 19 F.3d 1143 (7th Cir., 1994). Scott v. Henrich, 39 F.3d 912 (9th Cir., 1994).
FRANK J. GALLO
Policing and Critical Incident Teams
References [1] [2] [3] [4] [5]
West v. Atkins, 487 U.S. 42 (1988). Graham v. Connor, 490 U.S. 386 (1989). Tennessee v. Garner, 471 U.S. 1 (1985). Huffman v. County of Los Angeles, 147 F.3d 1054, 1058 (9th Cir., 1998). Stengel v. Belcher, 522 F.2d 438, 441 (6th Cir., 1975).
Police calls for service occasionally require the police to resolve high-threat or special-threat situations such as barricaded suspects, hostage situations, drug raids, or warrant services. Although infrequent, these events are significantly different from usual police work that is often less dangerous: They require some degree of
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special handling. In US law enforcement circles, such special teams have become known by the acronym SWAT, which stands for special weapons and tactics. In other countries, such special teams may be designated by other terms. Since the 1965 Watts riots in Los Angeles, California, the need for SWAT teams (at times called police paramilitary units, critical incident teams, special response teams, and other names in the police literature) to deal with special-threat situations that regular officers are traditionally unprepared to handle has become popular among American law enforcement agencies [1]. Police departments of all sizes have working SWAT teams and some are developing them [2, 3]. They most often employ, when available, their SWAT teams to deal with rare high-threat police call outs. Officers who are SWAT members receive special training to work as a team and to use special weapons and force tactics to handle the most dangerous call outs. Because their behaviors involve special uses of force, there are some common risks related to the legal process. The adequacy of a SWAT team and its training in particular uses of special weaponry, technology, and tactics to confront the most dangerous situations may give rise to a legal action when the team fails to train in the proper use of issued equipment and use of force tactics. When a SWAT team uses force, its choices must be “objectively reasonable.” In cases of alleged use of excessive force, criminal and civil liability can attach itself in the form of a team’s wrongful actions under Titles 18 and 42 of the US Code respectively. There are legal risks surrounding the intervention of a SWAT team to control and overcome hostage takers where the main concern is the protection of human life and the avoidance of hostage and bystander injuries.
Adequate Training Police departments that have SWAT teams often call upon them to resolve the most dangerous police–citizen contacts. SWAT teams commonly carry out high-threat warrant services where the police believe that suspects are armed and dangerous. They execute high-threat narcotics search warrants where drug dealers seem likely to defend their drugs and homes using weapons. Sometimes, SWAT team interventions require team members to confront, disarm, and arrest suspects who hold citizen prisoners.
To assist SWAT teams in handling and controlling extreme police callouts, police departments employ their SWAT team members with special weaponry that are not available to regular officers. For example, some police agencies issue high-powered rifles, automatic firearms, diversionary devices, ballistic shields, and chemical munitions [4]. They authorize their SWAT teams to carry out tactical operations that involve the use of special tactics such as warrant, warrantless, or “no-knock” forced building entries. Because police departments arm their SWAT teams with special weapons and tactics to help them to enforce laws and make arrests, they need to train them on their appropriate uses. A failure to train may amount to a “conscious choice” or “deliberate indifference” to the constitutional rights of citizens to be free from unreasonable uses by SWAT teams [5]. Without training, SWAT teams are likely to make mistakes when deploying SWAT such as using diversionary devices to help them to carry out no-knock warrants. It is not reasonable to expect common officers to know the right force option without training [6]. SWAT teams must receive training in specialized tasks they are likely to perform on-the-job [5]. A failure to train them might give rise to a federal cause of action. Community stakeholders could consider police agencies to be deliberately indifferent to the needs of SWAT teams to receive specialized training. In resolving the responsibility to train, police departments must focus on the adequacy of its training programs to meet the plausible conditions under which its SWAT teams works [5]. Courts suggest that training require officers to make judgments on the use of varying degrees of force [7] and present officers with situations that reflect real-life work conditions [8]. Knowing the prevalence of SWAT team call outs and the unique facts surrounding them can be the basis for making informed training decisions. Use of expert witnesses on the proper application of guidelines enacted by a department often provides the crucial factual information to courts when litigation ensues.
Reasonable and Excessive Force Free citizens raise a Fourth Amendment claim when they allege that a SWAT team used excessive force against them in a law enforcement capacity (see also Police Use of Force). The Fourth Amendment prohibits unreasonable searches and seizures. It protects
Policing and Critical Incident Teams free citizens from the police using excessive force against them. There is no prevailing definition of what is excessive force. The Supreme Court, however, imposed an “objective reasonableness” standard for reviewing claims of excessive force by the police [9]. In such cases and under the Graham rules [9], the trier (or judge) or triers (or jury) of facts must first weigh the rights of free citizens under the Fourth Amendment against the interests of the government to take action against them (or balancing test). The Fourth Amendment recognizes that the right to take action against free citizens is associated with the need to use some degree of physical coercion or threat [10]. Second, consider whether a well-trained officer under the same set of circumstances would observe and conclude that the actions by the police were reasonable (or objective test). Third, discount the subjective motivations of the police because they have no value in a court’s appraisal of excessive force (or subjective test). Evil intentions do not raise Fourth Amendment claims when force options were objectively reasonable. Good intentions do not make objectively unreasonable force options constitutional. Fourth, evaluate the circumstances of the police call out. That is, what is the severity of the crime, does the suspect pose an immediate threat to the police or others nearby, and is the person actively resisting or fleeing arrest (or totality of circumstances test). Because the “objective reasonableness” standard is not capable of providing an exact definition, its application requires attention to the totality of circumstances. Only circumstances known to the police before and at the time they use force are relevant [11]. The central question is whether the totality of circumstances justifies a particular use of force by the police. Fifth, recognize that not every push or shove by the police even if it later seems unnecessary violates the Fourth Amendment (or hindsight test). The standard of “objective reasonableness” makes allowances for errors made by the police who must at times make split-second decisions about force in situations that are tense and uncertain, and that evolve rapidly [12]. Finally, examine carefully at whether the severity of force by the police puts suspects at risk of death “or” serious bodily harm (or deadly force test). Under the Garner rules [13], police may deploy weapons or use tactics that amount to deadly force in three conditions. First, if deadly force is necessary to
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prevent escape (or necessary condition). Second, if the police have probable cause to believe that a suspect poses a significant threat of death “or” serious bodily harm to them “or” others nearby (or dangerous condition). In this condition, the court suggests that suspects who threaten the police or others with weapons and suspects who commit a crime and cause or threaten to cause serious bodily harm are dangerous because of their violent or potential violent behavior. Third, if possible, the police must warn a suspect of their intention to use deadly force against him or her (or warning condition). Whether SWAT teams use deadly or nondeadly force options against suspects of crimes, allegations of excessive force are possible especially when tactical operations involve the use of SWAT not employed by regular officers. For example, plaintiffs have argued that the uses of certain police tactics such as deploying diversionary devices are excessive. In numerous court cases, however, the courts have suggested that uses of diversionary devices are permissible under the Graham rules [9] when the totality of circumstances support their use, when the police use discretion and do not deploy them routinely as a matter of custom, and when the police receive training in their appropriate use [14–16]. A high-risk forced building entry by a SWAT team also raises concern of excessive force. In general, police need consent, exigent circumstances, or an arrest or search warrant to enter buildings. Carrying out a forced building entry will trigger a judicial review of its lawfulness and excessiveness especially when any injuries occur. The more on-scene time a SWAT team has with a police call out such as negotiating with a barricaded suspect, the less the team can rely on exigency to carry out a warrantless entry, search, or seizure. A SWAT team avoids some excessive force liability for using forced building entry tactics when it obtains prior judicial approval. Questions about excessive force may occur when police regularly execute as a matter of policy or custom warrantless building entries in critical incident situations regardless of the totality of circumstances. For example, in O’Brien v. City of Grand Rapids [17], the court held the city liable for a warrantless entry into the home of an armed barricaded suspect with whom the police had contact time for 6-hours. The police here had a custom of executing warrantless building entries in critical incidents regardless of the circumstances.
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Sometimes, when police fail to reevaluate prior to entry the circumstances justifying a no-knock warrant, it may be unreasonable or excessive to carry out the warrant. For example, in United States v. Singer [18], the court said that if during the period between obtaining a no-knock warrant and executing it the police receive reliable information that exigent or dangerous circumstances no longer exist, the police must reevaluate their plan of entering a home without first knocking and announcing. In cases of alleged use of excessive force, criminal and civil liability can attach itself in the form of a team’s wrongful actions under Title 18 of the US Code section 242 and Title 42 section 1983 respectively. Commonly referred to as sections 242 and 1983, police shall not deprive any citizen within their jurisdiction of any rights secured by the Constitution and laws while acting under the color of law. In an action of law (criminal action for deprivation of rights) or redress (civil action for deprivation of rights), police are liable to any persons injured under sections 242 and 1983. Civil liability can also come in the form of specific state statutes that are similar to those of the federal government. For those members of SWAT teams, call outs are at times fraught with certain legal – criminal or civil – problems, dangers, or difficulties.
Hostage and Bystander Injuries Police have the responsibility to safeguard the wellbeing of the community. There is the possibility of injuries, however, when tactics to handle dangerous police call outs involve the use of physical force to capture and arrest law violators. Generally, no deprivation of rights occurs when the police use reasonable care, but accidentally shoot hostages or bystanders during police–citizen encounters. For example, in Green v. Denison [19], a suspect fired a bullet that shattered glass, which blinded a bystander. An officer fired a bullet that accidentally hit the suspect’s girlfriend. Both injured persons sued and claimed that the police had a duty to protect them from harm. The court dismissed the claims and held that police officers are not liable for injuries or damages to the general public that arise from their acting within the scope of their authority or duty. It distinguished duty owed to the public from duty owed to particular persons targeted by the police. Protecting the police or
giving them official immunity from personal liability arising from making discretionary or best judgment decisions allows them to perform their job without distractions. In Lee v. Williams [20], a police deputy unintentionally shot a hostage during a shootout with armed suspects. Postincident litigation brought about a § 1983 civil deprivation of rights claim against the deputy. The court ruled that there was no Fourth Amendment seizure of the hostage because the deputy did not intend to shoot him, but did intend to shoot the armed suspects. For officers involved in making tactical decisions about handling hostage situations, the courts have established a philosophy of “human life is the main concern.” For example, in Downs v. United States [21], a Federal Bureau of Investigation (FBI) SWAT team carried out a forceful assault against armed suspects who hijacked an airplane, held passengers as hostages, but released some of them during negotiations. The outcome of the assault approach was the deaths of hostages. The court ruled that the safety of hostages is more important than the arrest of suspects. There is no constitutional obligation to have specially trained SWAT teams deal with nonnormal police calls for service such as hostage situations [22]. Actions by regular or non-SWAT officers, who generally do not possess the same training, experience, and equipment that SWAT officers posses to handle the most dangerous police call outs, might not automatically result in injuries or police behaviors that would shock the conscious of courts. For SWAT and non-SWAT officers involved in making tough tactical decisions, (see Aggression) postincident outcomes might involve criminal or civil action for deprivation of rights. Fourth Amendment principles (see Seizures: Behavioral) are equally applicable (see Threat Assessment: School) to both SWAT and non-SWAT officers who might injure citizens.
References [1]
[2]
Clark, J.G., Jackson, M.S., Schaefer, P.M. & Sharpe, E.G. (2000). Training SWAT teams: implications for improving tactical units, Journal of Criminal Justice 28, 407–413. Kraska, P.B. & Cubellis, L.J. (1997). Militarizing mayberry and beyond: making sense of American paramilitary policing, Justice Quarterly 14, 607–629.
Polymorphism: Genetic [3]
[4]
[5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22]
Kraska, P.B. & Kappeler, V.E. (1997). Militarizing American police: the rise and normalization of paramilitary units, Social Problems 44, 1–18. Williams, J.J. & Westall, D. (2003). SWAT and nonSWAT police officers and the use of force, Journal of Criminal Justice 31, 469–474. Canton v. Harris, 489 U.S. 378 (1989). Walker v. City of New York, 974 F.2d 293 (2nd Cir., 1992). Allen v. Muskogee, 119 F.3d 837 (10th Cir., 1998). Popow v. Margate, 476 F.Supp. 1237 (D.N.J. 1979). Graham v. Connor, 490 U.S. 386 (1989). Terry v. Ohio, 392 U.S. 1 (1968). Ford v. Childers, 855 F.2d 1271, 1276 (7th Cir., 1988). Johnson v. Glick, 481 F.2d 1028, 1033 (2nd Cir., 1973). Tennessee vs. Garner, 471 U.S. 1 (1985). Commonwealth v. Garner, 423 Mass. 735, 772 N.E.2d 510 (1996). Langford v. Gates, 43 Cal. 3d 21, 729 P.2d 822 (1987). United States v. Myers, No. 94-20013-01, 1194 WL 324582 (10th Cir., 1997). O’Brien v. City of Grand Rapids, 23 F.3d 990, 999 (6th Cir., 1994). United States v. Singer, 943 F.2d 758, 763 (7th Cir., 1991). Green v. Denison, 738 S.W.2d 861 (Mo. 1987). Lee v. Williams, 138 F.Supp.2d 748 (E.D. Va. 2001). Downs v. United States, 522 F.2d 990 (6th Cir., 1975). Salas v. Carpenter, 980 F.2d 299, 309–10 (5th Cir., 1992).
Related Articles Daubert v. Merrell Dow Pharmaceuticals Police Use of Force FRANK J. GALLO
Pollen see Palynology
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the number of loci considered increases. For profiling purposes, scientists use loci that comprise sequences with simple tandem repeats (STR) (see also Short Tandem Repeats). These are regions of DNA that have short sequences of DNA that are repeated as multiple blocks, like carriages of a train. Any one person will have two copies (alleles) of the locus, one from mother and one from father, and each allele will have its own number of STRs. These may be the same (homozygote) or different (heterozygote). DNA profiling tests the polymorphism, or variation, of the alleles at a set of loci for a sample. For the sake of convenience, the different alleles of any one locus are given a name that is the same as the number of STR contained within the allele’s DNA sequence. Thus, a person with profile D3/13,16 is a heterozygote with one allele at D3 that has 13 repeats and a second allele that has 16 repeats. Polymorphisms in a population have evolved as a result of mutations and the passage of time. In the case of STR, mutations are thought to be due to a low rate of slippage of DNA synthesis of the repeated sequences during the process of making sperm and egg cells. Such mutations are then passed on to a new generation and over time become a measurable proportion of a population. A rule of thumb for a polymorphism is that it occurs in at least 0.05% of a population. Exactly, how common any allele is depends on many factors, including chance, selective breeding, population size, intermingling of populations, and so on. The allele frequencies of a polymorphic locus will remain stable if the population is in Hardy–Weinberg equilibrium (see also Hardy-Weinberg Equilibrium), but are often different for different populations. SCOTT BADER
Polymorphism: Genetic Natural genetic variation, within a population, is seen by the existence of more than one type of allele for a locus. Loci with several commonly occurring alleles are useful for profiling purposes because, although some individuals may share the same at alleles at a locus, the probability of them sharing the same alleles at all loci reduces dramatically as
Popper Theory of Falsifiability see Falsifiability Theory
Postmortem see Autopsy
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Postmortem Biochemical Examinations
Postal: Going see Homicide: Multiple (Behavior)
Postmortem Biochemical Examinations Introduction Functional Causes of Death The diagnosis of functional causes of death is, on one hand, based on mostly sparse postmortem findings and, on the other hand, considerably on postmortem biochemical alterations, which frequently originate from illnesses with internal causes and subsequent dysregulations such as diabetes mellitus, alterations of kidney and liver function, and imbalances of water and electrolytes. It is not rare that combinations of such dysregulations with problematic overlappings are seen due to close physiological and biochemical links [1–4] (see also Cardiac and Natural Causes of Sudden Death; Natural Causes of Sudden Death: Noncardiac).
Postmortem Biochemical Estimations and Differences to Clinical Biochemistry Postmortem biochemical analyses may represent the main clue to the diagnosis of functional causes of death. One of the main problems is to be able to apply clinical biochemical values on postmortem conditions. On one hand, there are big unpredictabilities regarding general postmortem changes in body fluids. On the other hand, biochemical values in postmortem specimen may well represent more or less the results of changes taking place during agony or the early postmortem period. Contrary to clinical biochemical estimations, values obtained postmortem do not necessarily allow conclusions regarding the mechanism of death. Postmortem diagnostic procedures, therefore, require a critical way of looking at them [5].
Obtaining the Appropriate Specimen Body fluids are usually obtained during postmortem examination. In cases with a limited external examination specimen (e.g., cerebrospinal fluid (CSF), vitreous humor, blood, and urine) can also be taken by cannulation (suboccipital access, puncture of an eyeball, dissection of a femoral vein, and puncture of the urinary bladder). The cranial cavity and the eyeballs provide a relatively good protection of the enclosed body fluids against decomposition effects. After obtaining vitreous humor, the eyeballs should be refilled with water due to cosmetic reasons. The volume of CSF to be found varies from 50 ml (baby) to 135 ml (adult). A few milliliters are sufficient for the postmortem biochemical analyses and there is usually no problem to get blood-free CSF. Approximately 1–2 ml of vitreous humor can be obtained by the puncture of both eyeballs. Aspiration of small parts of the retina is of no further relevance. Postmortem blood should be taken from the heart and a (peripheral) femoral vein and urine from the bladder immediately after dissection (a few milliliters per specimen) [6].
“Near-Table” Methods During the postmortem examination, several screening tests with stripes and tablets can be carried out regarding glucose, bilirubin, or acetone. Furthermore, there are a number of electronic test devices on the market, which can be used for screening purposes. These “near-table” methods are useful to confirm or exclude certain differential diagnoses at the time of the autopsy (further information: http://www.rochediagnostics.com).
Glucose Metabolism and Diabetes Mellitus General Aspects of Diabetic Coma Diabetic coma is a life-threatening complication of diabetes mellitus. Owing to a relative or an absolute insulin deficit, there is a typical rise of blood sugar with the possibility of acute complications or damage to blood vessels and nerves after longer duration. Depending on the age group, the incidence of diabetes mellitus varies between 2 and 5%. Causes for coma may be the onset of an unknown diabetes, lack of insulin injections, or increased requirement of
Postmortem Biochemical Examinations Table 1
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Postmortem biochemical values in case of alterations of glucose metabolism
Dysfunction
Parameter
Compartment
Coma (in general)
Sum value(a)
Ketotic coma
HbA1c Glucose Acetone
Hypoglycemia
Sum value
Cerebrospinal fluid Vitreous humor Blood Urine Blood, cerebrospinal fluid Vitreous humor Urine Cerebrospinal fluid Vitreous humor
Results −1(b) > 415 mg dl−1(c) > 410 mg dl >12.1%(d) >25 mg dl−1(e) >21 mg dl−1(f) >5 mg l−1(f) −1 < 50–80 mg dl −1 < 100–160 mg dl
(a)
According to Traub: concentrations of glucose and lactate Mean value = 500–600 mg dl−1 (c) Mean value glucose = 300–950 mg dl−1 ; mean value lactate initially = 80–160 mg dl−1 , after 20 h = 210–260 mg dl−1 (d) Mean value = 13–15%, nondiabetics = 9.15% (e) Most of coma cases >50 mg dl−1 , partly 2000–4000 mg dl−1 (f) Coma: mean value = 100–150 mg l−1 (b)
insulin due to acute infections, poor diet, operations, gastrointestinal diseases, or myocardial infarction. Twenty-five percent of all diabetic comas are socalled manifestation comas with previous unknown diabetes. Infections are the most frequent triggers for coma onset (approximately 40% of the cases). The frequency of fatal coma among known diabetics is between 0.5 and 1.5% with a peak in the age group of 40–60 years. The overall lethality from coma varies from 5 to 25% and rises to 70% with coma of longer duration. Lethality of diabetic coma is tenfold in 70-year-old individuals compared to 30-year-old patients. Furthermore, the risk for coma in juveniles is four- to sevenfold higher than in adults [1, 2] (see Table 1).
Types of Diabetic Coma Typically, diabetes mellitus type I is associated with ketonemic coma, whereas hyperosmolar coma normally results from type II diabetes mellitus. A lack of insulin causes a rise of blood glucose with subsequent loss of fluids and electrolytes. In addition, increased lipolysis is used to compensate the deficit of energy resulting from the inhibition of glucose metabolism leading to increased levels of ketone bodies with metabolic acidosis. The latter may be excessive (500–1000 mg l−1 acetone or higher), whereas hyperglycemia remains mostly moderate (250–600 mg dl−1 ). Hyperosmolar coma is more rare (approximately 10–20% of the cases) and associated with relative lack of insulin causing reduced
peripheral utilization of glucose with simultaneous release of glucose from the liver. Low levels of insulin prevent ketosis due to inhibition of lipolysis. Therefore, it is typical to find excessive hyperglycemia (often above 1000 mg dl−1 ) with lacking or only mild ketosis. Diabetic coma may lead to fatal outcome via different pathophysiological pathways. There is a cardiovascular type with leading oliguria or a renal type with acute kidney failure. Moreover, there exists pseudoperitonitis type with the symptoms of an acute abdomen. Typical accompanying diseases of fatal diabetic decompensation may be myocardial infarctions, apoplexy, embolism, pneumonia, pancreatitis, pyelonephritis, and a predisposition for lactic acidosis [5]. The most important body fluids for postmortem diagnostic purposes are CSF and vitreous humor using the so-called sum value according to Traub, which provides a combined calculation to compensate postmortem alterations of blood glucose level due to glycolysis, accordingly [7].
Glucose The hourly metabolic decrease of glucose in CSF is about 10–15 mg dl−1 but may vary between approximately 5 and 45 mg dl−1 . The hourly rate is below 1 mg dl−1 100 h postmortem. Given normal metabolic conditions, therefore, zero levels are reached after 10–12 h. Longer persisting glucose levels are indicative of antemortem hyperglycemia [8].
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The speed of postmortem glycolysis depends on a number of factors, e.g., the temperature and duration of body storage. Postmortem glycolysis is slower in diabetics compared to nondiabetic individuals, whereas obesity accelerates degradation of glucose. Isolated assessment of elevated glucose levels in CSF requires critical reserve (normal range: ca. 50–90 mg dl−1 ), because multiple other dysregulations may be accompanied by the same symptom as carbon monoxide poisoning, acute cardiac death, brain trauma, strangulation, protracted agony, asphyxia, pneumonia, and pancreatitis. This aspect has also to be taken into account regarding other body fluids [6].
Lactic Acid (Lactate) The product of postmortem glycolysis is lactate (normal level in CSF ca. 9 mg dl−1 ). Its concentration increases postmortem with a rate of approximately 10–15 mg dl−1 up to the 10th hour after death. After this time, the increasing rates vary considerably. Under differential diagnostic aspects also other disorders may cause hyperlactacidemia, e.g., tumors, respiratory insufficiency, severe chronic inflammations, uremia, especially inflammations of the central nervous system or alcohol-induced with lack of thiamine, physical strain, and alimentary factors (e.g., strict fasting).
Sum Value This combined method, according to Traub, compensates arithmetically for the postmortem production of lactate from glucose by using a “sum value”. It is based on the fact that 1 mol of glucose produces, via glycolysis, two moles of lactate so that the concentrations can be added using milligrams per deciliter. If the “sum value” exceeds 362 mg dl−1 in CSF, the probability of fatal diabetic coma is about 89%, if other, e.g., toxicological and morphological, alterations can be excluded. In cases of diabetes mellitus, the “sum value” remains almost stable up to the 200th hour postmortem. If there are nondiabetic causes of death, the “sum value” increases up to the 30th hour postmortem, but remains nearly stable afterwards. Although the formula, according to Traub, has to be used under critical view, the “sum value” may be considered the most important criterion for the diagnosis of fatal diabetic coma. However, the author’s research
has revealed that it is more realistic to increase the limit “sum value” in CSF to 415 mg dl−1 (upper limit of the 95% confidence interval in cases of cardiac death), with cases of diabetic coma ranging on average between ca. 500 and 600 mg dl−1 [9, 10].
Vitreous Humor The calculation method according to Traub may also be applied on vitreous humor. The glucose level herein is about 50–85% of the serum glucose. Values for postmortem glucose concentrations vary from 20 mg dl−1 (nondiabetics) to 90 mg dl−1 (known diabetics), but wide variation ranges have to be taken into account. Owing to slower glycolysis in vitreous humor compared to CSF, normal glucose values may be found as long as two days postmortem. In cases of fatal coma, glucose values between ca. 300 and 950 mg dl−1 may be found. Lactate values are already around 80–160 mg dl−1 in the intramortal period and between 210 and 260 mg dl−1 approximately 20 h postmortem. The upper limit value is 410 mg dl−1 and if this is exceeded, it can be taken as a strong indication of fatal diabetic coma, given the condition that other possibly competing mechanisms can be excluded. The procedure is said to be applicable until the 10th postmortem day [11–15].
Blood Glucose Blood sugar levels alone are only of low diagnostic relevance, if at all limited to blood from the femoral veins within the 1st and 2nd hour postmortem in which the level is ca 40–100 mg dl−1 . Contrary to this, glucose levels in central blood (right ventricle) may easily reach 1000 mg dl−1 and over due to postmortem hepatic glycogenolysis. Normally, postmortem glycolysis (approximately 13 mg dl−1 h−1 ) results in complete metabolization of the blood glucose within 6–8 h. This leads to a corresponding increase of lactate up to 180 mg dl−1 after 1 h and ca. 450–680 mg dl−1 after 12–24 h. Especially due to postmortem diffusion of serum and its components from surrounding tissues into blood vessels, the “sum value” cannot be used [10].
Hemoglobin A1c This glycosylated fraction of hemoglobin represents an important parameter regarding a basic diagnosis of
Postmortem Biochemical Examinations diabetes mellitus. Owing to the fact that kinetics of its formation is depending on time and concentrations, HbA1c can be used as a long-term indicator of diabetic conditions (so-called blood sugar memory for ca. 120 days). Levels of 6–8% (maximum of 10%) are consistent with a normal glucose metabolism, whereas higher concentrations are indicative of inappropriate metabolic conditions (hyperglycemias in the past). Periods of increased blood sugar have to last 6–8 h minimum to cause significant rises of HbA1c due to its slow reaction kinetics. Furthermore, the prefinal and postmortem drop of the pH value in blood, due to formation of lactate, are likely to result in a reduction of HbA1c because of separation of its unstable component. Blood sugar also decreases rapidly after death. The stable part of hemoglobin A1c makes up approximately 90% of the whole. For example, hyperglycemia around 360 mg dl−1 takes around 12 h to cause an increase of HbA1c of 1.3% absolute. In reverse, a reduction of around 5% needs around seven days. There has been found a positive connection between “sum value”, urine glucose concentration, and HbA1c level. This means that there usually is a coincidence of elevated “sum value”, high urine glucose, and HbA1c . Hemoglobin A1c has proven to be relatively stable versus autolysis especially in hemolyzed blood and can be measured postmortem in frozen samples and also in samples stored in a normal fridge. It has been revealed that storage at temperatures between +4 and −80 ° C does not cause any relevant changes to the HbA1c concentrations. The result is independent from the actual total hemoglobin level because HbA1c is measured as percentage of the current hemoglobin value [16]. Falsely elevated hemoglobin A1c concentrations can be found due to increased HbF levels in cases of thalassemia or advanced renal failure. In principle, HbA1c has proven to be a reliable parameter for the basic diagnosis of diabetes mellitus without being too liable for interferences. It is also possible to measure other glycosylated proteins such as fructosamine, but assessment is rather difficult. The mean levels of HbA1c in cases of diabetes mellitus differ considerably from those in nondiabetic individuals and are around 12.1% in diabetic coma (range: ∼13–15%). However, the lower portion of the range in case of diabetes mellitus may overlap with the upper portions of the range in nondiabetic cases as it has been shown for the “sum value” [17].
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Ketone Bodies The ketotic type of diabetic coma is characterized by an increased level of ketone bodies in blood and other body fluids (acetone and acetylacetate ca. 25–35%, β-hydroxyl-butyrate ca. 65–75%; normal values for acetylacetate 0.8–2.4 mg l−1 , for β-hydroxyl-butyrate 2.5–9.8 mg l−1 ). Estimation of acetone may easily be carried out in connection with blood alcohol analysis using headspace chromatography. The normal concentrations for free acetone range from 2.3 to 2.5 mg l−1 in nondiabetic patients and may reach 23 mg l−1 in diabetics. The levels are almost independent from the postmortem interval [2, 5]. The level of acetone in CSF with diabetes mellitus differs considerably from those seen with nondiabetic causes of death, especially in cases of diabetic coma, with an obvious association regarding an elevated “sum value”. If other causes can be ruled out, acetone levels exceeding 5 mg l−1 are suspicious of diabetes mellitus. Ketotic coma may be associated with levels higher than 100 mg l−1 , but ketonemia is rarely seen if the blood glucose concentration is only 200 mg dl−1 and below. According to the author’s research, acetone levels in ketotic coma exceed 21 mg l−1 in most of the cases, with mean values in this group of 100–150 mg l−1 . Single cases may show levels of more than 1000 mg l−1 . Nondiabetic factors that might cause elevated ketone levels are, e.g., chronic hepatic and renal diseases, pancreatitis, shock, chronic alcoholism and isopropanol poisoning (levels up to 160 mg l−1 ) as well as protracted fasting (acetone levels may exceed 5000 mg l−1 ) [18].
Urine As the fourth column of postmortem diabetes mellitus diagnostics, an examination of urine can reveal important clues. Urine glucose levels higher than 25 mg dl−1 (maximum in healthy individuals) may be indicative of diabetes. Diabetic coma is sometimes associated with urine glucose concentrations above a few 1000 mg dl−1 , but usually higher than 500 mg dl−1 . These excessively high values only show very small overlapping with other cause of death groups, although positive findings for glucose in urine alone are only of lower value. Glucosuria is a rather frequent nonspecific symptom, e.g., due to brain trauma, myocardial infarction, intoxication, apoplexia, and leukemia. Likewise, glucosuria may
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be absent even in cases of manifest diabetes mellitus caused by diabetic glomerulosclerosis itself or postmortem degradation. Ketone bodies are likely to be found in urine longer than 24 h postmortem. Concentrations exceeding 0.5 mg dl−1 = 5 mg l−1 of free acetone may be indicative of ketotic dysregulation. However, a positive test for ketonuria is not a proof for ketonemia, because the kidneys have a relatively high clearance rate for ketone bodies. Furthermore, there are multiple conditions that might cause considerable ketonemia (see above). Hyperosmolar coma is typically characterized by a lack of ketonemia (approximately 30% of diabetic comas) [1, 2, 5].
Lactic Acidosis There are some secondary effects of lactic acidosis that might gain special forensic medical relevance. For example, moving potassium to the extracellular space may cause hyperkalemia (see below). Acidosis decreases the reactivity versus catecholamines with a negative-inotrope effect on the heart. Severe acidosis may result in massive reduction of the kidney blood circulation leading to acute renal failure. Diabetic coma can also cause acidosis by production of β-hydroxyl-butyrate and acetylacetate (see above). Lactic acidosis plays an important role, particularly regarding overlapping with postmortem diagnosis of diabetes mellitus. Considerable amounts of lactic acid are being released during shock and hypoxia, due to poor perfusion caused by diabetes mellitus, following renal failure, hepatic diseases, and ethanol/methanol intake, rarely as complication of a treatment with biguanides or due to severe lack of thiamine with chronic increased alcohol intake. The conditions can be exacerbated by chronic renal failure due to reduced excretion of acids and also by an increased loss of bicarbonate resulting from diarrhea and/or vomiting. The central causal mechanism is an increased concentration of pyruvate from protein catabolism together with a lack of oxygen, so that energy can still be provided by glycolysis. Accumulation of lactate happens more frequently in diabetics than in other patients what is due to disturbances of oxygen supply and alterations of metabolic activities. The clinical picture is characterized by gastrointestinal discomfort, muscular spasms, central nervous disturbances and deep frequent respiration. The severe type of biguanide-induced lactic acidosis shows a lethality rate of over 50%.
Patients suffering from chronic alcoholism represent a special risk group regarding fatal lactic acidosis and ketotic coma as well. There are often only very few and/or nonspecific morphological findings. On one hand, considerable ketonemia may follow acute alcoholization (free acetone from 74 to 400 mg l−1 ), but, on the other hand, high “sum values” may also result in this condition. Their range (ca. 294–594 mg dl−1 ) can also be associated with fatal diabetic coma. Given the precondition that diabetes mellitus and other competing mechanisms can be ruled out, ketotic coma or lactic acidosis has to be considered as a cause of death in such cases. The lower limiting values for the “sum value” are ca. 300–400 mg dl−1 , for acetone in blood around 90 mg l−1 and 6% for HbA1c [19, 20].
Hypoglycemia (Endogenous vs. Exogenous Hyperinsulinism) Although fatal hypoglycemia appears to be a rather rare event among forensically examined death cases, they might be the source of serious diagnostic problems. Under clinical conditions, hypoglycemia is diagnosed if the blood glucose level lies below 40 mg dl−1 or if the so-called Whipple’s triad can be found. It comprises blood glucose level below 45 mg dl−1 , symptoms of hypoglycemia, which disappear under administration of glucose. Multiple circumstances may be responsible for hypoglycemia in individuals with an empty stomach, e.g., insulinomas and other tumors, severe hepatic diseases, uremia and glycogenoses. The initial manifestation of diabetes mellitus may also be accompanied by reactive hypoglycemia as well as alterations of gastric mobility, vegetative instability, or massive alcohol intake with simultaneous lack of food due to inhibition of gluconeogenesis. The autonomous or glucopenia-associated spectrum of symptoms includes hyperorexia, nausea, restlessness, sweating, tachycardia, endocrine neuropsychologic disorder, primitive automatisms, risk of convulsions, and focal signs with apoplectiform symptoms. The final state with somnolence, coma, and central alterations of respiration and circulation until death has forensic medical relevance. Hypoglycemias due to exogenous causes are mostly seen with an existing diabetes mellitus. Important mechanisms are accidental or intentional overdosage of insulin or sulfonyl-urea derivates with
Postmortem Biochemical Examinations subsequent reactive hypoglycemia. Such a situation may arise from lack of regular alimentation due to intercurrent diseases without changing the doses of antidiabetic drugs. Other possibilities for hypoglycemias can be interferences with drugs which decrease the blood sugar level indirectly or unusual physical strains. However, types of hypoglycemia with a forensic medical impact are those caused by overdosages of antidiabetics. The so-called factitious hypoglycemia needs special attention. It is caused by (unnecessary) administration of insulin or sulfonyl-urea derivates and can be seen in connection with psychic alterations (e.g., borderline personality disorder) or suicidal intention. It is rare to find a primary criminal background, e.g., cases of homicide. The most important diagnostic criterion of this type of hypoglycemia is that it happens independently from alimentation. Affected persons often have relations to professional health care or are relatives of known diabetics [21]. The calculation procedure regarding a “sum value” can also be used for the diagnosis of hypoglycemia. Consequently, low sum values in CSF in vitreous humor below ca. 50–80 mg dl−1 or rather 100–160 mg dl−1 are strongly indicative of fatal hypoglycemia. This conclusion is particularly supported by simultaneously high insulin levels suggesting that estimation of insulin levels and also of c-peptide postmortem is essential. In case of endogenous secretion, insulin and c-peptide are both found elevated. If there is exogenous hypoglycemia due to administration of insulin, the level of c-peptide will be noted as much lower than normal. Contrary to this, there are usually increases of insulin and c-peptide concentrations following an intake of sulfonyl-urea derivates, but, in diabetic individuals, often rather high insulin levels can be seen without any indication of hypoglycemia. The procedure has also proven to be reliable in cases of suspected hypoglycemia in car drivers [22, 23]. Postmortem estimations of insulin levels can be carried out by radioimmune assay (RIA) and have revealed levels very similar to those of healthy individuals in blood from a femoral vein and also from the heart. Nevertheless, postmortem concentrations of insulin in blood from the right ventricle may be increased to about 10-fold of normal values due to release of insulin after death. Putrefaction may cause problems as well. Furthermore, single estimations have a wide variation and, therefore, cannot be used
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as the only criterion for the diagnosis of insulin-based hypoglycemia. Sometimes it is possible and useful to have a proof of suicidal insulin injection by analyses of the tissues close to the injection site. It is a strict rule that the postmortem diagnosis of hypoglycemias must be based on a combined assessment of different criteria and can only be made “per exclusionem”. According to this, especially cardiac diseases, cerebral hemorrhages, pulmonary embolism, strangulation/asphyxia, ruptures of vessels and intoxications have to be ruled out. Estimations of insulin should always be carried out in peripheral venous blood or CSF/vitreous humor because diffusion of insulin from the pancreas via the portal vein might take place postmortem. The “sum value” calculated from glucose and lactate levels is of special importance (see above) [24, 25].
Alterations of Liver Function In case of an advanced stage of hepatic cirrhosis from different causes, it is not rare that there develops an alteration of liver metabolism, often resulting in potentially reversible complications, due to retention of neurotoxic substances in blood with decompensation and final hepatic failure. Suspicion may arise from the previous medical history, desolate housing conditions, known alcohol abuse, and sometimes the presence of jaundice. Acute deterioration of hepatic insufficiency with a danger of hepatic coma originates from an increased production of ammonia due to a high portion of proteins in the intestinal contents that may be caused by gastrointestinal hemorrhages (especially esophageal varicosis due to alcoholism), protein-rich nutrition, febrile infections with increased protein catabolism and drugs (e.g., benzodiazepines, analgesics). Clinically, the advanced stage is characterized by permanent drowsiness but patients can be woken up, later on hepatic smell, and electroencephalogram (EEG) alterations. This picture leads to coma with unmistakable “foetor hepaticus” and massive EEG changes until fatal outcome with total hepatic failure [1, 2]. The terms acute hepatic insufficiency or endogenous hepatic coma describe a failure of the liver function without previously existing chronic liver disease. Contrary to the chronic hepatic failure, decompensation can occur suddenly without any indications from the medical history. Important morphological findings are dermal and scleral jaundice
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and, clinically, disturbances of blood coagulation and consciousness (somnolence, coma). It is especially the fulminant type with a duration of less than seven days, which may gain forensic medical relevance. Important causes are viral hepatitis (65%) and hepatotoxic substances (30%) such as medication (Paracetamol), drugs, chemicals (CCl4 ), or poisons from mushrooms (Amanita phalloides). This elucidates the importance of accompanying toxicological analyses. Potentially fatal complications may be brain edema (80%; most frequent cause of death), gastrointestinal hemorrhages (50%), as well as hypoglycemia and renal failure with electrolyte imbalances. The typical enzymes of liver metabolism represent important parameters, which can also be examined postmortem, as well as bilirubin. The daily bilirubin production comes to approximately 510 µmol l−1 (30 mg dl−1 ; normal value up to 1.1 mg dl−1 ). Hepatic failure is typically associated with an increased level of serum bilirubin causing jaundice if it exceeds 34 µmol l−1 (2 mg dl−1 ). A differentiation between direct bilirubin bound to biglucuronide and nondirect bilirubin bound to albumin is only useful under clinical aspects. Postmortem bilirubin levels may well be compared with those obtained antemortem. Differences are only ranging in the area of 0.1 mg dl−1 , especially in death cases showing jaundice. During the postmortem period, there can be seen a slight but steady increase (ca. 0.2 mg dl−1 after 2 h and 0.7 mg dl−1 after 20 h). Furthermore, there is an increase of enzymes typical for the liver (GPT glutamate pyruvate transaminase, GGT gamma glutamyl transferase, and AP alkaline phosphatase) as well as of ammonia (>100 mg dl−1 ; normal value below 0.05 mg dl−1 ) primarily not only in blood but also in other body fluids (CSF, vitreous humor). However, clinical reference ranges of values can only be used as a basis for assessment. Most of the bilirubin in CSF belongs to the conjugated type, often associated to hypokalemia and hypoglycemia [6].
Disturbances of Kidney Function Chronic renal failure represents the result of a nonreversible reduction of the function of both kidneys. Important causes are, e.g., diabetes mellitus (nephropathy, ca. 35%), hypertension (ca. 25%), chronic inflammations (ca. 15%) and abuse of analgetics (ca. 1%). The chronic reduction of the renal
function can also show acute decompensation leading to unexpected sudden death, which is not an unusual development during diabetic coma. The compensated chronic phase showing only a functional reduction of a low degree and the phase of compensated retention (azotemia, creatinine levels up to 6 mg dl−1 ) are not associated with symptoms of uremia. Preterminal renal failure with creatinine levels above 8 mg dl−1 plus symptoms of uremia is called decompensated retention. Terminal renal failure (uremia) showing creatinine levels over 10 mg dl−1 is associated with massive symptomatology of uremia. During the phase of decompensated retention (preterminal phase), there may be seen edematous changes, cardiac failure, gastroenteritis due to uremia and neuropathy. The terminal phase is characterized by acute life-threatening symptoms, such as neuropathy and encephalopathy, overhydration with pulmonary edema, bleeding tendency, coma, and death (see Table 2). Acute renal failure or acute renal insufficiency represents a mostly reversible reduction of the renal function with loss of urine production and increasing retention parameters (urea, creatinine). Fifteen percent of the cases with acute renal failure show polyuria or normuria with an increase of retention values being the only symptom. Without sufficient therapy, e.g., dialysis, acute renal failure mostly has a fatal outcome. Sometimes bilateral necroses of the renal cortex can be seen. There are multiple possible causes for acute renal failure, such as alterations of the blood circulation, toxins, medication (antirheumatics, cytostatics, and antibiotics), chemicals (glycols), and inflammatory or vascular processes. The most critical clinical phase is the third one with polyuria and extensive loss of water/electrolytes and simultaneous increase of urea and creatinine. Fatal complications may occur associated with other organs, e.g., shock lung, cardiac failure and arrhythmia, and cerebral edema with further central nervous complications. The most significant biochemical changes of acute and chronic renal failure are increased levels of urea and creatinine, electrolyte imbalances (often decreased with acute renal failure) and also a reduced concentration of urine [1, 2, 6].
Creatinine Under postmortem conditions, an increased level of creatinine in CSF and vitreous humor can be indicative of renal failure (normal value 0.6–1.4 mg dl−1 ).
Postmortem Biochemical Examinations Table 2
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Postmortem biochemical values in cases of renal failure (insufficiency)
Dysfunction
Parameter
Clinical values
Compensated retention Preterminal failure (f) Terminal failure RF ruled out
Creatinine
≤6 mg dl−1 >8 mg dl−1 >10 mg dl−1
Compartment
Results
CSF/VH
(First 13 hpm)
Blood and CSF
Creatinine 4.0 mg dl−1 Maximum 179 (83) mg dl−1 (mean value = 102 (47) mg dl−1 ) Maximum 197 (92) mg dl−1 (mean value = 89 (41) mg dl−1 >200 mg dl−1 (93)
CSF/blood (heart) Urea 200 mg dl−1
CSF Creatinine 4.0 mg dl−1
Blood (heart) Creatinine 4.5 mg dl−1
RF possible RF primary fatal Normal values (urea–nitrogen)/urea(a) )
Blood (heart)
CSF
Uremia (urea–nitrogen)/urea(a) ) dysfunction(b) ) RF ruled out RF possible RF primary fatal
RF, renal failure; CSF, cerebrospinal fluid; VH, vitreous humor; pm, postmortem (a) (b)
Urea–nitrogen × 2148 (mg dl−1 ) = urea (mg dl−1 ) Different method of assessment (see text and references)
During the early postmortem interval, the creatinine concentration is rather stable. In healthy individuals, the mean values are 1.6 mg dl−1 (8 h postmortem), 1–2 mg dl−1 (12 h postmortem) and 3–4 mg dl−1 (24 h postmortem). Therefore, reliable assessment is possible for pathological levels if the specimens are obtained during the early postmortem period. Renal failure can be ruled out if the creatinine level is below 2.5 mg dl−1 . It is possible if its concentration ranges between 2.5 and 4.0 mg dl−1 and renal failure is to be considered as the primary cause of death with levels exceeding 4.0 mg dl−1 , given CSF being obtained within the first hours postmortem. After death, the normal relation between creatinine levels in serum and CSF remains almost the same. On one hand, problems may arise from a connection between renal damage and creatinine level. On the other hand, high creatinine values are seen without any or only slight alterations of the
kidneys. However, there is also the possibility that advanced kidney damage coincides with levels below 4 mg dl−1 . It must be pointed out that disturbances of the circulation and toxicemia may cause creatinine retention but that partial renal function can still be in place during uremia [6].
Urea In case of renal failure, there exists a close relation between the levels of urea in serum and CSF (normal range: 13.8–34.6 mg dl−1 ). The urea level in CSF is approximately three fourths of the serum value. However, there have been reported reduced levels in CSF and also slight increases in blood from the femoral veins and also in liquor compared to antemortem values and also independent from the cause of death. If renal diseases can be excluded, such changes may be due to agonal or postmortem effects. Furthermore, there is a rising difference between the
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concentrations of urea in liquor and blood with the postmortem interval increasing. Often postmortem values are slightly higher compared to intravital estimations. However, this increase is lower if the intravital concentration has been rather high. In case of manifest renal insufficiency, possibly with uremia, there are usually considerable differences to the levels found in healthy individuals. There is an arithmetical connection between urea–nitrogen and urea, which is as follows: urea– nitrogen × 2.148 (mg dl−1 ) = urea (mg dl−1 ). Urea levels in CSF above 20 mg dl−1 (9.3 mg dl−1 urea– nitrogen) are indicative of renal disease, whereas the postmortem “normal values” for blood from the heart is 179 mg dl−1 maximum (83 mg dl−1 urea–nitrogen), with a mean value of 102 mg dl−1 (47 mg dl−1 urea–nitrogen). The corresponding concentrations in CSF are 197 mgYdl−1 (92 mg dl−1 urea–nitrogen) with a mean value of 89 mg dl−1 (41 mg dl−1 urea–nitrogen). Contrary to this, urea levels in CSF and blood from the heart do usually exceed 200 mg dl−1 (93 mg dl−1 urea–nitrogen) during the first 13 h postmortem in the case of uremia from all imaginable causes [26].
Diagnosis Postmortem estimation of creatinine and urea levels in blood from the heart (left ventricle preferred) and CSF have important relevance regarding the postmortem diagnosis of renal failure. The following ranges of values can be differentiated for a practicable combined diagnostic procedure: Urea below 100 mg dl−1 in CSF/blood, creatinine below 2.5 mg dl−1 in liquor and below 3.5 mg dl−1 in blood: renal failure can be excluded. Urea 100–200 mg dl−1 in CSF/blood: renal failure possible if there is an additional creatinine level of 2.5–4.0 mg dl−1 in liquor and of 3.0–4.5 m gdl−1 in blood from the heart. Urea above 200 mg dl−1 in CSF or blood: renal failure represents the primary cause of death if creatinine levels in liquor simultaneously exceed 4.0 and 4.5 mg dl−1 in blood from the heart [2, 6].
Water- and Electrolyte Imbalances The regulation of the water and electrolyte balance aims to maintain isotonia and isovolumia within
the intravasal space. Sodium, chloride, and bicarbonate show the highest extracellular concentrations, whereas potassium and phosphoric esters predominate in the intracellular space. Owing to the fact that the relation between extracellular fluid volume and water exchange is much lower in infants than in adults, water imbalances may develop much earlier and be life-threatening. It is not rare that electrolyte imbalances occur due to other diseases such as diabetes mellitus, chronic alcoholism, and nutritive disturbances. There are some types of dysregulations, which can lead to sudden unexpected death and may therefore be of forensic medical relevance. Isotonic dehydration is characterized by extracellular loss of sodium and water in isotonic relation, e.g., during the polyuric phase of acute and chronic renal failure, vomiting and diarrhea, pancreatitis and peritonitis, and due to dermal loss (following burn injuries). The main mechanism of hypotonic dehydration is salt depletion together with extracellular deficit of water. Delirium and convulsions are typical cerebral symptoms, which have to be considered as causes of sudden death. Hypertonic dehydration (with hypernatremia) leads to a deficit of free water in the extracellular and also in the intracellular space and is caused e.g., by a lack of water supply, dermal loss (sweating), and also via the lungs (e.g., hyperventilation from infections and fever), the kidneys (diabetic coma), and the gastrointestinal tract (diarrhea, vomiting). The typical morphology comprises tinting of the skin, sunken eyes, dry surface of the galea and/or dry cutting areas of organs. A biochemical pattern was proposed as diagnostic tool. The so-called dehydration pattern consists of an elevation of sodium >155 mmol l−1 , chloride >135 mmol l−1 , and urea >40 mg dl−1 . Persisting imbalances also result in corresponding alterations within the CSF (osmotic gradient) [27, 28]. Regarding the postmortem diagnosis of water and electrolyte imbalances, measurements of the pH is of no value. Estimations of electrolytes in CSF and vitreous humor can only be of limited meaningfulness. On one hand, the pH strongly depends on the state of the body, and, on the other hand, liquor often becomes sanguinolent when it is obtained so that there may be considerable alterations especially to electrolytes. Centrifugation may be of certain help, but cannot remove all components originating from damaged erythrocytes. This is why liquor from the lateral ventricles should be obtained, because after
Postmortem Biochemical Examinations 12–24 h there are no differences to lumbar liquor [29].
Potassium Disturbances of the potassium balance can gain forensic medical relevance because they have been described to occur not only isolated but also in connection with other diseases and sudden death (acute myocardial failure due to arrhythmias). Particularly, intestinal or renal loss or insulin treatment of diabetic coma are likely to result in hypokalemia (5.0 mmol l−1 ) are acute renal failure, chronic renal insufficiency, or extensive tissue damages. The main possible complications are disturbances of conduction, ventricular flutter, and fibrillation, which may lead to asystolia (acute danger to life with potassium levels >6.5 mmol l−1 ) [1, 2, 6]. Estimation of potassium in blood and serum specimens obtained postmortem have proven not to be reliable due to extremely fast and intense potassium release from cytolysis. In CSF, the potassium value can reach up to sevenfold of the normal level within the first 10 h postmortem, but the range of variation is rather wide. The potassium content of liquor is, to a large extent, independent from the serum level and in infants lower than in adults (normal range: ca. 2.1–4.6 mmol l−1 ). Contrary to this, the increase of the potassium concentration in vitreous humor has been reported to be regular. This can provide certain conclusions regarding the time of death within the first 12 h postmortem. There seem to be no other relevant disturbances from other diseases on the potassium content of vitreous humor except hepatic failure. Furthermore, there do not exist any comprehensible associations between the concentration differences of sodium and potassium, which appear to allow further reliable conclusions [30–34].
Sodium/Chloride There is an extracellular decrease of sodium parallel to an increase of potassium (see above) postmortem. As a general rule, there is a variation of the sodium level within CSF mostly corresponding to the serum concentration (ca. 128–157 mmol l−1 ), except situations with severe infections of the central nervous system.
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Without differentiation regarding the mechanisms of death, sodium levels in CSF and serum are usually found within the normal range, but the variation range differs considerably from intravital values (ca. 123–205 mmol l−1 ). Although there is a distinct decrease of sodium in CSF and serum after death, its concentration in vitreous humor remains rather stable up to 30 h postmortem, followed by an almost linear decrease in the following 50 h. Sodium levels above 155 mmol l−1 and below 130 mmol l−1 in adults and larger differences outwith the normal range in children can be indicative of hypernatremia or hyponatremia antemortem. Sodium levels in fluid obtained from the pericardial sac show distinct correlation to the postmortem interval, namely, a decrease of approximately 0.4 mmol l−1 during the first 85 h after death, but also with a wide range of variation. The level of chloride in CSF is approximately 20% higher compared to serum and shows a range of ca. 110–129 mmol l−1 in healthy individuals. The postmortem changes of chloride are comparable to those of sodium (see above), so that there happens also a typical decrease of the chloride concentration in plasma and CSF. The levels of chloride and sodium in vitreous humor appear to be almost “parallel” and remain nearly constant for over 30 h postmortem. However, any close correlations between chloride values and causes of death or time could not be identified postmortem.
Calcium The homoeostasis of calcium has an important impact onto the neuromuscular conduction. Hypocalcemia (total Ca 1.3 mmol l−1 ) are chronic osteolytic or endocrine processes in most of the cases, which may be the reason for sudden unexpected deaths via electrolyte imbalances with arrhythmias, somnolence, and coma. Under postmortem conditions, the serum calcium concentration is constant for ca. 10 h with a slight increase thereafter (normal range in healthy individuals: 1.96–2.60 mmol l−1 ). The calcium contents of CSF reflect approximately the serum level of ionized calcium. In vitreous humor, calcium levels are much more stable and there is less influence of agonal and postmortem effects [1, 2].
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Postmortem Biochemical Examinations
Diagnosis Postmortem diagnosis of imbalances of electrolyte and water metabolism cannot be based on isolated single parameters. Assessment must always include a synopsis of different values. Furthermore, the postmortem interval has to be taken into account in each case. Postmortem biochemical analyses regarding electrolyte imbalances are believed to be most successful in cases being characterized by elevations of parameters such as states of dehydration. One main disadvantage are the wide range of variation referred to single analyze results. This requires a combined interpretation of different values with consideration of all morphological and toxicological findings as well as the possibility of combined dysregulations (e.g., kidney and glucose metabolism).
quotients adrenaline/noradrenaline considerably1 are typical for short agony (e.g., myocardial infarction, head trauma) being indicative of higher adrenaline levels [38]. Additional analyses of volatile substances (ethanol, methanol, propanol-1, propanol-2, and acetone) usually show elevated acetone concentrations in all compartments being indicative of hypothermia, but basically only in cases that are ethanol-free. Acetone and propanol-2 are then altered equally. If relevant alcoholization is found, both substances can only be found in very low or physiological ranges that is indicative of an antilipolytic effect of ethanol (acetone >35 mg l−1 if blood alcohol level is 3 l kg−1 , and are sequestered in tissue and present in extracellular fluid are candidates for postmortem redistribution. Accordingly, amitriptyline exhibited significant postmortem distribution, whereas morphine and its glucuronides indicated only a trend for higher concentrations in heart blood compared with femoral or subclavian blood [37, 45, 46]. Many drugs are sequestered antemortem in organs, and postmortem redistribution may either occur by diffusion through blood vessels or from the lumen of a body cavity toward surrounding organs. The vascular pathway may depend on the blood remaining fluid after death. Investigations on postmortem
Major factors governing postmortem drug distribution
Physicochemical and pharmacokinetic properties of the drug
Environmental conditions
Size, shape, charge, pKa , partitioning behavior, lipophilicity, volume of distribution, binding to proteins and/or red cells, affinity toward tissues, decreasing or residual metabolic activity during the perimortem and early postmortem time period Initial concentration, pH, orientation of solute flux, temperature, time, blood coagulation and hypostasis, blood movement due to pressure and fluidity changes, position of the corpse, lysosomal enzyme activities, and bacterial invasion
Postmortem Toxicology: Artifacts diffusion from gastric residues in a human cadaver model using amitriptyline, paracetamol, and lithium carbonate revealed high concentrations in liver and lungs, whereas diffusion into gallbladder bile, cardiac, and aortic blood was less severe [47]. Diffusion of ethanol from the stomach into blood is not a problem in alcohol analysis. For an intact stomach containing 400 ml of 10% ethanol, contamination of a femoral vein sample was minimal [48]. However, it should be considered that regurgitation of alcohol or drugs from the stomach, esophageal sphincter relaxations, and severe blunt trauma resulting in the rupture of internal organs, especially of the stomach, facilitate postmortem diffusion processes. These circumstances may favor artificially elevated blood concentrations [49, 50]. Drugs accumulated in lungs are rapidly released inducing elevated drug concentrations in thoracic and heart blood samples as well as in liver specimens. These changes were assessed in animal and cadaver models, and were, e.g., also seen in methamphetamine-associated deaths [51]. Redistribution from the lungs seems more intense than redistribution from the gastrointestinal tract due to the large surface of the alveoli, the thin membranes, and the high vascularization. The early rise in dothiepin levels in thoracic blood in a rabbit model reflects postmortem redistribution from the lungs, where the drug was heavily concentrated [52]. Fuke et al. [53] observed that torso blood samples showed less toluene after gastric instillation than after tracheal instillation. Also, a higher toluene concentration was present in the left lobe of the liver than in the right with gastric instillation. The pleural and peritoneal fluids are regarded as vehicles for drug exchanges between the lungs and the liver [43]. The redistribution effects from the liver are far more complex, and may occur via the hepatic vessels or directly to adjacent organs, such as the stomach or the gall bladder [39]. Postmortem decreases in concentrations of fluoxetine and norfluoxetine, in both liver and lungs, occurred along with increases in blood concentrations in a dog model [54]. In rats, administered amitriptyline in the liver lobes had high but variable drug concentrations among tissues. Lobes lying closest to the stomach had the highest drug concentrations [55]. In general, a great part of the surface of the left liver lobe being in close contact with the stomach wall will be more involved in postmortem redistribution. Also, it may be difficult to
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correctly assign the source of hepatic concentrations postmortem [43]. A substantial increase in heart blood could be noticed for drugs, such as calcium channel blockers or cardiac glycosides, which are highly bound to cardiac tissue. In a series of digoxin cases, the drug concentration was invariably higher in heart blood specimens than in peripheral blood samples [56, 57]. The lungs, the liver, and the stomach may serve as further drug sources. A useful compilation of drug concentrations in heart and femoral blood has been published by Dalpe-Scott et al. [58]. Variations in postmortem drug concentration largely depend on both the time since death and the site of blood collection. Differences in drug concentrations collected from different anatomical sites have been reported for numerous drugs including imipramine, diphenhydramine and codeine [59], methadone [60, 61], doxepin, clomipramine, barbiturates [39], amitriptyline [45], cimetidine [62], methamphetamine [51], cocaine [63], digoxin [56], zopiclone [64], methylenedioxymethamphetamine, and methylenedioxyamphetamine [65]. A review on site-dependent differences is given by Prouty and Anderson [41] and Baselt [38]. It is evident that postmortem redistribution is governed by the postmortem time interval. Compared to studies on site-dependent differences, only few data on time-dependent differences are available. In a fatal case of dihydrocodeine intoxication, site-to-site differences of the parent drug and major metabolites were very small, probably due to steady state, an apparent volume of distribution of 1.0–1.3 l kg−1 for dihydrocodeine, the fluidity of blood as well as very early postmortem blood sampling [66]. Some case reports have determined that there is little evidence of time-dependent variability, which may be due to delayed sampling. Temporal changes in drug concentrations that have been studied in animal models revealed significant changes to occur already during the early postmortem period [55, 67–70]. The level of dothiepin in cardiac and pulmonary blood samples steadily increased to reach 400% of its original concentration at 8-h postmortem [71]. In a dog model, 2-h postmortem concentrations of fluoxetine and norfluoxetine were 2.2- to 6.0-fold higher than antemortem concentrations, but did not significantly differ from 12-h postmortem concentrations [54]. An overview on drugs in which redistribution is likely to occur or in which postmortem redistribution probably
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Postmortem Toxicology: Artifacts
does not occur is provided by Drummer [3], Leikin and Watson [4], and Baselt [38].
Major Changes of the Media and the Analyte Occurring after Death General Remarks. As indicated in the section “Postmortem Redistribution”, body fluids and tissues as well as drugs present in these specimens are subject to fundamental changes during the postmortem time period. Alterations of the media may considerably impact drug analysis. Decomposition of a corpse involves the processes of autolysis and putrefaction. Enzymes naturally present in the body induce autolytic changes; putrefaction is due to destruction by microorganisms. The onset of autolysis is rapid in cells with high concentrations of hydrolytic enzymes, such as the pancreas and the gastric mucosa, and is slower in the cells of the heart and the liver. Being the specimen of choice for detecting, quantifying, and interpreting drug concentrations, a more detailed review of postmortem changes in blood is given. Postmortem Changes of Blood with Regard to Drug Analysis. Blood is a complex mixture that contains solubilized proteins, dissolved fats, solids, and suspended cells. Serum or plasma is traditionally used in clinical settings because blood affords advanced handling in the laboratory procedures [6]. Drug concentrations provided in literature are usually determined from these fluids. Analytical results obtained from postmortem blood are compared valuably with levels previously reported in therapeutic and toxic conditions [38, 72–74]. However, separation of red blood cells from postmortem blood is usually not possible, and its composition may remarkably differ from a blood sample obtained from a living person. Changes may already occur during agony [75]. Hypoxia reduces the intracellular pH value, thus inducing an increased accumulation of basic drugs into the cells. Neutral or acidic drugs are less affected. Intracellular acidification and changes in ionic strength lead to a damage to the lysosomal membrane, and, subsequently, to enzymatic digestion of the cell membrane and components. Drugs that are concentrated in the cell are redistributed at this stage into the extracellular compartment. After death had occurred, there is a rapid progress in
postmortem redistribution processes due to disintegration of physiological and anatomical barriers (see the section “Postmortem Redistribution”). Postmortem vascular permeation has been shown in an in vitro model using morphine and its glucuronides [76]. In addition to the immediate postmortem dropping of the pH value up to 5.5, a decrease in blood–water content can often be observed [75, 77]. There exist strong variations in the water content of postmortem blood ranging from 59 to 89%. Both hemoconcentration and altered partition behavior affect original drug levels. As the permeability of all cell membranes increases, hemolysis occurs. In addition to hemolysis seen with most specimens, blood coagulates postmortem, and then becomes liquid again. The effectiveness of these two processes will determine whether postmortem blood is clotted, fluid or partially clotted, and partially fluid [78]. Blood clots distribute unevenly in the body. A few hours after death, hypostasis occurs by sedimentation of blood and serum to the lower parts of the body due to gravitation. As a result, concentration measured for any drug exhibiting unequal distribution between red cells and serum may be biased by blood hypostasis, irregular clotting, and hemolysis. Average distribution ratios between whole blood and plasma are given for major drugs in Table 3 [61, 79–88]. Further data of blood-to-plasma concentration ratios are provided by Baselt [38] and Iten [89]. For some drugs, varying blood-to-plasma ratios have been observed between individuals. In patients, chlorpromazine erythrocyte concentrations tended to correlate with plasma concentrations, but the erythrocyte/plasma concentration ratio varied from 0.61 to 2.00 among patients [90]. Ratios may not only vary between drugs but also differ between a particular drug and corresponding metabolites. Some caution is advisable using these data. Most of them are derived from in vitro partition experiments using systems composed of plasma water, plasma proteins, and erythrocytes. When spiked blood is diluted with autologous plasma water, erythrocytes always discharge the compound overproportionally, compared to plasma proteins [91, 92]. Also, ratios may differ depending on whether the sample had been collected from a living person or a corpse. For example, the plasma-to-whole blood concentration ratios of cannabinoids were found to
Postmortem Toxicology: Artifacts Table 3
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Blood-to-plasma concentration ratios for some drugs of forensic interest
Drug Amitriptyline Nortriptyline Cocaine Diazepam Oxazepam Ethanol Methadone Morphine Morphine glucuronides 9 - Tetrahydrocannabinol 11-Hydroxy-9 -tetrahydrocannabinol 11-Nor-9-carboxy-9 -tetrahydrocannabinol
be very similar and their individual coefficient of variation to be very low in samples taken from living individuals. However, data obtained postmortem suggest that the distribution of cannabinoids is scattered over a wider range of values compared to those determined in living subjects. Also, cannabinoids favored postmortem “serum”, the mean ratio between the blood supernatant and whole blood being 2.4, but only 1.6 in samples collected from living people [88]. Generally, the differences observed between blood or plasma are considered to be less important compared to the changes in concentration that may occur prior to sampling. Invasion of intestinal flora into tissues and body fluids occurs rapidly after death, especially at ambient or elevated temperatures. Postmortem blood samples taken 6 h after death in patients who had died of causes other than infectious diseases were tested positive for bacteria [93], whereas in a study on heart blood samples collected 85 h after death bacteriologic cultures gave negative results [94]. Microbial enzymes hydrolyze and transform lipids, carbohydrates, and proteins. As a result, the pH value of blood slowly increases again during the postmortem interval [75, 95]. Postmortem Alterations in Drug Concentrations. Degradation as well as formation of drugs during the postmortem interval as competing processes to postmortem redistribution has been observed. Drugs concentration may change due to chemical and physical degradation, metabolic formation or breakdown (Table 4). Problems also arise from interfering
Ratio 1.0–1.1 1.5–1.7 1.00 0.70 1.00 0.74–0.90 0.75 1.00 1.02 Dependent on hematocrit 0.55, 0.66 0.57, 0.58 0.62
Reference [79] [80] [79] [81] [82] [83] [61] [84] [85] [86, 87] [86, 87] [88]
substances that are endogenously produced during autolysis and putrefactive processes (see the section “Postmortem Redistribution”). Systematic investigations on the time dependence of detectability of drugs or poisons in a putrefying body do not exist. Some case reports revealed that drugs such as morphine or atropine may be identified in specimens from exhumed corpses or from stored tissues many months after death [96]. Comprehensive data on positive drug findings in putrefied bodies had been published by Arnold et al. [97]. For example, phenobarbital, bromazepam, sulpiride, and promethazine could be successfully identified in highly putrefied materials. The interpretative value of these measurements is limited, however. Recovery of organophosphorous pesticides, such as parathion or malathion, was less successful compared to paraquat, whereas recovery of organochlorine compounds was >72% from putrefactive materials [99, 100]. Stevens [95] studied the stability of 56 drugs and drug-related compounds added to drug-free liver homogenates. Degradation was elevated in samples exposed to fly-borne bacteria. From the results, the following molecular structures are assumed to be prone to putrefactive decomposition: oxygen that is bonded to nitrogen as in nitro groups or N -oxides, sulfur, which forms part of a heterocyclic ring, and aminophenol structures. A variable decomposition rate, which was observed for dothiepin in bacteria-contaminated liver and blood specimens, was suggested to be due to differences in bacterial activity [52].
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Postmortem Toxicology: Artifacts Table 4 to [98]
Possible mechanisms operating on drugs postmortem, examples modified according
Mechanism
Example(s)
Chemical instability Hydrolysis Oxidation
Heroin, cocaine, O-acyl-, and N -glucuronides Sulfur-containing drugs and morphine
Metabolic instability Esterases (endogenous)
Metabolic production
Hydrolysis of ester-type drugs Hydrolysis of phase-II metabolites Reduction, e.g., of nitrobenzodiazepines Oxidation, e.g., of thioridazine Ethanol, γ -Hydroxybutyrate, carbon monoxide, and cyanide
The possible role of enteric bacteria in the bioconversion of nitrobenzodiazepines was studied in detail by Robertson and Drummer [101]. It is well known, that in deaths involving flunitrazepam, considerably higher concentrations of 7-aminoflunitrazepam than that of the parent compound can be detected in blood [102]. The conversion of the respective 7-aminometabolites of nitrobenzodiazepines by individual bacteria in blood was species dependent. Significantly higher rates were found for obligate anaerobic species than for facultative anaerobic species, and there was little difference among the species for their ability to metabolize nitrazepam, flunitrazepam, or clonazepam. The conversion rate was slowed down by keeping the corpses at 4 ° C. The effect of pH variation on the metabolic activity of different bacterial species was variable. Postmortem degradation does also concern acidlabile conjugates, such as the ester glucuronides of 11-nor-9-carboxy-9 -tetrahydrocannabinol, propofol, or diflunisal [103, 104] as well as the more stable ether glucuronides [105]. Conversion of morphine glucuronides to free morphine by residual glucuronidase activity or some bacterial enzymes is a most prominent example [106]. The bacteria most likely involved are originating from the gastrointestinal tract. Being the most prominent among them, Escherichia coli is an important source of β-glucuronidase activity. Preferential hydrolysis of morphine-3-glucuronide to free morphine by bacterial enzymatic activity was ascertained in in vitro experiments, and was shown to depend on storage time, temperature, and initial degree of putrefaction [107]. Bacteria, yeast, and fungi can also produce some compounds in the postmortem blood, the most
prominent representative being ethanol. In contrast to drug metabolism, which may persist some time after death, the physiological metabolism of ethanol is assumed to cease at the time of death [108]. A considerable site-dependent variation of the ethanol concentration in blood samples had been observed even in cases where signs of putrefaction could not be noticed [109]. These differences were mainly attributed to death occurring during the absorptive phase where differences between arterial and venous blood exist. Ethanol absorbed from the gastrointestinal tract distributes throughout the body according to the water content of the corresponding tissue or body fluid. The postmortem change in blood alcohol content closely following the change in blood water content, correction for water content has been recommended [110]. In principle, the water content of blood decreases with the time after death. However, there are some exceptions, e.g., drowning experiments with animals indicated a dilution of alcohol in blood [111]. Postmortem changes of ethanol are well documented [112]. The majority of the cases attributed to neoformation did not have significant ethanol concentrations ( diethyl ether >> chloroform > toluene. Leaching of drugs into the fixing/storing solution is evident. In a sildenafil-related death, a comparison of the quantitative values of sildenafil in fixed tissues and those in the same tissues at autopsy revealed a mean decrease of 74%. However, the total recovery from both the fixed tissue and the particular formalin solution was 95% with regard to the original quantity in the same tissue before fixation [132]. Similar observation was reported on the detection and quantification of morphine and strychnine in fixed samples and formalin solutions [133, 134]. Analysis of fixed samples may create problems with regard to the isolation of the analyte and damage of the technical equipment. Iffland et al. [135] succeeded in determining carbon monoxide in clots of heart blood collected from an embalmed body following release of carbon monoxide from the sample by nitric acid. Phenobarbital was detected in fixed brain tissue as well as in the formalin solution in a poisoning case using ultraviolet (UV) spectrometry and thin layer chromatography, whereas gas chromatography (GC) was not applicable due to interferences and damage of the column [136].
Acquisition of Specimens General Considerations The purpose of sampling is to provide a representative part of the whole that is suitable for analysis and reliable interpretation. Sampling is the most important step in drug analysis because an analytical result
will never be better than the sample from which it is derived. Specimens available in postmortem toxicology investigations can be numerous and variable, and may be selected on the basis of the case history, requests, legal aspects, and availability in a given case. So far, a harmonized protocol for sampling in suspected poisoning or drug-related death has not been established [49, 137]. Generally, the specimens routinely collected at autopsy include fluids, such as blood from peripheral sites and heart blood, urine, bile, cerebrospinal fluid, vitreous humor and gastric contents, and organs, particularly liver [49, 138]. The main collection artifact is contamination, but can be reduced by sampling before the autopsy, if appropriate. It is difficult, if not impossible, to acquire quality specimens once autopsy has been completed. An appreciation of how contaminants may be introduced is also important.
Sampling Artifacts Incorrect Selection and Acquisition of Samples. Samples taken for analysis should always be chosen bearing in mind the disposition of the drug in the body. An incorrect or insufficient sampling will severely affect case investigation Toxicology: Analysis. In fatalities requiring quantitative determination, a blood specimen is preferably taken from the femoral vein prior to autopsy, for contamination may be avoided, and this site is less affected by postmortem changes (see the section “Changes Occurring after Death”). If the femoral vein is ligated prior to sampling, the sample is likely to be relatively uncontaminated by blood from the major organs [40]. Cardiac blood is regarded as unsuitable for quantitative analysis of drugs. Diffusion out of the stomach can artificially raise the cardiac blood concentration, and a sample may equally contain blood that has drained from the lungs, the vena cava inferior, the aorta, and the subclavian veins. If a heart blood specimen is sampled through the chest wall, one should be aware that the sample is contaminated with thoracic fluid and gastric contents. Postmortem specimens obtained from patients who have died several days after a drugrelated episode are likely to give negative results [2]. It is essential to perform toxicology investigations on specimens obtained on or soon after admission to hospital. In fire victims, blood that is not collected from body regions excluded from severe burning can contain falsely elevated carbon monoxide levels due
Postmortem Toxicology: Artifacts to diffusion of environmental carbon monoxide and binding to hemoglobin. Relying on a result from a single specimen may be misleading. It is recommended to collect blood from at least two different sites or, if not available, along with other specimens, at least. Urine is a valuable specimen, because it can easily be tested, and drugs and drug metabolites are usually found in high concentrations Drug Testing: Urine. A sample collected during autopsy may be contaminated by blood and should preferably be taken prior to autopsy by puncture of the abdominal wall. A positive identification indicates recent drug use, but does not indicate when or how much drug was ingested. There is little correlation between urine and blood concentrations. If death takes place quickly, urine findings can be negative. Analysis of a specimen may not be a reliable means to reveal ingestion of drugs, e.g., sertraline and norsertraline, which are present in very low concentrations or were not renally cleared [38]. Analysis of a urine specimen may reveal exposure to organophosphate compounds or analysis of toluene, xylene, and trichloroethylene via identification of their major metabolites in cases where blood analysis will fail to detect these compounds [38]. Local anesthetics, e.g., lidocaine, which are used on catheters, are a common finding in urine samples. Gastric contents are a useful specimen to rapidly discover drug overdose, for oral ingestion is the major administration route of prescribed drugs. The total amount of a drug or poison remaining in the gastric contents is far more important than its concentration. A low absolute amount does not rule out the possibility of an overdose. Also, a low drug concentration in the stomach may arise from passive diffusion from the blood into stomach contents. This phenomenon is frequently observed in drugs being weakly basic in nature [33]. Since the gastric contents can be largely inhomogeneous, the entire specimen should be submitted or mixed before an aliquot is taken. The odor of gastric contents or colored material can potentially point to a specific agent, although, e.g., blue stains may result from parathion or flunitrazepam ingestion. Bile represents a collection and storage depot for many xenobiotics and corresponding metabolites that have a biliary excretion and are subject to enterohepatic cycling. To avoid contamination of surrounding tissues, the gall bladder should be tied off
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before removing from the liver. Drug concentrations can be significantly higher in bile than in blood. The mean bile to blood ratios varied from about 1 for acetaminophen and amphetamine to about 2000 for desmethylclobazam. In several cases, a drug could be identified in bile, but was not detectable in blood [139]. A qualitative finding in bile may indicate previous or chronic exposure to a drug or poison. Cerebrospinal fluid and vitreous humor are aqueous and transparent fluids, which are useful to screen for a variety of drugs [140]. Both cerebrospinal fluid and vitreous humor also contain very little proteins. Therefore, drugs highly bound to proteins or lipophilic in nature tend to be found in lower concentrations in these fluids than in blood [49, 141]. A major limitation to the use of cerebrospinal fluids is the small database of reference values [142], whereas vitreous humor has been used to analyze a larger number of drugs [143–150]. Many studies have stressed the usefulness of vitreous humor for alcohol analysis [151]. However, the wide variation of vitreous humor to blood ethanol ratios must alert when results from vitreous humor are used to estimate the concentration in femoral venous blood [152]. Tissue specimens collected for postmortem toxicology investigations include liver, kidney, lung, brain, skeletal muscle, and adipose tissue [49, 151]. Tissue samples may be useful in cases with an extended postmortem time period and whenever body fluids are not available. Extensive data had been published for liver and kidney, less for brain and lung specimens [38, 153]. Drug concentrations in liver were found to be site dependent (see the section “Postmortem Redistribution”), and sampling from deep within the lobe has been recommended [154]. Concentrations in brain may also significantly vary from one region to another [155]. The within-case variability of drug levels observed in muscle specimens supports the opinion, that drug analysis on skeletal muscle is rather qualitative than quantitative in nature. Muscle specimens had also been considered for alcohol analysis, but the muscle to blood–ethanol concentration was found to depend on the time course of ethanol absorption, distribution, and elimination [156]. A skin specimen or a cube of muscle may support evidence of the route of drug administration [49]. As skin acts as a temporary drug reservoir, the specimen should always be excised together with a
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random specimen preferably taken from a similar site to act as control [157]. Hair is an ideal specimen for determining, e.g., chronic arsenic and mercury poisoning [158]. Also, numerous drugs and poisons have been detected in hair in recent years (see Hair: Toxicology) [159, 160]. The amounts deposited in hair are functions of both ingestion/exposure and of the metabolic regimen. Segmentation of the hair can assist in estimating the time of exposure. A decrease in drug concentration in the proximal sections of hair may indicate a decrease in tolerance to the drug. There are many factors that influence drug concentrations in hair: biological factors such as hair structure and pigmentation, individual factors such as drug use, customs culture or race including hair care, environmental factors, and also methodological factors [30]. External uptake of drugs from blood, vomit, or putrefactive fluids leads to artificially elevated drug levels in hair, which will not be fully removed by common wash procedures [31]. Specimen Containers and Preservation. The use of appropriate specimen containers and preservatives can be critical with regard to ultimately identify a substance in an individual specimen. Specimens must be collected in separate, clean containers, which should be filled up to minimize evaporation of volatiles and oxidative losses of drugs. The best materials to collect and store fluids or tissue specimens are glass containers. Sampling into a glass container is a must, if solvent abuse or an anesthetic death is suspected. Essential are also aluminum foil- or Teflon-lined lids to prevent gas escaping and to minimize drug adsorption. Solid tissue samples may also be placed in nylon bags, which are tightly sealed [138]. Most types of plastic containers are suitable for the collection of tissue specimens in drug-related fatalities. Disposable hard plastic tubes or Nalgene bottles with screw caps are also recommended for collection of body fluids for breakage of these containers upon freezing had not been observed [161]. The use of evacuated tubes is less desirable, for sample contamination from plasticizers used in their manufacture may occur. For collection tubes containing gel separators, a gross contamination by toluene, 1-butanol, ethyl benzene, and xylene has been reported [162]. Evaluating the container before
routinely collecting specimens in it might reduce production of artifacts. Obligatory recommendations for specimen preservations do not exist. Specimen preservatives are generally not required for specimens other than blood. In addition to a preserved blood sample, an unpreserved specimen available to the toxicologist is optimal, for preservation strategies depend on the target analytes and are not unique. Fluoride preservation with a final concentration of 1–5% sodium fluoride by weight is recommended for postmortem analyses of alcohol, cocaine, cyanide, and carbon monoxide. Postmortem synthesis of ethanol can be effectively inhibited, whereas hydrolysis of cocaine can only be slowed down by fluoride preservation [163]. A general problem with ester-type drugs is the presence of esterases; as degradation takes place even at 4 ° C, immediate freezing of specimens is recommended [164]. Artificial production of GHB has been observed in blood samples not collected in fluoride-containing tubes [165], and also in specimens collected in citrate buffer [121]. Fluoride preservation must not be used when organophosphorous chemicals are involved. For example, rapid degradation of metrifonate (dichlorvos) was found to be favored by the presence of sodium fluoride, esterases, elevated temperatures, and alkaline condition [166]. Early acidification of the specimen and storage at −80 ° C was recommended by Heinig et al. [167]. Acidification may also stabilize cocaine or labile conjugates such as N -glycosides [5, 168]. Ascorbic acid may be used as an antioxidant. For example, losses in olanzapine during storage at 4 ° C may be reduced by the addition of 0.25% ascorbic acid [169]. Apomorphine, like most catechols, is prone to oxidation to quinones, unless ascorbic acid is added as an oxidant [170]. However, the presence of an antioxidant may have reverse effects. During storage reduction of the N -oxide metabolites of chlorpromazine, of samples containing antioxidants, resulting in an increase in the concentration of the parent drug, has been observed [171]. Anticoagulants are not recommended for postmortem blood samples because these additives may also affect drug concentration. Blood concentration of morphine in ethylene diamine tetraacetic acid (EDTA) tubes was 4.8% higher than in heparin tubes [172], which also contain phenolic preservatives such as cresol [171].
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Stability During Storage In clinical chemistry, stability is defined as the capability of sample material to retain the initial value of a measured quantity for a defined period within specific limits when stored under defined conditions. The individual maximal permissible instability is preferably linked to the criteria of analytical imprecision, and is expressed as the critical difference [173]. This procedure allows defining the maximum permissible storage time for an analyte in a particular specimen at a given condition. In postmortem investigations, such consideration starts at the time of sampling and covers the time until analysis. The presence and extent of alterations since the time of death can only be estimated, part of them even cannot be avoided, and they cannot be undone. Therefore, knowledge on degradation mechanisms in a particular matrix and on resulting breakdown products is important. A review on poisons, drugs, and heavy metals suspected to be unstable is given by Leikin [4] and Ellenhorn [174]. Unfortunately, the particular biological matrix, which may play a role in the stability of an analyte, has not been considered. For example, in urine, cocaine is chemically stable at a pH of less than 7.0. In blood samples, even acidic conditions do not prevent cocaine to be metabolized by residual esterase activities. Interestingly, cocaethylene seemed to be more stable in postmortem specimens than cocaine. Muscle as well as brain tissues were considered to be the specimen of choice for testing both cocaethylene and cocaine [168]. Valuable information on artifacts is provided by Baselt [38] and Drummer [175]. Comprehensive data on the stability of drugs of abuse in blood were reported by Levine and Smith [176] already in 1989. A recent update was given by Skopp and P¨otsch [177]. Data on the stability of drugs in tissues are rare. In principle, all volatile compounds such as aerosol propellants, anesthetic gases, carbon monoxide, ethanol, and organic solvents are unstable during storage. Losses of up to 25% of blood toluene have been observed in glass tubes stored unopened for 7 days at room temperature, and considerably higher losses were noted in glass tubes with rubber stoppers [178]. There is an artifactual rise in carbon monoxide level in unpreserved blood specimens since bacterial action can result in both the production of carbon monoxide and the denaturation of hemoglobin
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[38]. The formation of toxicologically significant concentrations of cyanide in postmortem tissue has been demonstrated, which was attributed, in part, to conversion of thiocyanate to cyanide and breakdown of proteins [179, 180]. Conversely, a significant decrease in blood cyanide concentration has been attributed to mechanisms that include evaporation, thiocyanate formation, and reaction with specimen components [181]. Temperature and cyanide concentration are apparently important factors in these changes [182]. Another important consideration when measuring drugs is the stability of corresponding metabolites. Highly labile metabolites such as sulfate conjugates and N - and acylglucuronides may rapidly be converted back to the unconjugated compound and consequently result in falsely elevated concentrations. Examples are the N -sulfate metabolite of minoxidil, N -glucuronide metabolites of nomifesine, and 11-nor-9-carboxy-9 -tetrahydrocannabinol glucuronide [103]. Some of the degradation mechanisms seen during storage are similar to those observed during autolysis and putrefaction (see the section “Major Changes of the Media and the Analyte Occurring after Death”). Generally, degradation of a drug occurs through hydrolysis, oxidation or reduction processes, and is generally slowed down by decreasing storage temperatures and preservation of the sample (see the section “Specimen Containers and Preservation”). These processes are due to endogenous enzyme activities, e.g., esterases still operating in the sample, chemical reactions or to enzyme activities such as glucuronidase following bacterial invasion during the postmortem interval (see also Table 4) [98]. Experimental investigations on time-dependent changes give information on the reaction type involved in drug degradation [183], and may guide to a more proper estimation of the drug level at the time of sampling. Hydrolysis of ester-type drugs generally exhibited an apparent first-order reaction kinetic, whereas an oxidation can often be described by a second-order reaction kinetic. Investigations on the reaction type involved in the degradation of forensic relevant drugs have already been performed, e.g., for morphine, morphine glucuronides, cocaine, benzoylecgonine, ecgonine methyl ester, lysergic acid diethylamide (LSD), and 11-nor-9carboxy-9 -tetrahydrocannabinol glucuronide [103, 105, 163, 184].
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The mechanisms involved in the breakdown of benzodiazepines are poorly understood. Hydrolysis and reduction are suggested to be involved in their degradation. Degradation of nitrobenzodiazepines occurs very rapidly, whereas other benzodiazepines do not appear to be as unstable [101, 185]. Besides bacteria, major influence factors in the degradation of nitrobenzodiazepines are an increased temperature and the absence of sodium fluoride [186]. Chlordiazepoxide tends to form desoxychlordiazepoxide during storage, and further degrades to nordiazepam, which also represents a metabolite and an artifact in the analysis of the parent drug by GC [187]. Terbutaline was shown to be stable in spiked postmortem blood at room temperature for 7 days. In contrast, a loss of 83% was observed for fenoterol in spiked postmortem blood at the same conditions. Only 7% of the initial concentration was present after 6 months at 4 ° C. The instability of fenoterol is most likely a result of the presence of the phenolic group attached to the side-chain nitrogen atom, which is susceptible to oxidation [188]. There is evidence that different degradation mechanisms operate in blood depending on its source, either obtained from living individuals or collected from corpses. An experimental investigation on morphine and its glucuronides in spiked fresh blood and plasma revealed that oxidation primarily affected drug stability, whereas in postmortem samples stored under the same conditions, hydrolysis of morphine glucuronides was assumed to be the predominant reaction [105]. Sometimes, metabolites or breakdown products are far more stable than the parent drug. Complete degradation of furazolidone occurred in muscle tissue stored at 4 ° C during 24 h. Even storage in liquid nitrogen did not fully stabilize furazolidone [189] indicating that analysis of a metabolite, which is reasonably stable, may be favored [190]. The poor stability of cocaine, benzoylecgonine, and ecgonine methyl ester is well documented [163, 183, 191]. Alternate analysis for ecgonine representing a rather stable breakdown product may be performed in highly putrefied specimens or specimens stored for long periods of time. Most drugs or poisons are probably stable in biological materials for months, particularly if frozen and special arrangements may prevent loss of an analyte by degradation (see the section “Specimen Containers and Preservation”).
Analytical Artifacts Although the history of a sample appears to be most relevant to the production of artifacts, analytical artifacts may also be considered during the isolation and identification of an analyte. For most drugs and poisons, a two-stage testing is usually employed, comprising a preliminary screening test followed by confirmatory analysis, which should offer a higher degree of specificity for the analyte than the first test. A gross overview on common methods used in postmortem toxicology investigations has been given by Hearn and Walls [1] as well as by Drummer [3]. There is little to differentiate in analytical procedures used in other forms of forensic toxicology with respect to postmortem toxicology investigations. Available immunoassays can yield positive results in urine for metabolites from most of the common benzodiazepines, except lorazepam and flunitrazepam [1]. These drugs may not be detected until hydrolyzed [192]. Interaction with putrefactive amines is commonly seen in immunoassays for amphetamine-type drugs [193]. Interactions are not limited to matrix effects or the structural and conformational similarity of compounds. Further information on crossreactivity and potential mechanisms is given by Richardson [2]. In addition, turbid, highly colored, or opaque specimens can interfere with the detection principle affording an intensive preextraction step. Chromatography has been the mainstay of drug analysis for many years. Often, a special pretreatment or homogenization according to the specimen’s nature and/or a more sophisticated cleanup extraction of putrefied materials is required for all forms of chromatography. Extraction into an organic solvent for partial purification of a biological fluid or a tissue homogenate is still widely used. Lipophilic compounds will be readily extracted by nonpolar solvents. The more polar solvents being partially miscible with water will also remove water-soluble materials. As a result, drug conjugates are also transferred into the organic phase. If phase-II metabolites are subsequently hydrolyzed, this will lead to erroneously high levels of the parent drug [103, 194]. The phenomenon of conjugate instability is most common with labile conjugates such as N - or O-acyl-glucuronides [103, 104]. The chemical properties of a solvent can give rise to chemical reactions of the solvent itself and the insidious breakdown products or stabilizers it
Postmortem Toxicology: Artifacts may contain. For example, the effect of phosgene in chloroform has been reported as a cause of artifactual formation of carbamate derivatives during extraction of tricyclic antidepressants [195]. The problems associated with solvent extraction can be minimized by using solid-phase extraction. Because of its far greater variability, one must be well informed on the mechanisms of interaction to maintain proper control on the separation. If blood cells are not disrupted or if particles are still present in the sample, flow rates and reproducibility are altered. The extraction efficiency of a drug or metabolite from a postmortem specimen may be variable from case to case, or even from site to site within the same corpse. It may also be markedly different than from a particular blank specimen used for calibration. The use of stable isotope internal standards may provide a higher degree in the accuracy of the analytical results. Unfortunately, few deuterated standards are commercially available for drugs, metabolites, or artifacts. It is often necessary to evaporate extracts to reconstitute them into small volumes for transfer to chromatography. The most common routes of sample loss are adsorption onto glassware and volatilization of the drugs, e.g., of amphetamines. Adsorption losses can be prevented, e.g., by silanization of glassware or by including a polar solvent, such as amyl alcohols, as an additive to the extracting solvent or prior to evaporation. The problem of amphetamines’ volatilization can be solved by converting them to their nonvolatile hydrochloride salts [6]. Gas chromatography coupled to mass spectrometry (GC/MS) is generally accepted as unequivocal identification for most drugs, and provides best confirmatory information. Also, liquid chromatography coupled to mass spectrometry(LC/MS) is an emerging technique [3]. There are several drawbacks with GC/MS analyses; some of them are included in Table 5. It is now recognized that determination of major metabolites and degradation products along with the Table 5
Potential problems with GC/MS analyses(a)
Erroneous identification at a low analyte concentration Misidentification due to interfering substances Inadequate information due to similar (barbiturates) fragmentation behavior Production of low mass fragment ions only (tricyclic antidepressants) (a)
Reproduced from Ref. 1. Taylor & Francis Group, 1998
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parent drug is essential to avoid misinterpretation of the data due to artifacts [196]. Such a stabilityindicating assay is one that can accurately and selectively differentiate the intact drug from its potential decomposition products.
Conclusions Artifacts must be accepted as an integral part of postmortem toxicology, frequently interfering with a straightforward interpretation of the analytical results. Reporting all the details of the scene investigation and terminal events as well as of the social and medical history will aid to recognize important issues that may occur during the antemortem phase with respect to postmortem findings. There is general agreement that drug concentrations are site dependent and tend to change with time, most significant alterations occurring already perimortem or rapidly after death. Heart blood concentrations are often higher than those of peripheral specimens. However, there does not appear to be a way to predict the relationship between drug levels derived from various specimens nor the manner in which the concentrations may change with time. To circumvent the problem of postmortem redistribution, it is recommended that blood be sampled from a peripheral vessel along with at least a second specimen taken from a different site, liver from deep within the right lobe and lung rather from the apex than the base. Tissue samples can be of value to assess the significance of a drug in the death of an individual provided that a sufficiently large database has been established. Tables of therapeutic, toxic, or fatal ranges or correcting for blood-to-plasma ratio cannot be applied without restrictions. As the exact mechanisms of postmortem redistribution are not fully understood and most likely a combination of several factors, exact estimates of the dose are unreliable. Postmortem degradation as well as formation of compounds have been observed, and may vary between tissues and body fluids as well as from drug to drug. For example, ethanol may be formed in postmortem blood in variable and nonpredictable amounts. In severely putrefied, embalmed, or formalin-fixed tissue, fundamental changes of both the matrix and the drug should be considered. Complete degradation or even removal of a drug may have occurred.
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Sampling poses a high risk of contamination and/or production of artifacts. Correct sampling prior to or during autopsy is as essential as is the use of appropriate containers and preservatives including deep freezing. Some drugs or metabolites may undergo further decomposition during storage for several months. Changes in materials and target analytes often require modifications of routinely applied analytical procedures; the most valuable appears to be a stability-indicating assay. A thorough cooperation of the pathologist and toxicologist will enable to handle some of the problems addressed above. Some postmortem artifacts will never be resolved, whereas others are amenable to further elucidation from both case reports and experimental studies.
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GISELA SKOPP
Postmortem Toxicology: Interpretation
Postmortem Toxicology: Interpretation Introduction The detection of drugs and other substances in biological tissues, such as blood, represents the first stage in the application of toxicology to the forensic sciences. The presence of drug including situations where quantitative data are available requires careful interpretation. With few exceptions, interpretation requires a thorough understanding of the circumstances of the case and an advanced knowledge of how the substances detected by the analyses interact with the body. Thus, knowledge of both the pharmacokinetics (effect of drug) and the pharmacology of the substance is required and must be carefully related to the known circumstances of the case. This article provides an overview of the basic pharmacokinetics of drugs and how route of administration and the overall health of the person can influence the interpretation of toxicological results. Several examples are included to illustrate how toxicological data can be misinterpreted. Other articles in this encyclopedia provide details of the expected effects of substances; see sections on drug classes: alcohol, amphetamines, cocaine, benzodiazepines, and the opioids (opiates). (See also Behavioral Toxicology).
Basic Pharmacokinetics To understand the way substances such as drugs are absorbed and the time course of their presence in the body, it is necessary to understand some basic effects of drugs in the body, known as pharmacokinetics [1, 2]. The main pharmacokinetic phases can be segregated as follows: absorption, distribution, and elimination.
Absorption Drugs that are swallowed rely on the release of the drug or other dose form in the stomach or small intestine. This can occur through disintegration of
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a tablet or through a controlled release of drug from the tablet matrix. Controlled release of drugs is designed to slow the absorption, to (usually) prolong the drug’s actions, or sometimes to protect the stomach from potentially harmful drug (i.e., entericcoated tablets). Except for some acidic drugs (e.g., acetylsalicylic acid), drugs are primarily absorbed in the small intestine and then mainly in the upper sections (jejumen). The delay from swallowing to first appearance of drug in the blood stream can be typically 15–30 min and will occur over many hours. The time to the maximum blood (or serum) concentration is termed Tmax (units: time such as hours), while the concentration at this time is termed Cmax (units: mass per volume, i.e., milligrams per liter). Many drugs once absorbed (or their subsequent metabolites) can be excreted into the bowel through bile and become reabsorbed further down the gastrointestinal tract. This is known as enterohepatic recirculation and can lead to an apparent delay (or even a second peak) in the absorption of drugs. Morphine is a common example in which morphine glucuronide metabolites secreted into bile find their way back into the bowel and are subsequently reabsorbed. Unabsorbed drug is present in feces and can represent a significant proportion of the administered drug. A number of pharmaceutical formulations provide a controlled release of drug from a tablet matrix. This is used to control the absorption of drug into the body and provide a longer duration of action of the drug. This is typically used for drugs with short biological actions and has the net result in reducing the need for repeated doses within a 1-day period. For example, morphine and oxycodone can be given twice daily rather than four times daily when formulated into a sustained delivery tablet or capsule.
Distribution Once the drug is absorbed and has entered the blood stream, it is distributed to all parts of the body. The uptake of drug into tissues and organs will depend on access of drug to all parts of the tissue (e.g., blood supply) and the relative affinity of the drugto-tissue components. There is considerable variation of drug uptake for different drugs and also between individuals. For some drugs, the affinity of drug to a tissue can be manyfold higher than the blood (e.g., THC in fat and muscle tissue).
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Postmortem Toxicology: Interpretation
The distribution phase is variable but usually requires some hours or days of exposure before some form of steady-state situation is reached.
Elimination All foreign substances are eventually removed by the body; the rate depends on the drug and its ability to be metabolized (e.g., by liver) and excreted by the kidneys and other organs. Some drugs, e.g. cocaine, are rapidly metabolized to less active compounds and excreted within hours, whereas methamphetamine may only be excreted within days. The metabolism of drugs can be quite complex and often involve multiple pathways. In some cases, metabolites are also biologically active and contribute to the pharmacological response in a person (e.g., methamphetamine is metabolized to the active amphetamine) [3]. The time to halve the blood concentration (following the peak concentration) for methamphetamine can be over 1 day. This time is called half-life. This value applies to the terminal elimination phase once the drug has been fully absorbed and distributed to bodily tissues. There is considerable variation in half-lives among individuals, even for the same drug. Half-lives measured before the terminal elimination phase is dominant will generally underestimate the terminal elimination rate. Some pharmacokinetic data including terminal elimination half-lives for common drugs of abuse are given in Table 1. The term clearance is often used as another measure to quantify the removal of drugs from the body and represents a composite of all forms of drug removal. This includes a combination of kidney excretion, liver metabolism, and other sources of drug removal. For volatile substances, elimination can also occur through expiration, e.g., alcohol (ethanol), solvents, although this is still a relatively minor source of elimination compared to metabolism and excretion through the kidneys.
Route of Administration and Bioavailability The proportion of drug available to the body when compared with another route of administration is termed bioavailability. This term usually refers to the
Table 1 drugs
Typical pharmacokinetic data for some common
Drug Alprazolam Amphetamine Diazepam Cocaine Codeine MDMA Methadone Methamphetamine Morphine
Typical blood Dose range concentrations Half-life (days)(c) (mg)(a) (mg l−1 )(b) 0.5–4 From 10 5–40 From 25 8–60 50–150 5–120 From 10 From 5
0.05–0.2 0.1–0.2 0.1–0.6 0.1–0.5 0.1–0.3 0.1–0.3 0.1–0.3 0.05–0.2 0.1–0.4
0.3–1 0.3–1.5 0.8–2 0.6–4 0.1–0.2 0.4–1 0.6–3 0.5–1.5 0.1–0.4
(a)
Usual dose range Typical blood concentrations following common doses seen in forensic cases (c) Pharmacokinetic half-life of terminal elimination phase MDMA, 3,4-methylenedioxymethamphetamine (b)
comparative availability of drugs that are orally taken compared with the same dose given intravenously. Drugs that have a bioavailability of 100% are completely absorbed orally and are not metabolized prior to entering the blood supply. For example, morphine has a bioavailability of 25% when given orally as tablets, meaning that only 25% of morphine is available to the body after oral administration. In total, 75% is either not absorbed or is metabolized prior to entering the blood. When morphine is given by intravenous injection, the bioavailability is 100%. Moreover, the injection has delivered the drug to the blood stream almost instantaneously by passing the absorption phase. Drugs given by intravenous injection will have an immediate intense effect on the person. In abuse situations, such as in the use of heroin, this can precipitate a cardiorespiratory collapse and sudden death [4]. Substances given by other modes of administration, e.g., nasal insufflation (snorting), inhalation (volatile substance abuse), smoking, etc., have different rates of drug absorption.
Single versus Multiple Doses The pharmacokinetics of drugs do not generally change with repeated doses of drug; however, depending on the time between doses, there can be carryover from previous dose(s). For example, a drug with a half-life of 12 h will need about five times this
Postmortem Toxicology: Interpretation for the drug to be removed from the body. Hence, the administration of a further dose earlier than 60 h (5 × 12 h) will result in some accumulation of drug from dose to dose. In practice, multiple doses are given at least daily, and sometimes two or three times daily; hence, drugs with half-lives of more than a several hours will result in larger pharmacological responses on repeated dosing [1]. Methadone, a drug related to morphine, is used widely to treat dependency to heroin and other opioids. It has a half-life of about 24 h and when given once daily, the blood concentrations increase substantially over the first 5 days of treatment. This can cause potentially fatal toxicity if the initial doses are too high for the established tolerance to opioids [5]. To avoid this phenomenon, low starting doses are recommended, with daily monitoring for the first week of treatment to ensure optimal safety (and response) for the subject. The interpretation of blood concentrations in a person on a drug such as methadone is further complicated by the accumulation of drug with repeated doses. Hence, the only way a toxicological result can be properly interpreted is to establish whether the drug was likely to have been taken as one (larger) dose or by repeated (smaller) doses.
Predicting Blood Concentrations There is considerable variation in the way humans respond to drugs. A standard dose, even when corrected for body weight, will show considerable pharmacokinetic variability from one person to another and will even vary in the same person when
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the substance is given on separate days. This is because any one of the three processes (absorption, distribution, and elimination) will affect the plasma concentration versus time profiles. This difference is increased when the drug is given orally when compared with injection, since variability in absorption also occurs. Figure 1 illustrates schematically what would be expected of typical person-to-person variability for an orally administered drug when both Tmax and Cmax are quite different, and the overall area under the plasma concentration versus time profile indicates the amount of drug available to the body. It is important to understand that each drug has its own pharmacokinetic properties. These include the rate of absorption, the degree of distribution in bodily tissues, and the rate of metabolism and elimination. Standard texts provide details of the relevant pharmacokinetic factors to provide a guide as to the effects of the particular drug [2, 6]. A number of physiological factors can further affect blood concentrations of drugs. These include any disease that alters absorption, distribution, and elimination. The most common diseases are those of the liver and the kidneys, since these are the most important organs involved in the elimination of drugs. Liver is a major organ that metabolizes drugs to (more water soluble) metabolites that are more likely to be excreted by the kidneys [7]. Heart disease, such as congestive heart failure, can also affect drug clearance since blood flow through vital organs is reduced. Advanced age (over 70 year) will usually result in reduced organ function, leading to a reduced ability to process drugs. Older (but otherwise
Concentration (mg l−1)
3 2.5 2 1.5 1 0.5 0 0
2
4
6 Time (h)
8
10
12
Figure 1 Stylized blood concentration versus time profiles showing possible diverse profiles in two different persons given the same dose of drug orally
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Postmortem Toxicology: Interpretation
healthy) persons will often require lower doses for their weight than their much younger counterparts. The net consequence is that there is substantial variability in blood (and plasma/serum) concentrations for a given dose of substance even if the time of administration is known. In a great proportion of forensic cases, the time of dosage is unknown and in many instances the mode of administration (e.g., oral, intravenous, nasal insufflation, etc.) is usually assumed.
In situations involving the interpretation of toxicology results in deceased persons, it is probable that concentrations of drugs (and other substances) would have changed from the time of death [3, 8]. These changes have been described in Postmortem Toxicology: Artifacts.
Postcollection Artifacts Some substances are unstable chemically and can degrade postcollection, particularly, if optimal storage conditions are not maintained. This applies not only to volatile substances such as alcohol but also to nonvolatile substances that are not chemically stable under the storage conditions and, in particular, biological matrix.
Methamphetamine
Cocaine
(a) (b)
Table 2 summarizes examples of how a particular drug concentration in blood can be differentially interpreted based on the available information. See Cocaine; Opioids; Amphetamine.
In the case of methamphetamine, where the drug can accumulate with repeated use and produce much greater concentrations than after single doses, it is not possible to infer from a concentration the likely consequence of the drug. Similarly, with long-acting opiates such as methadone, accumulation occurs from one dose to another, leading to apparent elevated concentrations after some days of use. The interpretation is further compounded by the neuroadaptation that occurs to drugs with repeated use, leading to tolerance of potentially harmful effects [5]. The context of the death is critical to understanding the role, if any, of the drugs detected. For example, a person can die from the effects of using too much cocaine (usually from an adverse effect on the heart), but equally well a person can die from a
The effect of circumstances on the interpretation of toxicology results
Drug
Morphine
Examples
Repeated Use of Drugs
Postmortem Artifacts
Table 2
These changes have been described in Postmortem Toxicology: Artifacts.
Blood concentration Circumstances (mg l−1 )(a) 0.5
0.5 (free)
0.5
Likely interpretation(b)
Single oral dose, 2 h postdose
Moderate-to-high doses (100 mg) Moderate dose, potentially toxic (>50 mg) Moderate dose, potentially toxic (>50 mg) Low-to-moderate doses, likely to be safe (100 g)
Bile
(At least 5 ml or whole gall bladder)
Vitreous humor
(All available ∼2–5 ml)
Gastric contents Hair
(All)
Useful to confirm recent drug use and concentration, if a drug found, is useful for toxicological interpretation Mainly for alcohol and for analysis of some drugs requiring preservation Useful for broad class of drug screening but may not be useful on timing of drug administered Useful solid tissue samples to supplement blood data especially when blood is not available but limited literature data available Useful fluid for drug screening especially when urine is not available Useful in alcohol analysis and, if necessary, some other drugs (e.g., digoxin, glucose, urea nitrogen, uric acid, creatinine, and antipsychotic drugs) Indicative of recent drug administration
Identify distal and proximal end (>50 mg)
Lung
(50 g)
Brain
(50 g)
Blood
Drug use history provide information of drugs/poisons and metal exposure in scales of months For volatile substances (such as H2 S and chloroform poisoning) Brain may be useful in infant drug deaths or for volatile poison cases
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2.
3.
Postmortem Toxicology: Laboratory Analysis
should be seized as analysis of these items may be valuable for determining the subsequent type of analysis to be performed on the biological specimens. In some cases, household products, such as caustics, solvents, or pesticides, may also provide useful clues. While circumstantial evidence can provide hints, it can never substitute the analysis of body fluids or tissues because substance(s) found at the scene may not necessarily be connected to the death and often other substances are detected that are not obvious from the circumstances. A comprehensive list of medications (especially recent medications prescribed) given to the deceased with relevant medical history should be provided. Any physical abnormalities identified during autopsy may be indicative of intoxication or poisoning and a list of examples is given in Table 4 [6]. In this case, additional analysis targeting for the presence of possible toxic substances may be required.
Analytical Aspects in Postmortem Toxicology Ingested substances are metabolized, being broken down or transformed into other species before they Table 4 Useful findings related to toxic substances observable during autopsy Possible Indication Color of skin Cherry red to bright red Grayish to brownish Nasal/oral cavity Residues of powder or colored material
Oral cavity/ gastointestinal tract White, corrosive staining Black-brown, corrosive staining Glass-like, reddish necrosis
Carbon monoxide or cyanide Nitrate, nitrite or aniline Intransal drug use (e.g ketamine, cocaine), ingestion of tablet or capsule residues
Hydrochloric acid Sulphuric acid Alkaline agents (e.g. sodium hydroxide)
are excreted. Hence, identification of the original ingested material often involves considerable complications, for example, heroin is first metabolized into 6-acetylmorphine and then to morphine, while 9 -tetrahydrocannabinol (THC), an active ingredient in cannabis, is first converted to 11-hydroxy9 -tetrahydrocannabinol and then to 11-nor-9 tetrahydrocannabinol-9-carboxylic acid. In addition, the active constituent in a regular dose ranging from grams or milligrams is diluted to a concentration usually in the range of micrograms or nanograms per milliliter of body fluids or per gram of tissue by way of dispersion throughout the body. The analytical method to be utilized must be capable, both in terms of sensitivity and specificity, of detecting the target substances at low concentrations and in complicated biological matrices (see Postmortem Toxicology: Artifacts).
Analytical Techniques There are a wide variety of analytical techniques available for the analysis of toxic substances in biological specimens. The most common techniques used in modern toxicology laboratories include various immunoassays with different detection principles, color tests (e.g., Ferroin for CN, Marsh test for arsenic, etc.), instrumental chromatographic techniques using high-performance liquid chromatography (HPLC) and gas chromatography (GC) coupled with various detectors. To effectively apply chromatographic techniques, an extraction procedure is required to separate the intended drugs/poisons from biological matrices followed by reconstitution in appropriate solvents compatible with the requirements of the intended instrumentation. Immunoassays. A number of immunoassays intended for antemortem analysis can also be used for postmortem analysis especially when urine is available. Immunoassay is based on the principle that the drug is detected by its ability to displace or block the binding of a fixed amount of labeled drug molecules present in the reagent. The label can be a fluorescent molecule (e.g., fluorescence polarization immunoassay (FPIA)), an enzyme (e.g., cloned enzyme donor immunoassay (CEDIA), enzyme multiplied immunoassay technique (EMIT), and enzymelinked immunosorbent assay (ELISA)), a radioactive isotope (e.g., radioimmunoassay (RIA)) or other substance that can be detected by means of instrumentation. Some assays can distinguish between bound
Postmortem Toxicology: Laboratory Analysis
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and free labeled drug in a mixture are known as homogenous immunoassay, such as CEDIA, EMIT, and FPIA. For heterogenous immunoassays, such as ELISA and RIA, they require a washing step to separate the bound labeled complex from free labeled reagent prior to analysis. Thus, homogenous immunoassays are easier to be automated and less labor intensive than heterogenous ones. In general, immunoassays are fast, sensitive and, in homogenous immunoassays, direct detection can be achieved without sample purification. It is used for screening of common abused drugs, such as opiates, amphetamines, cocaine, cannabinoids, phencyclidine, and barbiturates. In addition, prescribed drugs, such as propoxyphene and tricyclic antidepressants, can also be screened with the use of specific reagents. For postmortem screening, antibodies having broad drug selectivity within a class of drugs (e.g., sympathomimetic amines) are preferred over those that are sensitive to a specific drug (e.g., methamphetamine) as it allows the screening of drugs within the same class. The sensitivity can be further increased by prior hydrolysis of glucuronide or sulfate conjugates of some drug classes, such as cannabinoids, opiates, and benzodiazepines. Cutoff values, often applied to workplace drug testing, especially for abused drugs should be used cautiously in postmortem cases since the presence of low drug concentrations can be of forensic significance. In an acute drug-related death, for instance, the drug may not have sufficient time to be excreted into urine before death resulting in a low drug concentration in urine. False positives may occur, either from structurally related drugs or from metabolites of other drugs that are recognized by the antibodies. For instance, phenethylamine, a common putrefactive product from decomposed bodies, can cause a false-positive response to the amphetamines class test when using immunoassays. Cross-reactivity can also be due to chemicals with similar structures to the intended analytes. For example, pholcodine gives rise to a positive response to the opiates reagent of FPIA. Thus, for those samples, which give positive screening results, confirmation tests should be performed, preferably using chromatographic techniques with MS detection.
LLE involves the selective partitioning of the compound of interest into one of two immiscible phases by a judicious choice of extraction solvents. Although there are some developments in SPE techniques, in recent years [19], the traditional LLE technique is still a common extraction method used in postmortem specimens. The method has the advantage of efficient extraction of drugs and poisons present in a wide concentration range and the absence of adsorption loss frequently associated with a solid surface. However, for some postmortem blood or tissues, problems associated with the formation of stable emulsion, variable extraction efficiency and endogenous interferences due to autolysis may occur. To extract acidic and basic/neutral drugs from biological fluids or tissues using LLE, separate extractions using appropriate organic solvent(s) with the addition of acidic and basic buffer, respectively, are required. Various methods using LLE for drug extraction in postmortem specimens show that there is a wide choice of solvents or mixture of solvents with similar extraction efficiency and selectivity [18, 20]. The mechanism of SPE based on the selective partition of one or more components between two phases, one of which is a solid sorbent while the second, mainly a liquid, is more complicated than LLE. Extraction is accomplished by adsorption of the analytes onto the solid sorbent followed by washing with an appropriate solvent to remove the unwanted matrix before eluting the analytes. Compared with LLE, SPE has the advantages of low solvent consumption, provision of cleaner extracts, and ease of automation and high extraction efficiency for certain specific drugs requiring a smaller sample volume. Thus, it provides an excellent alternative to the traditional LLE for the extraction of postmortem samples. Unlike LLE, untreated sample cannot be applied directly onto SPE. Pretreatment procedures, e.g., protein precipitation and centrifugation, may result in a significant loss of analytes due to adsorption or occlusion onto the precipitated constituents. Ion exchange resins have shown to be efficient in the extraction of acidic drugs [21]. On the other hand, mixed-mode SPE, being capable of extracting acidic, basic, and neutral drugs, is suitable for general unknown screening (GUS) [22] (see Toxicology: Initial Testing).
Extraction Techniques. The usual extraction techniques involve either liquid–liquid extraction (LLE) or solid-phase extraction (SPE).
Chromatographic Techniques. GC and HPLC, coupled with various detectors, are common instrumentations to screen for a wide range of organic toxic
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Postmortem Toxicology: Laboratory Analysis
substances. A combination of mass spectrometry with either GC or, more recently, HPLC is the definitive technique to establish proof of structure of unknown substances. With the extensive development of commercial MS technology at an affordable cost, gas chromatography mass spectrometry (GC-MS) and high-performance liquid chromatography mass spectrometry (HPLC-MS) (or liquid chromatography mass spectrometry (LC-MS)) become increasingly popular tools employed in toxicological analyses. GC is one of the most frequently used techniques for separating, identifying, and quantifying a parent drug and its metabolites, other coadministered drugs and endogenous compounds. This technique can be coupled with various detectors from the more universal flame ionization detector (FID) to specific detectors such as electron capture detector (ECD) and nitrogen phosphorus detector (NPD). FID is useful for the detection of alcohol, other volatile organic compounds and many other organic drugs and poisons. NPD is sensitive to nitrogen- and phosphorus-containing compounds and is useful for the detection of drugs and poisons, such as antidepressants, antipsychotic drugs, benzodiazepines, opiates, cocaine and its metabolites, organophosphorus insecticides, etc. The use of FID and NPD either alone [23–25] or in a combination of both [26] has been shown to be useful for GUS of organic drugs and poisons. ECD is particularly sensitive to halogenated compounds (e.g., chlorinated insecticides), nitriles (e.g., CN) or nitrogen-containing compounds (e.g., benzodiazepines, nifedipine, and zopiclone). Unfortunately, the above detectors can only provide retention time data without any additional information for structural identification. Thus, more sophisticated techniques, such as GC-MS or LC-MS, are recommended for confirmation (see Confirmation Testing: Toxicology). The high separation power of capillary GC coupled with a highly selective MS detector has been currently regarded as the “gold standard” in GUS for drugs and poisons. The availability of a wellestablished and standardized ionization technique (electron impact (EI) at 70 eV) has facilitated the construction of large databases of reference mass spectra for library search and many useful spectral libraries relevant to toxicological screening are now available. However, GC is not suitable for direct analysis of polar compounds although derivatization can partly solve the problem and mass spectral
libraries containing a practically complete coverage of trimethylsilyl (TMS) derivatives are available commercially [27]. HPLC is capable of dealing with the analysis of a wide range of both volatile and nonvolatile compounds. The reversed phase mode column is at present the most common separation method applied in toxicological screening. Unlike GC, derivatization is not necessary for the analysis of polar and thermolabile compounds and this advantage certainly promotes HPLC as a better alternative for compounds not amenable to GC. Detection is often aided by diode-array detectors (DAD), which acquire UV–visible spectra continuously during a chromatographic run and the chromatogram is extracted and plotted at preselected wavelengths. The combined technique of high-performance liquid chromatography diode-array detector (HPLC-DAD) is another suitable technique for GUS of compounds, covering a wide range of polarity, stability, and molecular masses. Since metabolic transformation, in many cases, does not affect the ultraviolet (UV) chromophores of the molecule, one of the added values of this technique in GUS for drugs and poisons is that the low selectivity of DAD facilitates the detection of metabolites. In addition, compounds belonging to the same class with similar chemical structures often display similar absorbance patterns allowing unknown compounds not previously identified are tentatively assigned for further analysis. However, one of the drawbacks of HPLC-DAD is that the resolution of HPLC is usually inferior compared with GC, and UV spectroscopy is less sensitive than that of MS. In addition, for compounds possessing weak UV–visible or without any characteristic UV–visible absorbency, identification using HPLC-DAD is difficult in terms of both sensitivity and specificity. LC-MS is useful for the analysis of compounds that are not amenable to GC-MS. These compounds include lysergic acid diethylamide (LSD), glucuronide conjugates, such as morphine-3 or 6glucuronide or for some very potent or large molecules that other techniques are not sufficiently sensitive for detection (e.g., colchicines, cardiac glycosides such as digoxin and digitoxin, β-agonists such as salbutamol and terbutaline) [26]. The most common ionization mode used in LCMS techniques is atmospheric pressure ionization (API), which mainly comprises of different versions of electrospray ionization (ESI) and atmospheric
Postmortem Toxicology: Laboratory Analysis pressure chemical ionization (APCI) interfaces. With simpler sample preparation, LC-MS is extended to certain analyses originally performed by the lessspecific HPLC-DAD or even GC-MS. For these reasons, LC-MS, which combines an almost universal separation process with the most specific and sensitive type of detector, has become a promising alternative approach to GC-MS and HPLC-DAD in toxicological analysis [28–30]. However, there are several drawbacks in the use of LC-MS. First, the ion-suppression effect, especially when operating in the ESI mode, is a well-known problem: signal of the intended analyte is often suppressed because of the presence of coeluting compounds/interferents so that the intended analyte may be underestimated or even overlooked. Thus, the effect of ion suppression on the signal of the intended analyte should be cautiously evaluated before use. If ion suppression does occur, changes in experimental conditions, such as the sample cleanup method, chromatographic conditions relating to the mobile phase, the elution column, and the internal standard, should be considered. Moreover, only certain volatile buffers and mobile phase can be used for LC-MS to be compatible with the MS requirement. Thus, the separation efficiency is often inferior compared with HPLC-DAD although it may not be a problem for tandem MS because separation of analytes can be made in the MS/MS mode.
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bile are useful qualitatively, quantification of drugs and poisons in these fluids usually has limited interpretative values. A comprehensive and systematic analysis for the presence of chemical substances of toxicological significance is termed systematic toxicological analysis (STA). There are thousands of potentially harmful substances ranging from poisonous gases (e.g., carbon monoxide and hydrogen cyanide (HCN), and hydrogen sulfides), food (e.g., ethanol), deadly poisons (e.g., CN salts and arsenic), abused drugs, pesticides, toxins from natural sources, a wide variety of prescribed drugs and even household products, etc. It is impossible to design a single analytical scheme to cover all these substances with distinctly different chemical and physical properties. Screening for a wide scope of drugs and poisons is, however, possible by grouping substances of similar properties for analysis. The most effective strategy includes a series of standard general screening procedures supplemented by as many special methods as required. A combination of immunoassays with chromatographic techniques is usually employed to detect a wide range of substances. Immunoassays detect classes of drugs with similar structures while chromatographic techniques detect large groups of drugs with similar extraction properties, polarity, and detection characteristics. General toxicological screening usually involves the following tests:
Systematic Toxicological Analysis The usual practice in toxicological examination begins with the preliminary identification of alcohol and screening of a wide spectrum of acidic, neutral, and basic organic drugs or poisons. If a toxic substance(s) is detected, confirmatory and, if necessary, quantitative testing has to be performed. In general, a positive identification is achieved using at least two independent analyses and preferably based on different analytical principles. Using GC-MS or LC-MS, confirmation and quantification can be simplified into one single analysis. Quantification of drugs in blood, liver, and gastric content as dictated by the case, provides more meaningful interpretative information. Reference concentrations of many compounds in blood in therapeutic, toxic, and even fatal levels have been published [7–10]. Although limited, useful references are also available for some compounds in liver [14]. It should be noted that while substances found in excretory fluids such as urine or
1. 2. 3. 4.
alcohol determination; immunoassay screening; GUS of organic drugs and poisons; other specific tests as required such as carboxyhemoglobin, CN, etc.
Table 5 shows the suggested screening tests based on different case nature. Since it is virtually impossible to screen for all toxic substances in every case, a rational selection of case-specific analysis in addition to STA will be necessary. In general, the additional analysis to be conducted is primarily based on the information provided or specific requests made by the relevant parties such as pathologists and the police. An example of an analytical scheme used for general toxicology screening and scope of analytes likely to be detected is shown in Figure 1. Alcohol Determination. Alcohol or ethyl alcohol (ethanol) is the most common drug found in
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Postmortem Toxicology: Laboratory Analysis
Table 5
Suggested analysis for sample collected(a)
Type of cases
Test conducted
Specimen tested
General cases
Alcohol Immunoassay drug screening General organic drugs/poisons screening Alcohol
Blood, urine, and vitreous humor Urine Blood (urine)
Immunoassay drug screening General organic drugs/poisons screening Plus general organic drugs/poisons screening Plus carboxyhemoglobin, cyanide Plus metal analysis Plus sulfide
Urine Liver/cavity fluid
Plus volatile organic
Blood, lung, and brain
General cases (blood not available)
Drug or poison suspected cases Fire death Heavy metal poisoning Gaseous and volatile organic related (a)
Urine and vitreous humor
Gastric content Blood Blood, kidney, and liver Blood, lung, and brain
Specific test(s) not covered may be added if deemed appropriate.
postmortem toxicology cases. In particular, ethyl alcohol is one of the leading causes of death by poisoning. In contrast to alcohol determination in living subjects, which is generally more straightforward, analysis of body fluids taken from cadavers is more likely to be contaminated with volatile substances, such as methanol and formaldehyde used in embalming processes, and abnormal metabolic products, such as acetone resulting from fasting or diabetic ketoacidosis. Therefore, techniques for analyzing postmortem alcohol are recommended to allow separation of most, if not all, low-boiling compounds eluting in the same range as ethyl alcohol [31]. Headspace GC coupled with FID is usually the method of choice and it can be used for simultaneous analysis of methanol, acetaldehyde, ethanol, isopropanol, and acetone using either n-butanol or n-propanol as an internal standard. A combination of blood (preferably femoral region), vitreous humor, and urine, if available, should be used for alcohol analysis to aid in the interpretation of the state of absorption and to avoid misinterpretation of blood alcohol concentrations due to diffusion of undigested alcohol from the stomach, and postmortem alcohol production due to bacterial action. The presence of significant amount of alcohol in blood together with the absence of alcohol in urine and vitreous humor cast doubt in the ingestion of alcohol prior to death and is indicative of endogenous alcohol production (see also Alcohol: Analysis).
Immunoassay Screening. Screening for drugs by immunoassays in urine is commonly pursued for the main classes of abused drugs (Figure 1), which include amphetamines, benzodiazepines, cannabinoids (metabolite of cannabis), benzoylecgonine (metabolite of cocaine), and opiates (morphine and codeine). The scope for drug screening can be extended to include opioids (e.g., methadone), barbiturates, and tricyclic antidepressants (e.g., amitriptyline/nortriptyline). As urine is not always available in postmortem cases, screening for drugs and poisons, especially abused drugs, in blood or plasma may be considered and may even be desirable to establish what substances may be affecting the person. Blood, plasma, or even specimens such as bile or liver homogenate can be screened by the urine-based immunoassay test kits, but pretreatment with solvent or protein precipitation are required and validation should be made before use. In addition, techniques intended for analysis of blood, such as RIA and ELISA can be used on postmortem samples, and they tend to be more sensitive than those kits designed for detecting drugs in urine but modified for testing blood. Screening of potent drugs like digoxin or structurally related cardiac glycosides, such as bufadienolides present in Chansu (a remedy from toad venom), can be effectively performed in plasma using a digoxin reagent by various immunoassay techniques [32].
Postmortem Toxicology: Laboratory Analysis
Urine
Vitreous humor
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Tissue homogenate or gastric content
Blood
Immunoassays: FPIA
Alcohol analysis: Headspace GC-FID
Acidic Screen: ∗ L–L extraction
Analytes: Amphetamines Benzodiazepines Benzyolecgonine Cannabiniods Opiates
Analytes: Methanol Ethanol Isopropanol Acetone
Analytes: Anticonvulsants Antidiabetics Barbiturates Benzodiazepines (less potent) Corticosteroids Diuretics Nonnarcotic analgesics Nonsteroidal anti-inflammatory drugs Opioids Xanthines
#
LC/DAD
Basic screen: ∗∗ L–L extraction ## GC-MS/NPD/ECD and/or # LC-DAD
Analytes: Anticonvulsants Antihistamines Antipsychotics and antidepressants Barbiturates Benzodiazepines (less potent) Cardiac drugs (nifedipine, wafarin detected as artifact in GC/MS) Hypnotics and sedatives Pesticides Non-narcotic analgesics Opiates (morphine and codeine) Opioids Stimulants (usually at toxic levels) Xanthines
∗
Phosphate buffer (pH 1), extracted with diethylether/toluene (1 : 1)
∗∗
Bicarbonate buffer (pH 9) extracted with dichloromethane: toluene: isobutyl alcohol (3 : 6 : 1)
LC-DAD: column: Lichrospher 60 RP-select B (5 µm,125 × 4.0 mm); mobile phase: Triethylamine in phosphate (pH 3)/acetonitrile #
GC-MS/NPD/ECD: column: HP5-MS (30 m × 0.25 mm × 0.25 µm); carrier gas: Helium
##
Figure 1
An example of general toxicology screening scheme
General Unknown Screening (GUS) for Organic Drugs and Poisons. As shown in Figure 1, acidic drugs can be extracted by adding an acidic buffer such as phosphate buffer (pH 1) to the samples followed by extraction with toluene: diethyl ether (1 : 1). Other methods, such as protein precipitation of blood with acetonitrile [33] or ammonium chloride salting-out of blood and other tissues with ethyl acetate followed by a washing step with hexane [34] can also be employed for the analysis of acidic and some neutral drugs. Analysis is usually made by HPLC-DAD
using a reverse-phase column in conjunction with a mobile phase at acidic pH with gradient elution. Identification is accomplished by automatic library search based on a preinstalled, commercially available, or an in-house developed UV–visible spectral library. The retention times are useful to aid in identification but it should be established in-house using authentic standards according to the type of column and the mobile phase used. Nonnarcotic analgesics (e.g., paracetamol, salicylic acid, mefenamic acid, and sometimes propoxyphene), nonsteroidal anti-inflammatory
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drugs (e.g., celecoxib, naproxen, and ibuprofen), diuretics (e.g., furosemide and hydrochlorothiazide), anticonvulsants (e.g., carbamazepine, phenobarbital, and phenytoin), antidiabetics (e.g., glicazide), opioids (e.g., methadone), barbiturates (e.g., secobarbital), corticosteroids (e.g., hydrocortisone), the less potent benzodiazepines (e.g., midazolam, diazepam, and sometimes estazolam), and xanthines (e.g., caffeine and theophylline) can be detected using HPLCDAD after acidic extraction. Drugs and their metabolites usually have similar UV–visible spectra because metabolic transformations, such as desmethylation and hydroxylation, do not usually affect the chromophores of the drugs. Yet, a drug and its metabolites usually have different retention times (e.g., midazolam and α-hydroxymidazolam, clomipramine, and desmethylclomipramine). Although it may be useful to extend the detection capability to drug metabolites even without the authentic standards, one should exercise caution to avoid misinterpretation when a peak slightly different in retention time and UV–visible spectrum from the parent drug is observed. As many drugs and poisons do not have characteristic UV–visible spectra, retention time becomes the main identification parameter. Thus, whenever standards of parent drugs and/or their metabolites are available, their retention times should be established in-house and their authenticity preferably confirmed by other techniques, such as GC-MS. Extraction of basic drugs is accomplished by a carbonate buffer (pH 9) followed by extraction with a dichloromethane/toluene/isobutyl alcohol (3 : 6 : 1) mixture. Other combinations of alkaline buffers and extraction solvents such as borate buffer (pH 8.5) extracted with dichloromethane/isopropanol (9 : 1) [35], and using SPE with suitable cleanup procedures compatible with GC analysis [18–20] are also applicable. The use of more than one type of detectors (e.g., NPD and MS) coupled to GC would definitely give a greater coverage of possible drugs and poisons. The extracted sample could be analyzed sequentially by injection into two GCs equipped with different types of detectors or by splitting the effluent of the sample from one GC into two different detectors for simultaneous detection. Examples of drugs and poisons found in the basic fraction include hypnotics and sedatives (e.g., zopiclone and zolpidem), benzodiazepines (e.g., diazepam, midazolam, estazolam, and
bromazepam), antihistamines (e.g., chlorpheniramine, brompheniramine, and promethazine), antipsychotics and antidepressants (e.g., amitriptyline/nortriptyline, cyclobenzaprine, sertraline, clomipramine, and trihexylphenidyl), opiates (e.g., codeine, acetylmorphine, and sometimes monomorphine), opioids (e.g., methadone and meperidine), anticonvulsants (e.g., carbamazepine, phenobarbital, and phenytoin), and pesticides (e.g., melathion, dimethoate, and tetramethylene disulfotetramine). Stimulants such as amphetamines and cocaine may be detected when present at high concentrations. In addition, artifacts due to the presence of certain cardiac drugs such as warfarin and nifedipine may be encountered. Some basic drugs that are too polar or thermally labile cannot be detected by GC and are not acid extractable for HPLC-DAD analysis. In such case, the basic extract can be analyzed using HPLC-DAD in addition to GC. Typically, the method permits the detection of cardiac drugs (e.g., warfarin, metoprolol, propranolol, dipyridamole, and amiodarone), anti-inflammatory drugs (e.g., ofloxacin), and herbal ingredients (e.g., tetrahydropalmatine). Alternatively, derivatization prior to GC analysis can increase the volatility and hence thermal stability for those drugs that are not easily detected by GC or GC-MS [36]. Among the available derivatization procedures, trimethylsilylation is the most common method because of its versatility for derivatizing many different functional groups such as hydroxyl, carboxyl, amidic, and some amine groups under relatively mild conditions. Furthermore, the additional mass gain by silylation improves the specificity of the mass spectral information [37]. Typical examples include morphine and sympathomimetic amines. Other derivatized agents such as trifluoroacetylation for basic and neutral drugs, and extractive methylation using methyl iodide or formation of ethereal diazomethane for acidic drugs are also applicable [38, 39]. Some compounds do not exhibit characteristic mass spectra in GC-MS. In this case, unambiguous identification can be difficult if mass spectral matching is solely relied on because many compounds can give seemingly high matching scores. Typical examples include amino-containing compounds with predominant base peaks at m/z 44 (C2 H6 N+ ) (e.g., amphetamine, methylenedioxyamphetamine MDA), 58 (C3 H8 N+ ) (e.g., doxepin, cyclobenzaprine), 72 (C4 H10 N+ ) (e.g., methadone, promethazine), or 98
Postmortem Toxicology: Laboratory Analysis (C6 H12 N+ ) (e.g., trihexylphenidyl, thioridazine) and usually associated with very low intensity fragments in the high mass range. If these compounds are well separated chromatographically, they can only be identified on the basis of their differences in retention time. For those substances having similar retention time in GC, however, another technique should be considered for confirmation. The application of LC-MS to GUS is still not extensive in spite of its versatile analytical capability as well as sensitive and specific detection of a wide range of drugs and poisons. One of the problems is the soft ionization of LC-MS, which produces mass spectra that are not compatible with those generated by EI at standardized 70-eV ionization potential. Hence, the very large libraries of standardized EI spectra of chemicals, drugs, poisons, and their metabolites applicable to GC-MS are not valid for LC-MS. Thus, a totally different strategy for mass spectral identification of compounds is required for LC-MS. Many efforts have been made to build up large mass spectral database applicable for GUS of compounds of toxicological interest on different types of LC-MS and promising progress has been demonstrated. Identification has been based on single quadrupole, ion trap, triple quadrupole, hybrid linear ion trap, and time of flight (TOF) [28–30]. The hybrid linear ion-trap LC-MS/MS showed promising development for building up a reference MS/MS library for the same type of instrument. This LCMS/MS technique is unique in that the third quadrupole of the triple quadrupole MS can be operated in either a standard quadrupole MS for multiple reaction monitoring (MRM) experiment or as linear ion trap to produce highly sensitive enhanced product ion (EPI) scan in an information-dependent acquisition (IDA) experiment [40, 41]. The first detection step involves IDA survey scan containing a number of preselected MRM target drugs and metabolites where ions are accumulated and then filtered in the third quadrupole. In case of a signal above a preset intensity threshold is detected for an MRM transition, the EPI scan of the precursor ion is triggered to yield product ion mass spectra at various preselected collision energies. Finally, the resulting EPI mass spectra are then searched against a prebuilt mass spectral library for identification of drugs present in the sample. Alternatively, LC-MS/TOF has provided a novel approach for comprehensive drug
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screening. The use of LC-MS/TOF method has the advantages to provide a relatively high mass accuracy (∼5 ppm) with reasonable resolution (5000–10 000 full width at half maximum). In this approach, a library is established to contain toxicological relevant compounds that consist of molecular formula and calculated monoisotopic accurate masses. Identification of drugs/metabolites was based on their accurate mass, retention time if a reference material is available, and drug metabolite patterns. Furthermore, the matching of theoretical and measured isotopic patterns of a compound introduces an additional parameter to allow unambiguous identification of compounds present in the sample. This approach allows substance identification even without any reference standards and retention time data [42] (see Confirmation Testing: Toxicology).
Other Specific Tests When analysis of specific types of drugs or poisons that are not covered under the general toxicology screening scheme is required, additional tests will have to be performed. Figure 2 shows some of the examples on the analysis of certain specific types of drugs and poisons.
Drug-detection Techniques Acid Back-Extraction. Although many basic drugs with amine functional groups such as those basic psychotropic drugs and antihistamines can be detected using aforementioned basic screening, an additional acid back-extraction after basic extraction can further improve GC-MS detection by producing a cleaner extract. Examples of psychiatric drugs include tricyclic antidepressants, phenothiazines antipsychotic drugs, tetracyclic antidepressants, butyrophenones, and serotonin reuptake inhibitors. In addition, better detection of other drugs like antiparkinson drugs (e.g., trihexylphenidyl) can also be achieved using this method (Figure 2). Ketamine, amphetamines, and their analogs can be detected at moderate-to-high level in the basic extract using GC-MS/NPD (Figure 1). To increase the detection sensitivity down to therapeutic or even subtherapeutic levels, a simple acid back-extraction cleanup after basic extraction with diethyl ether (Figure 2) coupled with LC-MS/MS (ion-trap MS) analysis can be considered.
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Postmortem Toxicology: Laboratory Analysis Urine/Blood/Tissue homogenate
Basic screen with acid back extraction: ∗ L–L extraction # GC-MS/NPD
Analytes: Antihistamines: chlorpheniramine, diphenhydramine, promethazine, and cinnarizine Phenothiazines Antipsychotic drugs: chlorpromazine, thioridazine, and trifluperazine Tricyclic antidepressants: carbamazepine, imipramine/desperamine, trimipramine, amitriptyline/nortriptyline, doxepin, and dosulepin clomipramine/desmethylclomip ramine Tetracyclic antidepressants: mianserin, and mirtazepine Butyrophenone: haloperidol Selective serotonin reuptake inhibitors: citalopram, fluoxetine, sertraline, and paroxetine Antiparkinson: trihexyphenidyl, amantidine, etc.
Basic screen with back extraction: ∗∗ L–L extraction ## LC-MS/MS
Analytes: Amphetamines: (amphetamine, methylamphetamine. MDA, MDMA, MBDB, and MDEA) Ephderine/pseudoephedrine Phentermine Ketamine
Basic screen with LC/MS: ∗∗∗
L–L extraction LC-MS/MS
##
Analytes: Benzodiazepines: 7-aminfluntrazepam, oxazepam, tamazepam, diazepam/nordiazepam, lorazepam, lormetazepam, estazolam, bromazepam, fluazepam, triazolam, chlordiazepoxide, pinazepam, nitrazepam, and niimetazepam Hynotic/sedatives: zopiclone and zoplidem Traditional Chinese medicines: aconitine, mesa-aconitine, bufalin, resibufogenin, cinobufagin, and cinobufotalin
∗
Bicarbonate buffer (pH 9) extracted with hexane/iso-amyl alcohol (98 : 2). Organic layer back-extracted with 1N HCl; pH being adjusted to pH 10 with saturated NaOH, followed by extraction with hexane
∗∗
Saturated bicarbonate (pH 9) extracted with diethyl ether and back extracted with 1N HCl Bicarbonate buffer (pH 9) extracted with dichloromethane : toluene : isobutyl alcohol (3 : 6 : 1)
∗∗∗ #
GC-MS/NPD: column: HP5-MS (30 m × 0.25 mm × 0.25 µm ID); carrier gas: Helium
#
LC-MS/MS: column: Alltech Altima C18 (5 µm, 150 × 2.1 mm); mobile phase: 0.01 M ammonium formate (pH 3)/acetonitrile
Figure 2
Examples of additional specific drug tests
Basic Extract Analyzed by LC-MS. LC-MS is complementary to the analysis of nonvolatile and thermally labile drugs/poisons that are not amenable to GC or GC-MS. In addition, LC-MS provides a superior sensitivity compared with the HPLCDAD method, a good example being the LCMS analysis of benzodiazepines: a structurally diverse class of pharmaceuticals. It is available
as prescribed drugs with some of them (e.g., diazepam, midazolam, and nimetazepam) having been widely abused. Benzodiazepines and their metabolites represent one of the most common drug types found in postmortem specimens. While the relatively less potent benzodiazepines (e.g., midazolam and diazepam/nordiazepam) can be screened by the general screening procedures, many
Postmortem Toxicology: Laboratory Analysis potent or thermally unstable benzodiazepines (e.g., lorazepam, triazolam, and oxazepam) cannot be readily detected by standard screening techniques (Figure 1). To cater for a more comprehensive screening of benzodiazepines, the basic fraction from general toxicology screening can be reconstituted into aqueous methanol and subjected to LC-MS analysis (Figure 2). The same extract can also be used for the analysis of a wide range of targeted basic/neutral drugs and poisons including traditional Chinese medicines (e.g., aconitine and mesa-aconitine) and toxic ingredients found in Chan Su (e.g., bufalin, resibufogenin, cinobufagin, and cinobufotalin). Analysis of Poisoning by Small Molecules. Carbon monoxide (CO), CN, and sulfide are well-known small and highly toxic molecules. Analysis of these molecules should be considered whenever poisoning due to these compounds is suspected. Carbon Monoxide (CO). Determination of carbon monoxide poisoning will be required when a known source of CO, such as coal gas, burnt charcoal, or automobile exhaust, is located at the scene. On the other hand, it would be of forensic interest to decipher whether a fire victim had died because of CO poisoning, or had already died before the fire broke out. The saturation ratio of carboxyhemoglobin (COHb) in blood is determined by (i) simultaneous spectrophotometric (e.g., CO-Oximeter) measurement of COHb level and total hemoglobin in blood [43] or (ii) analysis of COHb through the release of CO by adding saponin and potassium ferricyanide to blood, followed by catalytic conversion of CO to methane, which is quantified by gas chromatography flame ionization detector (GC-FID) [44]. Analysis of COHb should be made using blood samples; other biological fluids, such as pleural effusion, are not recommended because a considerable amount of postmortem CO can possibly be generated in these samples by bacterial action on hemin [45]. Hydrogen Sulfide (H2 S) and Its Metabolites. Analysis is performed when H2 S poisoning is suspected, usually in industrial accidents, sewers, or ship holds where H2 S poisoning together with oxygen deficiency is suspected. Analysis is mainly based on the detection of H2 S or its metabolite, thiosulfate. Sulfate is also produced due to H2 S
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exposure but endogenous levels of sulfate in blood and urine are relatively high making it not an analyte of choice. GC-MS analysis can be performed for the ionized form of H2 S after derivatization using pentafluorobenzyl bromide [46]. The pH of the derivatized mixture is made acidic to suppress the production of sulfide in the blood due to decomposition of sulfur-containing compounds, such as cysteine. A similar derivatization procedure prior to GC-MS method can also be used for the analysis of thiosulfate with the exception that tetradecyldimethylbenzylammonium, a phase-transfer catalyst used in H2 S determination is substituted by ascorbic acid/sodium chloride [46, 47]. Cyanide (CN). Potassium or sodium salts of CN are used in metallurgy and electroplating industries and are relatively easy to obtain. Thus, its involvement in suicide and even homicide is not uncommon in some parts of the world. In addition, incomplete combustion of nitrogen-containing compounds such as urethane at fire scenes can produce HCN as one of the poisonous gases. Thus for fire victims, in addition to measuring the COHb saturation, CN levels in blood should also be determined. Inhalation of HCN or ingestion of CN can be fatal through inhibition of cytochrome oxidase causing cellular anoxia. CN in blood can be determined by automated headspace gas chromatography electron capture detector (GC-ECD). Blood is acidified with sulfuric acid in the presence of silver sulfate to produce HCN, which is diffused into the headspace to react with chlorine produced by chloramine-T to form cyanogen chloride, which is analyzed by GC-ECD [48]. Volatile Analysis. In addition to the analysis of alcohols, determinations of other volatile chemicals including various organic solvents are also of forensic significance. Sudden death due to volatile substance abuse (VSA) is not uncommon particularly for an inexperience user because controlling of dose is often difficult. Solvent from thinners (e.g., toluene and xylene), halogenated solvents (e.g., chloroform and dichloromethane), hydrocarbons (both aliphatic and aromatic) such as gasoline and kerosene, and fuel gas (e.g., butane) are commonly abused substances. Apart from VSA, analysis of volatile substances may also be required in certain circumstances. For instance, chloroform is commonly used for industrial purposes such as solvent and extracting reagents, and death
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can occur accidentally and sometimes, in homicide cases, with the intent to incapacitate the victims. In addition, analysis for ingredients present in kerosene and gasoline may be useful in fire death cases. Most volatile substances are stable in blood. The specimens should be stored at low temperature (i.e., less than 4 ° C) in tightly sealed glass container, preferably with anticoagulant such as heparin. Analysis of tissues such as brain and lung may prove useful since high concentrations of volatile substances may be detected. Headspace GC-FID is the method of choice for volatile chemical analysis. If structural identification is required, GC-MS should be employed. The method used for alcohol determinations can be extended for the analysis of other volatile chemicals using same columns (e.g., Elite-BAC1 or BAC2) with some modification of experimental settings. Examples of compounds that can be analyzed are hexane, dichloromethane, chloroform, hexane, toluene, xylene, diethylether, and ethylacetate. For the analysis of low-boiling hydrocarbons, such as methane, ethane, propane, butane, and pentane, specific columns (e.g., GC-GASPRO) intended for analysis of volatile compounds can be used. Heavy Metal Analysis. Although many metals are known to cause toxic effects, only a few are regarded as important toxic hazards: these include arsenic, lead, cadmium, thallium, and mercury. In addition, lithium is a psychiatric drug used for the treatment of manic-depressive disorder. There are many methods available for metal analysis in biological specimens, such as electrochemical, atomic absorption, and flame emission spectrophotometry, inductively coupled plasma coupled with either emission spectroscopy (ICP-AES) or inductively coupled plasma coupled with mass spectrometer (ICP-MS). ICP-MS after digestion of the biological specimens with concentrated mineral acid, such as nitric acid, is recommended. It is because ICP-MS allows a simultaneous screening of both metals and nonmetals as well as selective quantification of a single element with low detection limits. The availability of stable isotopes for most of the metal further enhances the accuracy of metal quantification by isotope dilution method.
ensure that the results generated are accurate, reliable, and traceable. It is even more important for a forensic toxicology laboratory since the results will be closely scrutinized in the courts of law. A quality manual pertaining all policies and procedures relevant to the reliability and traceability of the analytical results should be clearly written. Criteria affecting the quality of analytical results include the quality of materials used (such as reference standards, reagents, and chemicals), analytical methods adopted such as procedures and instrumentations used and their validity, sampling, and the chain of custody. All analytical methods used must be properly validated. Suitable internal standards should be used in chromatographic assays, so that any systematic errors affecting the analyte can be compensated for by the internal standard. Compounds with chemical structures similar to the targeted analyte (e.g., deuterated analog) are preferably selected. For a batch of qualitative analyses, a negative control and a control representative of the analytes should be included. Any possible interfering factors that might adversely affect the analysis should be indicated. Quantitative analytical methods must be validated by determining the limit of detection, linearity range, precision, accuracy, and selectivity.
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WING-CHI CHENG
Postmortem Toxicology: Specimens see Toxicology: Analysis
Postpartum Psychosis Introduction Postpartum psychosis (PPP; also known as puerperal psychosis) was perhaps first described by Hippocrates in the fourth century BC. He described an acute onset of confusion, hallucinations, delirium, and insomnia [1, 2]. In 1865, the French physician Marce published his observations and study of perinatal disorders [3]. By the 1800s, symptoms of PPP were believed to be related to lactation, and the term milk fever was even used [1]. This “lactational insanity” was the basis for many Infanticide laws across the world. The Yellow Wallpaper, a monograph from 1899 [4], though controversial, may illustrate a woman’s struggles with PPP.
Postpartum Psychosis The time in a woman’s life when she is at greatest risk of psychosis or mental illness is in the postpartum period [5]. Fortunately PPP is rare, occurring after approximately 1–2 per thousand births. PPP often has a dramatic presentation, within the first several weeks of childbirth [6], but may begin within just days of giving birth. Early on, symptoms may include sleep disturbance and restlessness. Symptoms may evolve to include either depressed or elevated mood or both, agitation, delusions, hallucinations, and depersonalization. Women may believe they are being persecuted by the baby. Risks may include suicide, child neglect, or infanticide. PPP is considered a true psychiatric emergency, and mothers often require psychiatric hospitalization. Some specialized treatment units allow mothers to be hospitalized with their infants.
The Diagnosis of Postpartum Psychosis Though cases may begin during pregnancy [2], more often they begin shortly after childbirth. Most cases of PPP begin within a couple weeks of delivery, with an abrupt onset [1, 2, 7]. By this time the mother has most often been discharged home with her fragile infant, rather than remaining in the hospital. Sleep deprivation is a potential trigger [8]. Risk of PPP may be related to hormonal shifts after birth (primarily the drop in estrogen) [7], stressors (such as marital problems), biology (bipolar disorder), and family history – genetic studies are underway [9], and can also be triggered by menstruation or cessation of lactation [2]. Some researchers have reported that the first pregnancy is a risk factor for PPP [2, 10]. Reports of recurrence rates of PPP after further pregnancies range from one in seven to women with bipolar disorder or schizoaffective disorder have a 50% risk of another episode of PPP [7, 11]. However, this rate is modified by prophylactic medication treatment [12]. Delivery complications may also elevate risk [10]. Common symptoms of PPP include symptoms of psychosis, with an impaired concept of reality and fluctuating delirium. Confusion, bizarre delusions (fixed, false beliefs) and behavior, hallucinations (unusual perceptual experiences that can be tactile, olfactory, or visual in addition to auditory), mood lability (ranging from depression to euphoria), and disorganized thinking may occur [1, 13]. For
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example, a woman might be delusional that she has special powers, that God has chosen her baby to be sacrificed, or that the baby is defective. Because of the lack of insight, suspicion, or conspiracy theories, women may not reveal their symptoms to others. Among women with PPP, 72–88% have bipolar disorder or schizoaffective disorder, while 12% have schizophrenia [7]. In distinction to PPP, in schizophrenia delusional thinking and hallucinations often have a more gradual onset. The psychiatric reference book DSM-IV-TR [14] does not list a specific diagnosis for PPP. Some debate exists within the field. According to the DSM-IV-TR, brief psychotic disorder or psychotic disorder not otherwise specified are diagnoses used for PPP, or a woman’s symptoms may meet criteria for an affective (mood) episode [14]. Further even, the postpartum period is also defined differently depending on the group defining it; postpartum is 4 weeks according to the DSM-IV-TR, 6 weeks for ICD-10, 3 months in some epidemiological studies, and up to 1 year in some investigations [15].
Comparison with Postpartum Depression and Other Disorders Postpartum blues or “baby blues” occur in approximately half to three-quarters of mothers [7]. Baby blues are not synonymous with postpartum depression (PPD); they are transient and not as severe. Symptoms usually occur in the first week after giving birth, and are self-limited. Symptoms may include anxiety, mood swings from sadness to irritability, and insomnia. PPD symptoms are not the same as those of PPP. Approximately 10–15% of mothers experience PPD [3, 7]. Symptoms may occur within a few weeks to a year after giving birth. In PPD, a woman’s predominant mood is sad or depressed, and she may lose enjoyment in her activities. Other symptoms may include insomnia, even an inability to sleep when the baby is sleeping. Her appetite may be abnormal. She may be fatigued and have difficulty concentrating. She may lack the interest in caring for her appearance, or even for her baby. She may experience feelings of worthlessness or hopelessness, and may have difficulty bonding with the infant. She may experience suicidal thoughts or thoughts of harming the infant. Symptoms of anxiety often also occur.
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Psychiatrists must also differentiate psychotic thoughts and behavior from obsessive thoughts, which are also common in the postpartum [5, 7]. In obsessive compulsive disorder (OCD) or other anxiety disorders, women may experience intrusive thoughts that they have difficulty getting out of their head. These thoughts often represent worries, and the women, in distinction to women with psychosis, are not out of touch with reality. If these women have thoughts or fears, for example of harming someone, they usually realize that these thoughts are not of something that they would ever do and try to avoid the thoughts. In the evaluation of a postpartum woman with psychiatric symptoms, physicians may consider that the differential diagnosis includes medical problems such as thyroiditis, Late Onset Tay Sachs disease, and vitamin B12 deficiency. Laboratory tests, computed tomography (CT) scan, or magnetic resonance imaging (MRI) of the brain may be indicated to rule out alternative organic diagnoses.
Treatment of Postpartum Psychosis Because of the rapidly evolving and devastatingly severe nature of symptoms, PPP is often a psychiatric emergency. Women with a history of PPP or bipolar disorder have a 100-fold increase in psychiatric hospitalization during the postpartum [1]. In this disorder, treaters will often need to enlist help of family and other support. In some cases, child protective services may need to become involved. Mood stabilizing medications (such as valproate or lithium) are mainstays of treatment, related to the frequently underlying bipolar disorder. Electroconvulsive therapy (ECT) is another consideration. Though not without risks of its own, ECT may provide for a rapid symptomatic improvement. Atypical antipsychotics such as olanzapine may have a role in the treatment of PPP as well [15]. (These agents are increasingly being used for not only the treatment of psychotic disorders but also of mood disorders.) Typical (older) antipsychotic agents may not lead to remission of symptoms [5]. Side effects of medications, such as sedation, which could impair her ability to respond to her infant, should be considered. Because of the rarity of PPP, compared to other psychiatric disorders, there are fewer studies regarding evidence-based treatment. PPP is often considered to be a bipolar disorder unless proven otherwise.
Whether the mother is bottle-feeding or breastfeeding is another consideration, as different medications present different potential risks to breast-fed infants. The infant may require monitoring by a pediatrician. Other mothers may prefer to bottle-feed, to avoid any potential risk. With a supportive partner, bottle-feeding at least at night may have the added benefit of allowing the mother with PPP to sleep through the night. Healthcare providers should educate patients about PPP. Support of families may help alleviate some of the stress associated with PPP [11]. It is important to consider prevention of episodes in future pregnancies/postpartum periods. Women with bipolar disorder are often treated prophylactically, where possible, with lithium or another mood stabilizer [7].
Risks in PPP Mothers who experienced delusions that the baby is evil or a devil or not truly theirs were more likely to be abusive toward the infant [16]. Mothers with PPP “are at risk of injuring their children through practical incompetence or misguided delusions”. [1, p. 106] Women with childbearing-related onset of psychiatric illnesses have reported homicidal ideation more frequently [13]. Risk of suicide is also present in PPP [17]. Neonaticide is specifically the murder of the neonate by the parent in the first 24 h of life [18]. Obviously, as most PPP has not yet begun at the time of birth, but rather has an onset several days to weeks later, there is a lack of relation of PPP to neonaticide in the great majority of cases. However, some cases of neonaticide do involve psychotic mothers [19]. Infanticide is often considered to include the murder of infants less than 1 year of age at the hands of the parent. (However, infanticide is a nonspecific term; in Biblical times, murder of a child at the hand of the state may have been considered infanticide.) Filicide, more precisely, is the murder of a child by the parent. If a woman is suffering from PPP, the physician should consider her risk of harming herself and/or her infant. Though there have been reported cases of infant murder while in the hospital [20], the overwhelming majority of cases occur outside the hospital. In psychiatric studies, mothers who kill their children often have
Postpartum Psychosis experienced psychosis, suicidality, and depression [21]. Often, alcohol or substance use, limited social support, and a maternal history of abuse are found as well. The mother’s motive for killing her infant or child may fall into any of several categories: altruistic, acutely psychotic, fatal maltreatment, unwanted child, or spouse revenge [22]. In an altruistic filicide, the mother kills her child out of love. A mother who sees her child suffering from cerebral palsy or leukemia may feel that the loving thing to do is spare the child from suffering. Though difficult to fathom, because of her depressed or psychotic outlook on life, another mother may believe that it is in the child’s best interest to go to Heaven, rather than living an awful life on earth. The mother may be suicidal and not wish to leave her child in the hopeless world that she is departing. She may be psychotic, believing that if her child were to live, he or she would be tortured or raped or kidnapped, and may reason that the only humane choice is to kill him. Alternatively, in an acutely psychotic filicide, the mother kills her child for no comprehensible reason. She may be responding to hallucinated voices commanding her to kill. She may kill in the throes of epilepsy or the confusion of delirium. She may put the baby in the oven instead of the dinner, for no rational reason but borne out of severe confusion and illness. Fatal maltreatment filicide is the most common type of filicide overall. A child may die because of chronic abuse or chronic neglect. Certainly mothers suffering from psychosis or depression may be abusive, but so may many other mothers who do not have a mental illness. Too, mothers who are severely mentally ill and out of touch with reality may have difficulty providing for their infants’ many needs. In an unwanted child filicide, a child who is not desired is killed. In a spouse revenge filicide, the rarest type, a child is killed in order to cause emotional pain in the other parent. Newborns have a total dependence on their caregivers. If their caregiver is a woman with unidentified PPP, lacking in social support, that is highly concerning. A 4% risk of infanticide has been estimated in untreated PPP [23]. Even if a woman with PPP has support from her social network, if those who care do not understand the risks associated with PPP, there is cause for concern.
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Infanticide Laws and Defenses The British Infanticide Act was initially enacted in 1922, and was reformulated in 1938. The Act allows a woman, still recovering from giving birth, who kills her infant in the first 12 months of life to be charged with infanticide (akin to manslaughter) rather than murder, because “the balance of her mind is disturbed by reason of her not having fully recovered from the effect of giving birth to the child” [24]. Infanticide laws exist in over two dozen other nations, including Canada and Australia [25]. However, the legal criteria for infanticide vary across nations, including in New Zealand the murder of children up to age 10 [26]. In Luxembourg, there is a stricter penalty for child homicide. However, a causal connectional between mental illness and the crime does not always occur in practice [27]. And, if a psychotic postpartum mother kills her infant and her older child, she could be charged for murder of the older child and infanticide for the killing of the infant. Also, one acutely psychotic mother who killed her 13-month-old baby might not qualify for infanticide though another mother who killed her 11-month-old baby via fatal maltreatment borne out of frustration might. In the United States, there is no such infanticide legislation. The wake of the Andrea Yates child murder case led to proposals for American infanticide legislation [3, 28]. In the United States, the notguilty-by-reason-of-insanity (NGRI) defense is used in some cases of maternal filicide. Throughout the United States and the world, there are various laws regarding NGRI (see Insanity: Defense). NGRI laws often include that a mental illness caused an actor not to know her act was wrong, and may include that she was unable to conform her conduct to the requirements of the law. The diagnosis of PPP may be the mental illness on which the insanity defense is predicated. A woman with PPP and an alternative sense of reality may delusionally believe that she is doing what is right in killing her infant. Another woman may be unable to control her behavior because of manic psychosis. Still another may kill, believing that the hallucinations telling her to do so are from God. However, a mother who fatally abuses her infant may be unlikely to qualify for an NGRI finding because of the aforementioned requirements.
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PPP can be difficult to prove in the legal sense – symptoms may have rapid resolution prior to psychiatric evaluation, and there has existed disagreement in the field as well. Psychiatric evaluation may be expedited in cases where PPP is believed to be related to the murder.
Summary PPP may consist of symptoms including hallucinations, delusions, confusion, insomnia, mood swings, and loss of contact with reality. It must be differentiated from depression, anxiety, and medical disorders. Mothers may decompensate rather rapidly, within several weeks of delivery. Early recognition may be critical. These mothers often merit emergent treatment. Risks may include infant neglect, abuse, infanticide, or maternal suicide. Mothers with PPP who kill their infants may qualify for infanticide or insanity defenses.
[10]
[11]
[12]
[13]
[14]
[15]
[16]
References [1]
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[7]
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Attia, E., Downey J. & Oberman, M. (1999). Postpartum psychoses, in Postpartum Mood Disorders, L.J. Miller, ed, American Psychiatric Press, Washington, DC, pp. 99–117. Brockington, I. (1996). Motherhood and Mental Health, Oxford University Press, Oxford. Nelson, K.E. (2004). Postpartum psychosis and women who kill their children: making the punishment fit the crime, Developments in Mental Health Law 23, 23–36. Gilman, C.P. (1892). The Yellow Wallpaper. Wisner, K.L., Gracious, B.L., Piontek, C.M., Peindl, K. & Perel, J.M. (2003). Postpartum disorders: phenomenology, treatment approaches, and relationship to infanticide, in Infanticide: Psychosocial and Legal Perspectives On Mothers Who Kill, M.G. Spinelli, ed, APPI, Washington, DC. Kendell, R.E., Chalmers, J.C. & Platz, C. (1987). Epidemiology of puerperal psychoses, British Journal of Psychiatry 150, 662–673. Sit, D., Rothschild, A.J. & Wisner, K.L. (2006). A review of postpartum psychosis, Journal of Women’s Health 15(4), 352–368. Sharma, V., Smith, A. & Khan, M. (2004). The relationship between duration of labour, time of delivery, and puerperal psychosis, Journal of Affective Disorders 83(2–3), 215–220. Jones, I. & Craddock, N. (2007). Searching for the puerperal trigger: molecular genetic studies of bipolar affective puerperal psychosis, Psychopharmacology Bulletin 40(2), 115–128.
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Blackmore, E.R., Jones, I., Doshi, M., Haque, S., Holder, R., Brockington, I. & Craddock, N. (2006). Obstetric variables associated with bipolar affective puerperal psychosis, British Journal of Psychiatry 188, 32–36. Robertson, E. & Lyons, A. (2003). Living with puerperal psychosis: a qualitative analysis, Psychology and Psychotherapy 76(4), 411–431. Stewart, D.E., Klompenhouwer, J.L., Kendell, R.E. & van Hulst, A.M. (1991). Prophylactic lithium in puerperal psychosis, British Journal of Psychiatry 158, 393–397. Wisner, K., Peindl, K. & Hanusa, B.H. (1994). Symptomatology of affective and psychotic illnesses related to childbearing, Journal of Affective Disorders 30, 77–87. American Psychiatric Association (2000). Diagnostic and Statistical Manual, Text Revision, 4th Edition, American Psychiatric Association. Sharma, V., Smith, A. & Mazmanian, D. (2006). Olanzapine in the prevention of postpartum psychosis and mood episodes in bipolar disorder, Bipolar Disorders 8(4), 400–404. Chandra, P.S., Bhargavaraman, R.P., Raghunandan, V.N. & Shaligram, D. (2006). Delusions related to infant and their association with mother-infant interactions in postpartum psychotic disorders, Archives of Women’s Mental Health 9(5), 285–288. Lindahl, V., Pearson, J.L. & Colpe, L. (2005). Prevalence of suicidality during pregnancy and the postpartum, Archives of Women’s Mental Health 8(2), 77–87. Resnick, P.J. (1970). Murder of the newborn: a psychiatric review of neonaticide, American Journal of Psychiatry 126, 58–64. Putkonen, H., Weizmann-Henelius, G., Collander, J., Santtila, P. & Eronen, M. (2007). Neonaticides may be more preventable and heterogeneous than previously thought-neonaticides in Finland 1980–2000, Archives of Women’s Mental Health 10, 15–23. Mendlowicz, M.V., da Silva Filho, J.F., Gekker, M., de Moraes, T.M., Rapaport, M.H. & Jean-Louis, F. (2000). Mothers murdering their newborns in the hospital, General Hospital Psychiatry 22(1), 53–55. Friedman, S.H., Horwitz, S.M. & Resnick, P.J. (2005). Child murder by mothers: a critical analysis of the current state of knowledge and a research agenda, American Journal of Psychiatry 162, 1578–1587. Resnick, P.J. (1969). Child murder by parents: a psychiatric review of filicide, American Journal of Psychiatry 126, 73–82. Altshuler, L.L., Hendrick, V. & Cohen, L.S. (1998). Course of mood and anxiety disorders during pregnancy and the postpartum period, The Journal of Clinical Psychiatry 59(Suppl. 2), 29–33. Oberman, M. (1996). Mothers who kill: coming to terms with modern American infanticide, American Criminal Law Review 34, 2–109.
Posttraumatic Stress Disorder [25]
Friedman, S.H. & Resnick, P.J. (2007). Child murder by mothers: patterns and prevention, World Psychiatry 6, 137–141. [26] Dean, P.J. (2004). Child homicide and infanticide in New Zealand, International Journal of Law and Psychiatry 27, 339–348. [27] d’Orban, P.T. (1979). Women who kill their children, British Journal of Psychiatry 134, 560–571. [28] Connell, M. (2002). The postpartum psychosis defence and feminism: more or less justice for women? Case Western Reserve Law Review 53, 143.
SUSAN HATTERS-FRIEDMAN
Posttraumatic Stress Disorder Exposure to psychological trauma is thought to be a risk factor for the development of many mental health disorders including posttraumatic stress disorder (PTSD), acute stress disorder (ASD), other anxiety disorders, depressive disorders, somatic disorders, substance abuse disorders, and psychotic disorders. The specific mental health symptoms that typically become manifest following exposure to trauma appear to vary from culture to culture [1–3] and from era to era, e.g., somatic and psychotic symptoms were much more common in the traumatized World War II (WWII) combatants [4] than they were in traumatized Vietnam combatants [5]. The term PTSD was first introduced into the official Western classification of psychiatric disorders in 1980 with the publication of the third edition of the Diagnostic and Statistical Manual for Mental Health Disorders or DSM-III [6]. Prior to 1980, the disorder was referred to by a number of names including soldier’s heart in the Civil War, shell shock and traumatic neurosis in WWI, combat fatigue and war neurosis in WWII, and gross stress reaction in the 1970s [7]. PTSD has also been referred to by a number of somewhat pejorative terms to include secondary gain neurosis, compensation neurosis, and litigation neurosis owing to its association with malingering and factitious disorder [8, 9]. Malingering involves the intentional production or substantial exaggeration of physical or psychological symptoms and/or dysfunction in order
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to secure external incentives, e.g., avoiding work, evading criminal responsibility, and obtaining disability compensation [10]. Factitious disorder also involves intentional feigning or exaggeration of physical or psychological symptoms or dysfunction, but the motivation for doing so is to maintain the sick role, the victim role, or the wounded soldier role rather than obtaining external incentives [10]. Malingering and factitious disorder often coexist; and for the sake of brevity, the term malingering henceforth will be used to denote both malingering and factitious disorder. Six criteria currently define PTSD per the most recent edition of the DSM, the DSM-IV [10]. First, the person must have experienced, witnessed, or have been confronted with a traumatic event that involved an actual or threatened death or serious injury of someone, or involved a threat to the physical integrity of self or others. In addition, the person’s emotional response to the traumatic event must have involved intense fear, helplessness, or horror. Second, the person must persistently reexperience the traumatic event in the form of nightmares, intrusive recollections during the waking state, flashbacks (illusions and hallucinations) in which the person feels as if the event were reoccurring, and/or intense psychological distress or physiological reactivity upon exposure to stimuli that resemble an aspect of the traumatic event. Third, the person must persistently avoid stimuli associated with the traumatic event and/or experience a numbing of general responsiveness. Fourth, the person must experience persistent hyperarousal symptoms, e.g., hypervigilance, exaggerated startle reflex, and irritability. Fifth, the person must manifest reexperiencing, avoidance/numbing, and hyperarousal symptoms for more than one month posttrauma. Sixth, the person must manifest clinically significant distress or impairment in social, occupational, or other important areas of functioning. The diagnostic criteria for ASD are very similar to those for PTSD – the major differences being the presence of dissociative symptoms in ASD, but not in PTSD, and the PTSD symptom triad of reexperiencing, hyperarousal, and avoidance/numbing symptoms are experienced for less than one month in ASD, rather than for more than a month as they are in PTSD [10]. A voluminous amount of research has been conducted over the course of the past 25 years on psychological trauma, ASD, and PTSD. One of the
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more surprising findings is that most individuals in the United States will be exposed to one or more traumatic events in the course of their lifetime – between 68 and 90% depending on the criterion and measurement methods used [11–14]. Perhaps even more surprising is the finding that only a relatively small percentage of those individuals exposed to trauma go on to develop PTSD – between 9 and 14% depending on the stressor criteria and measurement methods used [11–16]. Individuals with certain characteristics have been found to be at greater risk than others to develop PTSD subsequent to trauma – namely, women [17] and individuals with a history of psychiatric disorders as well as individuals with a family history of psychiatric disorders [11–16]. Conversely, individuals with other characteristics appear less likely to develop PTSD subsequent to trauma – namely, men [17] and individuals with good intelligence [5, 15, 18] as well as those individuals with a substantial amount of a personality trait termed hardiness [19–22]. Hardy individuals are those who stay committed to life (as opposed to being alienated), who believe in their own ability to control and influence the course of events (as contrasted with a sense of being powerless), and who view negative life events as challenges to be met and overcome (as opposed to view these events as insurmountable threats). Similarly, some individuals respond to traumatic events and PTSD with enhanced mental health, altruism, empathy, spirituality, and prosocial values or what has been termed posttraumatic growth [23, 24]. Some types of trauma appear to be more pathogenic than the other types. The most pathogenic appears to be trauma that is repetitive and prolonged (as opposed to a single and brief), man-made (as opposed to natural catastrophes), and particularly gruesome such as is often found in combat, war atrocities, and torture situations [24–27]. Single, brief, and time-limited traumatic events also vary in terms of their pathogenic potential. For example, a situation in which an 18-month-old child is run over in his own driveway by a neighbor and thereafter dies shortly in the arms of his mother is far more likely to provoke PTSD in the neighbor and the mother than the bystanders who are horrified as they witness the tragedy but who have no personal involvement with the child, the mother, or the neighbor [24–27]. Another somewhat surprising finding is that those individuals who develop PTSD subsequent to trauma
often spontaneously remit or improve over time without the benefit of formal treatment to the point that they no longer meet the criteria necessary to be diagnosed with PTSD. Estimates vary, but approximately 50% of those with PTSD appears to spontaneously remit within two years posttrauma with the majority of the remission taking place in the first year [5, 12, 16, 28–31]. Those who do not remit spontaneously and who do not remit by way of treatment have an elevated risk to develop other mental health disorders and substance use disorders [11, 12, 14]. Those who do remit are at no greater risk to develop other mental health disorders than those who were never traumatized in the first place [11, 12, 14]. Another important finding is the level of vocational and social dysfunction varies considerably in the PTSD-afflicted individuals. Some individuals function at a high level vocationally and socially, and only experience occasional episodes of acute PTSD symptoms typically provoked by trauma anniversary dates or by severe situational stressors such as the death or serious illness of a loved one. Still others with PTSD are severely and chronically incapacitated emotionally, socially, and vocationally. This usually occurs when the individual has been exposed to a particularly severe trauma or to multiple traumas, has severe psychopathology prior to the trauma, and/or when severe comorbid disorders develop subsequent to the PTSD such as addictions, personality disorders, or psychosis [11–14].
Assessment Prior to the publication of the DSM-III in 1980 [6], PTSD was frequently misdiagnosed in the form of false negatives (PTSD was present but not diagnosed) simply because it was not recognized as a valid diagnostic entity. Since then, it appears that the frequency of PTSD diagnoses have steadily risen as has the misdiagnosis of PTSD in the form of false positives (PTSD is diagnosed as present when it is not). Described below are some of the errors that are frequently being made today.
Trauma One of the more common diagnostic errors being made is to equate stressful life events with trauma.
Posttraumatic Stress Disorder For example, a highly contentious divorce, being fired from a job, being betrayed by a close and trusted family member, or observing a tragic and deadly event unfold on television are often highly distressing and can generate many PTSD-like symptoms; but such events lack the critical element of being personally life-threatening and thus fail to meet one of the essential criteria necessary to diagnose PTSD [27]. For the same reason, being fearful while on sentry duty in a noncombat zone and learning of the deaths of other soldiers killed in a helicopter crash (but not being personally involved with them nor witnessing their deaths) generally does not constitute trauma. Malingers often fabricate traumatic events or they may fabricate their involvement with actual traumatic events. In either case, their stories often have inconsistencies in their retelling, inconsistencies with factual accounts of the traumatic events or in the events leading up to them, and/or implausibilities embedded within their stories [27]. For example, a malinger claiming to have been a sniper in Vietnam could not recall the manufacturer or power of the scope that was mounted on an unlikely weapon he said he employed – a rifle commonly used in Vietnam by infantrymen but generally considered to be inaccurate at long distances.
P TSD Symptoms Another common error is to diagnose PTSD on the basis of the presence of reexperiencing, hyperarousal, or avoidance/numbing symptoms by themselves [27]. None of these symptoms are unique to PTSD and all can be found in several other mental health disorders to include generalized anxiety disorder, phobia, panic disorder, and substance-induced mood and anxiety disorders. A causal link must be established between this triad of PTSD symptoms and a traumatic stressor before other mental health disorders can be safely ruled out and PTSD diagnosed. To do this, the triad of PTSD symptoms must have first become manifest after trauma exposure has occurred, not before. Most individuals who develop PTSD following trauma exposure will experience the initial onset of the triad of PTSD symptoms within days or weeks of trauma exposure. Occasionally individuals do delay the initial onset of PTSD symptoms for as long as a year or so posttrauma, but reports of delayed onset several years after trauma
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exposure should be suspect, particularly if the individual reports his or her mental health to be sound in the intervening period. The triad of PTSD symptoms typically wax and wane in concert with situationally induced stress once the symptoms first become manifest. Reports of severe PTSD symptoms that show little variability across time, stress, and situations should be suspect. Flashbacks wherein an individual with PTSD relives a traumatic experience in a delusional state and out of contact with reality do occur, but they are rare. When flashbacks do occur, they are typically provoked by high levels of situational stress coupled with substance abuse and poor sleep in individuals with a history of severe trauma and severe PTSD symptoms. Reports of frequent, prolonged, and unprovoked flashbacks should be suspect. Reexperiencing symptoms in the form of nightmares, in which the traumatic experiences are veridically recapitulated in the PTSD-afflicted individuals’ dreams, are typical. PTSD nightmares usually are accompanied by substantially more body movement than is found in conventional nightmares. PTSD nightmares also normally contain little in the way of fantasy at the outset; although as time progresses, PTSD nightmares may come to incorporate contemporary problems and issues in them as well as some fantastic elements. Conventional nightmares are largely fantastic and contain little in the way of realistic trauma material. Individuals with PTSD typically avoid situations that are connected with, or similar to, the traumatic events. Malingers generally do not avoid such reminders to the same extent. For example, malingers often relish telling war stories and often watch war movies and war footage on the news – things that most individuals with combat-induced PTSD would generally try to avoid. Malingerers tend to over-report or exaggerate the severity and frequency of hyperarousal and reexperiencing symptoms, and they tend to report these symptoms in interviews in an overly dramatic or histrionic fashion. On psychological tests that are sensitive to malingering, malingers tend to endorse obvious PTSD items but not subtle PTSD items; they also tend to endorse extreme but rare PTSD symptoms, and they tend to produce overall “fake-bad” test profiles. For a thorough review of the literature regarding psychological testing and malingering, see the article on forensic matters [32] in the text by Wilson and Keane [27].
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Disability The level of psychological, social, education, and vocational dysfunction related to PTSD varies considerably from one person to the other [27, 32]. Uncomplicated PTSD that is induced by a single, time-limited traumatic event in a mentally healthy adult who has good social support and who resides in a safe and healthy environment generally produces psychological distress in the neurotic (moderate) range along with mild to moderate dysfunction in social/educational/vocational functioning. The level of psychosocial dysfunction tends to markedly increase in those PTSD-afflicted individuals who heavily rely on substances and/or high levels of avoidance to cope with their PTSD symptoms [29, 30]. More psychosocial dysfunction is also generally seen in PTSD-afflicted individuals who have low social support and reside in unsafe, impoverished environments. The most severe psychosocial dysfunction is generally found among those PTSDafflicted individuals who have substantial pre-existing psychopathology and/or develop such pathology subsequent to the PTSD, e.g., substance abuse disorders, psychotic disorders, and personality disorders. Severe psychosocial dysfunction is also likely to be found in the PTSD-afflicted individuals whose PTSD was induced by prolonged, repetitive, and particularly gruesome trauma, e.g., atrocities, and torture. Psychosocial dysfunction should never be assumed if PTSD is present. It should always be independently assessed across vocational, educational, social, and recreational domains. Malingers tend to exaggerate their psychosocial dysfunction, and they often have marked discrepancies between their capacities for work and play. For example, a malinger claimed high levels of PTSD-related vocational dysfunction yet coached his son’s soccer team and routinely hosted social events in his home and in the community for team members and their parents.
Malingering Few, if any, studies have rigorously examined the prevalence of malingering in either clinical or forensic settings. There are, however, a number of case studies and studies that have employed samples of convenience that have estimated the prevalence to vary from 1% [33] to 50% [34] depending on the
setting and the population being examined. For a review of the literature in this regard, see the article on forensic matters [32] in the text by Wilson and Keane [27]. In most clinical settings, mental health professionals rely almost exclusively on individuals’ self-reports to diagnose PTSD that are taken by the way of unstructured interviews or structured interviews such as the Clinician-administered PTSD Scale [35]. Given clinicians’ general lack of skepticism and their desire to give clients the benefit of the doubt, many malingerers appear to be able to feign PTSD symptoms and trauma exposure well enough in such interviews to avoid being detected. This generally does not pose a problem provided the prevalence of malingering is low as it is in most clinical settings. However, in a few clinical settings and nearly all forensic settings, malingering is likely to be prevalent. This necessitates taking additional assessment measures to rule maligning out. Such measures usually entail collaborating clients’ self-reports of trauma exposure, collaborating their self-reports of PTSD symptoms, and collaborating their self-reports of psychosocial disability by way third party reports, reviews of public and private records (e.g., media accounts, police records, military records, and medical records), and the administration of structured interviews that are sensitive to dissimulation such as the Structured Interview of Reported Symptoms [36] as well as psychological tests that have scales that are sensitive to dissimulation such as the Minnesota Multiphasic Personality Inventory 2 (MMPI2) [37]. Gathering such information usually adds considerable time and expense to the assessment process. It is generally a good idea to rate individuals in terms of the malingering indicators listed below before diagnosing them with PTSD. The more malingering red flags that are present then the greater the likelihood of malingering. The number of red flags that should trigger efforts to collaborate individuals’ self-reports will vary from setting to setting depending on the costs for misdiagnosing PTSD if malingering is overlooked versus the costs for conducting the more thorough assessment necessary to rule out malingering. The costs will also be strongly influenced by the relative prevalence rates of PTSD versus malingered PTSD in the population of interest, which are likely to vary from time to time. For instance, malingered PTSD was probably relatively rare in veterans who approached the United States
Posttraumatic Stress Disorder Department of Veteran Affairs for services throughout the 1980s – about 5% according to one estimate [38]. Thus, the costs of occasionally misdiagnosing PTSD because malingering was overlooked were relatively small then. But clinical observation and some empirical evidence [39–41] now suggest that malingered PTSD is far more common in veterans seeking services from the US Department of Veteran Affairs than it once was. Consequently, the costs of misdiagnosing PTSD because malingering is overlooked are probably substantially greater than they once were. These costs not only include disability compensation being erroneously awarded to malingers but also include the costs of utilizing scarce clinical resources to treat malingers that could be better utilized if these resources were devoted to treating those in greater clinical need.
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6. Substance abuse disorder Malingering should be suspected when an individual presents with a substance abuse disorder. Substance abuse disorders sometimes do evolve as a consequence of PTSD so it is important to examine the individual’s substance usage before the trauma as well as after. 7. Marked disparities in psychosocial functioning Malingering should be suspected when an individual claims substantial vocational impairment subsequent to PTSD yet retains the capacity to successfully engage in social and/or recreational activities.
4. Antisocial personality disorder Malingering should always be suspected when an individual has an antisocial personality disorder or antisocial personality traits as evidenced by a long history of significant legal infractions and/or social irresponsibility.
8. Atypical presentational styles Malingering should be suspected if an individual presents with extreme emotional displays and/or bizarre symptoms when discussing their trauma. At the other extreme, malingering should also be suspected if an individual presents in a bland, matter-offact manner when discussing their trauma. Almost all PTSD-afflicted individuals will have some emotional distress and difficulty in discussing their trauma, but it will not be so severe as to disrupt the assessment process nor will it have a histrionic quality to it. Malingerers tend to present themselves as victims and tend to externalize, condemn, and blame others for their misfortune with accompanying anger, whereas individuals with PTSD tend to internalize and perceive themselves as being primarily responsible for their misfortune with accompanying guilt and shame. Malingering should also be suspected when an individual idealizes their life and work prior to the trauma while simultaneously attributing any and all shortcomings they currently have to the trauma and/or PTSD. Malingering should also be suspected when an individual behaves in an evasive, noncooperative, or hostile manner during the assessment. Such presentational styles are atypical of PTSD-afflicted individuals in most assessment settings.
5. Poor work history Malingering should be suspected when an individual is functioning as a marginal member of society as manifested by a poor work history, no permanent address, a vagabond lifestyle, etc. Severe PTSD or PTSD complicated by severe comorbid disorders can result in a poor work history so it is important to examine an individual’s work history prior to the trauma as well as after.
9. Atypical trauma Malingering should be suspected when traumatic events cannot be independently verified. Malingering should also be suspected when the traumatic events contain one or more implausible elements or when there are significant inconsistencies noted from one retelling of the trauma story to the next. Malingering should also be suspected when severe PTSD is claimed, the individual has no
Malingering (Factitious Disorder) Red Flags 1. Criminal proceedings Malingering should always be suspected when a diagnosis of PTSD is likely to mitigate an individual’s criminal culpability. 2. Disability proceedings Malingering should always be suspected when a diagnosis of PTSD is likely to result in disability compensation for an individual. 3. History of disability claims Malingering should always be suspected when an individual has a history of filing disability claims.
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pre-existing psychopathology, and the trauma is a single, brief, and not a particularly gruesome tragedy. 10. Atypical PTSD symptoms Malingering should be suspected when an individual reports a number of atypical symptoms or symptom patterns to include: substantial time delays between traumatic events and the initial onset of the PTSD symptom triad, the complete cessation of the PTSD symptoms for substantial periods of time owing to the heavy use of substances, PTSD symptoms that fail to vary in frequency and severity in concert with situational stressors, the presence of rare PTSD symptoms such as flashbacks occurring in the absence of high stress and substance abuse and a history of severe PTSD symptoms, nightmares that contain substantial fantasy and little trauma content, little in the way of avoidance of situational stimuli associated with the traumatic events, the endorsement of obvious PTSD symptoms but not subtle PTSD symptoms on psychological tests as well as overall fake-bad test profiles.
Treatment Treatment for individuals with PTSD takes a variety of forms depending on the severity and chronicity of the PTSD symptoms, the severity and type of any comorbid disorders that might be present, the characteristics of the community and prevailing mental health service delivery system, and the characteristics of the individuals themselves, e.g., motivation, secondary gain, age, ethnicity, and gender [42, 43]. PTSD that is of recent onset and is uncomplicated by other mental health disorders or problematic environmental circumstances (e.g., homelessness or dangerous environments) generally can be effectively treated on an outpatient basis with antidepressant medications [42, 43] and exposure-based cognitive-behavior therapy [42, 43]. Exposure-based CBT safely exposes PTSD-afflicted individuals to trauma-related stimuli in imagination and/or in vivo while simultaneously facilitating the assimilation of their traumatic events into healthy beliefs or cognitive schema regarding themselves and their world [42, 43]. It is also often beneficial to treat PTSD-afflicted individuals’ cooccurring situational problems by way of supportive problem-solving while simultaneously treating their
uncomplicated, recent onset PTSD way of antidepressants and CBT – exposure. This is particularly true in the case of soldiers recently returning from a war zone. Nearly all returning soldiers will be struggling with the task of transitioning from the military back into civilian life, with all of its attendant housing, job, education, family, and social support stressors; and some of the soldiers will be struggling with recent onset PTSD symptoms as well. In most cases, the stress of their readjustment issues will aggravate and prolong the PTSD symptoms of those who have them. By reducing the readjustment-related stress, the PTSD symptoms are likely to be lessened and the spontaneous remission process is likely to be strengthened. Hospitalization for the treatment of PTSD is seldom necessary. With the possible exception of one study [44], most of the evidence suggests that there is little sustained therapeutic benefit from treating chronic PTSD in specialized inpatient PTSD units [45–49]; and such hospitalizations appear to have iatrogenic effects for a significant minority of those who undergo such treatment [44–49]. Treatment of PTSD complicated by severe comorbid disorders is usually dictated by the nature of the comorbid disorders rather than the PTSD per se [42, 43]. For example, those with PTSD accompanied by severe depression and significant suicidal risk usually require hospitalization to treat the depression and suicidal threat before beginning treatment for the PTSD. In other cases of chronic, severe, and highly complicated cases of PTSD, it is sometimes best to approach treatment as one would approach an incurable and chronic medical illness. That is, the treatment should focus on palliative care and try to help the individual manage his or her psychiatric symptoms rather than directly focus on the traumatic events and PTSD symptoms in an effort to eliminate them, as would be the case with exposure-based CBT [42, 43].
Summary In summary, approximately 75% of all adults will be exposed to one or more traumatic events during the course of their lives. About 10% of those exposed to trauma will develop PTSD subsequent to the trauma, and about 50% of those who do develop PTSD will spontaneously remit within two
Posttraumatic Stress Disorder years posttrauma. Those who do not remit are at increased risk to develop additional disorders such as mood disorders and substance abuse disorders. Some individuals are at greater risk to develop PTSD than the others, particularly those with pre-existing psychopathology. Multiple trauma that is gruesome, prolonged, and man-made is more pathogenic than is less repetitive and less gruesome forms of trauma. The psychosocial dysfunction stemming from PTSD varies greatly from person to person depending on the severity of the trauma, the severity of the PTSD symptoms, and the type and severity of the comorbid disorders that are often present. Recent onset PTSD can be effectively treated by way of CBT exposure-based psychotherapy and antidepressant medications on an outpatient basis. The treatment of chronic PTSD in specialized PTSD inpatient units appears to be largely ineffective and possibly harmful for a significant minority of those who undergo it. PTSD appears to be frequently misdiagnosed in the form of false positives today. Malingering should always be suspected in forensic settings. Malingering should also be suspected in clinical settings when a significant number of malingering red flags are present. Collaborating clients’ self-reports of trauma, PTSD symptoms, and psychosocial dysfunction are usually required to rule out malingering.
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Wilson, J. (2006). The Posttraumatic Self, Routledge, New York. Roth, S., Newman, E., Pelcovitz, D., van der Kolk, B. & Mandel, F. (1997). Complex PTSD in victims exposed to sexual and physical abuse, Journal of Traumatic Stress 10(4), 539–555. Yehuda, R., Southwick, S. & Giller, E. (1992). Exposure to atrocities and severity of chronic posttraumatic stress disorder in Vietnam combat veterans, American Journal of Psychiatry 149(3), 333–336. Wilson, J. & Keane, T. (2004). Assessing Psychological Trauma and PTSD. Guilford, New York. Green, B. (1994). Psychosocial research in traumatic stress: an update, Journal of Traumatic Stress 7(3), 341–362. Perkonigg, A., Pfister, H., Stein, M., Hofler, M., Lieb, R., Maercker, A. & Wittchen, H. (2005). Longitudinal course of posttraumatic stress disorder and posttraumatic stress disorder symptoms in a community sample of adolescents and young adults, American Journal of Psychiatry 162, 1320–1327. Karamustafalioglu, O., Zohar, J., Guveli, M., Gal, G., Bakim, B., Fostick, L., Karamustafalioglu, N. & Sasson, Y. (2006). Natural course of posttraumatic stress disorder: a 20-month prospective study of Turkish earthquake survivors, The Journal of Clinical Psychiatry 67, 882–889. Shlosberg, A. & Strous, R. (2005). Long-term followup of PTSD in Israeli Yom Kippur war veterans, The Journal of Nervous and Mental Disease 193, 693–696. Wilson, J. & Moran, T. (2004). Forensic/clinical assessment of psychological trauma and PTSD in legal settings, in Assessing Psychological Trauma and PTSD, J. Wilson & T. Keane, eds, Guilford, New York, pp. 603–636. Keiser, H. (1968). The Traumatic Neurosis, JB Lippincott Co., Philadelphia. Miller, H. & Cartlidge, N. (1972). Simulation and malingering after injuries to the brain and spinal cord, Lancet 1, 580–585. Blake, D., Weathers, F., Nagy, L., Kaloupek, D., Klauminizer, G., Charney, D. & Keane, T. (1990). Clinician – Administered PTSD Scale, National Center for PTSD, West Haven. Rogers, R., Bagby, R. & Dickens, S. (1992). Structured Interview of Reported Symptoms, Psychological Assessment Resources, Odessa. Butcher, J., Dahlstrom, W., Graham, J., Tellegen, A. & Kaemmer, B. (1989). Minnesota Multiphasic Personality Inventory-2 (MMPI-2): Manual for Administration and Scoring. University of Minnesota Press, Minneapolis. Lynn, E. & Belza, M. (1984). Factitious posttraumatic stress disorder, Hospital and Community Psychiatry 35, 697–701. Frueh, B., Hamner, M., Cahill, S., Gold, P. & Hamlin, K. (2000). Apparent symptom overreporting in combat veterans evaluated for PTSD, Clinical Psychology Review 20(7), 853–885.
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Frueh, B., Smith, D. & Barker, S. (1996). Compensation seeking status and psychometric assessment of combat veterans seeking treatment for PTSD, Journal of Traumatic Stress 9(3), 427–439. Freuh, B., Gold, P. & de Arellano, M. (1997). Symptom overreporting in combat veterans evaluated for PTSD: differentiation on the basis of compensation seeking status, Journal of Personality Assessment 68, 369–384. Wilson, J., Friedman, M. & Lindy, J. (2001). Treating Psychological Trauma and PTSD, Guilford, New York. American Psychiatric Association (2004). Practice Guideline for the Treatment of Patients with Acute Stress Disorder and Posttraumatic Stress Disorder, APA Press, Washington, DC. Creamer, M., Morris, P., Biddle, D. & Elliott, P. (1999). Treatment outcome in Australian veterans with combat-related PTSD, Journal of Traumatic Stress 12(4), 545–558. Fontana, A. & Rosenheck, R. (1997). Effectiveness and cost of the inpatient treatment of PTSD, American Journal of Psychiatry 154, 758–765. Creamer, M., Forbes, M., Biddle, D. & Elliott, P. (2002). Inpatient versus day hospital treatment for chronic, combat-related PTSD, The Journal of Nervous and Mental Disease 190(3), 183–189. Fontana, A., Rosenheck, R. & Spencer, H. (1993). The Long Journey Home: The Third Progress Report on Specialized PTSD Programs, Northwest Program Evaluation Center, Department of Veteran Affairs Medical Center, West Haven. Johnson, D., Rosenheck, R., Fontana, A., Lubin, H., Charney, D. & Southwick, S. (1996). Outcome of intensive inpatient treatment for combat-related PTSD, The American Journal of Psychiatry 153, 771–777. Hammarberg, M. & Silver, S. (1994). Outcome of treatment for posttraumatic stress disorder in a primary care unit serving Vietnam veterans, Journal of Traumatic Stress 7(2), 195–216.
Related Articles Behavioral Science Evidence Deception: Detection of Disaster Mental Health Malingering: Forensic Evaluations Rape Trauma Syndrome Recollective Accuracy of Traumatic Memories Syndromes: Psychological LARRY D. SMYTH
Premenstrual Syndrome
PowerPlex [3]
Introduction The ability of polymerase chain reaction (PCR)based short tandem repeat (STR) multiplexes to successfully analyze human DNA from a diverse range of circumstances is at the cornerstone of forensic DNA science. A contemporary version of these sophisticated systems has been the GenePrint PowerPlex range of multiplex STR systems (Promega Corporation, Madison, WI; Table 1). These systems originally emerged in 1997 with PowerPlex 1.1 and progressed iteratively towards the current 16-locus PowerPlex 16 autosomal STR multiplex PCR system. The PowerPlex 16 offers extremely high discriminating power due to the combination of 15 STR loci plus the sex marker amelogenin [1, 2]. There is also the PowerPlex Y male-specific STR multiplex [3], which has specific advantages for the analysis of sex-assault cases and population genetic testing. The PowerPlex range of tests has shown its applicability to all forms of human identification casework, including kinship and disaster victim identification cases.
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J.M., Masibay, A., Rabbach, D.R., Amiott, E.A. & Sprecher, C.J. (2002). Validation of a 16-locus fluorescent multiplex system, Journal of Forensic Sciences 47, 773–785. Krenke, B.E., Viculis, L., Richard, M.L., Prinz, M., Milne, S.C., Ladd, C., Gross, A.M., Gornall, T., Frappier, J.R., Eisenberg, A.J., Barna, C., Aranda, X.G., Adamowicz, M.S. & Budowle, B. (2005). Validation of male-specific, 12-locus fluorescent short tandem repeat (STR) multiplex, Forensic Science International 151, 111–124.
Related Articles Microsatellites SIMON J. WALSH
Predecisional Bias: Jury see Jury Dynamics
Premenstrual Syndrome
References The Medical Perspective [1]
Spreecher, C.J., Krenke, B., Rabbach, D., Hennes, L., Amiott, E., Nassif, N. & Mandrekar, P. (2000). The PowerPlex 16 system: development and validation, in Proceedings of 11th International Symposium on Human Identification, Promega Corporation, Madison, WI. [2] Krenke, B., Tereba, A., Anderson, S.J., Buel, E., Culhane, S., Finis, C.J., Tomsey, C.S., Zachetti,
Table 1
The idea that hormones control a woman’s emotional state has been entrenched in populist thinking. For centuries, physicians tried in vein to link the cyclical hormonal pattern of estrogen and progesterone to
GenePrint PowerPlex STR multiplex systems produced for use in forensic DNA profiling
Name
No. of loci
Target loci included
PowerPlex (1.1 and 1.2) PowerPlex 2.1
8 9
PowerPlex ES
9
PowerPlex 16
16
PowerPlex Y
12
TH01, TPOX, CSF1PO, vWA, D16S539, D13S317, D7S820, D5S818 Penta E, D18S51, D21S11, TH01, D3S1358, FGA, TPOX, D8S1179, vWA. D3S1358, TH01, D21S11, D18S51, vWA, D8S1179, FGA, SE33 (also known as ACTBP2 ), Amelogenin D3S1358, vWA, FGA, TH01, TPOX, CSF1PO, D5S818, D13S317, D7S820, D8S1179, D21S11, D18S51, D16S539, Penta D, Penta E, Amelogenin DYS19, DYS385a, DYS385b, DYS389I, DYS389II, DYS390, DYS391, DYS392, DYS393, DYS437, DYS438, DYS439
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premenstrual syndrome (PMS). After all, it seemed so logical. Despite these efforts, medical science was never able to make the connection work. Attempts to treat PMS with hormonal treatments continuously failed. Hysterectomy and oopherectomy rarely afforded significant relief. The breakthrough came with the discovery of serotonin, a ubiquitous neurotransmitter, now well established to underlie moodiness, anxiety, irritability, and hostility – symptoms commonly seen in PMS. Consequently, on 6 July 2000, fluoxetine became the first food and drug administration (FDA) recognized and approved treatment for the severe form of PMS, known as premenstrual dysphoric disorder (PMDD).a So, the answer was not hormones – it was serotonin. Despite an understanding of the chemical etiology, PMS itself is a remarkably common experience and cannot itself be considered abnormal or pathological. Most women who experience PMS have mild or moderate symptoms and are not socially or occupationally impaired by them. However, a small subset of women experience significant impairment and disability in the premenstrual phase. Psychiatry has chosen to define the women suffering from this severe form of PMS as having PMDD. While deemed as an area of interest and research, PMDD is not considered to be a mental illness. It can be classified alternatively as a depressive disorder, not otherwise specified (coded 311); this category includes disorders with depressive features that do not meet the criteria for major depressive disorder. The sensitivity of the political correctness of this issue is obvious. The american psychiatric association (APA) has established diagnostic criteria, which are provided in the box below.
Legal Usage In the 1980s, two British cases raised PMS as the basis for a diminished capacity defense reducing the quantum of guilt assessed against the accused.b First, in November, 1981, Sandie Smith was put on three years’ probation after conviction of threatening to kill a police officer and for carrying a knife. She suffered from PMS and had committed almost 30 crimes, including arson, assault, and manslaughter, during the premenstrual period. Smith responded to progesterone therapy, advocated by English gynecologist Dr
Katharine Dalton, to curb PMS. Dalton was a pioneer researcher who used her patients as a source of information for formulating what she and Dr Peter Green, a fellow researcher, named “premenstrual syndrome” in 1953. Then, that same month Christine English pleaded guilty to manslaughter by reason of diminished responsibility. She drove her car into her lover after an argument that occurred while she was suffering from severe PMS [1]. She was conditionally discharged for 12 months. One court martial case and an unreported US decision admitted PMS evidence as grounds for a defense. In United States v. Morton, the accused was charged with assault with a dangerous weapon, communicating a threat, and unlawfully carrying a concealed weapon. She pled not guilty by reason of insanity due to PMS. Morton had to establish by clear and convincing evidence that her PMS was so severe that she was unable to know and appreciate the consequences of her conduct [2]. The court held that she failed to establish insanity. It is unlikely that any US jurisdiction would allow PMS as an insanity defense. In People v. Santos [3], the defendant testified in a preliminary hearing that she beat her child while in a “blackout” induced by PMS [4]. She was able to get a favorable plea bargain based on diminished capacity. Diminished capacity is an excuse defense that shifts the burden to the prosecution to disprove the excuse beyond a reasonable doubt once evidence of the excuse is admitted.c American states that recognize a diminished capacity defense might permit evidence of PMS to be admitted to show diminished capacity [5]. However, several states have abolished the diminished capacity defense.d Some states permit a diminished capacity defense murder prosecutions [6], following United States v. Brawner [7]. Other states permit a diminished capacity defense when the accused is charged with any crime of specific intent [8]. Federal practice under the 1983 Insanity Defense Reform Act [9] permits expert evidence on diminished capacity. Alaska allows expert testimony on diminished capacity that would permit PMS evidence during the guilt phase of trial.e Diminished capacity must be established by expert opinion evidence that shows that the defendant both suffers from PMS and committed the crime charged while under the influence of PMS. Half
Premenstrual Syndrome the statesf and the Federal courts follow Daubert v. Merrell Dow Pharmaceuticals Inc. [10] and exclude expert opinion evidence if the expert’s underlying scientific principles fail to meet a four-part test [11]: 1. 2. 3. 4.
Has the theory been tested by other researchers? Has the theory been published? What is the error rate? Is the process generally accepted?
An expert in a Daubert jurisdiction must testify that PMS is a mental illness as diagnosed using diagnostic and statistical manuel of mental disorders, fourth edition, Text Revised (DSM-IV and DSMIV(TR)) and explain the DSM-IV(TR) criteria for PMS (see Box). The expert must state that the diagnosis and criteria for PMS have been published and subject to peer review. She/he must assert the error rate for making the diagnosis of PMS. Finally, the expert should state that the criteria for diagnosing PMS and diminished responsibility are generally accepted (see Expert Opinion: United Kingdom, Canada, and Australia). Some states follow the Frye rule (see Frye v. United States) that requires the underlying scientific principles be “generally accepted” before an expert gives an opinion based on those principles [12]. Others have adopted a modified Frye rule with modifications using some or all of the Daubert factors [13]. In the Frye states and mixed states, the expert must testify that psychotherapists generally accept that PMS causes the sufferer to be unaware of the consequences of her action or to distinguish right from wrong. Expert opinion evidence on PMS should be freely allowed during the sentencing phase of any trial. According to ¶ Section 5K2 of the Federal Sentencing Guidelines, the court may make a downward departure from the statutory maximum sentence for a convicted defendant on the ground of diminished capacity.g
Concerns about the use of PMS in the Courtroom The forensic use of PMS has generated global controversy. Some of the principle arguments are as follows.
•
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PMS is yet another sexist “woman as mad” explanation for female criminality Historically, deviant women have often been characterized as either “bad” or “mad” since their antisocial behavior conflicted with certain socially defined and desirable female personality traits and roles. Medical theory, from at least the mid 1800s, espoused that women’s reproductive organs controlled their minds, bodies, and personalities. Such biological determinism was strongly endorsed and promulgated by psychiatry: in Freud’s model of psychoanalysis, sexual temperament was conceived as a function of biology [14]. Accordingly, the nineteenth century doctors and lawyers agreed that menstruation and uterine malfunction could lead a woman to insanity or criminality. As an example, in the 1867 case United States v. Harris, attorneys called a psychiatrist and six other physicians who testified that the defendant was “morally insane” at the time of the homicide due to painful dysmenorrhea that led to mental derangement and hysteria. After a brief deliberation, the jury returned a verdict of not guilty by reason of insanity.h English courts also recognized some form of mental derangement related to the menstrual cycle as an excuse for criminality before Harris [15, 16]. One woman was acquitted of shoplifting in 1845 while two others were acquitted of murder in 1851. All three were found to have acted with temporary insanity due to “suppression of menstruation” [17]. One of these women had murdered her lover who had rejected her. A doctor testified that her wild eyes indicated problems with her uterus [18]. The specifics of the sociomedical theoretical explanations for female deviance shifted with time as the understanding of the female reproductive system evolved from the uterus to ovaries and then to hormones in the 1920s. With the UK cases of Smith and English discussed above, the focus in the early 1980s became PMS and its relationship to female criminality. In part, this undoubtedly reflected the growing interest in studying the female offender and etiology since statistics during the 1970s were reflecting an increasing number of crimes committed by women or, at the least, a higher number of arrests or prosecutions [19]. To some of its detractors, PMS is therefore the latest in a long line of anatomical deterministic theories of female criminality that have prevailed as
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a substitute for looking at how entrenched gender inequality might contribute to crime. Instead, women’s deviance has been linked with the anatomical parts that differentiate them from males and which allow them to fulfill their primary gender role of reproduction. •
Its usage in court could stigmatize women as a whole and/or affect their equal participation in the public sphere There is concern that if PMS is raised as exculpatory grounds, people might generalize from the few and negatively stereotype all women or at the least those who experience any premenstrual symptoms [20]. Sensationalist captions such as “raging hormones”, “premenstrual frenzy”, and “Dr Jekyll and Ms Hyde” that appeared in British newspapers during the English and Smith cases can fuel imagery of women as periodically unstable and therefore unsuitable for some employment positions and/or responsibilities. As with all medical disorders, a whole class of people with similar maladies could be stigmatized. As discussed earlier, the syndrome is fairly common, although only a minute percent manifest the symptoms that can substantially impact on their actions. •
Its use relies upon acceptance of the legitimacy of PMS and PMDD and advocates/specialists All medical practitioners do not share in Dalton’s belief in temporary psychosis as a symptom of the most severe PMS cases [21, 22]. The medical literature is confusing in its diversity of opinion concerning the possible connection of PMS to criminal behavior with no universally accepted medical consensus about the correlation of the severe variant with antisocial behavior. In some countries like Australia where PMS is not raised except very infrequently in sentencing mitigation,i it continues to be referred to as premenstrual tension (PMT) and lacks acknowledgment as a legitimate medical condition. This is illustrated in a popular news feature story on PMS: Despite the popular belief that “it is all in the hormones”, there is no convincing evidence that women with severe PMS have different hormonal fluctuations than other women . . . cause of PMS are still unknown . . . [23].
A number of female medical practitioners are quoted in the article articulating the view that women who think they have PMS may actually have clinical depression. Yet to use it successfully a forensic expert is required. With insanity the defense must show that PMS is a disease of the mind and that the sufferer did not know the nature or quality of the act or that it was wrong (McNaughton Rule). Doing so with PMS can be highly problematic. To raise automatism (a state in which the mind or the will does not accompany physical acts) by arguing that certain women with PMS who go hours without eating produce an excess amount of adrenalin that causes a hypoglycemic state of impaired consciousness requires an expert like Dalton to testify that hypoglycemia can be a symptom of PMS and that the defendant possessed that abnormality. The defense with diminished responsibility or capacity must show that PMS prevented the accused from having the specific intent (mens rea) with hazy thinking, and impairment of self-control, judgment and willpower. Again, proof is problematic. Plus, there are several legal issues since the defense has to show that PMS is an abnormality of the mind (which is difficult since the symptoms of PMS are not even universally accepted), that it arose from an inherent cause, and that it substantially impaired the defendant’s mental responsibility [24]. With potentially lengthy sentences, the convicted has the added stigma of mental illness [25]. •
It could be misused and or abused by defendants There is concern that PMS might be used as grounds for a defense by non-bona fide sufferers – either charlatans and/or women who experience some of the more mild PMS symptoms. However, the diagnosis of PMDD can be substantiated by a heavy burden of proof, with medical evidence showing a clinically demonstrable physical disorder. A causal connection must be shown between the premenstrual symptom(s) and the criminal act. Additional evidence could include personal diaries, medical records, prior arrest record that could illustrate deviant activity correlation with the individual’s premenstrual time of her cycle, and evidence by family and friends of marked premenstrual behavioral changes.
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PMDD APA Diagnostic Criteria [26] In most menstrual cycles during the past year, symptoms (e.g., markedly depressed mood, marked anxiety, marked affective lability, decreased interest in activities) regularly occurred during the last week of the luteal phase (and remitted within a few days of the onset of menses). These symptoms must be severe enough to markedly interfere with work, school, or usual activities and be entirely absent for at least 1 week post menses. The essential features are symptoms such as markedly depressed mood, marked anxiety, marked affective lability, and decreased interest in activities. These symptoms have regularly occurred during the last week of the luteal phase in most menstrual cycles during the past year. The symptoms begin to remit within a few days of the onset of menses (the follicular phase) and are always absent in the week following menses. Five (or more) of the following symptoms must have been present most of the time during the last week of the luteal phase, with at least one of the symptoms being one of the first four: 1) feeling sad, hopeless, or self-deprecating; 2) feeling tense, anxious or “on edge”; 3) marked lability of mood interspersed with frequent tearfulness; 4) persistent irritability, anger, and increased interpersonal conflicts; 5) decreased interest in usual activities, which may be associated with withdrawal from social relationships; 6) difficulty concentrating; 7) feeling fatigued, lethargic, or lacking in energy; 8) marked changes in appetite, which may be associated with binge eating or craving certain foods; 9) hypersomnia or insomnia; 10) a subjective feeling of being overwhelmed or out of control; and 11) physical symptoms such as breast tenderness or swelling, headaches, or sensations of “bloating” or weight gain, with tightness of fit of clothing, shoes, or rings. There may also be joint or muscle pain. The symptoms may be accompanied by suicidal thoughts. This pattern of symptoms must have occurred most months for the previous 12 months. The symptoms disappear completely shortly after the onset of menstruation. The most typical pattern seems to be that of dysfunction during the week prior to menses that ends mid-menses. Atypically, some females also have symptoms for a few days around ovulation; a few females with short cycles might, therefore, be symptom free for only 1 week per cycle. Typically, the symptoms are of comparable severity (but not duration) to those of a Major Depressive Episode and must cause an obvious and marked impairment in the ability to function socially or occupationally in the week prior to menses. Impairment in social functioning may be manifested by marital discord and problems with friends and family. It is very important not to confuse long-standing marital or job problems with the dysfunction that occurs only premenstrually. There is a great contrast between the woman’s depressed feelings and difficulty in functioning during these days and her mood and capabilities the rest of the month. These symptoms may be superimposed on another disorder but are not merely an exacerbation of the symptoms of another disorder, such as Major Depressive, Panic, or Dysthymic Disorder, or a Personality Disorder. The presence of the cyclical pattern of symptoms must be confirmed by at least 2 consecutive months of prospective daily symptom ratings. Daily symptom ratings must be done by the woman and can also be done by someone with whom she lives. It is important that these diaries be kept on a daily basis rather than composed retrospectively from memory. Delusions and hallucinations have been described in the late luteal phase of the menstrual cycle but are very rare. Although females with the combination of dysmenorrhea (painful menses) and premenstrual
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dysphoric disorder are somewhat more likely to seek treatment than females with only one of these conditions, most females with either of the conditions do not have the other condition. A wide range of general medical conditions may worsen in the premenstrual or luteal phase (e.g., migraine, asthma, allergies, and seizure disorders). There are no specific laboratory tests that are diagnostic of the disturbance. However, in several small preliminary studies, certain laboratory findings (e.g., serotonin or melatonin secretion patterns, sleep EEG findings) have been noted to be abnormal in groups of females with this proposed disorder relative t o control subjects. It is estimated that at least 75% of women report minor or isolated premenstrual changes. Limited studies suggest an occurrence of “premenstrual syndrome” (variably defined) of 20%–50%, and that 3%–5% of women experience symptoms that may meet the criteria for this proposed disorder. There has been very little systematic study on the course and stability of this condition. Premenstrual symptoms can begin at any age after menarche, with the onset most commonly occurring during the teens to late 20s. Those who seek treatment are usually in their 30s. Symptoms usually remit with menopause. Although symptoms do not necessarily occur every cycle, they are present for the majority of the cycles. Some months the symptoms may be worse than others. Women commonly report that their symptoms worsen with age until relieved by the onset of menopause. Research criteria for premenstrual dysphoric disorder A. In most menstrual cycles during the past year, five (or more) of the following symptoms were present for most of the time during the last week of the luteal phase, began to remit within a few days after the onset of the follicular phase, and were absent in the week postmenses, with at least one of the symptoms being either (1), (2), (3), or (4): (1) markedly depressed mood, feelings of hopelessness, or self-deprecating thoughts (2) marked anxiety, tension, feelings of being “keyed up”, or “on edge” (3) marked affective lability (e.g., feeling suddenly sad or tearful or increasedsensitivity to rejection) (4) persistent and marked anger or irritability or increased interpersonal conflicts (5) decreased interest in usual activities (e.g., work, school, friends, hobbies) (6) subjective sense of difficulty in concentrating (7) lethargy, easy fatigability, or marked lack of energy (8) marked change in appetite, overeating, or specific food cravings (9) hypersomnia or insomnia (10) a subjective sense of being overwhelmed or out of control (11) other physical symptoms, such as breast tenderness or swelling, headaches, joint or muscle pain, a sensation of “bloating”, weight gain. Note: In menstruating females, the luteal phase corresponds to the period between ovulation and the onset of menses, and the follicular phase begins with menses. In nonmenstruating females (e.g., those who have had a hysterectomy), the timing of luteal and follicular phases may require measurement of circulating reproductive hormones. B. The disturbance markedly interferes with work or school or with usual social activities and relationships with others (e.g., avoidance of social activities, decreased productivity and efficiency at work or school). C. The disturbance is not merely an exacerbation of the symptoms of another disorder, such as Major Depressive Disorder, Panic Disorder, Dysthymic Disorder, or a Personality Disorder (although it may be superimposed on any of these disorders). Criteria A, B, and C must be confirmed by prospective daily ratings during at least two consecutive symptomatic cycles. (The diagnosis may be made provisionally prior to this confirmation.)
Premenstrual Syndrome
End Notes
References
a.
[1]
The Massachusetts Institute of Technology holds the patent for this treatment. b. The English Homicide Act of 1957 provides that “Where a person kills or is a party to the killing of another, he shall not be convicted of murder if he was suffering from such abnormality of mind . . . as substantially impaired the mental responsibility for acts and omissions in doing or being a party to the killing.” 5 and 6 Eliz. 2, ch. 2, § 2[1], 1957. c. LaFave § 9.8(f)(4). d. Arizona, California, Florida, Georgia, Maryland, Ohio, Oklahoma, Rhode Island, and South Carolina have abolished diminished capacity. See, e.g., State v. Doss, 568 P.2d 1054 (Ariz. 1977) (en banc) Cal. Penal Code § 25. Section 2.02 of the Model Penal Code abolished specific intent and diminished capacity. e. See Alaska Stat. § 12.47.020. f. Alaska, Colorado, Connecticut, Delaware, Idaho, Indiana, Iowa, Kentucky, Louisiana, Maine, Michigan, Mississippi, Nebraska, New Hampshire, New Mexico, North Carolina, Ohio, Oklahoma, Oregon, Rhode Island, Tennessee, Texas, West Virginia, and Wyoming. See, e.g., State v. Coon, 974 P.2d 386 (Alaska 1999); People v. Shreck, 22 P.3d 68 (Colo. 2001); Springfield v. State, 860 P.2d 435 (Wyo. 1993). g. 18 U.S.C. Appendix Ch. Five Determining the Sentence, part K Departures 5K2.13. Diminished Capacity (Policy Statement). h. See Clephane, J.O. Trial of Mary Harris Indicted for the Murder of Adoniram Burroughs Before the Supreme Court of the District of Columbia, 10–12 (opening statement of Joseph Bradley) (W.H. & O.H. Morrison, Washington, DC. 1865); Goldstein, A. (1997). Nineteenth Century Gender Roles and the Murder Trial of Mary Harris; Kaye, N.S. (1997). Feigned Insanity. i. A search of Australian law databases such as LexisNexis and AUSTLII and the archives of the two major Australian newspapers The Sydney Morning Herald and The Age newspapers was conducted. No cases were reported in which PMS or PMT was used in an Australian court during that time period. Legal practitioners report its infrequent mention in sentencing.
[2] [3] [4]
[5]
[6]
[7] [8]
[9] [10] [11] [12]
[13]
[14] [15] [16]
[17]
[18]
[19]
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British Legal Debate: Premenstrual Tension and Criminal Behavior, New York Times, 29 Dec 1981, at http://www.nytimes.com/ (accessed 1 Jun 2007). 2001 CCA Lexis 202, (NMCM 99 00830 17 Jul 2001). No 1KO46229 (N.Y. Crim. Ct. 3 Nov 1982). (1983). Recent decisions: criminal law – premenstrual syndrome: a criminal defense, Notre Dame Law Review 59 253. United States v Pohlot, 827 F2d 889 (3rd Cir. 1987); cert denied, U.S. 98 L Ed 2d 660, 108 S Ct 710 (1988) LaFave, § 9.1(a). North Carolina, Massachusetts, Oregon, New York, and Pennsylvania. See, e.g., State v. p., 488 S.E.2d 225 (N.C. 1997). People v. Segal, 429 N.E.2d 107, 444 N.Y.S.2d 588 (N.Y. 1981). 471 F.2d 969 (D.C. Cir. 1972). Hawaii, Kansas, Massachusetts, Minnesota, Mississippi, Missouri, and Tennessee. See, e.g., State v Baker, 691 P2d 1166 (Hawaii 1984). State v. Grose, 982 S.W.2d 349 (Tenn. Crim. App. 1997) appeal denied (May 11, 1998). United States v. Brown, 326 F.3d 1143 (10th Cir. 2003); 18 U.S.C.S. § 17 (2007). 509 U.S. 579, 113 S.C.t. 2786, 125 L.Ed.2d 469 (1993). Daubert, 509 U.S. 593–594 (1993). Frye v. United States, 293 F. 1013, 34 A.L.R. 145 (App. D.C. 1923) States following this rule include Arizona, California, the District of Columbia, Florida, Illinois, Kansas, Maryland, Minnesota, Missouri, Nebraska North Dakota, Pennsylvania, and Washington. See, e.g., People v. Superior Court, 137 Cal. App. 4th 353, 40 Cal. Rptr. 3d 365 (2d Dist. 2006). Com. v. Crews, 536 Pa. 508, 640 A.2d 395 (1994). State v. Peters, 192 Wis. 2d 674, 534 N.W.2d 867 (Ct. App. 1995) These states include Alabama, Georgia, Hawaii, Massachusetts, Nevada, Oregon, South Carolina, Utah, Virginia, and Wisconsin. See, e.g., Turner v. State, 746 So. 2d 355 (Ala. 1998). Chodorow, N. (1989). Feminism and Psychoanalytic Theory, Yale University Press, New Haven. Riley, T.L. (1986). Premenstrual syndrome as a legal defense, Hamline Law Review 9, 193–194. D’Orban, P.T. (1983). Medicolegal aspects of the premenstrual syndrome, British Journal of Hospital Medicine, 30, 404–406. Spitz, A. (1987). Premenstrual syndrome: a critical review of the literature, Indiana Medicine 80(4), 378–382. Meehan, E. & MacRae, K. (1986). Legal implications of premenstrual syndrome: a Canadian perspective, Canadian Medical Association Journal 135, 601–608. Horney, J. (1978). Menstrual cycles and criminal responsibility, Law and Human Behaviour 2(1), 25–36.
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[21] [22] [23] [24] [25]
[26]
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Easteal, P. (1991). Women and crime: premenstrual issues, Trends and Issues in Crime and Criminal Justice 31, 1–8. Dalton, K. (1980). Cyclical criminal acts in premenstrual syndrome, Lancet 1070–1071. Dalton, K. (1986). Premenstrual syndrome, Hamline Law Review 9(1), 143–154. Sweet, M. (1996). Periods of joy, Sydney Morning Herald, 1 April, p. 11. Mc Sherry, B. (1993). The return of the raging hormones theory, Sydney Law Review 15, 309–310. Scutt, J. (1982). Premenstrual tension as an extenuating factor in female crime, The Australian Law Journal 56, 99–100. American Psychiatric Association, (1994) Diagnostic and Statistical manual of Mental Disorders 4th ed., (Text Revision). Washington, DC.
Related Articles
Privilege see Duty to Warn
Product Standard of Insanity see Insanity: Defense
Professional Judgment: Structured see Risk Assessment: Patient and Detainee
Temporary Insanity PATRICIA EASTEAL, NEIL S. KAYE
AND
TOM REED
Preventative Law see Therapeutic Jurisprudence
Primer Discharge Residue: Cartridge Discharge Residue see Firearm Discharge Residue: Analysis of
Printing Devices in Document Examination see Writing Instruments and Printing Devices
Professional Responsibility Codes for Forensic Scientists see Ethics: Codes of Conduct for Expert Witnesses
Profiles: Psychological and Behavioral Profiles are most closely associated with psychological models developed by the Federal Bureau of Investigation (FBI) in their early searches for serial murderers [1] (See Serial Homicide). The term has since been applied to a great many diverse compilations of information, as well as to what are little more than stereotypes. Over the past decade or so, “profilers” have been a favorite topic of crime dramas and novels and in the process have been glamorized and misrepresented to the point where the facts have often been obscured. Of particular concern for the justice
Profiles: Psychological and Behavioral system, however, has been the introduction of “profiles” as a component of psychological syndromes that have suggested new categories of “victims” and alleged profiles of the perpetrators responsible for their victimization (see Syndromes: Psychological; Deception: Truth Serum).
Profiles as an Aid in Law Enforcement In 1987, Judge Charles Becton published a law review article that drew attention to a seemingly chameleon-like way in which drug courier profiles adapted to any particular set of observations [2]. Within months, the Court of Appeals for the Ninth Circuit incorporate Judge Becton’s arguments into United States v. Sokolow [3]; a case which it had debated for over 2 years. By the late 1980s, however, criminal profiles had become a staple of law enforcement. Even the US Supreme Court could not stand by and watch them wiped out in a single sweep of a judicial pen. The High Court went back to basics, and they found their foundation in Terry v. Ohio [4]. Officer McFadden, and his detention of two men casing Zucker’s clothing store on an Ohio day in 1963, had given rise to the Terry Stop “stop and frisk” exception to the Fourth Amendment and the reasonable suspicion test, which provided justification, short of probable cause, under which police officers could initiate limited investigatory action. The Supreme Court knew that it could not allow any decision that it could make in Sokolow to turn profiles into unrestricted hunting licenses for overenthusiastic enforcement officials, nor was it willing to set up an entirely new bureaucracy to review the constitutionality of each and every profile. The Court also recognized that profiles changed over time, and that their effectiveness would evaporate if they became frozen and subject to public scrutiny. This solution requires that every law enforcement intervention, regardless of whether or not it was set in motion by a profile, must be justifiable through the same articulation of facts – the “totality of the circumstances” – required for a Terry stop. Searches made under Sokolow are reviewed on a case-by-case basis and have been overturned if they fail to meet appropriate standards [5]. In this single decision, the Court recognized the validity of the
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probabilistic assumptions underlying the application of behavioral science techniques in justice administration, yet made it impossible to elevate criminal profiles into a license for Fourth Amendment abuse. Criminal profiles continue to serve as a tool in law enforcement, but more importantly, profiles are a means of leveraging investigative expertise, training investigative and enforcement officials, and applying systematic methodologies to the fast-changing and highly mobile environment that characterizes contemporary criminal operations. Once the intervention has been initiated, however, the profile is of no further probative relevance. Arrest and even the issuance of a search warrant require probable cause, and prosecution of any resulting charges must be based upon substantive evidence of guilt. The original profile is inadmissible in support of guilt, and is presumed to be inherently prejudicial [6]. The temptation to push these limits was brought home to the British public in a highly publicized 1995 case. Three years earlier, 23-year-old Rachel Nickell took her 2-year-old son and dog for a walk. She selected Wimbledon Common as her south London destination because of its reputation for safety, but, less than an hour later, she was found soaked in the blood of some 49 stab wounds, her child clinging to her lifeless body crying “get up mummy”. Police responded with the biggest murder investigation in London history – and one of the nation’s early attempts at using the new science of psychological profiling. England’s first encounter with the behavioral sciences in criminal investigation came in the 1985 “Railway Rapist” case. Although profiling had become well established in the United States through the work of the FBI Behavioral Science Unit, both serial killers and the methods for catching them were only just then taking hold in Britain. David Canter, professor of investigative psychology at Liverpool University, had a background in the psychology of building design, human behavior during fires, and the psycholinguistics of hoax fire calls; but the rigor of his science prepared him well to become that nation’s leading criminal profiler. His methodical work led to the conviction of John Duffy, and inspired the Robbie Coltrane character in the hit television detective series Cracker [7]. By the time of the Nickell murder, however, the publicity surrounding criminal profiling had attracted
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a host of psychologists who had been bitten by the detective bug. It was one of these who claimed the case, produced a profile, and eventually took over much of the day-to-day police operations directed toward conviction of the suspect, Colin Stagg, targeted by the profile. Through an attractive blond undercover policewoman, the psychologist initiated an 8-month liaison with the 31-year-old Stagg in which she shared violent sexual fantasies, confessed to the ritual sexual murder of a baby and a young woman, and egged him on to match her stories; even telling him that she wished he were Nickell’s murderer because “That’s the kind of man I want.” Stagg never claimed credit for the killing, but from 700 pages of letters and transcribed telephone conversations and public meetings, the psychologist concluded that Stagg’s fantasies, modeled upon information fed to him by those familiar with the details of the crime, revealed unique knowledge of the crime scene that could be known only by the murderer. Dragged before a judge in open court at the Old Bailey, defense quickly pointed out that Stagg had not even made good guesses – he did not know the location of the crime and had wrongly asserted that the victim had been raped. Up until that point, Great Britain had never felt the need for an entrapment statute, but the judge recognized a “honey trap” when he saw one. Clearing the accused and acknowledging the understandable pressure on the police, the judge was, nevertheless, forced to conclude that the operation betrayed “not merely an excess of zeal, but a blatant attempt to incriminate a suspect by positive and deceptive conduct of the grossest kind”. Stagg left the chaotic courtroom vowing to sue everyone involved, the police were the butt of press ridicule, and David Canter observed with typical English understatement that pulling in some “media recognized expert” can undermine “more effective, longer term development of a professional discipline” [8]. It is not just the newcomers who can make mistakes. The 1996 Summer Olympics began in the wake of the first case of suspected air terrorism on American soil, and as the investigation of the TWA flight 800 crash off New York moved ahead with commendable precision, a bomb blast rocked the Olympic festivities in Atlanta. Unwilling to stand by in the face of two national assaults, an inexperienced FBI
agent allowed the press to get word that a psychological profile had identified the private security guard who first spotted the bomb as the likely perpetrator. In moments, Richard Jewell went from hero to the object of media scrutiny and scorn. After a week of publicized investigation, in which the entire world got to see Jewell live on CNN sitting forlorn on his own front steps as the FBI picked through his apartment, the investigation yielded nothing more than a few pathetic souvenirs of a man’s only moment of glory. Pressed for an explanation, an FBI spokesperson on the scene curtly informed the press that “We don’t make apologies”. FBI director Louis Freeh, called before a congressional investigating committee, tried to put a better face on the public relations disaster but confided privately that “We wish we never heard of Richard Jewell”. [9, 10]. This is not to say that mention of a profile, or court testimony that overlaps in any way with a profile, is necessarily prohibited. Testimony can mention a profile in the context of background as to how and why a defendant was stopped and searched, if such testimony is confined to the preliminary stop and not the actual investigation, and the fact that the individual satisfied the profile is not used to impugn the defendant [11]. Moreover, the expertise reflected in profiles can be the subject of expert testimony to refute assertions by the defendant [12], to supply factual information helpful to the trier of fact in placing the case in context [13], or to establish motive, intent, absence of mistake or accident, or identity of a common scheme or plan [14].
Profiles as Evidence at Trial By their tentative and proximal nature, profiles pose serious issues of both scientific and probabilistic validity [15]. Their use, and the term itself, are therefore most appropriately restricted to investigative tools. As evidence, profiles easily become little more than a means to either link a defendant to undesirable traits or stereotypes; or for the defense to attribute by association positive or sympathetic attributes to a defendant. Behavioral science is relevant to justice because it can assist the trier of fact to understand a party in litigation as an individual (see Risk Assessment),
Profiles: Psychological and Behavioral while profiles are a tactic to attribute the qualities of a grouping to an individual. There are circumstances in which this tactic can be attractive to either side of a case, and the law has established guidelines to restrict potential abuse. Entrapment, the affirmative defense that alleged crimes were in reality induced by government persuasion or trickery, is a good example. An entrapment defense, as with defenses to most serious criminal charges, turns on the defendant’s mental state: was the defendant an active participant or simply a passive bystander to conduct actually carried out by a government operative? Although early cases tended to hold that a defendant asserting the affirmative defense of entrapment could not establish their state of mind through expert testimony, the courts now generally consider such testimony an appropriate aid to the triers of fact [16, 17]. Most other attempts to enlist expert testimony regarding a defendant’s personality profile to help disprove a criminal charge have been less successful. Introduction of psychiatric testimony regarding the “dependent personality disorder” of a defendant was excluded, for example, as support of her assertion that she was unaware that computer equipment that she sold was, in fact, stolen. Here, the court felt that imprimatur of such an official-sounding label was neither necessary nor helpful to the jury in making its assessment of the defendant’s mental state [18]. Similarly, the psychological profile of a murder and robbery defendant was excluded as possible support that his crime could not have been deliberate and premeditated, holding that the profile appeared to be simply a narration of the defendant’s social history with little or no rational bearing on issues of premeditation and intent [19]. Such personality testimony has also been excluded as a defense to armed robbery and assault [20], and manslaughter [21], where the defendants sought to establish that they were simply not the “type” to use a weapon. In many instances, the testimony is simply a way in which to introduce character evidence. Testimony in support of good character is generally permissible [22], but the courts are leery of according it scientific stature [23]. Nevertheless, in two controversial decisions, lay character witness testimony has been upheld in a child molestation case [24], and a psychologist’s opinion was upheld as appropriate testimony concerning a defendant charged with lewd
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and lascivious acts upon a child, noting that the testimony was based, at least in part, upon standardized testing [25]. Most frequently, however, courts have excluded expert testimony aimed simply at ruling out a defendant as the guilty party. This has been the case in proposed testimony as to “peaceableness” [26], psychiatrist testimony as to lack of characteristics “likely to result in abuse of infant victim” [27], psychiatrist testimony that defendant had made previous false confessions and may therefore be mentally ill and his confession untrustworthy [28], expert testimony as to defendant’s remorse or lack of remorse [29], and that the defendant had undergone a religious conversion and therefore could be rehabilitated [30]. Expert testimony is also typically not allowed as to mitigation of an offense [31]. Often, such expert testimony is proffered in place of the defendant taking the stand on his or her own behalf, thus becoming subject to cross-examination. The jury system quite correctly assumes that a defendant is his own most revealing character witness, and that if character is to be made an issue it is best presented by the defendant himself [32]. Expert behavioral testimony on behalf of a defendant can also end up working against that defendant. For example, in State v. Hunt [33], the defendant claimed that a borderline personality prevented him from being able to form the necessary intent to be guilty of a shooting charge. The court ruled that this assertion opened the door for broad inquiry into his mental condition, and allowed the prosecution to counter the claim with expert testimony that the defendant was actually suffering from nothing more than “antisocial personality disorder”. To explain how this conclusion was reached, the expert was further permitted to recount for the jury defendant’s difficulties in interpersonal relationships, including his prior “bad acts”. If profile evidence has had little impact upon the ability of the accused to fashion a defense, it has provided a potentially devastating weapon in the hands of the prosecution. The case of Sgt. Russell Banks illustrates just how powerful and insidious prosecution profile testimony can become, even when the “expert” does not testify as to a personal conclusion about the guilt or innocence of the defendant. In this instance, a pinpoint profile that could only describe the defendant – a stepfather living with his wife
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and her young daughter – combined with the known limitations of a child witness, and an aggressive child “therapist” able to lead that witness and allowed to testify as to her own conclusions, created a direct path to the defendant, which a jury would be hard pressed to ignore. In its Banks holding [34], the Court of Military Appeals noted that its reversal of Sgt. Banks conviction for child rape and sodomy was consistent with the case law in both federal and state courts that has severely criticized attempts to introduce “profile” evidence to establish either guilt or innocence. As the Supreme Court of Kansas noted in the 1989 case of State v. Clements, “Evidence which only describes the characteristics of a typical offender has no relevance in determining whether the defendant committed a crime in question, and the only inference which can be drawn from such evidence, namely that the defendant who matches the profile must be guilty, is an impermissible one” [35]. This conclusion has been reached in cases as diverse as child molestation [36], child abuse [37], murder [38], rape [39], and shoplifting [40]. This is not to say that expert profile testimony may never be used by the prosecution. If the defendant places his own personality and character at issue, the prosecution can call experts to help rebut defense assertions [41]. In a Washington state case, a defendant who stuttered pointed to the fact that the person he allegedly assaulted was unable to identify his assailant as a stutterer. The prosecution was permitted to introduce to the jury expert scientific testimony as to the statistical percentage of probability that a stutterer would not exhibit that particular speech anomaly in certain situations [42]. Expert profile testimony as to a lack of profile can also be admissible when a defendant deviates significantly from the expectation that a lay jury may hold about people who commit particular types of crimes [24]. Finally, background testimony that does not specifically address guilt or innocence of a defendant but instead enables the jury to understand evidence that does go to guilt or innocence has been held to be permissible profile evidence.
suspects and establish reasonable suspicion necessary to justify an action in the field. Reasonable suspicion is reviewed on a case-by-case basis to assure protection of suspect rights. As evidence at trial, profiles easily become little more than a means to either link a defendant to undesirable traits or stereotypes; or for the defense to attribute by association positive or sympathetic attributes to a defendant. Although behavioral science evidence may be proffered for use at trial, including statistical compilations, such evidence should have relevance to the applicable party as an individual, and the term profile avoided when possible. Expert testimony concerning a trait of an accused may only be used as evidence that the accused possesses such a trait. It must be left to the jury to determine whether and how such a trait may influence the facts of the case [43]. While the term profile may appear to give behavioral evidence an aura of scientific respectability, such labels themselves do nothing to enhance the stature of the substantive underlying observations. In fact, if anything, good science and credible observation are more readily accepted without them [44].
References [1]
[2] [3] [4] [5]
[6]
[7]
Conclusions
[8]
The often misused term profile is best restricted to investigative tools used to narrow down likely
[9]
For a critique of FBI profiles and a plea that behavioral evidence is admissible by the defense, see George, J.A. (2008). Offender profiling and expert testimony: scientifically valid or glorified results? Vanderbilt Law Review 61, 221–260. Becton, C.L. (1987). The drug courier profile, North Carolina Law Review 65, 417–480. United States v. Sokolow, 490 U.S. 1 (1989). Terry v. Ohio, 392 U.S. 1 (1968). An interesting look at the kind of reasoning used by the appellate courts in overturning a Sokolow search is provided in People v. Pullman, (Not Reported in Cal.Rptr.2d, 2002) WL 31230831 Cal.App. 1 Dist., (2002). People v. Hubbard, 530 N.W.2d 130 (Mich. Ct. App. 1995); United States v. Williams, 957 F.2d 1238 (5th Cir., 1992); United States v. Wilson, 930 F.2d 616 (Minn. 1991); United States v. Beltran-Rios, 878 F.2d 1208 (Cal. 1989); United States v. Hernandez-Cuartas, 717 F.2d 552 (Fla. 1983). Crace, J. (Feb 17, 1995) Inside the criminal mind, New Statesman & Society, 29; (1995 WL 14340484). Guardian (London) (1995). Sept 15 (1995 WL 9944184, 9944234, 9944240, 9944195 and 9944268). Yoder Jr., E.M. (Aug 2, 1996) Olympic park bombing, San Diego Union Tribune, B8.
Psychological Autopsy [10]
[11] [12]
[13] [14] [15]
[16] [17]
[18] [19] [20] [21] [22] [23]
[24] [25] [26] [27] [28] [29] [30] [31] [32]
[33] [34] [35] [36] [37] [38] [39] [40] [41] [42]
Sack, K. (Oct 29, 1996) Jewell lambastes FBI, media for 88-day ordeal as suspect, Austin American-Statesman A1. United States v. Hernandez-Cuartas, 717 F.2d 552 (Fla. 1983). People v. Lopez, 26 Cal. Rptr. 2d 741 (Ct. App. 1994); United States v. Robinson, 978 F.2d 1554 (N.M. 1992); United States v. Wilson, 930 F.2d 616 (Minn. 1991); United States v. Beltran-Rios, 878 F.2d 1206 (Cal. 1989). United States v. Khan, 787 F.2d 28 (N.Y. 1986). Wilson v. State, 871 P.2d 46 (Okl. 1994). An analysis of issues of probability as they relate to criminal profiles appears in Risinger, M. (2002). Three card monte, Monty hall, modus operandi and ‘offender profiling’: some lessons of modern cognitive science for the laws of evidence, Cardozo Law Review 238, 193–284. State v. Woods, 484 N.E.2d 773 (Ohio Com. Pl. 1984);United States v. Hill, 655 F.2d 512 (Pa. 1981). Moore, C.D. (1995). The elusive foundation of the entrapment defense, Northwestern University Law Review 89, 1151–1188. United States v. DiDomenico, 985 F.2d 1159 (Conn. 1993). Hartless v. State, 611 A.2d 581 (Md. 1992). People v. Watkins, 440 N.W.2d 36 (Mich. App. 1989). State v. Hensley, 655 S.W.2d 810 (Mo. App. 1983). Green, E.D. & Nesson, C.R. (eds) (1966). Federal Rules of Evidence, Little, Brown, Boston, pp. 51–58. Mendez, M.A. (1996). The law of evidence and the search for a stable personality, Emory Law Journal 45, 221–238. People v. McAlpin, 812 P.2d 563 (Cal. 1991). People v. Stoll, 783 P.2d 698 (Cal. 1989). State v. Arnold, 421 A.2d 932 (Me. 1980). State v. Screpesi, 611 A.2d 34 (Del. Super 1991). Stano v. Dugger, 883 F.2d 900 (Fla. 1989). Clenney v. State, 344 S.E.2d 216 (Ga. 1986). People v. Moya, 350 P.2d 112 (Cal. 1960). People v. Masor, 578 N.E.2d 1176 (Ill. Ct. App. 1991). Mueller, C.B. & Kirkpatrick, L.C. (1996). Evidence Under the Rules, 3rd Edition, Little, Brown, Boston, pp. 677–679. State v. Hunt, 555 A.2d 369 (Vt. 1988). United States v. Banks, 36 M.J. 150 (CMA, 1992). State v. Clements, 770 P.2d 447, 448 (Kan. 1989). United States v. Gillespie, 852 F.2d 475 (Cal. 1988). Sloan v. State, 522 A.2d 1364 (Md. Ct. App. 1987). Sanders v. State, 303 S.E.2d 13 (Ga. 1983). State v. Percy, 507 A.2d 955 (Vt. 1986). State v. McCoy, 294 N.E.2d 242 (Ohio Ct. App. 1973). United States v. Gillespie, 852 F.2d 475 (Cal. 1988); State v. Hunt, 555 A.2d 369 (Vt. 1988). State v. Briggs, 776 P.2d 1347 (Wash. Ct. App. 1989).
[43] [44]
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State v. Hicks, 649 P.2d 267 (Ariz. 1982). Hadden v. State, 670 So.2d 77 (Fla. Ct. App. 1996).
CARL N. EDWARDS
Profiling: Drugs see Drug Profiling
Profiling: Mitochondrial DNA see Mitochondrial DNA: Profiling
Property Crime see Firesetting
Pseudoseizures see Seizures: Behavioral
Psychodynamic Diagnostic Manual (PDM) see Psychopathology: Terms and Trends
Psychological Autopsy Origins The psychological autopsy originated in approximately 1958 as a result of the Los Angeles County Medical Examiner’s Office consulting the Los Angeles Suicide Prevention Center for assistance in distinguishing drug-related accidental overdoses from suicides [1]. This collaboration laid down the basic principles of the psychological autopsy procedure. Edwin Schneidman, a director of the LA Suicide
2162 Table 1 • • • • • •
Psychological Autopsy Commonalities of suicide
Purpose: seek a solution Stimulus: unbearable psychological pain Stressor: frustrated needs Emotion: hopelessness, helplessness Cognition: ambivalence Perception: constriction
Adapted from Schneidman, 1996
Prevention Center, is credited with coining the term psychological autopsy. Schneidman’s initial definition of the psychological autopsy was “a thorough retrospective investigation of the intention of the decedent” [2]. The process was partially based on his observations that many suicides shared certain common characteristics that could help identify a suicidal individual. Table 1 lists some of Schneidman’s “commonalities of suicide”. Over the past 50 years, the procedure has become familiar to most suicidologists, suicide researchers and major city homicide investigators. However, a single standard definition has yet to be formally agreed upon. This article uses the following definition for the psychological autopsy: “A postmortem investigative procedure requiring the identification and assessment of suicide risk factors present at the time of death, with the goal of enabling a determination of the manner of death to as high a degree of certainty as possible”. Thus, the psychological autopsy can be conceptualized as synonymous with a postmortem suicide risk assessment. The strength of framing the psychological autopsy in this manner lies in the fact that performing formal suicide risk assessments on patients who are at risk for suicide is endorsed by overwhelming clinical consensus [3], and will be further clarified below in the section on current controversies. Regardless of the definition or method used, the quality of the assessment will depend heavily on the training, knowledge, experience and clinical judgment of the investigator. In the push toward standardization, the psychiatric autopsy has evolved through a number of iterations. Initially, Schneidman developed a list of 14 areas of inquiry to guide the investigator when conducting a psychological autopsy [2]. In the late 1980s, the Centers for Disease Control established a list of 22 criteria to assist forensic investigators, called the Operational Criteria for the Determination of Suicide
(OCDS) [4]. Shortly afterwards, suicide researchers developed the Empirical Criteria for the Determination of Suicide (ECDS). This instrument subsumed the OCDS, as well as other important criteria from the research literature [5]. While the Department of Defense had long employed the psychological autopsy method, in 2002 it published a sample model curriculum for conducting them, along with recommendations for training and peer review [6]. Finally, in 2006, leading suicidology experts and researchers proposed an initial standard protocol for lines of inquiry to improve reliability and validity [7]. This protocol, which has been further amended with the assistance of an expert from this research group (Berman, A. Personal communication, 2007), is presented toward the end of this article. Despite progress in psychological autopsy research, some deaths (i.e., drug-related fatalities [8, 9]) continue to frustrate medical examiners (MEs). Thus, the psychological autopsy methods and protocol must continue to be vigorously pursued and tested.
Purpose Psychological autopsies are an invaluable tool for assessing equivocal deaths. An “equivocal death” may be one in which the manner of death is questionable, or the circumstances surrounding the death are otherwise unclear [7]. Typical equivocal death scenarios are listed in Table 2. When MEs perform autopsies, they attempt to classify the death into one of four categories or “modes”: natural, accidental, suicide, or homicide (NASH) [10]. When a death cannot be immediately classified, it is often officially referred to as undetermined. Table 3 lists the basic elements of death classification. Table 2 • • • • • • • •
Typical equivocal death scenarios
Drug-related deaths Autoerotic asphyxia Self-induced asphyxia (e.g., the “choking game”) Drownings Vehicular deaths “Russian Roulette” “Suicide by cop” Staged death scenes
Psychological Autopsy Table 3
Death classification
1. Cause: gunshot, poisoning, etc. 2. Mode: circumstances leading to cause a) Natural b) Accidental c) Suicide d) Homicide 3. Motive: reasons for the action 4. Lethality: probability of death as a result of method and circumstances chosen (low, medium, and high) 5. Intent: what the decedent wanted to happen at the time
The goals of the psychological autopsy include obtaining an in-depth understanding of the decedent’s personality, behavior patterns, and possible motives for suicide. The investigator strives to obtain an objective analysis of the decedent’s suicide risk enhancing and protective factors. In certain cases, an experienced investigator can use the method to help sort out the degree of risk, intent and causal factors at the time of death [3]. Ultimately, this should allow for a well informed assessment of whether or not the deceased was a likely candidate for suicide. Table 4 lists some of the more important goals of the psychological autopsy. The psychological autopsy has utility in a variety of settings. Table 5 gives a list of some of its more common uses. As noted, it can be an extremely helpful tool for assisting MEs and homicide investigators. It has been shown to have a significant impact on MEs determination in equivocal cases [11]. It has been used for several decades to collect valuable research data about suicide that ultimately informs prevention efforts [12–14]. The vast majority of these studies suggest that mental disorder is present in a preponderance of suicides. The first generation of Table 4 • • • • • • • •
Psychological autopsy goals
Identify behavior patterns – stress reactions, adaptability, habit, or routine changes Establish presence or absence of mental illness Identify possible precipitants Determine presence or absence of motives Determine presence or absence of suicidal intent Determine suicide risk factors – both mitigating and aggravating Perform a postmortem suicide risk assessment Establish whether or not the deceased was a likely candidate for suicide
Table 5 • • • • • • • • •
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Psychological autopsy uses
Assist medical examiners with “equivocal” deaths Research on suicide Insurance claims Criminal cases Estate issues, contested wills Malpractice claims Worker’s compensation cases Product liability cases Organizational suicide prevention efforts
research driven by psychological autopsies found that more than 90% of completed suicides suffered from mental disorders, mostly mood disorders and substance use disorders [3, 15]. The second generation of psychological autopsy research has employed casecontrol designs, resulting in better estimations of the role of various risk factors for suicide [16]. The psychological autopsy method has also been used in a forensic context in both criminal and civil courts. While courts have admitted testimony based on psychological autopsies in many civil cases, criminal courts have been more hesitant [17]. The issue of the psychological autopsy’s legal admissibility will be further discussed below. In criminal cases, the psychological autopsy may be used to establish whether a decedent was likely to have committed suicide, or whether the matter should be viewed as a homicide. In some criminal cases, most notably Jackson v. State (Fla. 4th DCA 1989), the psychological autopsy has been used to help analyze whether an abusive relationship played a role in a suicide [18]. In the criminal case U.S. v. St. Jean (US Ct. of Appeals for Armed Forces, 1996), the psychological autopsy was used by the prosecution to assist in determining whether or not a suspected homicide victim had been a likely candidate for suicide. In civil cases, the psychological autopsy has been used to help determine whether benefits are owed to the decedent’s beneficiaries [10]. This often involves life insurance payments, where many policies hold that a suicide precludes benefits. However, some policies permit payment if it can be proven that the decedent’s death was an “insane suicide”. “Insane suicide” is a legal term that was defined by the US Supreme Court in the case of Mutual Life Insurance Company v. Terry (US 1872; 82: 580). The Court held that a suicide was “sane” when the “assured, being in the possession of his ordinary reasoning faculties,
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from anger, pride, jealousy, or a desire to escape from the ills of life, intentionally takes his own life.” In contrast, an “insane” suicide was defined as “when his reasoning faculties are so far impaired that he is not able to understand the moral character, the general nature, consequences, and effect of the act he is about to commit, or when he is impelled thereto by an insane impulse, which he has not the power to resist . . .” Thus, a sane suicide implies the decedent had a rational understanding that his acts would result in his death, whereas an insane suicide implies the decedent was so emotionally disturbed that he did not have a rational appreciation of his actions [10]. Worker’s compensation cases generally involve allegations that the decedent’s employer was somehow legally responsible for his suicide. Similarly, product liability cases allege that the decedent’s use of a particular product (e.g., medication) caused him to commit suicide. In psychiatric malpractice cases involving suicide, the plaintiff must prove that the doctor’s negligence was a proximate cause of the decedent’s suicide [19]. In addition to determinations regarding the standard of care, a postmortem suicide risk assessment must be conducted to determine the decedent’s overall suicide risk and the foreseeability of the suicide. Another potential use for the psychological autopsy may be its clinical utility in helping surviving family members better understand the tragedy and begin the grieving process [20]. The psychological autopsy may be used for other clinical purposes, such as informing an institution’s morbidity and mortality conference after a client’s suicide. For historical purposes and interest, psychological autopsies have been conducted on numerous public figures such as Ernest Hemingway [21], Vince Foster, (Berman, A. Personal communication, 2007), Howard Hughes and Marilyn Monroe.
Methods The psychological autopsy method involves collecting and analyzing all relevant information on the deceased. This means that all applicable records are reviewed, including medical records, psychiatric records, police records, and autopsy findings. A visual inspection of the death scene via photographs is necessary, and occasionally a visit to the scene will be required. A thorough review of the decedent’s
writings in the form of diaries, journals, e-mails and internet correspondence is vital. The suggested protocol at the end of this article provides a list of other important sources of data. In addition to reviewing records, structured interviews of family members, relatives or friends are necessary. Thus, a psychological autopsy synthesizes data from multiple informants and records. When performed in a comprehensive manner, the method may take anywhere from 20 to 50 or more hours to complete. The overriding principle is that the greater the amount of relevant data analyzed, the more accurate the investigator’s conclusions are likely to be. Suicide risk factors vary among different populations [22]. The investigator should consider any special nuances of the deceased, such as age group [23], mental health diagnosis, gender [24] and other factors that may allow for a more precise consideration of risk factors associated with that group. This requires keeping up to date with the evolving psychiatric and suicidology literature, which is steadily becoming more detailed about risk factors in distinct diagnostic categories such as depression [25], bipolar disorder [26], and persons who are outside the care of mental health services [27]. Some individuals may display unique, individualized behaviors suggestive of increased or decreased suicide risk that will be known only by close social contacts or treating mental health professionals [22]. Thus, an understanding of the decedent’s individualized risk factors and past stress reaction patterns becomes important.
Suicide Notes There is a considerable literature on suicide notes. Research suggests that suicide notes are left only by a minority, approximately 10–33% of all suicides [15]. Regarding persons who do leave notes, available research has not found any significant differences when compared to suicides who do not leave notes. A few studies have suggested that whites and women are slightly more likely to leave suicide notes. At least one study has suggested there are no significant differences in the themes of notes between male and female suicides [28]. Themes of love and relationships were found to be more common than achievement themes in both men and women [29]. Another study found that suicide notes written by young people were longer and rich in emotions, whereas notes
Psychological Autopsy written by the elderly were shorter, contained specific instructions, and were less emotional [30]. In a study of 42 suicide notes, the most common themes were: “apology/shame” (74%), “love for those left behind” (60%), “life too much to bear” (48%), “instructions regarding practical affairs postmortem” (36%), “hopelessness/nothing to live for” (21%), and “advice for those left behind” (21%) [31]. The common usage of computers, the Internet [32] and various electronic types of messaging have introduced another important source of data for the psychological autopsy. The investigator should not fail to inquire about these potential sources of information, as they may provide critical insight into the decedent’s state of mind and intentions. One important caveat regarding suicide notes is the possibility that they have been fraudulently prepared and left by another person attempting to disguise a homicide. While there has been some attempt to develop a method for distinguishing genuine from simulated suicide notes [33], more research in this area is required. In such cases, collaboration with a forensic handwriting analysis expert might be considered. Another important consideration for the investigator is the possibility that family members or others who find a suicide note may destroy it or remove it from the death scene for various motives.
Collateral Interviews The importance of collateral interviews as part of the psychological autopsy method cannot be overstated. Careful interviews of the decedent’s family members and other relevant social contacts distinguish a proper psychological autopsy from a mere analysis of demographic data and police reports. Most experts recommend a structured or semistructured approach to collateral interviews. At least one study has developed a semistructured interview for the psychological autopsy which has demonstrated inter-rater reliability [34]. For research purposes, there has been a trend toward using modified instruments such as the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, 4th ed.-Text Revision Disorders (SCID), as well as a life events calendar method, which helps identify and quantify the burden of events that may be associated with suicide [35]. Regardless of method used, collateral interviews often reveal critical information about the decedent
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that cannot be obtained elsewhere. Recent theories about suicide have stressed that psychiatric illness alone is not enough to fully explain an individual suicide. Rather, a stress-diathesis model has been proposed, in which the risk for suicidal acts is determined by the interplay of biopsychosocial factors and situational variables [36]. According to this model, a diathesis may be reflected in an individual’s tendency to have maladaptive responses to stressors, such as acting impulsively. Such information is most likely to be obtained via collateral interviews. Ethics and Sensitivity. An important ethical and practical consideration related to gathering collateral data is the manner in which collateral sources should be contacted and interviewed. Interviewing surviving family and friends is a very sensitive matter that must consider the survivor’s reactions. Ideally, the investigator should have adequate clinical experience in order to handle survivors’ reactions with appropriate sensitivity [37]. For “research purposes”, it has been recommended that a two to six-month time interval between the suicide and interview be used [37]. There does not appear to be a significant relationship between the timing of the interview and the quality of information obtained when this time frame is used [38]. While a concern about untoward emotional reactions to the interview is an obvious concern, some have noted that survivors appeared to have benefited from the interview experience in terms of being able to express their feelings and receive a mental health referral if needed [37]. Presently, there is no clearly agreed upon method for initiating contact with survivors. Investigators performing a psychological autopsy for forensic legal purposes will likely be supplied with relevant phone numbers and/or addresses of potential interviewees. Often, attorneys will have previously informed the interviewees that an investigator will be contacting them. Investigators seeking interviews for research purposes may consider a letter followed by a phone call, or vice versa [10].
Postmortem Suicide Risk Assessment A comprehensive postmortem suicide risk assessment is necessary because of the fact that there is no single pathognomonic risk factor for suicide [22]. Single risk factors do not have adequate statistical power on which to base conclusions. Particularly in the context
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of forensic expert testimony, the postmortem suicide risk assessment approach is recommended [3]. This involves a careful identification and assessment of suicide risk factors present at the time of death. Risk enhancing factors (both proximal and distal) should be carefully weighed along with risk reducing factors. When thoughtfully analyzed in the context of the totality of the decedent’s circumstances, the investigator should be able to arrive at conclusion about the decedent’s overall risk of suicide near the time of death. This ultimately informs the investigator’s opinion about whether or not the decedent was a likely candidate to commit suicide at the time in question. Testimony that focuses on whether the psychological autopsy yielded results consistent with an individual who committed suicide is more likely to be found admissible in court. In contrast, overreaching opinions that conclude the decedent did or did not commit suicide are more likely to be found inadmissible. For example, in the case of State v. Guthrie (2001 SD 61, 627 N.W. 2d 401), the court found that the expert’s testimony became inadmissible when it “shifted from discussing typical suicide characteristics”, to a “bold declaration” that the decedent did not die by suicide [39].
Limitations and Controversies In both research and forensic legal settings, mental health professionals are legally and ethically obligated to note the limitations of their methods. In the case of the psychological autopsy, controversy over its limitations has existed for as long they have been performed [40]. Commonly cited controversies involving the psychological autopsy are listed in Table 6. The limitations largely involve the fact that there is no unanimously accepted standardized protocol for conducting a psychological autopsy. However, dedicated efforts are currently underway to resolve this issue [7]. Progress in this area may Table 6 • • • • • •
Current controversies [42]
Lack of standardized protocol Lack of standardized suicidology nomenclature Methodological problems Reliability of assessment instruments Lack of homogeneity among studies Bias among collateral informants
be somewhat dependent on the field of suicidology developing a standard, comprehensive nomenclature. For example, even the basic term suicide attempt may have different meanings to different investigators [41]. Controversy surrounding admissibility and meeting Daubert standards may be best resolved by adopting the postmortem suicide risk assessment approach. The reasoning for this is as follows: (i) in clinical practice, the standard of care requires the clinician to gather relevant information and assess the patient’s level of suicide risk; (ii) performing such suicide risk assessments on patients considered to be at risk for suicide is endorsed by overwhelming clinical consensus (i.e., it is “generally accepted”); and (iii) the psychological autopsy is similar in that it is the assessment of suicide risk factors present in the decedent near the time of death [3]. This approach to the psychological autopsy should meet the process-driven Daubert criteria, particularly where Kumho Tire Co. v. Carmichael (1999 536 U.S. 137, 141) has held that Daubert standards are not limited only to scientific evidence, but may include “technical, or other specialized knowledge” [43]. In the event that a court found that the postmortem suicide risk assessment did not meet Daubert criteria, it should at least meet the Frye v. U.S. (DC COA, 1923) criteria of “general acceptance” among mental health professionals. This line of reasoning was adopted by a Louisiana appeals court when it found the psychological autopsy admissible under Daubert. The case, In re Succession of Pardue (La Ct. App. 2005 915 So. 2d 415), involved estate issues and testamentary capacity. The court held that the methodology used in the psychological autopsy was sufficiently reliable and generally accepted in psychiatry. In federal court where expert testimony is governed by the Federal Rules, opinions on the basis of the postmortem suicide risk assessment method would appear to comply with Federal Rules 703 and 702, which allows expert opinions if they are “of a type reasonably relied upon by experts in the particular field”, and if the testimony is “the product of reliable principles and methods” [44]. An obvious criticism of the psychological autopsy is the problem of not being able to interview the decedent so as to more accurately determine intent. One response to this issue is that the comprehensive nature of the psychological autopsy, with its
Psychological Autopsy wide net of collateral data, may ultimately allow a reasonable approximation or inference of intent. Additionally, it has been argued that having no prior contact with the decedent removes the vagueness and subjectivity inherent in an interpersonal relationship with the decedent [18]. Therefore, one might argue that psychological autopsies may be more objective and less controversial than the analysis of living patients. To date, only a restricted number of research studies have relied on standardized instruments, making the comparison of findings problematic [42]. Current studies are increasingly using the SCID, but this approach has yet to be conclusively validated for administration to proxies. However, at least two studies (of psychiatric inpatients admitted following a suicide attempt) have suggested that proxies are good judges of past history of suicide attempts, level of suicidal intent and data leading to a psychiatric diagnosis [45, 46]. The issue of bias in collateral informants requires a cautious approach by investigators. Informants’ reports may be biased by many factors such as their own personal attitudes toward suicide and their emotional state at the time of the interview. Further, their recollection of circumstances may be impacted by the emotional trauma of the death of their loved one [42]. The demeanor and interpersonal style of the investigator may also become a factor. It is possible that informants may react to the investigator’s personal characteristics, which may then influence the amount and type of information they are willing to divulge. In summary, there is a considerable need for further research efforts aimed at improving the validity and reliability of the psychological autopsy [17]. There is concern that testimony based on a faulty or inadequate psychological autopsy may result in a “miscarriage of justice” [47]. Forensic experts who give testimony in court on the basis of psychological autopsy findings must be prepared to concede any relevant limitations.
Toward a Standard Protocol In the interest of improving validity and reliability, forensic suicidology must continue to work toward an accepted, standardized protocol for the psychological autopsy [7]. Below is a recommended template that
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was developed by expert consensus [7], (Berman, A. Personal communication, 2007) and further enhanced according to relevant research and clinical findings [5–7, 10, 20, 48–50]. The protocol may be used to guide areas of investigation and lines of inquiry for collateral interviews. Use of a standardized protocol can serve as a framework for conducting a psychological autopsy. Ultimately, a standard protocol will enhance admissibility, and aid in the testability of the method [7]. The psychological autopsy method allows for a “polyperspective” that can help illuminate key aspects of an equivocal death [51]. However, the light that it shines may also be distorted by the perspective of the investigator. Therefore, it is critical that the individual performing the psychological autopsy possess adequate training. This includes having sufficient knowledge in the fields of suicidology, related mental health concepts, and basic death scene investigation. Data obtained from the death scene and physical autopsy are often highly determinative, and meticulous inspection of the death scene and related items may be necessary in certain forensic legal cases. For example, in cases of suspected “simulated suicidal hanging”, there may be important evidence suggesting a homicide that was staged to appear as though it was a suicide [52]. Detailed investigation of body position, ligature placement and knot formation may be required to distinguish a suicide from a homicidal hanging [53]. Further, in cases of suspected autoerotic asphyxiation, researchers have noted characteristic death scene findings (see Appendix 1) [54]. Finally, the problems inherent in assessments of suicidal intention require that the investigator be cognizant of the limits of the data and corresponding conclusions. This is primarily because of clinical observations that suicidal individuals are often ambivalent, and may even have multiple intentions at the same time [55]. In certain cases, the presence and degree of suicidal intent may be difficult to determine because of ambivalence, denial, minimization or confusion. In contrast, the nuances of other cases may present a rather straightforward inference that the decedent’s intent was to die. In difficult cases, the investigator may choose to simply report on the results of the postmortem suicide risk assessment, or provide reliable evidence that “Natural”, “Accidental” and “Homicidal” causes of death can be excluded [56].
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Psychological Autopsy Protocol Records and documents • Medical records • Mental health records • Police records and related witness statements • Legal records • Criminal records • School records • Financial records • Military records • Suicide note(s), communication or video • Decedent’s journals, diary • Electronic data: E-mails, text messages, instant messages, and websites • Forensic computer analysis report if available • Autopsy report • Toxicology report Death scene • Photos of death scene and site visit if necessary • Presence of atypical wounds (see Appendix 1) • Decedent’s relationship to site • Evidence of rescuability versus precautions taken against • Evidence of planning and/or rehearsal • Evidence of staged manner of death (see Appendix 1) Demographics • Socioeconomic status • Employment status • Financial status • Age/gender/race/height/weight • Marital status • Educational status • Religion and religiosity • Adopted vs. biological family status • Immigrant status – acculturation issues • Residence relative to recent mobility Recent symptoms and behaviors • Appeared depressed, sad, tearful, or moody • High risk depressive symptoms [25] – Insomnia – Appetite loss – Weight loss
• • • • • • • • • • • •
Feelings of worthlessness and/or inappropriate guilt – Physical agitation – Depression comorbid with anxiety Expressed suicidal ideation or preoccupation with death Appeared to have made a change for the better Appeared anxious, or complained recently of anxiety or panic attacks Appeared agitated Behaved in an impulsive manner Displayed uncontrolled rage or aggressive behavior Demonstrated constricted thinking or “tunnel vision” Disclosed feelings of guilt or shame Appeared confused, disoriented or psychotic Expressed feelings of hopelessness, helplessness or worthlessness Engaged in excessive risk-taking behaviors Mental Status evidence of: – Impaired memory – Poor comprehension – Poor judgment – Hallucinations or delusions – Inflated sense of self or signs of magical thinking
Precipitants • Significant losses (relationships, job, finances, prestige, self-concept, family member, moving, or anything of importance) • Significant (or perceived) disruption of a primary relationship • Legal troubles or difficulties with police • Traumatic events • Significant life changes (negative or positive, birth of child, promotion, etc.) • Completed or attempted suicide by a family member or loved one • Anniversary of important death, loss, etc. • Exposure to suicide of another via media or personal acquaintance • Preparations for death (e.g., gave away prized items, settled personal accounts, updated will, and said “goodbye” to loved ones) • Expression of wish to reunite with a deceased loved one, or to be “reborn” Psychiatric history • Prior suicidal behaviors
Psychological Autopsy – – – – –
• • • • • • • •
Total number of past attempts Dates Precipitants Method, lethality What stopped event, if anything? How found – Attitude and behavior after found Prescribed psychotropic medications Observed adverse reactions to psychotropic medications Lack of compliance with psychotropic medications Efficacy of treatment (e.g., subtherapeutic doses, poor or incorrect agent choice, inadequate blood level, etc.) Psychiatric hospitalization (reasons, dates, diagnoses, and treatment) Outpatient treatment (psychiatrist, psychologist, therapist, and Primary Care Physician PCP) Psychotherapy at time of death (duration, quality of alliance, compliance, and diagnosis) Expressing concerns about “going crazy” or losing cognitive function
Physical health • Recent visit to physician (reasons) • Chronic pain • Chronic, fatal or debilitating disease • Recent reduction in physical/functional capabilities • Current medications (compliance or recent changes) Substance abuse • History and pattern of alcohol, drug abuse • Recent attempts to discontinue use • Recent increase in pattern of use • Degree of use at time of death (binge drinking, etc.) • History of “accidental overdose” (when and type of drug) Family history • Suicide or attempted suicide • Nonnatural deaths • Level of support or observed closeness in nuclear and extended families • Physical, sexual, or emotional abuse • Substance abuse • Violent behavior • Affective or other psychiatric disorders
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Firearm history (if relevant) • Ownership • Recent purchasing or obtaining (stated purpose?) • Recent movement of gun (from where to where?) • Pattern of weapon care and cleaning • Pattern of storage and use • Accidental discharges Social Supports and Attachments • Ability to create and maintain close personal relationships • Ability to express feelings as needed in relationships • Recent talk about feeling unsupported, uncared for, unimportant • Relative success in personal relationships • Relative success in work • Attachment to hobbies, interests, religion, etc. • Recent change in any of the above attachments/supports Emotional reactivity • History of violence toward others • Impulsive behaviors • Excessive rage or aggression Lifestyle/character • Typical coping patterns, pattern of reaction to stress • Perfectionism • Self-destructive behaviors (self-mutilation, deliberate self-harm, driving while intoxicated, etc.) • Frequent crises • Victimization behaviors (bullied or abused) • Tendency to dissembling (hiding emotions or stoicism) Access to care • History of help-seeking behaviors • Barriers to healthcare (no insurance or no accessible caregiver) Other • • • • •
areas of inquiry Occupational history Personal interests, hobbies Gambling history Degree and type of religiosity Description of activities/behaviors in last days before death
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Factors associated with suicide risk reduction • Evidence of future-oriented thinking or behaviors (doctor’s appointments, job interviews, etc.) • Responsibility for a child under 18 (stronger for women vs. men) • Absence of suicidal ideas or intent • Hopefulness • Willingness to accept help and/or treatment for psychiatric conditions • Low symptom severity • Good therapeutic alliance with mental health professional • Stable, supportive marriage or spouse • Religious prohibition Collateral interviews For each interview, note the following: • Relationship to deceased • Time interval between death and interview • Reactions to the death (surprise, acceptance, and beliefs) • Attitudes about suicide • Potential biases (pending lawsuits, insurance claims, denial, etc.) • Assessment instruments used
Appendix 1 Evidence of Alternative or Staged Manner of Death •
Presence of Autoerotic Characteristics [57] • Body partially supported by ground • Ligature with self-rescue mechanism (slip knot, etc.) • Bondage items and/or sexual masochistic behavior (genitals, nipples, etc.) • Male wearing female attire • Protective padding between ligature and body • Sexual paraphernalia (vibrator, pornography, and mirrors) • Evidence of previous autoerotic practices
•
Presence of Atypical Self-Inflicted Gunshot Wounds [58] • More than one gunshot injury • Gunshot injury without contact or near contact • Uncommon entrance wound sites (back of neck or head, ear, and eye)
•
Uncommon bullet paths (downward and back to front)
Acknowledgment The authors would like to acknowledge Alan L. Berman, PhD for his expertise and assistance, particularly with the Psychological Autopsy Protocol.
References [1]
Schneidman, E. (1996). The Suicidal Mind, Oxford University Press, New York. [2] Schneidman, E. (1981). The psychological autopsy, Suicide and Life-Threatening Behavior 11, 325–340. [3] Simon, R. (2002). Murder, suicide, accident, or natural death? Assessment of suicide risk factors at the time of death, in Retrospective Assessment of Mental States in Litigation, R. Simon & D. Shuman, eds, American Psychiatric Publishing, Washington, D.C, pp. 135–153. [4] Rosenberg, M., Davidson, L., Smith,J.C., Berman, A.L., Buzbee, H., Gantner, G., Gay, G.A., MooreLewis, B., Mills, D.H., Murray, D., O’Carroll, P.W. & Jobes, D. (1988). Operational criteria for the determination of suicide, Journal of Forensic Sciences 33(6), 1445–1456. [5] Jobes, D., Casey, J. & Berman, A. et al. (1991). Empirical criteria for the determination of suicide manner of death, Journal of Forensic Sciences 36(1), 244–256. [6] Ritchie, E. & Gelles, M. (2002). Psychological autopsies: the current department of defense effort to standardize training and quality assurance, Journal of Forensic Sciences 47(6), 1370–1372. [7] Snider, J., Hane, S. & Berman, A. (2006). Standardizing the psychological autopsy: Addressing the daubert standard, Suicide & Life-Threatening Behavior 36(5), 511–518. [8] Cone, E. et al. (2004). Oxycodone involvement in drug abuse deaths. II. Evidence for toxic multiple drugdrug interactions, Journal of Analytical Toxicology 28(7), 616–624. [9] Wolf, B.C., Lavezzi, W.A., Sullivan, L.M. & Flannagan, L.M. (2005). One hundred seventy two deaths involving the use of oxycodone in palm beach County, Journal of Forensic Sciences 50(1), 192–195. [10] Scott, C., Swartz, E. & Warburton, K. (2006). The Psychological autopsy: solving the mysteries of death, The Psychiatric Clinics of North America 29(3), 805–822. [11] Jobes, D., Berman, A. & Josselson, A. (1986). The impact of psychological autopsies on medical examiners’ determination of manner of death, Journal of Forensic Sciences 31(1), 177–189.
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M.A., Frank, E., Perlis, R.H., Martinez, J.M., Fagiolini, A., Otto, M.W., Chessick, C.A., Zboyan, H.A., Miyahara, S., Sachs, G. & Thase, M.E. (2006). Prospective predictors of suicide and suicide attempts in 1, 556 patients with bipolar disorders followed for up to 2 years, Bipolar Disorders 8, 566–575. Owens, C., Booth, N., Briscoe, M., Lawrence, C. & Lloyd, K. (2003). Suicide outside the care of mental health services: a case-controlled psychological autopsy study, Crisis 24(3), 113–121. Salib, E., Cawley, S. & Healy, R. (2002). The significance of suicide notes in the elderly, Aging and Mental Health 6(2), 186–190. Canetto, S. & Lester, D. (2002). Love and achievement motives in women’s and men’s suicide notes, The Journal of Psychology 136(5), 573–576. Ho, T., Yip, P., Chiu, C. & Halliday, P. (1998). Suicide notes: what do they tell us? Acta Psychiatrica Scandinavica 98(6), 467–473. Foster, T. (2003). Suicide note themes and suicide prevention, International Journal of Psychiatry in Medicine 33(4), 323–331. Baume, P., Cantor, C. & Rolfe, A. (1997). Cybersuicide: the role of interactive suicide notes on the Internet, Crisis 18(2), 73–79. Lester, D. & Linn, M. (1998). Joseph Richman’s signs for distinguishing genuine from simulated suicide notes, Perceptual and Motor Skills 87(1), 242. Werlang, B. & Botega, N. (2003). Semistructured interview for psychological autopsy: an inter-rater reliability study, Suicide & Life-Threatening Behavior 33(3), 326–330. Seguin, M., Lesage, A., Turecki, G., Bouchard, M., Chawky, N., Tremblay, N., Daigle, F. & Guy, A. (2007). Life trajectories and burden of adversity: mapping the developmental profiles of suicide mortality, Psychological Medicine 37(11), 1575–1583. Mann, J.J., Waternaux, C., Haas, G.L. & Malone K.M. (1999). Toward a clinical model of suicidal behavior in psychiatric patients, The American Journal of Psychiatry 156, 181–189. Beskow, J., Runeson, B. & Asgard, U. (1990). Psychological autopsies: methods and ethics, Suicide & Life-Threatening Behavior 20(4), 307–323. Brent, D.A., Perper, J.A., Kolko, D.J. & Zelenak, J.P. (1988). The psychological autopsy: methodological considerations for the study of adolescent suicide, Journal of the American Academy of Child and Adolescent Psychiatry 27(3), 362–366. Kern, J. & Swier, S. (2004). Daubert, kuhmo, and its impact on south dakota jurisprudence: an update, South Dakota Law Review 49, 217–249. Hansen, M. (2000). Suicidal Missions: psychological autopsies to uncover motivation in suspicious deaths are themselves now suspect, ABA Journal 86, 28–29. Silverman, M. (2006). The language of suicidology, Suicide and Life-Threatening Behavior 36(5), 519–532.
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Pouliot, L. & De Leo, D. (2006). Critical issues in psychological autopsy studies, Suicide and Life-Threatening Behavior 36(5), 491–510. Kumho Tire Co. V. Carmichael, 536 U.S. 137, 141 (1999). Federal Rules of Evidence, Available at 2008. http:// www.law.cornell.edu/rules/fre/rules.htm#Rule703. Conner, K., Conwell, Y. & Duberstein, P. (2001). The validity of proxy-based data in suicide research: a study of patients 50 years of age and older who attempted suicide. II. Life events, social support and suicidal behavior, Acta Psychiatrica Scandinavica 104(6), 452–457. Conner, K., Duberstein, P. & Conwell, Y. (2001). The validity of proxy-based data in suicide research: a study of patients 50 years of age and older who attempted suicide, I Psychiatric Diagnosis Acta Psychiatrica Scandinavica 104(3), 204–209. Ormerod, D. (2001). Psychological autopsies: legal applications and admissability, The International Journal of Evidence and Proof 5, 1–31. Moscicki, E. (1997). Identification of suicide risk factors using epidemiologic studies, Psychiatric Clinics of North America 20(3), 499–517. American Psychiatric Association (APA) (2003). Practice guideline for the assessment and treatment of patients with suicidal behaviors. The American Journal of Psychiatry Available at http://www.psych.org/psych pract/treatg/pg/SuicidalBehavior 05-15-06.pdf. Shea, S. (2002). The Practical Art of Suicide Assessment: A Guide for Mental Health Professionals and Substance Abuse Counselors, John Wiley & Sons, New Jersey. Berman, A. (1993). Forensic suicidology and the psychological autopsy, in Suicidology: Essay in Honour of Edwin S. Schneidman, A. Leenaars, ed, Aronson, New York. Hazelwood, R. & Napier, M. (2005). Crime scene staging and its detection, International Journal of Offender Therapy and Comparative Criminology 48(6), 744–759. Vanezis, P. & Busuttil, A. (1996). Suspicious Death Scene Investigation, Arnold, London, p. 153. Byrard, R., Hucker, S. & Hazelwood, R. (1990). A comparison of typical death scene features in cases of fatal male and autoerotic asphyxia with a review of the literature, Forensic Science International 48(2), 113–121. Andriessen, K. (2006). On “Intention” in the definition of suicide, Suicide and Life-Threatening Behavior 36(5), 533–538. O’Carrol, P., Berman, A., Maris, M., Moscicki, E., Tanney, B. & Silverman, M. (1996). Beyond the tower of babel: a nomenclature for suicidology, Suicide and Life-Threatening Behavior 26, 237–252. Hazelwood, R., Dietz, P. & Burgess, A. (1983). Autoerotic fatalities, Lexington Books, Lexington, MA. Karger, B., Billeb, E., Koops, B. & Brinkman, B.(2002). Autopsy features relevant for discrimination between suicidal and homicidal gunshot injuries, International Journal of Legal Medicine 116, 273–278.
Further Reading Legal Citations Campbell v. Young Motor Co, 211 Mont. 68, 684 P.2d 1101 (1984). Daubert v. Merrell Dow (USSC., 1993). Frye v. United States (D.C. COA., 1923). In re Succession of Pardue (La Ct. App. 915 So. 2d 415 2005). Jackson v. State, 553 So. 2d 719 (Fla. 4th DCA., 1989). Kumho Tire Co. v. Carmichael 536 U.S. 137, 141 (1999). Mutual Life Insurance Company v. Terry (U.S. 82, 580 1872). State v. Guthrie (SD 61, 627 N.W. 2d 4012001). United States v. St. Jean (U.S. Ct. of Appeals for Armed Forces, 1996).
Additional References Cavanagh, J., Carson, A., Sharpe, M. & Lawrie, S. (2003). Psychological autopsy studies of suicide: a systematic review, Psychological Medicine 33(3), 395–405. Conner, K., Cox, C., Duberstein, P., Tian, L., Nisbet, P. & Conwell, Y. (2001). Violence, alcohol, and completed suicide: a case-control study, The American Journal of Psychiatry 158, 1701–1705. Conwell, Y., Duberstein, P., Cox, C., Herrmann, J., Forbes, N. & Caine, E. (1996). Relationships of age and axis I diagnoses in victims of completed suicide: a psychological autopsy study, The American Journal of Psychiatry 153, 1001–1008. Fruehwald, S., Matschnig, T., Koeni, F., Bauer, P. & Frottier, P. (2004). Suicide In custody: case-control study, The British Journal of Psychiatry 185, 494–498. He, X.Y., Felthouse, A.R., Holzer, C.E., Nathan, P. & Veasey, S. (2001). Factors in prison suicide: one year study in Texas, Journal of Forensic Sience 46(4), 896–901. Kovasznay, B., Miraglia, R., Beer, R. & Way, B. (2004). Reducing suicides in New York State correctional facilities, Psychiatric Quarterly 75(1), 61–70. Litman, R. (1989). 500 psychological autopsies, Journal of Forensic Sciences 34(3), 638–646. Malone, K.M., Oquendo, M.A., Haas, G.L., Ellis, SP., Li, S. & Mann, J.J. (2000). Protective factors against suicidal acts in major depression: reasons for living, The American Journal of Psychiatry 157, 1084–1088. Marttunen, M., Henriksson, M., Isometsa, E., Heikkinen, M., Aro, H. & Lonnqvist, J. (1998). Completed suicide among adolescents with no diagnosable psychiatric disorder, Adolescence 33(131), 669–681. Ohberg, A. & Lonquist, J. (1998). Suicides hidden among undetermined deaths, Acta Psychiatrica Scandinavica 98(3), 214–218. Owens, C., Booth, N., Briscoe, M., Lawrence, C. & Lloyd, K. (2003). Suicide outside the care of mental health services: a case-controlled psychological autopsy study, Crisis 24(3), 113–121.
Psychological Testing Shaw, J., Baker, D., Hunt, I.M., Moloney, A. & Appleby, L. (2004). Suicide by prisoners: National clinical survey, British Journal of Psychiatry 184, 263–267. Spellman, A. & Heyne, B. (1989). Suicide? Accident? Predictable? Avoidable? The psychological autopsy in jail suicides, The Psychiatric Quarterly 60(2), 173–183. Weinberger, L.E., Sreenivasan, S., Sathyavagiswaran, L. & Markowitz, E. (2001). Child and adolescent suicide in a large, urban area: Psychological, demographic, and situational factors, Journal of Forensic Science 46(4), 902–907.
Related Articles Autoerotic Deaths Accident Reconstruction Crime Scene Investigation Mass Grave Investigation Suicide (Behavior) JAMES L. KNOLL, IV AND ROBERT R. HAZELWOOD
Psychological First Aid see Disaster Mental Health
Psychological Profiles see Profiles: Psychological and Behavioral
Psychological Syndromes see Syndromes: Psychological
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Psychological Testing Introduction Psychological testing is best understood within the larger context of psychological evaluation or assessment that, in turn, is seen as one discipline’s approach to a more general and shared task of information collection. The APA Dictionary of Psychology [1] defines psychological assessment as “the gathering and integration of data in order to make a psychological evaluation, decision, or recommendation” (p. 751). Multiple tools of assessment are listed including interview, behavioral observations, tests, and other specialized instruments. A psychological test is a “standardized instrument (i.e., a test, inventory, or scale)” used for the purpose of measuring any of a variety of abilities, aptitudes, or attributes (p. 753). This article includes discussion of psychological testing and differentiates it from other types of assessment and focuses on one area of personality testing (see, in contrast, Neuropsychological Assessment; Neuropsychological Assessment: Child; Head Injury: Neuropsychological Assessment). While general information is applicable to examinees of all ages, most of the tests that are discussed here were developed for use with adults.
Clinical Assessment and Formal Testing Evaluation or assessment is used in all clinical disciplines and may involve elaborate, sophisticated technology, such as magnetic resonance imagery (MRI) to look for the presence of a brain lesion, or may depend on more informal, intuitive ways of combining personal observations to form hypotheses or conclusions, such as surmising a person acts depressed. Different clinicians within mental health “work up” a client or patient using common as well as unique tools and methods associated with the specialized training and expertise of the particular discipline. For example, almost all mental health clinicians assessing someone not only interview the person by asking common questions about mood, sleep, appetite, and daily functioning but also probe other areas more selectively. Psychiatrists are more likely to consider medical or biological factors potentially contributing to emotional problems, whereas social workers may spend
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more time exploring the person’s interchanges with social systems. Family therapists may look more acutely at the history of family relationships and alliances, and psychologists are more likely to use inventories and psychological testing. Each discipline’s approach is a blend of commonly shared tools, literature, and research arising from several disciplines as well as unique resources based on clinical specialization and scope of practice for that particular discipline.
Differences between Psychiatric and Psychological Testing Clinical psychologists and psychiatrists both provide assessment and treatment services in the field of mental health, but the differing educational and clinical training routes shape distinct elements that each group uses for these services (see Behavioral Science Evidence). Psychiatrists, like other physicians, attend medical school for four years during which time they focus on studying chemistry, anatomy, and physiology as well as work in a wide variety of medical speciality placements before getting the MD (medical doctor) degree. They also may take courses in research, statistics, and learning theories. During psychiatric rotations in medical school and later in residency specialization (3 or 4 years), they learn about medical tests and clinical diagnostic techniques for mental health problems, study personality theories and human development, and acquire skills for treating mental illness. For most psychiatrists, treatment is heavily based on biological and chemical factors that medicines affect (see Psychopharmacology; Psychopharmacology: Child and Adolescent). Assessment is therefore oriented toward finding biological factors or markers for which medical or somatic intervention is well matched. Psychiatric assessment relies heavily on clinical observation (something physicians are well trained to do) and the use of mental status evaluation (see Mental Status: Examination). A mental status evaluation involves assessing a person’s orientation (knowledge of place, time, and self); ability to attend to environment and to communicate; mood and expression of feelings; and congruence or incongruence within the situation (appearing to hallucinate or act delirious). Depending on the nature of the hypothesized mental health problem, the psychiatrist may use brief tests or inventories to support or exclude
certain diagnoses. These instruments may include behavioral inventories designed to collect information about classroom behavior of children; self-reported symptoms on a depression checklist; or a brief cognitive status exam looking for signs of dementia. More elaborate psychiatric testing is usually medically or biologically oriented as the psychiatrist reaches into his/her medical training to refine diagnosis (e.g., radiological tests looking for brain tumor; electroencephalogram (EEG) to document seizures or to find unusual electrical patterns in the brain; and blood tests to measure hormone levels or to check for problems such as anemia). Psychologists, on the other hand, begin their training by attending a university graduate school for four or more years taking courses in personality theory and human development, measurement theory and test development, research statistics, learning theories, methods of mental health interventions, and principles of social contexts and human interactions. To a lesser degree, course work includes anatomy and physiology of the nervous system, human biochemistry, and genetics. Students in a psychology Ph.D. (doctor of philosophy) program complete both a masters level research project and a doctoral dissertation. Clinical training involves multiple placements in clinical sites during graduate school followed by a 12-month internship in a mental health setting prior to graduation. Some states require an additional year of postgraduate supervised clinical work before licensure, and several areas of professional specialization offer residency training for one or two years. Some areas of specialization are clinical psychology (dealing with application of psychological knowledge and principles to address mental health problems), neuropsychology (study of brain–behavior relationships), experimental psychology (basic physiological or social factor research), and forensic psychology (application of psychological knowledge and principles to address legal issues). Each of these areas makes heavy use of assessment and testing. When psychologists conduct an evaluation, they also rely on the common tools of observation and interview with the person and collateral sources (family members, teachers, institutional staff who have information about the person’s behavior). As do psychiatrists, they conduct mental status evaluations and may also use brief inventories, checklists, or simple tests to support or dismiss diagnostic hunches. However, when psychologists proceed to more elaborate
Psychological Testing testing, they rely most heavily upon the tools their discipline has developed. For the most part, these tests involve either measurement of cognitive abilities (e.g., intelligence, memory, and academic skills) or personality factors (e.g., traits and emotional states). Cognitive Testing. Cognitive testing may be thought of as a way to measure how well the brain is functioning. Neuropsychology, a speciality with its own postgraduate training and certification, has developed a vast array of tests that measure not only basic intelligence but also learning and memory, sensory perception and sensorymuscle integration, reasoning and problem solving skills, language and communication abilities, and basic academic skills such as reading (see Neuropsychological Assessment; Neuropsychological Assessment: Child). Cognitive testing is able to identify and to document the level of skill or the degree of impaired functioning of a person. It is often used in conjunction with neurological or radiological testing that documents impaired structure of the brain or nervous system. Findings from cognitive testing may be used for such tasks as assisting with decisions about academic placement or need for special education resources (see Mental Retardation); rehabilitation treatment planning after head injury or neurosurgery (see Head Injury: Neuropsychological Assessment); diagnosis of conditions having subtle onset such as early stage dementia; measurement of progress or lack of response to remediation efforts after head injury or stroke; or documentation of progression of effects of diseases such as Parkinson’s or Multiple Sclerosis. Neuropsychologists are often called upon in forensic cases involving head injury, toxic exposure, or questions of competency or capacity (see Capacity to Stand Trial; Capacity Assessment; Guardianships of Adults). Personality Testing. If cognitive testing is thought of as a way to measure the brain’s work, personality testing may be thought of as a way to assess the mind of the person. Whereas one deals with neurophysiology and often uses physical measures, the other deals with psyche and uses measures of emotion, attitude, and traits. Personality testing explores intrapsychic (internal aspects of self, value conflicts and ambivalence, moods, motivation) and interpersonal issues (social behavioral clusters, styles of interaction, orientation toward others).
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Personality testing is often used to gather information to allow psychologists to describe what a person is like; how a person is different from others and to what degree; how the person functions or is likely to function with others; whether there is significant psychopathology; extent to which a person is open and transparent in self-presentation or guarded or even deceptive (see Deception: Detection of and Brain Imaging; Deception: Detection of); Malingering: Forensic Evaluations) and prognosis for improvement with treatment for mental health problems. Psychologists are often called upon in forensic cases to use personality testing to address questions involving risk assessment (see Dangerousness: Risk of); mental illness diagnosis and treatment recommendations; competency and capacity; tort cases where emotional distress claims are made (see Posttraumatic Stress Disorder); and criminal cases where mental illness factors are being presented (see for example Insanity: Defense; Temporary Insanity).
Properties of Formal Testing Testing, which is a relatively circumscribed activity involving use of tests to obtain specific scores, is one part of an overall assessment that collects information from multiple sources using multiple methods. Information usually includes records that place a person’s current performance in historical context, referral information that places a person in a situational context, behavioral observations, interviews, and consideration of the person’s test taking attitudinal factors (fatigue, rapport, motivation, exaggeration, or defensiveness). The person–context information can be as important as the test result information, for instance when the person is observed to be disengaged from the task or hostile toward the examiner. As a result of such situational data, the psychologist interprets data cautiously or may even disregard the scores as being invalid measures. This person–situation information, whether obtained from direct observation or from validity scales embedded within tests, helps determine if test results are considered valid for interpretation. Together with information from these other sources, test results are then used to assist in diagnosis, to identify areas for intervention, or to provide information about current functioning.
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These results are integrated into a cohesive and comprehensive understanding of the person to communicate it to others including the person being tested. Indeed, providing feedback to the person often serves as an intervention itself and can be a very important part of treatment. Formal testing refers to an assessment process using standardized instruments that have rules for administration and for scoring responses, normative information for comparing scores, and guidelines for interpretation of results. Holding these test factors constant means there should be minimal “noise” produced so that it may be logically assumed that most of the variability of scores between examinees is a result of something associated with differences between the individual test takers. Just as the use of an accurately calibrated thermometer allows a physician to verify or rule out the presence of fever to help refine diagnostic hunches, the use of psychological testing allows psychologist to verify or rule out abnormalities and to refine diagnostic hunches on the basis of test score patterns and known psychological conditions.
Reliability Reliability is the term used to indicate the concept of score consistency on a test. It is a measure of how closely clustered or how far apart a person’s scores would be with repeated administrations of the same test or with alternate versions of the test. Reliability is a measure of how much error (or “noise” as compared to “signal”) is present in test scores [2, 3].
Validity Validity is the term used to designate the concept of score accuracy of a test. It tells how well a test works in measuring what it purports to assess. Validity may be determined by comparing a test with a “gold standard” in the field, by seeing how well test scores discriminate between known groups on a particular factor, or by how well a test covers relevant aspects of a construct but avoids tapping other constructs. Just as a rifle must shoot true before a marksman can attain target accuracy, a test must have reliability (consistency of measured scores) before its validity (accuracy of measured scores) can be established [2, 3].
Standardization Standardization refers to the process whereby a test and its components are made standard or routine in details of administration. Test items, the order of administration of items, ways of recording and scoring responses, and ways of instructing examinees about how to take the test must become standard or fixed. Standardization and adherence to instructions regarding the test should decrease the “noise” associated with a person’s scores so that differences between examinees (or the same person tested at different times) should be related to actual differences rather than to errors involved in the process of obtaining the scores [2, 3].
Norms Norms refer to the collection of scores that represent a sample group’s responses on a test. Norms can be obtained when many people take the test under the same standard conditions. The mean (average) and standard deviation (SD) (measure of variability of scores) can be calculated and used to evaluate a particular person’s obtained score in relation to the cluster and range of scores produced by the norm group. Raw scores are often transformed to standard scores (mean = 100, SD = 15), T -scores (mean = 50, SD = 10), or scale scores (mean = 10, SD = 3) to create a shorthand way of conveying a person’s score in relation to the sample group’s norms. A welldeveloped test has a heterogeneous (mixed gender, ethnicity, and socioeconomic status) group of individuals whose scores are used to calculate the norms. As a result, the sample group norms should be more representative of the entire population of interest than if only a homogenous group was tested and scores calculated. By having good normative data, it is possible to determine to what degree the examinee is similar to or different from the average person taking the test. By having test data from differing groups of people with a known condition or factor, it is possible to use a person’s test results to refine diagnostic hypotheses about the examinee. By using information about a person’s score in relation to the norms, the psychologist can then analyze and interpret test score data. Analysis of test data can occur at three levels: specific details about skills, deficits, or symptoms based on actual scores; level of performance or
Psychological Testing information about severity of problem or level of skill based on relationship of score to group norms; and syndrome or pattern of scores, which generalizes to life context, based on research literature and clinical knowledge [3, 4]. Testing offers advantages over interview or observation alone by providing empirically quantified information that is usually more precise than interview impressions. Testing may cover a variety of constructs, and, in the case of personality testing, it covers a large array of traits in an efficient manner. Standardized administration and scoring means a common yardstick is used for measuring a person, and behavior is observed in a uniform context. Test norms allow scores to be compared to known groups, and research with such known groups provides the psychologist with a stimulating backdrop from which to generate and evaluate hypotheses related to test scores [5].
History of Psychological Testing A brief history of psychological testing can provide a useful context for understanding its current state. A very influential English figure was Sir Francis Galton who in 1869 published “Classification of Men According to Their Natural Gifts” [6]. Galton pioneered use of questionnaires and rating scales, developed statistical methods for analysis of individual differences, and popularized forms of psychological testing. At the International Health Exhibition in London (1884), he and his assistants tested individuals willing to pay to learn about their vision and hearing sensitivity, muscle strength, reaction time, and memory. This focus of attention on individual abilities was in contrast to the emphasis on group data being collected by others. Wilhelm Wundt, a German psychologist who had established the first psychology lab in Leipzig five years before, considered individual differences to be errors and was far more interested in measures of perception that portrayed information about the species as a whole [7]. In the same tradition as Galton, James M. Cattell established a testing lab at the University of Pennsylvania (1888) and used tests to measure sensitivity to pain, perceptual discrimination, memory, and other cognitive skills as ways to study individual differences in intelligence. Cattell was the first to use the term mental test to describe his techniques [7]. In
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general, testing in clinical psychology testing has continued to focus more on individual distinctives, whereas measurement in physiological or experimental psychology has focused more on data that add to knowledge about collective or group characteristics of humans and other animals. Psychological testing took a major leap forward in 1905 when Alfred Binet, a French psychologist, and Theodore Simon, a psychiatrist, collected 30 brief cognitive tests to use as an intelligence scale for the purpose of determining school entry for Parisian children. They later revised their collection of tests and developed the concept of mental age (the age at which an average child could pass a particular test). In the United States, Lewis Terman added some other tasks and developed the concept of intelligence quotient (IQ) that was found by dividing the attained mental age by the person’s chronological age. Eventually, IQ came to be calculated in a different manner on the basis of comparison to group information and how far from the group mean a person’s scores were [8]. Another major advancement in psychological testing occurred in 1917 when the US Army had to classify World War I (WWI) recruits for their suitability for military service as well as for possible officer training. In a period of two years, 1.7 million inductees were given group administered intelligence tests based on alterations of the Binet and Terman tests. For those literate in English, the Alpha version (verbal tests) was used; for illiterate or non-English speaking recruits, the Beta version (nonverbal tests) was used. Nonverbal or language free tests had been used in the United States at Ellis Island for screening immigrants for mental defects and had also been used in Chicago with unschooled juvenile delinquents. David Wechsler, a psychology graduate student, enlisted in the Army and was trained to conduct individual intelligence tests for the 5% of recruits who failed one of the group-administered versions. Many years later as psychologist at Bellevue Psychiatric Hospital in New York City, he developed a different approach to intelligence testing that combined verbal and nonverbal tasks to result in a single score. He also collected normative data on a large group from the general population and compared each person’s score to the group average (mean). This deviation derived IQ score (relationship of person’s score to group average) provided information about how far a person’s score was above or below the mean score for
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the group. In 1939, he contracted with Psychological Corporation for production and sale of his test [8]. Psychological Corporation, formed in 1921, had already been marketing intelligence tests (termed scholastic aptitude tests) and other specialized aptitude tests to schools and industries after the war, but the number of psychological tests had been rather limited until the mid-1930s. Oscar Buros’ first edition of Educational, Psychological, and Personality Tests of 1933 & 1934 had been only 44 pages, but his 1938 edition of what became Mental Measurements Yearbook was more than 400 pages long and covered 4000 tests. The current edition is multivolume and covers thousands of tests [9]. The entry of the US military into World War II brought with it the need for testing four million recruits for military assignments. Once again, a national crisis produced a surge of testing emphasis which propelled psychological testing from academic or clinical environments into the larger culture. A similar peacetime surge occurred in the Cold War with a strong focus on achievement and aptitude testing when the space race was initiated with the launch of the Russian satellite Sputnik. These intelligence, aptitude, and achievement tests fall into the general category of cognitive testing [10].
designed to measure test taking attitude (defensiveness, exaggeration of symptoms, and subtle defensiveness) [7, 11]. From this line of development has come a wide range of objective tests that provide information about personality traits (e.g., introversion, dominance, and self-constraint); emotional states (anger, anxiety, and depression); behaviors (substance abuse, risktaking, and antisocial acts); and interpersonal orientation (psychopathy, altruism, and cooperativeness). Often these tests are pencil and paper or computer administered self-report measures that have validity scales to assess manner of self-presentation. As the tests are usually in written form, it is important to assess the examinee’s reading level to assure it is sufficient for the task. The results of the tests are thought to be explicit self-representations of the test taker. Test items are seen as stimuli, and self-report statements of endorsement or denial of particular items are seen as responses that define and describe the person. Some tests are also designed to be completed by collateral sources who know the person, and this information can be quite useful in assessment of children or when the examiner wants to know how others perceive the person [3].
Projective Tests Objective Tests In a different line of development, another contribution out of the WWI era was the self-report inventory that formed the basis for objective personality testing. Robert Woodworth’s personal data sheet was developed too late for military use in the war but was used afterwards in civilian life to screen for seriously disturbed individuals. The inventory was basically a self-report of recognized symptoms associated with psychiatric problems. This approach culminated in the 1943 publication of the Minnesota Multiphasic Personality Inventory (MMPI). Starke Hathaway, a psychologist, and Charnley McKinley, a psychiatrist, had developed the set of test items empirically by selecting those items that successfully differentiated known patient groups from a general population sample (both genders but all Caucasian samples comprised mostly of hospital visitors, some airline workers, and civilian conservation corps workers in Minnesota). The inventory was remarkable for this use of empirical research that served as a basis for item selection and for its use of three validity scales
A different approach to personality assessment is the use of projective tests, best typified by the inkblots used by Hermann Rorschach, a Swiss psychiatrist. Others had previously used vague or ambiguous stimuli to elicit a person’s responses, which then were interpreted on the basis of the assumption that the subject’s internal struggles, fantasies, and needs were being projected onto this ambiguous but neutral stimulus material. Rorschach began experimenting with inkblots around 1910 and established a system for eliciting and scoring responses, which he published along with 10 inkblots in Psychodiagnostik (1921). This line of assessment was further elaborated by the work of Henry Murray in the development of the Thematic Apperception Test (TAT) (picture cards used to elicit short stories from the subject), Goodenough’s draw a person test (originally used as an intelligence measure), and various sentence completion or word association tests. Often projective tests are administered directly by the examiner who records responses of the examinee, but some projective tests are also self-administered
Psychological Testing (house–tree–person drawings and sentence completion tasks). Regardless of the manner of administration, the stimuli are used to evoke behavior that is thought to contain implicit information that must be discovered and interpreted by the trained examiner [12].
Personality Testing The study of the nature of personality has a long lineage dating back at least to early Greek philosophers and playwrights. In the mid-nineteenth and early twentieth centuries, scientists such as Galton, Wundt, and James moved psychology away from being a philosophical exercise to the study of actual human behavior, many times trading erudite speculation for humble inquiry. Much of the physiological and cognitive research work of the European psychologists was laboratory based study of normal behavior but lacked a theory of person. In contrast was the work of Freud, a psychiatrist who was a seminal figure in the history of personality theory who worked with disturbed patients and searched for a model of the psyche combining understanding of normal and abnormal personality that would fit neurological evolution. His treatment approach and psychoanalytic theory came from his clinical model of inquiry and observation, and his major contributions were related to abnormal personality.
Issues in Personality Test Theory There remains a basic division in personality research regarding whether personality is known by studying normal or abnormal behavior. In the United States, Gordon Allport studied the individual and the unique combination of the individual’s normal traits. Henry Murray (who developed the TAT) studied individual differences seen in normal drives or traits and how they were integrated in the person. Both assumed personality is defined by traits that are independent of psychopathology, but both taught that the individual cannot be understood by fragmenting these traits. Eysenck, who proposed a two factor theory of neuroticism/emotional stability and extroversion/introversion, and Cattell, who developed the 16 Personality Factor (16 PF) test, carried on this line of work that now has given rise to the five factor model of Costa and McCrae [13]. This model is the
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basis for the NEO-Personality Inventory (NEO-PI) [14]. In contrast, developers of inventories such as the MMPI [11] or the Personality Assessment Inventory (PAI) [15] have paid more attention to clinical groups and abnormal personality. Those who attempt to reconcile normal and abnormal personality research must address the question articulated by Paul Meehl as to whether personality traits (enduring characteristics in contrast to temporary states) occur in a dimensional spectrum that ranges from normal to abnormal extremes or occur in categorical divisions (taxons or uniquely different groups). The thinking behind the Diagnostic and Statistical Manual of Mental Disorders (DSM) approach to diagnosis assumes distinct categorization. Some trait theorists such as Millon posit a dimensional approach where either extreme of a trait may be pathological [16, 17]. Those who study personality are also divided as to whether traits actually exist independent of models of thought (constructive-realist) and are largely determined by physiology or whether traits are only psychological explanations of behavior, actually determined by social domains affecting expression of biological needs (socioanalytic). The debate comes out in discussion about nature versus nurture causing behavior but goes beyond to attempt to answer whether there are really inherent basic trait domains (such as hardwired extroversion/introversion or even psychopathy) or only differences evident in the way people respond to or cope with biological needs based on social factors [18].
Atheoretical Approaches to Personality Testing In addition to the trait research, other American work has significantly influenced personality testing from an atheoretical model. Coming out of the medical exam/psychiatric interview methodology, Hathaway (psychologist) and McKinley (psychiatrist) in the 1930s and early 1940s developed the MMPI in an attempt to find an empirically derived test that would differentiate medical patients with psychopathology from normal individuals. Even though self-report methodology, which had been developed by Woodworth in World War I with the Personal Data Sheet, had come to be criticized as too easily manipulated, Hathaway and McKinley used the technique anyway. They collected a large pool of items that were associated with psychiatric and medical symptoms
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and asked individuals to respond to each by endorsing or denying its occurrence in their own lives. The MMPI authors, aware that responses might be affected by efforts to distort self-presentation, created validity scales to be used in interpretation of scores. They disregarded theoretical constructs and attempted to use only empirical means to identify those particular items that produced scores able to distinguish between specific diagnostic groups of patients and nonpatients. The original hope and early emphasis with the work at the University of Minnesota and later at Menniger Clinic in Kansas was to develop a tool capable of providing psychiatric diagnosis using a practical, empirically derived approach [19, 20]. The work on the MMPI was part of a postWorld War II interest in testing. Similar to the demands of WWI, the military during wartime had responded to the task of classifying millions of recruits. After the war, in the United States there was a large number of nonmedically trained mental health providers, mainly clinical psychologists, who were equipped and ready to apply science, which had been optimistically embraced by the nation, to the study and treatment of mental health problems. Testing was valued in clinical, educational, industrial, and correctional settings and was seen as a way to bring efficiency, empiricism, and objectivity to tasks in these fields. During the rise and reign of behaviorism (1960s and early 1970s), there was strong challenge to the concept of “personality”, something that was intangible and considered an unnecessary and useless myth in explaining behavior. There was no need for the concept of “self” as there was exclusive focus on what an organism did in response to particular stimuli. Testing did not go away, but there was a much stronger emphasis on behavioral assessment – identifying particular behaviors of interest and recording the circumstances and frequency of their occurrence. In the past few decades, there has been modification of this model that now includes cognitive as well as behavioral aspects of assessment and treatment [21]. With this cognitive-behavioral approach there is focus on specific assessment using specialized instruments (Beck Depression Inventory and Beck Anxiety Inventory) that make no effort to describe the person as an integrated personality or even to provide a comprehensive clinical picture. Some have suggested that these brief rating scales and inventories, which are limited in scope, represent a third type
of personality assessment: rapid personality assessment instruments [3]. Currently, in many settings outside the teaching or research environments, comprehensive personality assessment is often not seen as important or is not viewed as essential even if important. In addition, managed care of mental health services has often taken a restrictive stance toward more comprehensive testing. A survey of psychologists assumed to be in private practice found that 25% did not do personality testing at all. Of the ones who did such testing at least sometimes, about half used one or both of the two widely recognized tests (MMPI and Rorschach Inkblots) although the most utilized personality test reported was sentence completion [21].
Current Psychological Test Usage Other surveys of psychologists have likewise documented a decided trend toward less testing in recent years. Psychologists in 1959 said 44% of their time was spent in assessment, but that figure was down to 22% in 1982. In 1971, 5 of the top 10 most often used psychological tests were projective personality tests; 1 was an objective personality test (MMPI), and 3 others were IQ tests. The core of the most popular tests remained stable through the early 1990s, but the amount of time devoted to assessment declined markedly. By the end of the decade, a study on test usage conducted for the American Psychological Association (APA) found fewer than 20% of clinical psychologists spent as much as 5 hours a week doing testing although about three-quarters of neuropsychologists spent at least that much time testing. Of those clinical psychologists with at least 5 hours a week devoted to testing, approximately 40% of their service was devoted to IQ or achievement testing and one-third to personality testing. Neuropsychological testing was the next highest category of time spent (about 20%) but was (as expected) the major use of time for neuropsychologists who also spent about 20% of their time doing personality assessment. The MMPI/MMPI-2 was the most widely used test in the combined two groups with an IQ test (Wechsler Adult Intelligence ScaleRevised (WAIS-R)) placing second overall. Clinical psychologists also tended to use the Rorschach Inkblots (ranked fourth), but neuropsychologists did not (ranked eighteenth). No other personality tests
Psychological Testing were popular with neuropsychologists, but at least half of clinical psychologists in the survey used the TAT (ranked sixth in frequency of use) [22].
Psychological Testing in Forensic Context In addition to neuropsychology, another area of psychology that relies heavily on assessment and testing is forensic psychology. A survey of state directors of mental health resulted in information for 41 state corrections departments. Of those responding, 40 used testing at intake while 25 used it also for pre-parole work-ups. Of those testing at intake, 26 (65%) used MMPI/MMPI-2, 18 (45%) used intelligence tests, and five (12.5%) used Rorschach Inkblots in their department protocols. Of the 25 using testing for preparole evaluations, 24 (96%) used MMPI/MMPI-2, eight (32%) used intelligence tests, and nine (36%) used Rorschach Inkblots [23]. Results of a survey of 152 forensic psychologists who were members of American Psychology-Law Society (AP-LS) or diplomates of the American Board of Forensic Psychology (ABFP) indicated they averaged 56% of their time doing forensic work, presumably largely assessment, with almost a third (29%) being spent in actual testing. When asked about most frequently used tests in particular types of adult assessments, the top five in order of weighted frequency of usage across referral questions were: MMPI-2, one of the Wechsler intelligence or memory, one of the Hare Psychopathy Checklist versions (see Psychopathy Checklists) Structured Interview of Reported Symptoms (SIRS), and PAI [24]. Another survey of 64 diplomates of ABFP asked which tests were considered acceptable for use in six areas of forensic assessment. Across areas, both the MMPI-2 and the Wechsler Adult Intelligence Scale, Third Edition (WAIS III) showed strong acceptance as did the PAI to a lesser but still major degree. The Millon Clinical Multiaxial Inventory, Third Edition (MCMI-III) was rated as acceptable in only one area (mental status at time of offense). The Rorschach inkblots was rated as unacceptable by the majority (52–60%) of the respondents in five of the six areas (equivocal for use in exploration of mental status at time of offense) while other projective tests were deemed unacceptable in all areas by a significant majority (60–95%). Two neuropsychological batteries (Halstead-Reitan and Luria-Nebraska) were
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reported to be acceptable in half of the areas as was another IQ test (Standford-Binet) [25].
Forensic Assessment: Psychology and Law Historical Developments Hugo Munsterberg, considered the founder of applied psychology, was the first director of the psychology lab at Harvard after leaving the University of Leipzig where he had been a student of Wilhelm Wundt. He was an early pioneer of the study of eyewitness testimony and a strong advocate of application of psychology to law. In his book On the Witness Stand (1908), he chastised attorneys and judges for not embracing the research findings of psychology and using them in the courtroom. He was strongly criticized and his ideas mocked, but in the 1920s law schools began hiring psychologists to teach courses. Psychology was involved in courts largely in relation to treatment and disposition of children, and psychiatrists were more involved with competency and sanity questions. But psychologists and other social scientists were involved in Brandeis briefs, the most famous being the work of Kenneth Clark and colleagues in Brown v. Board of Education (1954) [26]. Only after Jenkins v. United States (1962) [27] was the way open for psychologists to provide expert testimony on mental health issues. Other more recent legal rulings that have significantly impacted the practice of forensic psychology have been Daubert v. Merrell Dow Pharmaceuticals, Inc. (1993) [28], which replaced Frye (1923) criteria and defined the standards for consideration of scientific expert testimony; General Electric v. Joiner (1997) [29], which established the authority for the trial judge to determine what proffered testimony met Daubert standards; and Kumho Tire Co., LTD v. Carmichael (1999) [30], which expanded Daubert criteria to other fields of technical and specialized knowledge. Although these rulings only apply to federal courts, states have their own case law decisions in these areas [31].
Prevalence of Forensic Psychological Assessment No data were found that indicate the current extent of psychological assessment utilization by US courts, but a conservative estimate of Competency to Stand
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Trial evaluations in 1993 was 50 000 [32]. A more recent work cited research indicating 4–7% of criminal cases involved referral for these competency evaluations, the most prevalent mental health evaluation for criminal courts [33]. Civil courts often refer custody case participants for psychological evaluations, and personal injury cases frequently involve mental health expert testimony. Although the data are not available, it is obvious that a significant number of legal cases involve psychological or other mental health assessment. This reliance on psychology appears to be growing as evident with the publication of this volume that verifies Munsterberg’s foresight. The practice of forensic psychology, which is heavily dependent on psychological research and assessment tools, is one of the speciality areas in which the American Board of Professional Psychology (ABPP) offers board certification or diplomate status. The APA Division 41 (AP-LS) is devoted to exploration of the interface of psychology and law. Several well respected, refereed journals (including Law and Human Behavior; Behavioral Sciences and the Law; Psychology, Public Policy, and Law ) are devoted exclusively to publication of research in this area of disciplinary overlap.
Tensions between Clinical and Forensic Assessment Perspectives Forensic assessment in some important ways differs from traditional clinical assessment as discussed by Melton et al. [34], Heilbrun [35], and Archer et al. [31]. Some of the major ways include purpose, scope, and understanding of who is being served (broad understanding of purpose and scope in mental health evaluation where examinee is also the client being served versus forensic assessment addressing specific legal or quasilegal question(s) regarding the examinee to assist the decision maker who is considered the client). In addition, forensic examinees are frequently mandated for an evaluation and often assumed to have significant reasons to be purposefully selective in self-disclosure so that a much stronger focus must be placed on examiner objectivity and assessment of examinee’s response style (pattern of selfpresentation). Because of the threats of conscious deception or selective self-presentation in forensic evaluations, there is more emphasis on use of multiple sources of data to create hypotheses or to verify information as well as strong reliance on external
sources (collateral observations, historical records, and reports of others) apart from the formal assessment interactions with the examinee. While there are some instruments specifically developed for forensic use, these tend to be structured interviews, rating scales, or tests designed for use with a particular legal application in mind (e.g., Competence Assessment Instrument for Standing Trial (CAI), Psychopathy Checklist-Revised (PCLR), and Competence Assessment for Standing Trial for Defendants with Mental Retardation (CAST/MR)). Quite frequently other instruments, developed for nonforensic purposes, are used in a forensic assessment because of the vast research on the instruments, validity indicators built into some of the instruments, or ability for these tests to contribute to a broad understanding of the person to develop hypotheses related to factors bearing on the legal question(s). Obvious examples would include well researched personality tests, tests of malingering, and cognitive tests including IQ measures. When any test is considered for forensic evaluation, these factors are important to consider: sufficient research and norms with a population similar to that of the examinee, adequate test development and psychometric properties, and ability to link test results to conclusions regarding the referral question [35]. A major risk inherent with use of clinical tests is overinterpretation of results where adequate validity research (relating test scores to real world conditions or outcomes) does not demonstrate clear connections between the test data and specific legal question(s) [34]. This problem was pointed out in a marked way by Jay Ziskin and David Faust, two psychologists, in the 1970s and 1980s (Coping with Psychiatric and Psychological Testimony; The Limits of Scientific Reasoning). They criticized mental health providers for going beyond the data and research by offering forensic opinions based on personal impressions rather than scientific conclusions. As a more recent writer noted, the task should be to provide “the best that psychology has to offer but also to be candid about the limits of our science and our expertise” (p. 131) [36].
Tensions between Psychological and Legal Perspectives Even though psychologists are often used to conduct assessments and to provide relevant information
Psychological Testing to the courts about psychological factors having a bearing on legal issues, there remains basic tension between psychology (which is experimental, descriptive, and probabilistic in its orientation to pursue scientific truth) and law (which is adversarial, prescriptive, and decisive in its orientation to pursue social and individual justice) [34, 37]. Psychology operates from a perspective of determinism (i.e., behavior can be predicted by some combination of genetic, biological, social, interpersonal, and environmental factors) whereas law operates on an assumption of free will (i.e., behavior is the result of personal choice and responsibility as each person is a free moral agent). Other differences are evident as law applies broad terminology to specific cases, and psychology seeks to define and operationalize terminology into quantifiable form. Questions arise about legal terms for which there are no operational definitions either in law or psychology (e.g., reasonable degree of certainty pertaining to professional opinions, best interest of the child, reasonable degree of rational understanding for competency, unable to appreciate the nature and quality or wrongfulness of acts for criminal responsibility) or where the meaning of words or use of concepts differ (insanity as a legal construct and psychosis as a mental health concept). Despite the sometimes illfit of the two systems of thought, courts continue to rely on psychologists for help; and psychologists continue to explore better ways to respond to the task by developing methods to tie psychological data to legal constructs in a rational manner that can be logically followed [38].
Brief Overview of Major Personality Tests Minnesota Multiphasic Personality Inventory (MMPI and MMPI-2) The original 550 items and norms were developed by Hathaway and McKinley in the 1930s, mostly with patients and visitors at the University of Minnesota Hospital. The instrument was developed to aid in psychiatric and medical screening [7]. A revision (MMPI-2) was published in 1989 with updated items (66 modified, 90 omitted, and 107 newly created) and contemporary norms (2600 subjects of which 5% were current psychiatric patients). Individuals in the new norm group were from seven states representing a geographic diversity and were roughly balanced for gender (56% female).
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Although ethnic and socioeconomic diversity was sought, Hispanic and Asian American groups are underrepresented in the norms. The normative sample is also skewed with college graduates comprising a larger percentage than is present in the US population [20]. The current 567 item true/false inventory requires an eighth grade reading level according to the 1989 version of the manual or a sixth grade reading level according to the revised edition of the test manual published in 2001 [11]. In addition to the original three validity scales (L, F, K), there are now several others measuring tendency to acquiesce, marking responses randomly, or subtly presenting self in a consciously distorted manner. Although well respected and popularly used, the inventory is criticized for its scales being too highly intercorrelated and therefore not distinct because many items are used simultaneously for scoring on different scales. The MMPI was originally constructed for diagnostic classification purposes, but it proved to be disappointing in that regard when used in replication studies. Meehl was influential in adapting interpretation to a larger context by focusing on patterns of scores (profiles) and code types (based on scores of highest scales in a person’s profile). These profiles and code types were researched to provide psychiatric descriptions for the major groups. While code type or group profile descriptions came to be widely used, research revealed problems with temporal instability of the code types when individuals were retested [19]. Another way of using test results from the MMPI has grown through the development and use of content scales, which are comprised of items that seem to be consistently related to a similar construct. This approach led to content scales providing descriptive rather than diagnostic information about a person and has more recently led to innovations such as Restructured Clinical (RC) scales (basic clinical scales with a general demoralization factor removed) and Restructured Form (MMPI-2RF) with RC scales and newly developed specific problem (content) scales in a shorter version. These innovations also removed the use of K-corrections in calculating scores and removed item overlap within the basic scales [19].
Personality Assessment Inventory (PAI) The PAI, a self-report inventory comprised of 344 items to which a person marks one of four choices
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about how well each item applies to self, produces scores on 22 scales and 31 conceptually derived subscales. Scales were devised based on content and internal consistency and no item is scored on more than one major scale. Raw scores are transformed to T-scores using norms from a group of 1000 community dwelling subjects matching 1995 US census projections. Comparison clinical norms are also available based on a group of 1246 patients. Construction of the PAI was based on the assumption that normal personality constructs are distributed for both patients and nonpatients according to a bell-shaped (normal) curve. However, abnormal symptoms and constructs differ markedly within the two populations and occur very infrequently in the general population. The PAI requires a fourth grade reading level. It has four validity scales measuring positive and negative self-presentation, random responding, and overendorsement of unusual items [15, 39].
NEO-Personality Inventory-Revised (NEO-PI-R) A third objective personality measure is the NEOPersonality Inventory-Revised (NEO-PI-R) that measures five basic stable dimensions of personality based on the work of Tupes and Christal who analyzed data that had been collected by Cattell in his work on normal personality traits. These personality domains are neuroticism, extroversion, openness to ideas, agreeableness, and conscientiousness. These five scales each have six subscales that have been developed by logical and factor analytic strategies utilizing known research on normal personality traits. This inventory is comprised of 240 items marked with one of five possible responses (strongly disagree to strongly agree). It contains no validity scales. Norms were developed using 500 males and 500 females selected to match 1995 US census projections. Forms are available for both self-rating and ratings by collateral persons who know the examinee [13, 14].
is that self-report only describes behavior, but this projective task actually produces behavior that can be observed, recorded, scored, and analyzed. Over the next five decades after Rorschach’s publication, several different systems for scoring and interpretation emerged in both Europe and the United States. John Exner, influenced by Meehl’s writings about actuarial rather than intuitive approaches to test interpretation, set out to standardize rules for scoring responses so that empirical data could be developed and used in interpretation. His comprehensive system of coding caught on and has largely shaped the use of this instrument since its introduction in the mid-1970s. Use of Exner’s system [40] leads to specific data that can be related to norms and empirical research to provide information about a person’s ability to control stress; ways to process information or make sense of the world; patterns of thinking about self and the world; emotional state; and ways of perceiving events and relationships. Despite criticisms and disfavor of projective tests in general, the Rorschach Inkblots, especially when scored and interpreted using the Exner system, has remained a respected instrument for personality assessment and has passed Daubert scrutiny enabling expert testimony based on its findings. It provides limited information about diagnosis with the notable exception of thought disorder but provides a wealth of information to enable an understanding a person as an individual [41].
Other Resources Clinical and forensic uses of these and other personality tests are discussed at length in Butcher [42, 43], Goldstein [44], Meyer and Deitsch [45], Maruish [46], Strack [47], and Archer [48].
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Rorschach Inkblots This projective test, a standard set of 10 inkblots, was published by Swiss psychiatrist Hermann Rorschach in 1921 and is based on the assumption that personality can best be assessed through analysis of responses to ambiguous stimuli. Such implicit knowledge is less confounded by conscious distortion than is explicit information obtained by self-report. The assumption
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Harkness, A.R. & Hogan, R. (1995). The theory and measurement of traits: Two views, in Clinical Personality Assessment, J.N. Butcher, ed, Oxford University Press, New York, pp. 28–41. Ben-Porath, Y. (2006). Differentiating normal from abnormal personality with the MMPI-2, in Differentiating Normal and Abnormal Personality, S. Strack, ed, Springer, New York, pp. 337–382. Pope, K., Butcher, J. & Seelen, J. (1993). The MMPI, MMPI-2, and MMPI-A in Court, American Psychological Association, Washington, DC. Exner Jr, J.E. (1995). Why use personality tests? A brief historical view, in Clinical Personality Assessment, J.N. Butcher, ed, Oxford University Press, New York, pp. 10–18. Camara, W., Nathan, J. & Puente, A. (2000). Psychological test usage: Implications for professional psychology, Professional Psychology: Research and Practice 31, 141–154. Gallagher, R.W., Somwaru, D.P. & Ben-Porath, Y. (1999). Current usage of psychological tests in state correctional settings, Corrections Compendium 24, 1–3, 20. Archer, R.P., Buffington-Vollum, T.K., Stredny, R.V. & Handel, R.W. (2006). A survey of psychological test use patterns among forensic psychologists, Journal of Personality Assessment 87, 84–94. Lally, S.J. (2003). What tests are acceptable for use in forensic evaluations? A survey of experts, Professional Psychology: Research and Practice 34, 491–498. Brown v. Board of Education, 347 U.S. 483 (1954). Jenkins v. United States, 307 F.2d 637 (1962). Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993). General Electric v. Joiner, 522 U.S. 136 (1997). Kumho Tire Co. Ltd. v. Carmichael, 526 U.S. 137 (1999). Archer, R.P., Stredny, R.V. & Zoby, M. (2006). Introduction, in Forensic Uses of Clinical Assessment Instruments, R.P. Archer, ed, Lawrence Erlbaum, Mahwah, pp. 1–18. Skeem, J., Golding, S., Cohn, N. & Berge, G. (1998). Logic and reliability of evaluations of competence to stand trial, Law and Human Behavior 22, 529–547. Stafford, K. (2003). Assessment of competence to stand trial, in Handbook of Psychology: Vol. 11, Forensic Psychology, I. Weiner, (Series Editor) A. Goldstein, (Volume Editor), John Wiley, Hoboken, pp. 359–380. Melton, G.B., Petrila, J., Poythress, N.G. & Slobogin, C. (2007). Psychological Evaluations for the Courts: A Handbook for Mental Health Professionals and Lawyers, 3rd Edition, Guilford, New York. Heilbrun, K. (2001). Principles of Forensic Mental Health Assessment, Kluwer Academic, New York. Nicholson, R.A. (1999). Forensic assessment, in Psychology and Law: The State of the Discipline, R. Roesch, S.D. Hart & J.R.P. Ogloff, eds, Kluwer Academic, New York, pp. 121–173.
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Ogloff, J.R.P. & Finkelman, D. (1999). Psychology and law: an overview, in Psychology and Law: The State of the Discipline, R. Roesch, S.D. Hart & J.R.P. Ogloff, eds, Kluwer Academic, New York, pp. 1–20. Grisso, T. (2003). Evaluating Competencies: Forensic Assessments and Instruments, 2nd Edition, Kluwer Academic, New York. Morey, L.C. & Hopwood, C.J. (2006). The Personality Assessment Inventory and the measurement of normal and abnormal personality constructs, in Differentiating Normal and Abnormal Personality, S. Strack, ed, Springer, New York, pp. 451–471. Exner Jr, J.E. (2003). The Rorschach: A Comprehensive System, 4th Edition, John Wiley, Hoboken. Ganellen, R.J. (2006). Rorschach assessment of Normal and Abnormal Personality, in Differentiating normal and abnormal personality, S. Strack, ed, Springer, New York, pp. 473–500. Butcher, J.N. (ed) (1995). Clinical Personality Assessment, Oxford University Press, New York. Butcher, J.N. & Miller, K.B. (2006). Personality assessment in personal injury litigation, in The Handbook of Forensic Psychology, 3rd Edition, A.K. Hess & I.B. Weiner, eds, John Wiley, New York, pp. 140–166. Goldstein, A. (ed) (2007). Forensic Psychology: Emerging Topics and Expanding Roles, John Wiley, Hoboken. Meyer, R.G. & Deitsch, S.E. (1996). The Clinician’s Handbook: Integrated Diagnostics, Assessment, and Intervention in Adult and Adolescent Psychopathology, 4th Edition, Allyn and Bacon, Boston. Maruish, M.E. (ed) (2004). The Use of Psychological Testing for Treatment Planning and Outcomes Assessment, 3rd Edition, Lawrence Erlbaum, Mahwah. Strack, S. (ed) (2006). Differentiating Normal and Abnormal Personality, Springer, New York. Archer, R.P. (ed) (2006). Forensic Uses of Clinical Assessment Instruments, Lawrence Erlbaum, Mahwah.
PAUL ANDREWS
Psychological Trauma see Posttraumatic Stress Disorder
Psychopathology see Compulsion, Firesetting
Psychopathology: Terms and Trends Introductoin Society cannot exist without norms, and yet the definition of what is normal proves to be a thorny task for both social science and the field of mental health. In particular, at the interface of behavioral sciences and the law, forensic assessment requires clarity regarding threshold issues in the determination of the presence or absence of pathology and psychical suffering. Whether societal norms are identical to norms of psychical functioning or whether these two norms diverge from one another in specific and definable ways, the line between mental health and mental illness always necessarily implies an appreciation of the individual’s ability to function effectively within his environment. This environment, however, is not a biological one but rather is societal. An individual’s ability to function in the social environment is mediated through his subjective interpretation of its laws and imposed constraints, that is, his perception of and ability to integrate norms. A forensic evaluator’s role is precisely to introduce and assess this subjective point of view within the parameters of legal proceedings; parameters are designed to apply to all cases equally while providing for individual differences.
Norms and Normality Psychopathology refers to the description, explanation, and logical formulation of the individual’s mental state and mental processes, with the aim of characterizing abnormalities or guiding interventions in the context of treatment. Psychoanalysis has traditionally played an important role in psychopathology, along with cognitive science, neurobiology, and epidemiology (the study of diseases within populations). The overarching aim of psychopathology is the task of demarcating mental health and mental illness, two concepts whose meanings are inextricably bound up with one another, in reference to a norm. In an article in the September 1967 issue of Archives of General Psychiatry, Sabshin outlines four perspectives on normality: (i) normality as health
Psychopathology: Terms and Trends or adequate functioning; (ii) normality as utopia or optimal functioning; (iii) normality as average or statistically common behavior; and (iv) normality as process or constant redefinition of the human condition relative to advances in civilization [1]. Canguilhem offers an additional viewpoint, defining normality as the individual’s capacity to adjust his relationship to the environment toward the restitution of a norm, when confronted with “error” or deviation due to an anomaly or defect [2]. As cited by Sabshin, Freud’s work, Civilization and its Discontents [3], describes civilization’s impact on human nature as an intrinsic potential source of pathology. The imposition of culture upon the biological organism necessarily induces discomfort, though not always illness. To the extent that society’s norms are evolving and imperfect, absolute conformity to such norms would entirely efface the individual’s initiative. Normality, thus involves the negotiation of desires within social parameters and the law.
Values, Theory, and the Problem of Stigma In the previously cited issue of Archives of General Psychiatry, medical sociologist Strauss argued that deviant behavior becomes pathological through “visibility,” through public attention [4]. Deviant behavior is assigned significance through societal attribution of harm or potential harm – a judgment of value. The process of distinguishing between deviant behaviors that are due to mental health problems and behaviors that are not due to mental pathology has been subject to complex debate. Wakefield [5, 6] is a key contemporary author in this debate, who introduced the concept of harmful dysfunction as a criterion for disorder. Although a detailed summary of the debate is beyond the scope of this article, the concept of harmful dysfunction has gained credence and acceptance and requires elaboration. Among other topics, Wakefield has addressed the advantages of an approach to diagnosis that emphasizes the development of a common vocabulary for improved communication between clinicians and for research purposes, and which thereby allows for the clarification of causation of symptoms using multiple explanatory theories. Wakefield developed the concept of harmful dysfunction in response to a lack of clarity regarding
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the definition of a “disorder.” Although clinicians utilize the concept of disorder and are able to reach a consensus about what is and is not a disorder, the formulation of an operational definition of disorder remains problematic. The concept of harmful dysfunction involves two separate elements, both of which must be present in order for there to be a mental disorder. First, there must be harm of some kind to the individual or others. This is a value judgment, in reference to societal norms. However, harm alone would not define a mental disorder, since many forms of harmful behavior are simply social evaluative judgments. The second element dysfunction implies a cause that is in some way internal to the functioning of the individual – in other words, a disturbance of an evolutionary capacity from which the resulting harmful behavior flows. If there is dysfunction but no harm, then there is no disorder. Similarly, if there is harm but no dysfunction, there is no mental disorder. Klein agrees with Wakefield and adds the “involuntary” nature of the dysfunction [7]. In a disorder, harm arises from a process that occurs without the individual choosing it. Spitzer remarks that the current diagnostic criteria may be overly inclusive of nonpathological syndromes, and that the testing of diagnostic criteria according to the harmful dysfunction analysis would result in more precise definitions of disorders. With regards to adjustment disorder (symptoms which arise in the context of life stressors) he writes, “the degree of distress . . . is a poor marker for discriminating disorder from nondisorder. What would be more helpful would be the issue of whether the individual’s response to the stressor helped or hindered the individual in dealing with the stressor. . . . If the reaction, even if associated with marked distress, facilitated dealing appropriately with the stressor, then a judgment of nondisorder would be appropriate.” [8]. Separation of harm from dysfunction as components of mental disorder allows for clarification of the nature of psychopathology, as defined by norms that are not entirely determined by judgments of social value. The definition of disorder as a combination of harmful manifestations and underlying dysfunction may reduce the tendency toward stigmatization of the mentally disordered person, since disorder is, thus, attributed neither to social norms nor to causes that are beyond the individual’s control [9].
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Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision (DSM-IV-TR) In the United States, there is consensus by mental health forensic experts on the use of the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM) for attribution of diagnoses in legal proceedings, despite the fact that the DSM explicitly indicates that it is not designed for this purpose [10]. The first edition was issued in 1952, and involved narrative, descriptive paragraphs according to categories from the psychoanalytic orientation of psychopathology at that time. The second edition, with some revisions, was issued in 1968 and continued the previous edition’s characterization of disorders through narrative paragraphs. A major conceptual shift occurred in 1980 with the release of the third edition, shaped in parallel with the research diagnostic criteria (RDC), which identified disorders according to specific criteria, which were required in order to assign the diagnosis. This was a significant step in the international standardization of diagnosis for the purposes of biomedical research, and the DSM was also applied in clinical and public mental health settings [11]. The strict set of criteria present for establishing a diagnosis were designed to focus on the phenomenology, or symptom description, rather than the underlying theory or causal explanation of the symptoms. The same conceptual basis was retained in subsequent revisions, the DSM-III-R (R for revised), the DSM-IV and the DSM-IV-TR (TR for text revision, indicating that the accompanying text was updated without changing the criteria). However, the two editions of the DSM-IV emphasized empirical evidence, including field trials of the diagnostic criteria and classification, as well as data from published research [12]. A dramatically different system of classification, with a new conceptual basis, is likely in the forthcoming fifth edition of the DSM (see below). The DSM-IV-TR divides mental disorders into broad categories and defines within each grouping a set of specific disorders with symptom lists and other criteria that must be met in order to assign the diagnosis. While some diagnoses are excluded or superseded by the presence of symptoms meeting criteria for another disorder, other diagnoses allow for the presence of multiple other disorders, sometimes with overlapping symptoms. Although the definitions
require clinical judgment in assigning diagnosis, the method of arriving at a diagnosis specifies that if the clinical manifestations do not meet all of the necessary criteria for a given diagnosis, the diagnosis cannot be assigned. For this reason, many clinically significant syndromes do not fit into specific DSM disorders, and the DSM provides for these through “not otherwise specified” diagnoses within each large category. The “not otherwise specified” diagnoses generally focus on a predominant symptom, such as anxiety or depressed mood, and indicate that such symptoms are present, without the individual meeting full criteria for a specific disorder. Diagnoses with the suffix “not otherwise specified” should not be taken to be less meaningful than specific diagnoses, since the individual’s level of impairment may be as significant as that of a person who meets the criteria for a specific diagnosis. The reality of clinical practice suggests that disorders arise on a continuum with gradations from subtle to more severe and marked manifestations; the existence of “not otherwise specified” diagnoses reflects the reality that some symptomatic individuals with clinically significant distress or impairment do not fit neatly into the criteria which define research categories, but nevertheless closely resemble them.
The International Classification of Diseases, 10th Edition (ICD-10) The International Classification of Diseases (ICD) includes diagnostic codes and criteria for all medical disorders, including mental health disorders [13]. The ninth version of the ICD was finalized 1 year after the task force for DSM-III was formed, without coordination of the criteria or nomenclature [14]. The preparation for a 10th edition of the ICD began well in advance of the work of the DSM-IV task force, making it impossible for the two systems to become identical [15]. During the subsequent development of the ICD-10 and the DSM-IV, international groups worked to improve the concordance between the two [15]. When both systems of classification are present in legal proceedings (e.g., where expert opinions are expressed in terms of DSM-IV-TR criteria and medical records contain ICD-10 coding), possible differences in specific criteria used to assign diagnoses should be clarified.
Psychopathology: Terms and Trends
Beyond the Clinical Interview Although the clinical interview and the mental status examination (see Mental Status: Examination) form the basis of diagnostic assessment, the examiner often has recourse to additional information, including documents, such as prior hospital records. Some of the criteria required for assigning a DSM diagnosis are difficult to confirm or disaffirm through the evaluee’s self-report of symptoms or past behavior alone.
Parallel History Some disorders are characterized by a lack of awareness of symptoms. Individuals with disorders such as schizophrenia or a personality disorder often manifest symptoms that they themselves are unable to perceive. Their symptoms are more readily perceived by others in their entourage. For this reason, information obtained from sources other than the evaluee (family members, employers, or the individual’s treating physician) may be of value in determining the nature of the psychopathology. In addition, diagnostic criteria for some disorders include the time course of symptoms, and parallel history obtained from family members or others may be useful, for example, in confirming whether or not the symptoms of schizophrenia have been present for six months or longer, or whether elements suggestive of a personality disorder do in fact represent a life-long pattern, present from the time of childhood or adolescence.
Psychometric Validation Although a large number of rating scales and standardized diagnostic instruments are available for the assessment of psychopathology (see Psychological Testing), the use of such techniques is not obligatory in forensic clinical practice for the determination of the presence of a mental disorder. Some examiners routinely administer psychometric tests, whereas others have recourse to them only in cases where there is ambiguity in the examination or where findings in the clinical interview suggest the presence of malingering (see Malingering: Forensic Evaluations). Caution must be exercised in relying too heavily upon the results of standardized testing, because the results are calibrated upon findings within a defined population as statistical probabilities and not as probabilities
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in an individual case. Even reporting of a highly validated and reliable examination such as the Minnesota Multiphasic Personality Inventory-2 (MMPI2) is usually expressed in terms such as “Individuals with this profile tend to . . ., ” suggesting that the result indicates a trend that is relevant to the particular case only after appreciation in the context of findings upon clinical examination. However, the diagnosis of a mental defect (see Mental Retardation) such as mental retardation or dementia (disturbance of memory and either language, motor activity, or complex task completion) (see Neuropsychological Assessment) does require testing beyond the clinical examination. By definition, these mental defects involve deficits in cognitive function that are sometimes subtle and require detailed evaluation with psychometrically validated techniques. In some cases, dementia may be so evident upon clinical examination that confirmation through specialized testing is unnecessary.
Genetics Efforts in the field of neurobiology to determine the genetic basis of mental disease (see Genomics and Behavioral Evidence) have yielded results that are as yet unreliable, though some researchers propose classification of psychopathology on a genetic basis in the future [16–18]. Owing to variability in the expression of genes and environmental factors in disease causation, it appears unlikely that genetic typing will supplant clinical examination as a basis for diagnosis at any time in the near future. Even a disease with strong genetic underpinnings such as schizophrenia is present in both identical twins only approximately 50% of the time [19, 20]. Should genetic evidence in support of a diagnosis become admissible in courts, it will likely have a status similar to that of psychological testing, as data that supplements the clinical impression and not as definitive proof of diagnosis.
Neuroimaging Recent developments in structural and functional magnetic resonance imaging (MRI) have led some jurisdictions to permit testimony from experts in brain imaging (see Deception: Detection of and Brain Imaging) as an aid in the assessment of psychopathology, though the future use of such
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techniques in legal proceedings remains uncertain at the time of writing of this article.
Structural Approaches The concept of structure refers to the underlying organization of internal psychical functioning, at a level beyond what is manifest. Structure is interpreted in different ways by various schools of thought, particularly within psychodynamic psychiatry and psychoanalysis. The notion refers, in general, to latent relationships between different elements of the psyche, viewed as a set [21]. Recent articles utilize the concept of structure to describe the underlying organization of psychopathology, including the integration of temperament, personality, and symptoms [22–24]. Although the various conceptualizations of structure are valuable in clinical practice, they pertain to enduring patterns relating to personality diagnosis and are seldom relevant to specific legal adjudications such as insanity at the time of the criminal act. Structural assessment of a forensic evaluee is challenging under evaluation conditions, since accurate formulation may require serial interviews over a significant period of time. Hypotheses regarding structural diagnosis may lead the forensic examiner to identify traits or historical features that he may then integrate into formulations that are pertinent to criminal mitigation or the assessment of civil damages. In addition, preliminary hypotheses regarding structural diagnosis may lead to further exploration of an individual’s points of vulnerability in the setting of assesment of fitness for duty or of risk for future violence.
Psychodynamic Diagnostic Manual (PDM) In 2006, a task force representing six psychoanalytic organizations published the result of their collaborative effort to develop a system of diagnostic classification to “complement the DSM and ICD efforts of the past 30 years in cataloguing symptoms by explicating the broad range of mental functioning,” and with a wider appreciation of the patient as a “whole person” with a complex and rich life history [25]. Prior to the Psychodynamic Diagnostic Manual (PDM), some authors provided cogent psychoanalytic perspectives on DSM-IV diagnoses, reflecting the perceived need for enhanced formulations of the processes underlying descriptive diagnostic categories
[26, 27]. Although the PDM includes syndromes that are recognizable to readers of the DSM-IV, it also describes other syndromes and classifies them in a manner that allows the clinician to find a basis to link diagnoses that are commonly co-occurring. In other words, in the PDM disorders are not considered as separate categories but as identifiable manifestations of the individual’s underlying internal functioning. The PDM is likely to be useful to treating clinicians, but is unlikely to supplant the DSM as a basis for expert opinion, a use for which it is not explicitly intended. The authors state quite clearly that it is not their intention to displace the DSM as a scientific classification necessary for research studies. Only time will determine whether forensic experts will refer to the PDM in supplementing their case formulations when arriving at an opinion or testifying in court. The PDM represents a consensus statement that supports what careful forensic mental health professionals already do – that is to say, to seek in detail the case-specific factors that are at issue in explaining past behavior and the likely future evolution of an individual within his personal history and in terms of idiosyncratic subjective experience.
Dimensional Approaches: the DSM-V and Beyond Planning for the DSM-V began in 1999 and resulted in the publication in 2002 of A Research Agenda for DSM-V [28]. After a review of the existing literature, DSM-V workgroups were formed in 2007, with an aim to publish DSM-V by as early as 2011 [29]. A major conceptual revision of the DSM is anticipated, in light of numerous observations regarding the DSM-IV, which utilizes a categorical system of classification of disorders, in which the particular disorder is either present or absent. Clinicians have noted that disorders do not easily conform to such a system, since symptoms that partly meet criteria may result in significant impairments that are susceptible to treatment. Researchers have noted that categorical diagnosis may exclude individuals from studies, resulting in a skewed picture of underlying pathological processes [30]. In order to remedy such difficulties, the DSM-V workgroups began to consider the feasibility of a dimensional approach to diagnosis, which would
Psychopathology: Terms and Trends retain the categorical diagnoses currently in use, with modifiers to indicate the milder versions or partial syndromes, which are nonetheless related to the primary diagnosis. This approach is based on the assumption that psychopathology exists on a continuum, although there are characteristics which define a “prototype” of the disorder [31, 32]. Previously, the terms “categorical” and “dimensional” were most widely used in the diagnosis of personality disorders, where a wide range of assessment instruments were developed, alternately defining disorders using strict criteria for determining the presence or absence of a specific entity (“borderline personality disorder” or “antisocial personality disorder”) versus defining disorder according to the predominance of traits that were deemed to be more or less characteristic of the individual’s life pattern. The clarification of relevant dimensions in disorders other than personality disorders is likely to require the development of consensus through empirical study of the types of dimensions most characteristic of the “prototype” for each specific disorder [33, 34]. The DSM-V may also include a reorganization of disorders into spectra, of related disorders. Beyond the identification of relevant dimensions for specific disorders, the spectrum approach seeks to group together disorders that share similar underlying processes [35, 36]. For example, pathological gambling, eating disorders, and substance abuse could be conceptualized as disturbances arising from an underlying process of compulsion (see Compulsion), and these might therefore be more likely to occur together in the same individual. Although the process of DSM revision is lengthy and careful, including field testing of the criteria prior to finalization, commentators observe that the major conceptual change will likely require further refinement after the DSM-V is published [12, 37]. After extensive discussion, the final published criteria for DSM disorders summarize only the essential findings of the committees. For this reason, the DSM-IV Sourcebook [38] – a summary of debates prior to arriving at final criteria – is a useful reference when clarification is needed, and provides further information for assessment of the intended meaning of DSM diagnoses. Hopefully, the DSM-V will also be accompanied by such a companion sourcebook to aid the reader.
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Relevance to Legal Proceedings At first blush, a dimensional approach to the diagnosis of mental disease would appear to be contraindicated in the context of legal proceedings. Case law has defined, for example, what diagnoses are eligible for consideration as a “severe mental disease” leading to criminal nonresponsibility, implying that adjudications require clear thresholds provided by categorical diagnosis. However, closer scrutiny reveals that a dimensional approach is compatible with the process of expert evaluation in cases involving mental disorders, to the extent that forensic opinions do not rely solely upon diagnosis, but rather present the relationship between particular symptoms and specific behavior or distress, along a continuum of severity. A term such as “severe mental disease” is, thus, a legal term of art that can accommodate evolution in the professional standards regarding mental pathology, in accordance with contemporary scientific definitions.
Conclusion Psychopathology is a complex and evolving field of study, with a long historical tradition that merits a closer examination than is possible in this article. Systems of classification of mental disorders have been constructed in accordance with changing needs and new findings in research. Although manuals such as the DSM and the PDM are commercially available for purchase, works such as these should be viewed as guides for use by mental health professionals in light of their education, experience, and intuition based on clinical reasoning and the specifics of each case. Through research and consensus, it has been possible to define categories of psychopathology using standardized criteria that serve as a common language, across theoretical orientations. However, debate continues as to the adequacy of these categories, particularly given the wide variety of clinical manifestations and underlying mental processes involved in the experience of each person, and efforts are under way to revise the existing classifications in light of new findings.
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Canguilhem, G. (1989). A new concept in pathology: error (1963–1966), The Normal and the Pathological, Zone Books, New York. Freud, S. (1930, 1953). Civilization and its Discontents in J. Strachey, ed, The Standard Edition of the Complete Psychological works of Sigmund Freud, Hogarth Press and The Institute of Psycho-Analysis, London, Vol. 21. Strauss, A. (1967). A sociological view of normality, Archives of General Psychiatry 17, 265–270. Wakefield, J.C. (1997). Diagnosing DSM-IV – Part I: DSM-IV and the concept of disorder, Behaviour Research and Therapy 35(7), 633–649. Wakefield, J.C. (1999). The concept of disorder as a foundation for the DSM’s theory-neutral nosology: response to Follette and Houts, part 2, Behaviour Research and Therapy 37, 1001–1027. Klein, D.F. (1999). Harmful dysfunction, disorder, disease, illness, and evolution, Journal of Abnormal Psychology 108(3), 421–429. Spitzer, R.L. (1999). Harmful dysfunction and the DSM definition of mental disorder, Journal of Abnormal Psychology 108(3), 430–432. Dain, N. (1994). Reflections on antipsychiatry and stigma in the history of American Psychiatry, Hospital and Community Psychiatry 45(10), 1010–1014. American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision, APA Press, Washington, DC, pp. 32–33, 37. First, M.B. (2002). The DSM series and experience with DSM-IV, Psychopathology 35, 67–71. Regier, D.A., Narrow, W.E., First, M.B. & Marshall, T. (2002). The APA classification of mental disorders: future perspectives, Psychopathology 35, 166–170. World Health Organization (1990). International Classification of Diseases and Related Health Problems, 10th Revision, Geneva. Widiger, T.A., Frances, A.J., Pincus, H.A., Davis, W.W. & First, M.B. (1991). Toward an empirical classification for the DSM-IV, Journal of Abnormal and Social Psychology 100(3), 280–288. Kendell, R.E. (1991). Relationship between the DSM-IV and the ICD-10, Journal of Abnormal Psychology 100(3), 297–301. Gottesman, I.I. & Gould, T.D. (2003). The endophenotype concept in psychiatry: etymology and strategic intentions, The American Journal of Psychiatry 160, 636–645. Cannon, T.D. & Keller, M.C. (2006). Endophenotypes in the genetic analyses of mental disorders, Annual Review of Clinical Psychology 2, 267–290. Bearden, C.E. & Freimer, N.B. (2006). Endophenotypes for psychiatric disorders: ready for primetime? Trends in Genetics 22, 306–313. Cardno, A.G. & Gottesman, I.I. (2000). Twin studies of schizophrenia: from bow-and-arrow concordances to Star Wars Mx and functional genomics, The American Journal of Medical Genetics 97, 12–17.
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Psychopathy special section, Journal of Abnormal Psychology 114(4), 551–556. [38] Widiger, T.A., Frances, A.J., Pincus, H.A., First, M.B., Ross, R. & Davis, W. (1994). DSM-IV Sourcebook, American Psychiatric Association, Washington, DC, 3 Vols.
SUZANNE YANG
AND
FRANCOIS ¸ SAUVAGNAT
Psychopathy Psychopathy or psychopathic personality disorder is referred to as antisocial personality disorder in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders or DSM-IV [1] and as dissocial personality disorder in the tenth edition of the International Statistical Classification of Diseases and Related Health Problems or ICD-10 [2]. Previously, it was referred to as sociopathy or sociopathic personality disorder.
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Assessment and Diagnosis In the DSM-IV and ICD-10, the diagnostic criteria for psychopathy focus primarily on symptoms from the behavioral organization domain, especially those related to violation of explicit social norms. In many civil psychiatric settings, these diagnostic criteria have adequate reliability (e.g., stability or consistency across evaluators and time) and validity (e.g., prognostic value with respect to poor treatment response, institutional misbehavior, or community violence) [1, 5]. In forensic settings, however, the DSM-IV and ICD-10 criteria are less useful. Their heavy focus on criminality leads to extremely high prevalence rate – typically 50–75% or higher – in correctional offenders and forensic psychiatric patients [1, 5]. For this reason, many forensic mental health professionals prefer more comprehensive diagnostic criteria, such as the Hare Psychopathy Checklist Revised or PCL-R [6] and its progeny, such as the Screening Version or PCL:SV [7] and the Youth Version or PCL:YV [8]. These latter tests yield a lifetime prevalence rates of ∼15 to 25% – about one-third the rate observed using the DSM criteria for antisocial personality disorder [5, 6] – and also have superior reliability and validity (see Psychopathy Checklists).
Clinical Description
Course
According to clinical descriptions over the past 200 years [3, 4], psychopathy is characterized by a broad range of symptoms in several major domains of personality functioning. In the domain of behavioral organization, they include lack of perseverance, unreliability, recklessness, restlessness, disruptiveness, and aggressiveness. The emotionality domain includes lack of anxiety, lack of remorse, lack of emotional depth, and lack of emotional stability. The domain of interpersonal attachment includes detachment, lack of commitment, and lack of empathy or concern for others. The domain interpersonal dominance includes antagonism, arrogance, deceitfulness, manipulativeness, insincerity, and glibness or garrulousness. The cognitive domain includes suspiciousness, inflexibility, intolerance, lack of planfulness, and lack of concentration. Finally, the self domain includes self-centeredness, self-aggrandizement, selfjustification, and a sense of entitlement, uniqueness, and invulnerability.
Symptoms of psychopathy may emerge as early as age 6–10 [9], and it is common for adults with psychopathy to have been diagnosed in childhood or adolescence as suffering from one of the disruptive behavior disorders. Indeed, the DSM-IV diagnostic criteria for antisocial personality disorder require that the person met the criteria for a conduct disorder before age 15 [1]. Unfortunately, the majority of children or adolescents so diagnosed – 50 to 75% or more – spontaneously desist antisocial behavior and do not go on to develop psychopathy as adults [9, 10]. Consequently, it is recommended not to diagnose psychopathy before the beginning of early adulthood, at least 18 years old or possibly even 25 years old [1, 2]. The course of the disorder during adulthood is characterized by relative stability. For example, there is evidence of moderate diagnostic stability across periods of several months to several years [6], persistence of symptoms across adulthood [11, 12], and long-term risk for negative health outcomes
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such as morbidity and mortality [13]. But there is also evidence that symptom severity may fluctuate substantially over time [14].
Prevalence Epidemiological research in the United States indicates that the lifetime prevalence of psychopathy in the general population, according to DSM-IV or similar criteria, is ∼1.5 to 3.5% [15, 16]; in correctional offenders, the rate is 50–75% [6]. When more comprehensive diagnostic criteria are used, the prevalence rate is considerably lower. For example, research using the PCL-R with correctional offenders and forensic psychiatric patients in the United States has reported lifetime prevalence rates of ∼15 to 25% – about one-third the rate observed using the DSM criteria [6].
Gender, Age, and Sociocultural Factors Lifetime prevalence rates of psychopathy vary across three major group factors: gender, age, and culture. First, with respect to gender, the male : female sex ratio in diagnosis is typically about 3 : 1 [15, 16]. This gender difference is not limited to a few clinical features, but is evident across the full range of symptomatology. Second, with respect to age, some epidemiological research in the United States using DSM-III and DSM-III-R criteria has reported a cohort effect, with higher lifetime prevalence rates in younger generations than in older generations [17]. Third, with respect to culture, anthropological and epidemiological research indicates that psychopathy is found across cultures [18], but there is evidence of cross-cultural differences in prevalence. For example, according to general population studies, the lifetime prevalence of psychopathy in Taiwan is much lower than that reported in the United States [19], and according to studies of correctional offenders and forensic psychiatric patients, the prevalence of psychopathy is higher in the United States than in Europe [20.] These group differences may be due to cultural facilitation [20, 21]. In highly individualistic cultures such as the United States, norms and values that emphasize the importance of distinctiveness, status, self-confidence, honor, competition, and freedom from obligations to others may also foster the
development of extreme manifestations of the same characteristics – for example, conceit, manipulativeness, irresponsibility, pathological dominance, and aggressiveness. Similarly, within a dominant culture, the expression of symptoms of psychopathy may be facilitated in certain subgroups, such as males or younger generations, that subscribe to more individualistic norms and values. The group differences may also be due to inadequacies in diagnostic criteria. The current diagnostic criteria for psychopathy may be biased to reflect its prototypical manifestation in young males from individualistic cultures; if this is true, any differences due to gender, age, and culture may be smaller than suggested by research to date [20].
Comorbidity Psychopathy has a high rate of comorbidity with substance use disorders [15, 22, 23]. This comorbidity may reflect a common etiological mechanism, or it may be that in some cases substance use disorders are a consequence or complication of psychopathy. Psychopathy also has a high rate of comorbidity with other personality disorders, specifically, borderline, the Cluster B narcissistic, and histrionic personality disorders in DSM-IV or emotionally unstable and histrionic personality disorders in ICD-10 [24, 25]. The high rate of comorbidity among them almost certainly reflects inadequacies in their diagnostic criteria (i.e., a failure to “carve nature at its joints”), as well as common etiological factors. Low rates of comorbidity are observed between psychopathy and certain other personality disorders, specifically the Cluster C avoidant, dependent, and obsessive–compulsive personality disorders or anxious/avoidant, dependent, and anankastic personality disorder in ICD-10 [24, 25]. The low rates of comorbidity among the disorders suggest they have independent or even competing etiologies. The rates of comorbidity between psychopathy and most other disorders are inconsistent, unclear, or unremarkable [15, 24, 25].
Etiology The etiology of psychopathy is unknown. Theoretical models of etiology can be divided into two main categories based on whether they view psychopathy
Psychopathy as a true disorder, that is, a bona fide form of mental abnormality. Theoretical models of psychopathy as mental abnormality have focused on the potential causal influence of social and biological factors. Overall, the research literature supports the relative importance of biological over social factors. With respect to social factors, there are no child-rearing experiences, familial dysfunctions, or adverse life experiences that are found both frequently and specifically in people with psychopathy compared with people with other personality disorders. As noted previously, however, sociocultural factors certainly appear to play a role in the expression of the disorder [20, 21]. With respect to biological factors, researchers have reported elevated rates of prenatal trauma, neurotransmitter abnormalities, and structural abnormalities of the brain associated with symptoms of psychopathy [26–28], but none of these factors is clearly pathognomonic. Also, some adoption research has reported that the heritability of psychopathy is substantial [11, 29], but molecular genetic research has not identified genetic markers. A common theme underlying many etiological theories that focus on biological factors is that psychopathy is associated with impaired ability to experience emotions and integrate them in executive functions; this core emotional deficit results in a failure of attachment to others, inattention to cues of impending punishment, and insensitivity to reward or punishment. Other theoretical models reject the notion that psychopathy is a mental abnormality at all. First, some interpersonal and behavioral genetic theories view psychopathy as an extreme variant of the same personality traits found in all people [30, 31]. According to these theories, psychopathy is not associated with any unique or specific causal influences and any differences between people with versus without the disorder are quantitative rather than qualitative in nature – that is, the differences are a matter of degree rather than of kind. Second, some sociobiological and evolutionary theories view psychopathy as an adaptation [32]. According to these theories, the human species has the genetic capacity to express traits associated with psychopathy. In sociobiological theories, the genetic capacity exists in only a minority of humans and its manifestation is only partially dependent on environmental circumstances; in evolutionary theories, the genetic capacity exists in all humans, but is manifested in only a minority of
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humans who are exposed to specific environmental circumstances. In both the theories, people with psychopathy have an evolutionary advantage in terms of an increased likelihood of producing offspring.
Treatment There is no methodologically sound research on the treatment of psychopathy, and so there no good evidence that it can be successfully treated [33]. Notwithstanding methodological limitations, there is evidence that psychopathy is associated with increased risk for disruptive behavior during treatment, treatment dropout, and posttreatment recidivism [34].
Forensic Relevance Psychopathy does not appear to impair cognitive abilities to the extent that it is relevant in the assessment of psycholegal competencies or capacities. With respect to civil-forensic evaluations, psychopathy generally is not considered by either research or law to be relevant to issues such as competence to consent to treatment, enter into contracts, or testify. With respect to criminal forensic evaluations, it is generally not considered relevant to issues such as competence to confess or stand trial, or to ability to form criminal intent. In contrast, psychopathy does appear to impair volitional abilities to the extent that it is relevant to the assessment of risk for serious crime, and, in particular, for violence. A large body of research indicates that psychopathy is a major risk factor for disruptive behavior while institutionalized and for recidivism upon release to or while under supervision in the community [35, 36]. Explanations include the following [35]: 1. Psychopathy increases the perceived benefits of serious crime. For example, interpersonal symptoms may make demeaning, controlling, and hurting other people rewarding; and behavioral symptoms may make exciting, risk activities rewarding. 2. Psychopathy decreases the perceived costs of serious crime. For example, attachment symptoms, emotional deficit, and self symptoms may
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result in failure to be deterred by anxiety, empathy, remorse, or self-punishment. Psychopathy destabilizes general psychosocial adjustment. For example, all symptoms of psychopathy may increase problems in daily living, decrease social integration or cohesion, or otherwise increase interpersonal conflict.
Given the association between psychopathy and serious crime, as well as the lack of demonstrably effective treatment for psychopathy, it is understandable that psychopathy is potentially relevant in a wide range of psycholegal evaluations involving risk for serious crime. With respect to civil-forensic evaluations, psychopathy is relevant to issues such as parental capacity (i.e., risk for child abuse), employee discipline and dismissal (i.e., risk for workplace violence), and civil commitment as a sexually violent predator (i.e., risk for sexual violence). With respect to criminal forensic evaluations, it is relevant to issues such as pretrial release, sentencing, correctional classification, and community registration, notification, and supervision.
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Forth, A.E., Kosson, D.S. & Hare, R.D. (2003). Hare Psychopathy Checklist Revised: Youth Version (PCL:YV), Multi-Health Systems, Toronto. Goldstein, R.B., Grant, B.F., Ruan, W.J., Smith, S.M. & Saha, T.D. (2006). Antisocial personality disorder with childhood – vs adolescence-onset conduct disorder: results from the national epidemiologic survey on alcohol and related conditions, The Journal of Nervous and Mental Disease 194, 667–675. Simonoff, E., Elander, J., Holmshaw, J., Pickles, A., Murray, R. & Rutter, M. (2004). Predictors of antisocial personality: continuities from childhood to adult life, The British Journal of Psychiatry 184, 118–127. Burt, S.A., McGue, M., Carter, L.A. & Iacono, W.G. (2007). The different origins of stability and change in antisocial personality disorder symptoms, Psychological Medicine 37, 27–38. Hare, R.D., McPherson, L.E. & Forth, A.E. (1988). Male psychopaths and their criminal careers, Journal of Consulting and Clinical Psychology 56, 710–714. Repo-Tiihonen, E., Virkkunen, M. & Tiihonen, J. (2001). Mortality of antisocial male criminals, Journal of Forensic Psychiatry 12, 677–683. Lenzenweger, M.F., Johnson, M.D. & Willett, J.B. (2004). Individual growth curve analysis illuminates stability and change in personality disorder features: the longitudinal study of personality disorders, Archives of General Psychiatry 61, 1015–1024. Compton, W.M., Conway, K.P., Stinson, F.S., Colliver, J.D. & Grant, B.F. (2005). Prevalence, correlates, and comorbidity of DSM-IV antisocial personality syndromes and alcohol and specific drug use disorders in the United States: results from the national epidemiologic survey on alcohol and related conditions, Journal of Clinical Psychiatry 66, 677–685. Narrow, W.E., Rae, D.S., Robins, L.N. & Regier, D.A. (2002). Revised prevalence estimates of mental disorders in the United States using a clinical significance criterion to reconcile 2 surveys’ estimates, Archives of General Psychiatry 59, 115–123. Robins, L.N., Tipp, J. & Przybeck, T. (1991). Antisocial personality, in L.N. Robins & D.A. Reiger, eds, Psychiatric disorders in America: The epidemiological catchment area study, Free Press, New York, USA, pp. 258–290. Cooke, D.J. (1996). Psychopathic personality in different cultures: What do we know? What do we need to find out? Journal of Personality Disorders 10, 23–40. Compton, W.M., Helzer, J.E., Hwu, H.G., Yeh, E.K., McEvoy, L., Tipp, J.E. & Spitznagel, E.L. (1991). New methods in cross-cultural psychiatry: psychiatric illness in Taiwan and the United States, American Journal of Psychiatry 148, 1697–1704. Cooke, D.J., Michie, C., Hart, S.D. & Clark, D.A. (2005). Searching for the pan-cultural core of psychopathic personality disorder: Continental Europe and North America compared, Personality and Individual Differences 39, 283–295.
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Paris, J. (1998). Personality disorders in sociocultural perspective, Journal of Personality Disorders 12, 289–301. Grant, B.F., Stinson, F.S., Dawson, D.A., Chou, P.S., Ruan, W.J. & Pickering, R.P. (2004). Co-occurrence of 12-month alcohol and drug use disorders and personality disorders in the United States: results from the national epidemiologic survey on alcohol and related conditions, Archives of General Psychiatry 61, 361–368. Hemphill, J., Hart, S.D. & Hare, R.D. (1994). Psychopathy and substance use, Journal of Personality Disorders 8, 32–40. Hart, S.D. & Hare, R.D. (1989). Discriminant validity of the psychopathy checklist in a forensic psychiatric population, Psychological Assessment 1, 211–218. Hildebrand, M. & de Ruiter, C. (2004). PCL-R psychopathy and its relation to DSM-IV Axis I and II disorders in a sample of male forensic psychiatric patients in the Netherlands, International Journal of Law and Psychiatry 27, 233–248. Coccaro, E.F. (2001). Biological and treatment correlates, in Handbook of Personality Disorders: Theory, Research and Treatment, W.J. Livesley, ed, Guilford, New York, pp. 124–135. Neugebauer, R., Hoek, H.W. & Susser, E. (1999). Prenatal exposure to wartime famine and development of antisocial personality disorder in early adulthood, Journal of the American Medical Association 282, 455–462. Rainze, A., Lencz, T., Bihrle, S., LaCasse, L. & Colletti, P. (2000). Reduced prefrontal gray matter volume and reduced autonomic activity in antisocial personality disorder, Archives of General Psychiatry 57, 119–127. Cadoret, R., Troughton, E., Bagford, J. & Woodworth, G. (1990). Genetic and environmental factors in adoptee antisocial personality, European Archives of Psychiatry and Neurological Sciences 239, 231–240. Livesley, W.J. (1998). The phenotypic and genotypic structure of psychopathic traits, in Psychopathy: Theory, Research, and Implications for Society, D.J. Cooke, A.E. Forth & R.D. Hare, eds, Kluwer Academic Publisher, Dordrecht, pp. 69–79. Miller, J.D., Lynam, D.R., Widiger, T.A. & Leukefeld, C. (2001). Personality disorders as extreme variants of common personality dimensions: can the five-factor model adequately represent psychopathy? Journal of Personality 69, 253–276. Mealey, L. (1995). The sociobiology of sociopathy: an integrated evolutionary model, The Behavioral and Brain Sciences 18, 523–599. Dolan, B. & Coid, J. (1993). Psychopathic and Antisocial Personality Disorders: Treatment and Research Issues, Gaskell, London. Hemphill, J.F. & Hart, S.D. (2002). Motivating the unmotivated: psychopathy, treatment, and change, in Motivating Offenders to Change, M. Mc Murran, ed, John Wiley & Sons, Chichester, pp. 193–219.
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Hart, S.D. (1998). The role of psychopathy in assessing risk for violence: conceptual and methodological issues, Legal and Criminological Psychology 3, 121–137. Douglas, K.S., Vincent, G.M. & Edens, J.F. (2006). Risk for criminal recidivism: the role of psychopathy, in Handbook of Psychopathy, C.J. Patrick, ed, Guilford, New York, pp. 533–554.
Related Articles Dangerousness: Risk of Psychopathy Checklists Risk Assessment: Patient and Detainee STEPHEN D. HART
Psychopathy Checklists Psychopathy is a specific form of personality disorder (see Psychopathy). The Hare Psychopathy ChecklistRevised (PCL-R) [1, 2] and the Screening Version of the Hare Psychopathy Checklist-Revised (PCL:SV) [3] are standardized psychological tests of lifetime psychopathic symptoms in adults. They have proven to be particularly useful forensic mental health evaluations and are in wide use, both in the original English and in numerous foreign language translations.
History In the mid-1970s, Robert Hare was dissatisfied with the assessment procedures for psychopathy then in use, as they focused primarily on impulsive, irresponsible, and antisocial behavior and had only low-tomoderate correlations with each other [4]. Hare began work on the development of measures that were more comprehensive and reliable. His first attempt, the Psychopathy Checklist (PCL), was distributed informally starting in about 1980 [5] and stimulated considerable interest among researchers and forensic mental health professionals. The manual for the revised PCL, or PCL-R, was published in 1991 [1] and updated in 2004 [2].
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Several derivations of PCL-R were developed by Hare and colleagues. One of these was PCL:SV, which is shorter and easier to administer than PCLR, as well as being appropriate for use in general community and civil psychiatric settings [3]. Development of PCL:SV began in the mid-1980s, concurrent with the revision of the PCL, and a test manual was published in 1995.
Format PCL-R and PCL:SV are multi-item observer rating scales designed to assess the lifetime presence and severity of psychopathic symptoms. Ratings are based on personal interviews and third-party information (e.g., collateral interviews and official records). Each item reflects a different symptom or characteristic of psychopathy, defined in the test manual, and is rated on a 3-point scale (0 = absent, 1 = present to a limited extent, 2 = present and severe). A small number of items can be omitted if insufficient information is available to rate them. Items are summed (and prorated, if necessary) to yield total scores. Total scores can be interpreted dimensionally, relative to norms from various comparison groups, or cut-off scores can be used to make categorical diagnoses. Items can also be summed to yield factor scores, although these are used primarily for research purposes. PCL-R is intended for use with adult correctional offenders and forensic psychiatric patients, male or female. It comprises 20 items, some of which reflect pathological personality traits and others that reflect specific forms of antisocial conduct. Item definitions average about 200 words or so in length. Total scores range from 0 to 40; a cut-off score of 30 and higher is used to diagnose psychopathy. Norms are available for a variety of reference groups. Scores can be calculated for two superordinate factors or four subordinate factors. PCL : SV is intended for use with adults in general community and civil psychiatric settings, in addition to adult correctional offenders and forensic psychiatric patients, male or female. It comprises 12 items, all of which tap relatively broad pathological personality traits. Each item is either a simplified version of a PCL-R item or a combination and simplification of two PCL-R items. Item definitions are shorter than in PCL-R, averaging about 50 words. Total scores
range from 0 to 24, with scores of 18 and higher used to diagnose psychopathy. Norms are available for reference groups of male or female correctional offenders, forensic psychiatric patients, civil psychiatric patients, and community residents. Scores can be calculated for two factors, isomorphic to the superordinate factors of PCL-R. In forensic settings, PCL:SV can be used in conjunction with PCL-R as a screening test for psychopathy; most evaluators, however, tend to use PCL-R if the person being evaluated has a history of serious criminality (e.g., chronic or long-sentence offenders), and PCL:SV when the person does not (e.g., first-time, short-sentence, or less serious offenders; mentally disordered offenders; and forensic psychiatric patients).
Administration PCL-R and PCL:SV are usually administered as part of a comprehensive psychodiagnostic evaluation. It takes about 20–30 min to score and interpret PCL-R, and about 10–15 min to score and interpret PCL:SV in these circumstances. Single-use assessment guides are available for both PCL-R and PCL:SV, which include a semistructured interview and space for recording relevant third-party information. It is possible to administer the tests solely on the basis of third-party information if a person refuses or is otherwise unable to be interviewed, provided the quantity and quality of this information is sufficient. This procedure may, however, result in a score that is substantially lower than would have been obtained if the person had been interviewed. It is not possible to administer PCL-R or PCL:SV without access to third-party information, except for certain research purposes.
Test User Qualifications PCL-R and PCL : SV are controlled psychological tests. Independent use of the tests for clinical purposes is limited to people who are legally entitled to use psychological tests to assess and diagnose mental disorder. Test users also should have advanced education and training in individual assessment and psychological testing that would qualify them to practice as a mental health professional (e.g., graduate or medical degree). PCL-R manual also recommends
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that test users should have at least 2 years experience working in forensic settings. Completion of training workshops and supervised practice in the use of PCL-R and PCL:SV is recommended, but not required. Similarly, the manuals recommend completion of 5–10 practice cases prior to clinical use of the tests.
may be due to the effects of cultural facilitation, with symptoms of psychopathy being expressed more often in highly individualistic societies. There is no evidence, however, of metric bias between ethnic majority versus minority groups within a dominant culture [11]. Only recently have researchers started to investigate metric bias across gender and age.
Psychometric Properties
Association Between PCL-R and PCL:SV
The psychometric properties of PCL-R and PCL:SV have been evaluated extensively within the framework of classical test theory [2, 3, 6]. The most relevant forms of reliability for the tests are structural, inter-rater, and test–retest reliabilities. Structural reliabilities are good to excellent: Item adequacy, as indexed by corrected item-total correlation, is typically 0.40–0.50; item homogeneity, as indexed by mean inter-item correlation, is typically 0.20–0.30; and internal consistency, as indexed by Cronbach’s α, is typically 0.85–0.90. Inter-rater reliabilities also are good to excellent: For items, the intraclass correlation coefficient (ICC1) is typically between 0.60 and 0.80; for total scores, ICC1 is typically 0.80–0.90; and for categorical diagnoses, inter-rater agreement, as indexed by κ, is typically 0.50–0.75. Test–retest reliability of total scores and diagnoses has been examined infrequently, but appears to be good to excellent over periods of 1 week to 1 month and at least fair over periods of 6 months to 2 years. More recently, the tests have been evaluated within the framework of item response theory (IRT) by Cooke, Hare, and colleagues [2, 7, 8]. The interpersonal, affective, and behavioral symptoms have good discriminating power; in contrast, the discriminating power of antisocial behavioral items is weaker. The interpersonal symptoms discriminate the latent trait at high levels (i.e., psychopathy), affective symptoms at moderate levels, and behavioral symptoms, at low levels. IRT is also being used to examine potential metric bias in PCL-R and PCL : SV scores. Some researchers have reported evidence of a small but statistically significant metric bias across dominant cultures, with offenders and patients in the United Kingdom and other European countries scoring lower on PCL-R than those in Canada and the United States, given equivalent standing on the latent trait [9, 10]. This
Cooke and colleagues have evaluated the derivation of PCL:SV using IRT methods [8]. They found a strong association between corresponding PCL-R and PCL:SV items or item pairs. They also found that PCL:SV items had a discriminating power as good as or better than the corresponding PCL-R items or item pairs. Total scores on PCL-R and PCL:SV are also strongly associated. Cooke and colleagues [8] reported a high correlation (r = 0.94) between scores on the latent trait underlying both tests according to IRT analyses, and Guy and Douglas [6] reported similar high correlations (r = 0.94–0.95) between (raw) total scores on the tests in forensic samples. Guy and Douglas [6] also found that PCL:SV had good validity as a screening test for high-PCL-R scores in the same two forensic samples, with large areas under the curve (AUC = 0.98) according to receiver operating characteristic (ROC) analyses.
Factor Structure Initial investigations of the dimensionality of PCL-R and PCL:SV used exploratory factor analysis (EFA) methods. The only consistent finding was the absence of a simple, unidimensional latent variable underlying the tests. Hare and colleagues proposed a structure comprising two orthogonal (i.e., correlated) factors: one reflecting interpersonal and affective symptoms, and the other reflecting behavioral symptoms and antisocial conduct [1]. Cooke and Michie [12] overcame the limitations of EFA by using confirmatory factor analysis (CFA) methods. After omitting PCL-R and PCL:SV items tapping antisocial conduct, they found strong evidence of a hierarchical three-factor structure, comprising a superordinate general factor (psychopathy) underpinned by three correlated subordinate factors (interpersonal, affective, and behavioral symptoms).
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The hierarchical three-factor structure was replicable across diverse samples of offenders and forensic psychiatric patients from different nations. Importantly, it was even found when factor-analyzing diagnostic criteria for psychopathy other than PCL-R and PCL:SV. Subsequent to Cooke and Michie’s article, several researches have found support for the three-factor hierarchical structure. But others, including Hare and his colleagues, have argued that the entire item pools of PCL-R and PCL:SV should be included in factor analyses, which they say results in the addition of a fourth subordinate factor, reflecting antisocial conduct; this view was reflected in the updated PCL-R test manual [3]. Debate continues on whether antisocial conduct should be considered a primary symptom of psychopathy versus a secondary symptom, sequela, or consequence of the disorder [13].
Validity As PCL-R and PCL:SV have been used in virtually hundreds of published studies, only a general review of research is presented here; and as the tests are strongly associated, they are reviewed together. One important line of research has evaluated the concurrent validity of PCL-R and PCL:SV, that is, their association with other procedures for assessing psychopathy. Total scores on the tests have moderate to large correlations with clinical diagnoses made using other criteria, and moderate correlations with self-report measures of psychopathy [2, 3]. Both clinical diagnoses made using other criteria and self-report measures tend to correlate more highly with PCL-R and PCL:SV items reflecting behavioral symptoms and antisocial conduct than with items reflecting the interpersonal and affective features [2, 3]. With respect to predictive validity, total scores on PCL-R and PCL:SV are reliably associated with serious antisocial behavior, including violence, in both institutional and community settings. Summarizing a number of reviews in recent years [14, 15], several general conclusions may be drawn. First, the predictive validity of PCL-R or PCL:SV with respect to serious antisocial behavior is typically moderate in magnitude, r = 0.20–0.30. Second, the predictive validity tends to be larger in community settings than institutional settings. Third, the predictive validity tends to be larger when the outcome reflects
general but serious antisocial conduct (e.g., “any violence”), rather than more specific or less serious antisocial conduct (e.g., “sexual violence” or “any misconduct”). Fourth, the predictive validity of psychopathy, as measured by PCL-R and PCL:SV, typically is higher than that of other established demographic, criminal history, and clinical risk factors (e.g., age, prior antisocial conduct, substance use); indeed, PCL-R and PCL:SV predict antisocial conduct about as well as do multifactor risk assessment procedures constructed theoretically or statistically. Fifth, the predictive validity of PCL-R and PCL:SV is not attributable solely or even primarily to the inclusion of items reflecting past antisocial conduct. With respect to other aspects of construct validity, PCL-R and PCL:SV have been used to study the course, comorbidity, etiology, and treatment of psychopathy [16]. (See also Psychopathy.)
Forensic Applications In the practice of forensic mental health, PCL-R and PCL:SV are used most often as part of comprehensive assessments of risk and treatability for sentencing, civil commitment, institutional classification, and release decision making. This application is supported by research on the prediction of serious antisocial conduct and on treatment response. Indeed, PCL-R and PCL:SV are incorporated explicitly into several procedures for assessing violence risk (see Dangerousness: Risk of and Risk Assessment: Patient and Detainee). Forensic mental health professionals should be aware of some important limitations of PCL-R and PCL:SV [17, 18]. First, as observer ratings scales, the tests may be susceptible to distortion – unconscious or deliberate – by evaluators. To safeguard against this, evaluators should closely follow the administration instructions in the test manuals; training and supervised practice in the use of the tests may also be helpful. Second, although the tests have good psychometric properties in adult male offenders and forensic psychiatric patients in the United States and Canada, the possibility of bias due to culture and gender has not yet been ruled out. Third, the tests reflect the lifetime presence of psychopathic symptoms; this means they cannot be used to measure changes in the presence or severity of symptoms over time, or used to determine whether the person currently suffers
Psychopharmacology from psychopathy. Fourth, although comprehensive, PCL-R and PCL:SV are not exhaustive in content and relatively heavily saturated with items reflecting antisocial conduct. Evaluators should consider using PCL:SV instead of PCL-R in cases where the person being assessed does not have a serious history of criminality. Fifth, although psychopathy is a robust risk factor for antisocial behavior, PCL-R and PCL:SV scores cannot be used – either on their own or in combination with other factors – to estimate the specific probability or absolute likelihood that a given person will commit a criminal or violent act with any reasonable degree of scientific certainty.
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References Hare, R.D. (1991). Manual for the Hare Psychopathy Checklist – Revised, Multi Health Systems, Toronto. [2] Hare, R.D. (2003). Manual for the Hare Psychopathy Checklist – Revised, 2nd Edition, Multi Health Systems, Toronto. [3] Hart, S.D., Cox, D.N. & Hare, R.D. (1995). Manual for the Hare Psychopathy Checklist: Screening Version (PCL:SV), Multi-Health Systems, Toronto. [4] Hare, R.D. (1996). Psychopathy: a clinical construct whose time has come, Criminal Justice and Behavior 23, 25–54. [5] Hare, R.D. (1980). A research scale for the assessment of psychopathy in criminal populations, Personality and Individual Differences 1, 111–119. [6] Guy, L.S. & Douglas, K.S. (2006). Examining the utility of the PCL:SV as a screening measure using competing factor models of psychopathy, Psychological Assessment 18, 225–230. [7] Cooke, D.J. & Michie, C. (1997). An item response theory analysis of the Hare psychopathy checklistrevised, Psychological Assessment 9, 3–14. [8] Cooke, D.J., Michie, C., Hart, S.D. & Hare, R.D. (1999). Evaluating the screening version of the Hare psychopathy checklist-revised (PCL:SV): an item response theory analysis, Psychological Assessment 11, 3–13. [9] Cooke, D.J., Michie, C., Hart, S.D. & Clark, D.A. (2005). Assessing psychopathy in the United Kingdom: Concerns about cross-cultural generalisability, British Journal of Psychiatry 186, 339–345. [10] Cooke, D.J., Michie, C., Hart, S.D. & Clark, D.A. (2005). Searching for the pan-cultural core of psychopathic personality disorder: Continental Europe and North America compared, Personality and Individual Differences 39, 283–295. [11] Cooke, D.J., Kosson, D.S. & Michie, C. (2001). Psychopathy and ethnicity: structural, item and test generalizability of the psychopathy checklist revised (PCL–R) in Caucasian and African-American participants, Psychological Assessment 13, 531–542.
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Cooke, D.J. & Michie, C. (2001). Refining the construct of psychopathy: Towards a hierarchical model, Psychological Assessment 13, 171–188. Cooke, D.J., Michie, C., Hart, S.D. & Clark, D.A. (2004). Reconstructing psychopathy: clarifying the significance of antisocial and socially deviant behavior in the diagnosis of psychopathic personality disorder, Journal of Personality Disorders 18, 337–357. Hart, S.D. (1998). The role of psychopathy in assessing risk for violence: conceptual and methodological issues, Legal and Criminological Psychology 3, 121–137. Douglas, K.S., Vincent, G.M. & Edens, J.F. (2006). Risk for criminal recidivism: the role of psychopathy, in Handbook of Psychopathy, C.J. Patrick, (ed), Guilford, New York, pp. 533–554. Patrick, C.J. (ed) (2006). Handbook of Psychopathy, Guilford, New York. Hare, R.D. (1998). The Hare PCL-R: some issues concerning its use and misuse, Legal and Criminological Psychology 3, 99–119. Hemphill, J.F. & Hart, S.D. (2003). Forensic and clinical issues in the assessment of psychopathy, in Comprehensive Handbook of Psychology: Vol. 11. Forensic Psychology, I. Weiner (series editor) & A.M. Goldstein (volume editor), eds, John Wiley & Sons, New York, pp. 87–107.
Further Reading Patrick, C.J. (ed) (2006). Handbook of Psychopathy, Guilford, New York.
Related Articles Dangerousness: Risk of Psychopathy Risk Assessment: Patient and Detainee STEPHEN D. HART
Psychopharmacology Psychopharmacology is the study of the effects of drugs on psychological function. It is a branch of pharmacology, which focuses on the nervous system. Clinical psychopharmacology is the portion of psychiatric practice, which pertains to the use of medication as a tool to treat mental disorders [1, 2].
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Clinical psychopharmacology involves an assessment process, development of a treatment plan, and subsequent assessment of the effects of treatment [3]. Psychopharmacologic testimony is often relevant in both civil and criminal cases. Establishing standard of care, and causation of damages in cases alleging negligent prescription, evaluating complex disability claims, and testamentary competency are some areas for psychopharmacological consultation. Cases of suspected poisoning or suicide may also warrant psychopharmacological consultation. Since many crimes are committed under the influence of substances (see Substance Abuse), the effect of those substances on the defendant’s mental state may be relevant (see Insanity: Defense; Temporary Insanity; Mitigation Testimony). Even though voluntary intoxication may not negate a mental state in many jurisdictions, the distinction between intoxication, mental illness, and “settled insanity” [4] requires psychiatric evaluation. Defendants who are incompetent as a result of mental disorder (see Capacity to Stand Trial) may often be restored to competence through treatment. If the defendant refuses treatment, psychopharmacological evaluation is necessary to inform the court that medication is substantially likely to render the defendant competent to stand trial and substantially unlikely to have side effects that will interfere significantly with the defendant’s ability to assist counsel in conducting a defense [5]. Basic principles of psychopharmacology are outlined in this article, along with an overview of psychotherapeutic agents, and some clinical and medical legal issues related to them. Substance abuse and dependence are reviewed in Substance Abuse; Addictions. The study of pharmacology includes an understanding of pharmacokinetics, pharmacodynamics, and drug mechanisms. Pharmacokinetics describes what happens to a drug when it enters the body. How a drug is absorbed, metabolized, activated or inactivated, and excreted, influences how much of a drug is available at the site of action. Pharmacodynamics explains the effect of drugs on the sites of action [6]. Drug effects may vary as a result of the route of administration. For example, intravenous benzodiazepines can reliably cause short-term amnesia, which is useful to anesthesiologists. The same dose of drug ingested orally will usually not have the same effect.
Once a drug is absorbed, it enters the bloodstream to be carried through the body. Most psychoactive drugs are lipid (fat) soluble. They do not dissolve well in water. Thus, they are carried through the bloodstream bound to protein. Many drugs are metabolized through interactions with enzymes in the liver (many are metabolized throughout the body). When a drug is metabolized, it is altered, often to an inactive or water soluble form. Sometimes the metabolites are themselves active drugs. If the drug is ingested by mouth, after it is absorbed in the intestines, it goes through the portal system to the liver for first pass metabolism, and then to the general circulation, where it can effect other organs. Drugs that are inactivated to an efficient degree by the liver are not effective when administered orally. First pass inactivation can be bypassed through alternative routes of administration: intravenous, sublingual, or intranasal. Drugs and their metabolites are excreted through urine, feces, and perspiration. The time required for the plasma concentration of a drug to fall by one half is the half-life of the drug (t1/2 ). When the amount of drug administered in a given time equals the amount eliminated, the drug has reached steady state. In order for a drug to act on the brain, it must cross the blood–brain barrier. Factors that affect a drug’s ability to enter the brain include size and charge of the drug molecule, and its lipid solubility. For example, L-Dopa will cross the blood–brain barrier, while Dopamine (DA) will not. A drug may have a nonspecific effect on the nervous system when it affects energy metabolism, or membrane stability. Specific drug effects arise from interaction with identifiable molecular mechanisms unique to target cells, which bear receptors for that drug. Sometimes a drug with specific effects at a low dose has general effects at a higher dose. Alcohol and general anesthetics are general depressants of the central nervous system, while drugs such as caffeine can be general stimulants [6]. Psychoactive drugs generally affect psychological function through interaction with the normal function of the nervous system [1, 6–8]. The brain contains billions of neurons supported by glia. Glia are considered supporting tissue for the nerve cells. Some form myelin, which facilitates axon function. Others are involved in metabolic activity, and the formation of the blood-brain barrier. Ongoing research suggests
Psychopharmacology that glia may, in fact, serve a more active role in brain function than previously believed [3]. The cell body contains the nucleus of the neuron. It is the center of metabolic activity. Dendrites extend and branch from it, and connect to the terminal processes of other neurons to form synapses. The axon is a single, often long, process, which arises out of the cell body to connect to other neurons. The concentration of ions, like potassium, sodium, chloride, and calcium within the cell is not equal to the concentration outside the cell. As a result, the cell membrane carries a charge across it, like a microscopic battery. When a nerve fires, the membrane allows ions to cross, depolarizing it briefly. The depolarization travels down the length of the axon (an action potential). At the terminal process, packets of chemicals – neurotransmitters – are released across the membrane into the synapse, where the terminal process connects to the dendrite of another neuron. The surface of the dendrite contains special proteins called a postsynaptic receptor. The axon may contain presynaptic receptors as well. Each receptor is specialized to react to a specific neurotransmitter. The effect may be to excite the neuron or to make excitation more difficult – to inhibit it (depending on the neurotransmitter and receptor). When the sum of excitatory minus inhibitory stimulation exceeds a threshold, the nerve will fire. The system is regulated through feedback mechanisms mediated by (presynaptic) autoreceptors and secondary messengers. When stimulated, autoreceptors on the presynaptic neuron signal the cell to stop release of neurotransmitter. Secondary messengers within the postsynaptic neuron modulate metabolic processes in the cell, including protein production. This controls neural plasticity, including long-term potentiation, long-term depression, down regulation and up regulation of receptors. Neurotransmitter molecules are removed from the synapse by the presynaptic neuron (which released them) through a reuptake process. Once removed, the neurotransmitter does not interact with the receptor, until it is released again. Some neurotransmitter is inactivated through enzyme-assisted metabolic degradation. The synapse is the site of action of most psychoactive drugs. Neurons are organized in circuits, with specialized function. The systems that are most interesting to the
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psychiatrist are the limbic system, the basal ganglia, and the thalamocortical system. The limbic system is involved with the experience and expression of emotion. Basal ganglia are involved in both motor and cognitive function. The thalamocortical system is involved in sensation, movement, and cognition. Drugs of abuse affect DA circuits in the nucleus acumbens, an area of the brain involved in learning and motivation. The reinforcing effect of such stimulation is difficult to overcome, as reflected in the rates of lapses and relapses in recovering addicts (see Addictions). A non-comprehensive list of neurotransmitters follows: • • • • • • • • • •
Dopamine (DA); serotonin (5-HT); acetylcholine (ACh); norepinephrine (NE); gamma aminobutyric acid (GABA); glutamate (Glu); endorphins; enkephalins; histamine; and aspartate.
Therapeutic Classes of Drugs Drugs are often classified in terms that identify the target syndrome or symptoms for which the particular drug was first marketed. Thus, we have antipsychotic drugs, antidepressants, sedative hypnotics, stimulants, mood stabilizers, and cognitive enhancers. Over the course of time, however, drugs are often used effectively for purposes other than those for which they were initially marketed. Some antipsychotic drugs can be used for anxiety, depression, and mood stabilization. Some antidepressants are used for first line treatment of anxiety disorders. Other classification schemes based upon chemical structure or target chemical systems are sometimes employed by practitioners. Thus, various drugs may be described as benzodiazepine, or tricyclic, or selective serotonin reuptake inhibitor (SSRI).
Antipsychotic Medication The practice of psychiatry was revolutionized in the 1950s with the introduction of chlorpromazine, the
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first effective antipsychotic drug. Its use reduced the need for restraints, seclusion, and locked psychiatric facilities [6]. As the only effective treatment for psychosis at the time, it was accepted rapidly, despite its side effects. The success of chlorpromazine stimulated the development of other phenothiazine drugs: thioridazine, fluphenazine, perphenazine, and trifluoperazine. In attempts to increase potency while reducing side effects, the pharmaceutical industry developed butyrophenones (haloperidol), thioxanthenes (thiothixene), dihydroindolones (molindone), and dibenzoxazepines (loxapine). By the 1980s, clozapine was recognized as an effective treatment for psychotic illness, which had not responded to other medications. Its significant toxicity (agranulocytosis) necessitated weekly blood counts, and precluded its use as a first line treatment in the United States. However, its atypical neurochemical profile, its lack of movement side effects, and its affect on negative symptoms of schizophrenia, suggested significant advantages over older line medications. Olanzapine, risperidone, quetiapine, ziprasidone, and aripiprazole were developed in attempts to provide clozapine’s therapeutic advantages without potentiating agranulocytosis. These second-generation antipsychotics, also known as atypical antipsychotics are now used more frequently than neuroleptics for treatment of chronic psychosis, as their side effects are generally milder and more easily tolerated by patients. Antipsychotic medication is indicated for treatment of schizophrenia, schizoaffective disorder, schizophreniform disorder, or psychotic symptomatology caused by medical disorders. Symptoms of schizophrenia can be divided into positive and negative symptoms. Atypical antipsychotics are more effective than first-generation drugs for negative symptoms, which include flat or blunted affect, inactivity, diminished pleasure in activities, and poverty of thought. First-generation drugs primarily affect positive symptoms, including delusions, hallucinations, confusion, and anxiety [9–12]. Blockade of some DA receptors (D2 ) is associated with both the antipsychotic effect and movement side effects of these drugs. (In fact, the first psychiatrists to use chlorpromazine did not expect to see antipsychotic effects without an extrapyramidal syndrome.) The blockade of some serotonin receptors (5-HT2 ) is associated with relief of negative
symptoms, as well as mitigation of movement side effects [1, 6, 7]. Side effects of antipsychotic medication include sedation, orthostatic hypotension, dry mouth, constipation, blurry vision, urinary hesitancy, extrapyramidal effects, weight gain, and metabolic effects. First-generation antipsychotics were differentiated from each other on the basis of their side effect profiles, rather than their efficacy. These side effects, related to the drugs’ effects on cholinergic, adrenergic, and histamine receptors [1] were understood in relation to differences in the structures of the side chains of these molecules. Anticholinergic effects include dry mouth, constipation, blurry vision, confusion, and urinary hesitancy. Adrenergic blockade may cause changes in blood pressure, and cardiac rhythm, as well as symptoms of dizziness. Histamine blockade is associated with sedation, drowsiness, and weight gain. Extrapyramidal side effects are caused by DA blockade. DA and ACh are neurotransmitters of the extrapyramidal motor system, involved in posture and coordinated movement. Excessive blockade of DA receptors in this system may lead to an imbalance, and one of four extrapyramidal syndromes: Akathisia, dystonia, Parkinson’s syndrome, or tardive dyskinesia. Akathisia is an uncontrolled sense of inner restlessness, which must be distinguished from anxiety. If it is mistaken for anxiety, and treated with increased dose of medication, it will be worsened. Dystonia is spasm of the muscles, usually of the head and neck. Parkinson’s syndrome includes muscular rigidity, tremor, slowed motor responses, and diminished facial expression. Tardive dyskinesia is an often irreversible effect of antipsychotic medication characterized by involuntary movements of the mouth and tongue, as well as of the trunk and extremities. Akathisia, dystonia, and Parkinson’s syndrome may be treated as they emerge through the use of anticholinergic agents, minor tranquilizers, or adjustment in dose of antipsychotic medication. While various drugs have been used to diminish symptoms of tardive dyskinesia, there is no cure. Discontinuation of the antipsychotic medication will
Psychopharmacology lead to initial worsening of dyskinesia. Over time, symptoms often will remit. Atypical antipsychotic drugs are less frequently associated with tardive dyskinesia, or other extrapyramidal side effects, than older first-generation antipsychotics. Significant weight gain is a common problem with antipsychotic drugs, and appears to be associated with an increased risk of diabetes. Aripiprazole and ziprasidone are less likely than other agents to be implicated in weight gain. Neuroleptic malignant syndrome is a rare complication of antipsychotic drug use. It is characterized by severe muscular rigidity, fever, increased blood pressure, increased heart and respiratory rate, and changing levels of consciousness. Laboratory testing show elevations in creatine phosphokinase (CPK), sometimes along with altered liver functions, and myoglobin (a muscle protein) in the blood or urine. Immediate treatment with supportive symptomatic measures and discontinuation of antipsychotic medication is necessary when this diagnosis is made. Treatment with DA agonists as well as benzodiazepines should be considered with high fevers.
Antidepressants Iproniazid was an antituberculous agent developed after World War II. After its mood-elevating qualities were noticed, it was investigated, and then marketed as an antidepressant in the late 1950s. The therapeutic action was a result of inhibition of monoamine oxidase (MAO) enzymes, which break down serotonin and NE. Iproniazid was withdrawn because of toxic effects on the liver. Other MAO Inhibitors were developed, but their use was limited because of the need for dietary restrictions to avoid potentially fatal hypertensive reactions. Recently a transdermal form of selegiline was developed, allowing fewer dietary restrictions. Around the same time that iproniazid was developed, phenothiazine-like drugs were being tested for antipsychotic effects, with the hope that new drugs could be found without the side effects of chlorpromazine. One, imipramine, was relatively ineffective in calming psychotic patients. However, it did have a therapeutic effect on depressed patients, especially those characterized by regression and inactivity. It was marketed as the first tricyclic antidepressant.
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Over the following years, several other tricyclic antidepressants were developed: desipramine, amitriptyline, nortriptyline, clomipramine, trimipramine, doxepin, protriptyline, amoxapine, and maprotiline (a tetracyclic). All block the reuptake of NE into nerve terminals. Imipramine, amitriptyline, doxepin, nortriptyline, and especially clomipramine, also block reuptake of serotonin (5-HT). These drugs are all pharmacologically “dirty”. In addition to their desired effects, they bind to a host of other receptors, with resultant unwanted side effects, including faintness, cardiac arrhythmias, constipation, dry mouth, sedation, and weight gain. SSRIs or SRIs represent an important pharmacological advance in the treatment of depression, as pharmacologically cleaner drugs, their safety, and tolerability have led to their becoming the predominant class of prescribed antidepressants. Venlafaxine and duloxetine, serotonin and norepinephrine reuptake inhibitors (SNRIs) may be more useful than SSRIs in treating chronic pain. Bupropion effects DA and NE reuptake. Trazodone and nefazodone block a portion of the serotonin receptors. Mirtazapine blocks some alphaadrenergic and serotonergic receptors. These drugs are less likely to cause sexual side effects than other antidepressants. All antidepressants are indicated for treatment of major depression, including vegetative symptoms of appetite and sleep disturbance, fatigue, diminished sex drive, anhedonia (loss of the ability to experience pleasure), agitation, restlessness, or psychomotor retardation. In addition, many are effective for generalized anxiety disorder, panic disorder, posttraumatic stress disorder, insomnia, and enuresis. Tricyclic antidepressants and SNRIs are effective in chronic pain conditions. SSRIs and clomipramine are effective in obsessive compulsive disorder [13–15]. Bupropion can reduce craving for cigarettes, probably as a result of its dopaminergic effect on the nucleus accumbens. The mechanism of action of antidepressants is not fully understood. While antidepressant drugs exert immediate effects on brain receptors, the therapeutic effect is delayed, usually 2–6 weeks. This suggests that the therapeutic effects arise from a cascade of adaptive processes to repeated administration of the drug. Increased availability of serotonin and/or NE
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in the synapse evokes negative feedback mechanisms to restore homeostasis. This includes downregulation and desensitization of receptors, and alterations in tonic inhibition and stimulation mediated through secondary messengers in the neuron, which signal formation of new protein. Newer antidepressants present fewer, less toxic side effects than older tricyclics and MAO Inhibitors. As a result, patients are more likely to comply with treatment long enough to obtain a therapeutic effect than those prescribed tricyclic antidepressants. Patient acceptability and relative safety in overdose have contributed to the popularity of these drugs. Tricyclic antidepressants cause side effects related to their effects on the autonomic nervous system. These include dry mouth, dizziness, palpitations, blurry vision, constipation, tachycardia, orthostatic hypotension, and cardiac arrhythmias. MAO Inhibitors may cause postural hypotension. Drug and diet interactions may precipitate hypertensive crisis or serotonin syndrome, which includes restlessness, muscle twitching, sweating, shivering, and tremor [16]. SRI and SNRI side effects include nausea, headache, delayed ejaculation, and impaired orgasm. Bupropion can cause anorexia, insomnia, and agitation. Trazodone can cause priapism. Mirtazapine is sedating and can cause weight gain. Patients with bipolar disorder treated with antidepressants may be at risk of switching from depression to a hypomanic or manic state [17–19].
Mood Stabilizers Cade first described the therapeutic effects of lithium on mania in 1949. It was first approved by the US FDA for treatment of acute mania in 1970s, and for prophylaxis of bipolar disorder in 1974. While lithium is quite toxic, it is very effective for treatment of both manic and depressive phases of bipolar disorder. Several large-scale studies have demonstrated significant reduction in suicide risk associated with lithium therapy [20, 21]. There is an increase in suicide risk after discontinuation of lithium [22]. Adverse effects include acne, leucocytosis, hypothyroidism, hypoparathyroidism, nephrogenic diabetes insipidus, and kidney damage. Signs of toxicity include tremor, weakness, fatigue, nausea,
vomiting, cardiac arrhythmias, hypotension, shock, stupor, coma, and even death. Safe use of lithium requires monitoring of blood levels, since the therapeutic dose is close to the toxic dose. Evaluation of serum electrolytes, thyroid, parathyroid, renal, and hematological function is necessary at the commencement of treatment and periodically during the course of therapy. Valproate was approved by the FDA for treatment of acute mania in 1994. It is less toxic, and easier to prescribe than lithium. It consequently has been prescribed more frequently than lithium, even though the evidence of its effectiveness for prophylaxis is not robust. In 2003, the FDA approved the use of lamotrigine for long-term treatment of bipolar disorder. This anticonvulsant demonstrates little effect on acute mania. However, it shows antidepressant effect and prophylactic effects in bipolar patients. Other anticonvulsants, which are used as mood stabilizers, include carbamazepine, gabapentin, pregabalin, topiramate, tiagabine, oxcarbazepine, and zonisamide. Antipsychotic drugs such as olanzapine, aripiprazole, and quetiapine are also termed mood stabilizers because of their demonstrated roles in treatment of bipolar disorder [23].
Anxiolytics Chlordiazepoxide and diazepam were the first benzodiazepines, introduced in the early 1960s. They were soon widely prescribed by physicians for pathological anxiety, because they were effective and safer than meprobamate and barbiturates. Other benzodiazepines were subsequently developed and marketed, including clorazepate, alprazolam, oxazepam, and clonazepam. All benzodiazepines exhibit anxiolytic, sedative hypnotic, muscle relaxant, and anticonvulsant effects. The primary differences among them are a result of pharmacokinetic properties, including rates of absorption and elimination. Benzodiazepines bind to specific receptors in the brain – the GABA – BZ complex. GABA is a primary inhibitory neurotransmitter in the brain. When it is bound to its receptor, a chloride channel on the membrane is opened a little, making depolarization of the nerve more difficult. GABA works more effectively in the presence of a benzodiazepine.
Psychopharmacology Sedation and drowsiness are common side effects of benzodiazepines. Motor impairment may occur, as may memory impairment. Tolerance may occur, and physical dependence is common with prolonged treatment. Abuse and dependence (see Substance Abuse; Addictions), as defined by Diagnostic and Statistical Manual of Mental Disorders-IV (DSM-IV) [24], are less common, but may still be problematic. Buspirone is a unique nonsedating nonbenzodiazepine anxiolytic drug, which appears to exert its effect through actions on a subset of serotonergic receptors (5-HT1A ). It is effective for generalized anxiety disorder, but not for panic attacks. Its effect builds up slowly, over several weeks. Side effects may include dizziness, headaches, and nausea. Addition of buspirone to an antidepressant can be beneficial for patients with inadequate or poor responses to an initial trial of antidepressant treatment [25–28].
Stimulants Amphetamines and methylphenidate stimulate the release of DA and NE at the synapse. They are useful for the treatment of attention deficit disorder [29–32] (see Psychopharmacology: Child and Adolescent), and have been used for appetite suppression, fatigue, and treatment of poststroke depression. Side effects include nervousness, insomnia, and agitation. Arrhythmias and seizures may occur. Hallucinations and delusions are uncommon with stimulants administered orally at usually prescribed doses. They are a frequent complication of inhaled or injected amphetamines. Stimulant psychosis, including visual hallucinations, disorientation, agitation, pacing, and thought disorder, may persist for months after cessation of amphetamine use. Modafinil is similar to stimulants, in that it increases wakefulness. It does not increase reinforcement, like other stimulants. Thus it is, in a class by itself, a “wakefulness promoting agent”. It is indicated for narcolepsy, and the fatigue associated with shift work and sleep apnea.
Drug Interactions Concurrent use of more than one drug, or a drug with other substances, may lead to altered pharmacological
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effect – a drug interaction. Pharmacokinetic interactions occur when an agent alters the absorption, distribution, or metabolism of a drug. Pharmacodynamic interaction involves changes at the receptor, or the biologically active site. The absorption of buspirone and ziprasidone are enhanced in the presence of food. Antacids may decrease absorption of some antibiotics. Drugs that are bound strongly to protein, like fluoxetine, will displace other protein-bound drugs, possibly enhancing their action or leading to toxic effects. Excretion of lithium is diminished with certain diuretic drugs, leading to increased serum concentration. Grapefruit juice may inhibit Cytochrome P450 enzymes, which break down imipramine, leading to increased serum concentration. These are all pharmacokinetic interactions. Many drugs are metabolized by the Cytochrome P450 family of enzymes, predominantly found in the liver, the gut, and the brain. The activity of these enzymes, in turn, is enhanced or inhibited by many drugs. Many significant pharmacokinetic drug interactions are mediated by changes in these enzymes [33]. Much variability in individual sensitivity to therapeutic agents can be explained by variations in the concentrations and activities of these enzymes. Pharmacodynamic interactions can cause increased or decreased pharmacological effect. For example, alcohol can potentiate the sedative effect of hypnotic drugs. Lithium can potentiate the effect of antidepressant drugs. MAO Inhibitors can provoke a serotonin syndrome when administered with an SSRI. Attention to the potential for drug interactions allows a psychopharmacologist to safely and effectively provide rational treatment.
Drug Testing For most psychotherapeutic drugs, the relationship between serum concentration and clinical effect has not been established. Lithium, valproate, carbamazepine, and nortriptyline are important exceptions. The difference between the therapeutic dose and a toxic dose of lithium is small. Periodic measurement of serum concentration is necessary to safely prescribe it. The interactions of carbamazepine and valproate with the Cytochrome P450 enzymes necessitate blood testing to establish an appropriate therapeutic dose. Sometimes physicians will check on the
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concentration of other prescribed drugs when toxicity is suspected. Sometimes less expensive qualitative testing can confirm or refute suspicions of noncompliance. Generally, however, adjustment of doses of psychotropic medication is made on clinical grounds. Qualitative testing for the presence of drugs in blood, urine, saliva, or hair samples is often part of a treatment program for patients with substance use disorders (see Drug Testing: Urine; Amphetamine; Benzodiazepines; Cannabis; Cocaine; Opioids). Serum concentration is often presented to the forensic psychopharmacology consultant for interpretation (Toxicology: Forensic Applications of). Substances associated with dependence tend to evoke tolerance over time. Thus, without additional data, one cannot usually determine from a single sample of body fluid, the level of intoxication experienced by a user. Was the blood level the result of one use or many over time? How was the drug ingested? How long ago? Were blood levels on their way up, or down? Or was this steady state? Concentrations of drugs obtained during necropsy are often quite different than those obtained during life (Postmortem blood has been described as a fluid resembling blood that is obtained from the vasculature after death [34]). A drug that has been concentrated in solid organs and tissues will diffuse into the blood after death, increasing its concentration. This was demonstrated in the case of a man who committed suicide by ingesting an overdose of imipramine. Concentrations of imipramine and its active metabolite, desipramine, obtained during postmortem examination 7 h after death were compared with concentrations in blood samples obtained in the emergency room 2 h prior to death. Postmortem imipramine concentrations ranged from 1.8 to 7.9 times the concentration of the emergency room sample (depending on the site in the body from which the blood was drawn), while desipramine ratios ranged from 1.6 to 6 [35]. The Volume of distribution (Vd ) is a hypothetical volume of body fluid that would be necessary if the total amount of drug in the body were distributed uniformly in the same concentration as in the plasma. In general, lipophilic drugs have a high volume of distribution. Caffeine, which dissolves equally in water and in fat, has a Vd of 1 l kg−1 . For imipramine, it is 11–16 l kg−1 . For sertraline, it is in the range of 50–80. Drugs with a high volume of distribution
will show the greatest change in concentration postmortem (see Toxicology: Analysis).
References [1]
Schatzberg, A.F. & Nemeroff, C.B. (2004). The American Psychiatric Press Textbook of Psychopharmacology, 3rd Edition, American Psychiatric Press, Washington, DC. [2] Nemeroff, C.B., Heim, C.M., Thase, M.E., Klein, D.N., Rush, A.J., Schatzberg, A.F., Ninan, P.T., McCullough, J.P., Weiss Jr, P.M., Dunner, D.L., Rothbaum, B.O., Kornstein, S., Keitner, G & Keller M.B (2003). Differential responses to psychotherapy versus pharmacotherapy in patients with chronic forms of major depression and childhood trauma, Proceedings of the National Academy of Sciences of the United States of America 100(24), 14293–14296. [3] Sadock, B.J. & Sadock, V.A. (2004). Kaplan and Sadock’s Comprehensive Textbook of Psychiatry, 8th Edition, Lippincott Williams & Wilkins. [4] Feix, J. & Wolber, G. (2007). Intoxication and settled insanity: a finding of not guilty by reason of insanity, The Journal of the American Academy of Psychiatry and the Law 35(2), 172–182. [5] Sell v. United States, 539 U.S. 166 (2003). [6] Brunton, L., Lazo, J. (2005). Goodman and Gilman’s the Pharmacological Basis of Therapeutics, 11th Edition, McGraw Hill. [7] Seeman, P. (2004). Atypical antipsychotics: mechanism of action, Focus 2(1), 48–58. [8] Nemeroff, C.B. (1998). Psychopharmacology of affective disorders in the 21st century, Biological Psychiatry 44(7), 517–525. [9] Keefe, R.S.E., Silva, S.G., Perkins, D.O. & Lieberman, J.A. (1999). The effects of atypical antipsychotic drugs on neurocognitive impairment in schizophrenia: a review and meta-analysis, Schizophrenia Bulletin 25(2), 201–222. [10] Lieberman, J.A., Stroup, T.S., McEvoy, J.P., Swartz, M.S., Rosenheck, R.A., Perkins, D.O., Keefe, R.S.E., Davis, S.M., Davis, C.E., Lebowitz, B.D., Severe, J & Hsiao, J.K. The Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) Investigators, (2005). Effectiveness of antipsychotic drugs in patients with chronic schizophrenia, New England Journal of Medicine 353(12), 1209–1223. [11] Rosenheck, R., Cramer, J., Xu, W., Thomas, J., Henderson, W., Frisman, L., Fye, C. & Charney, D. The Department of Veterans Affairs Cooperative Study Group on Clozapine in Refractory Schizophrenia (1997). A comparison of clozapine and haloperidol in hospitalized patients with refractory schizophrenia, New England Journal of Medicine 337(12), 809–815. [12] Volavka, J., Czobor, P., Sheitman, B., Lindenmayer, J.-P., Citrome, L., McEvoy, J.P., Cooper, T.B., Chakos,
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M. & Lieberman, J.A., (2004). Clozapine, olanzapine, risperidone, and haloperidol in the treatment of patients with chronic schizophrenia and schizoaffective disorder, Focus 2(1), 59–67. Greist, J.H., Jefferson, J.W., Kobak, K.A., Katzelnick, D.J. & Serlin, R.C. (1995). Efficacy and tolerability of serotonin transport inhibitors in obsessive-compulsive disorder. A meta-analysis, Archives of General Psychiatry 52(1), 53–60. Kaplan, A. & Hollander, E. (2004). A review of pharmacologic treatments for obsessive-compulsive disorder, Focus 2(3), 454–461. Kobak, K.A., Greist, J.H., Jefferson, J.W., Katzelnick, D.J. & Henk, H.J. (2004). Behavioral versus pharmacological treatments of obsessive compulsive disorder: a meta-analysis, Focus 2(3), 462–474. Looper, K.J. (2007). Potential medical and surgical complications of serotonergic antidepressant medications, Psychosomatics 48(1), 1–9. Altshuler, L.L., Suppes, T., Black, D.O., Nolen, W.A., Leverich, G., Keck Jr, P.E., Frye, M.A., Kupka, R, McElroy, S.L., Grunze, H., Kitchen, C.M.R. & Post, R. (2007). Lower switch rate in depressed patients with bipolar II than bipolar I disorder treated adjunctively with second-generation antidepressants. Focus 5(1), 107–110. Judd, L.L., Akiskal, H.S., Schettler, P.J., Endicott, J., Maser, J., Solomon, D.A., Leon, A.C., Rice, J.A. & Keller, M.B. (2002). The long-term natural history of the weekly symptomatic status of bipolar I disorder, Archives of General Psychiatry 59(6), 530–537. Leverich, G.S., Altshuler, L.L., Frye, M.A., Suppes, T., McElroy, S.L., Keck Jr, P.E., Kupka, R.W., Denicoff, K.D., Nolen, W.A., Grunze, H., Martinez, M.I. & Post, R.M. (2006). Risk of switch in mood polarity to hypomania or mania in patients with bipolar depression during acute and continuation trials of venlafaxine, sertraline, and bupropion as adjuncts to mood stabilizers. American Journal of Psychiatry 163(2), 232–239. Tondo, L., Jamison, K. & Baldessarini, R. (1997). Effect of lithium maintenance on suicidal behavior in major mood disorders, Annals of the New York Academy of Sciences 836, 339–351. Tondo, L., Hennen, J. & Baldessarini, R. (2001). Lower suicide risk with long-term lithium treatment in major affective illness: a meta-analysis, Acta Psychiatrica Scandinavica 104, 163–172. Baldessarini, R., Tondo, L. & Viguera, A. (1999). Discontinuing lithium maintenance treatment in bipolar disorders: risks and implications, Bipolar Disorders 1, 17–24. Bauer, M.S. & Mitchner, L. (2004). What Is a “mood stabilizer”? an evidence-based response, American Journal of Psychiatry 161(1), 3–18. American Psychiatric Association (1994). The Diagnostic and Statistical Manual of Mental Disorders, (DSM IV), 4th Edition, American Psychiatric Association, Washington, DC.
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Thase, M.E., Friedman, E.S., Biggs, M.M., Wisniewski, S.R., Trivedi, M.H., Luther, J.F., Fava, M., Nierenberg, A.A., McGrath, P.J., Warden, D., Niederehe, G., Hollon, S.D. & Rush, A.J. (2007). Cognitive therapy versus medication in augmentation and switch strategies as second-step treatments: a STAR*D report, The American Journal of Psychiatry 164(5), 739–752. Fava, M., Rush, A.J., Wisniewski, S.R., Nierenberg, A.A., Alpert, J.E., McGrath, P.J., Thase, M.E., Warden, D., Biggs, M., Luther, J.F., Niederehe, G., Ritz, L. & Trivedi, M.H. STAR*D StudyTeam, (2006). A comparison of mirtazapine and nortriptyline following two consecutive failed medication treatments for depressed outpatients: a STAR*D report, The American Journal of Psychiatry 163(7), 1161–1172. Nierenberg, A.A., Fava, M., Trivedi, M.H., Wisniewski, S.R., Thase, M.E., McGrath, P.J., Alpert, J.E., Warden, D., Luther, J.F., Niederehe, G., Lebowitz, B., ShoresWilson, K. & Rush, A.J. STAR*D Study Team, (2006). A comparison of lithium and T3 augmentation following two failed medication treatments for depression: a STAR*D report, The American Journal of Psychiatry 163(9), 1519–1530. Rush, A.J., Trivedi, M.H., Wisniewski, S.R., Nierenberg, A.A., Stewart, J.W., Warden, D., Niederehe, G., Thase, M.E., Lavori, P.W., Lebowitz, B.D., McGrath, P.J., Rosenbaum, J.F., Sackeim, H.A., Kupfer, D.J., Luther, J. & Fava, M. (2006). Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: a STAR*D report, The American Journal of Psychiatry 163(11), 1905–1917. The MTA Cooperative Group (1999). Moderators and mediators of treatment response for children with attention-deficit/ hyperactivity disorder: the Multimodal Treatment Study of Children with attentiondeficit/hyperactivity disorder, Archives of General Psychiatry 56(12), 1088–1096. The MTA Cooperative Group (1999). A 14-month randomized clinical trial of treatment strategies for attention-deficit/hyperactivity disorder, Archives of General Psychiatry 56(12), 1073–1086. Spencer, T., Wilens, T., Biederman, J., Faraone, S.V., Ablon, J.S. & Lapey, K. (1995). A double-blind, crossover comparison of methylphenidate and placebo in adults with childhood-onset attention-deficit hyperactivity disorder, Archives of General Psychiatry 52(6), 434–443. Goldman L.S., Genel M., Bezman R.J., Slanetz P.J., for the Council on Scientific Affairs AMA (1998). Diagnosis and treatment of attention-deficit/hyperactivity disorder in children and adolescents, The Journal of the American Medical Association 279(14), 1100–1107. Nemeroff, C., DeVane, C. & Pollock, B. (1996). Newer antidepressants and the cytochrome P450 system, The American Journal of Psychiatry 153(3), 311–320. Klaasen, C.D. (2001). Casarett & Doull’s Toxicology: The Basic Science of Poisons, 6th Edition, McGraw-Hill, New York.
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Pounder, D. & Jones, G. (1990). Postmortem drug redistribution – A toxicological nightmare, Forensic Science International 45, 253–263.
SAMUEL I. MILES
Psychopharmacology: Child and Adolescent Psychopharmacology’s Role in Treatment of Child and Adolescent Mental and Behavioral Disorders Psychopharmacology is the study of drug–behavior relationships and the use of medications to influence affective and emotional states and thoughts. In children and adolescents, psychotherapeutic medications are best used in conjunction with a holistic bio-psycho-social approach to identify youth’s problems and at times in combination with specific nonmedication-based therapies [1]. Transactions between individual genetics, environmental, family and social stresses, and protective factors are currently considered integral to the development of or protection from psychiatric illness. The use of psychotherapeutic medication, when based on scientific evidence, has an important role in fostering improved adaptation in the face of an individual’s lowered threshold toward disease. Psychotherapeutic medications are not intended to affect a cure but rather to help by reducing problematic behaviors or relieving mentally painful symptoms. If a biologic predisposition to a mental disorder lowers the threshold at which a disease becomes evident, then understanding the nature of the risk exposure, while not always immediately evident in the chain of causality, is important. Examples include how the toxic effects of lead and mercury on the development of human nervous system lead to disease states, learning disabilities, and behavioral disorders. Likewise, fetal alcohol effects are discussed as public policy issues, while families, pediatricians, child and adolescent psychiatrists, teachers and the juvenile, and adult justice system attempt to mitigate the damage at a more individual level.
Our knowledge of the pernicious effects of multigenerational cycles of physical and mental maltreatment in childhood, leading to states of affective dyscontrol beginning in childhood and continuing throughout the life span, has expanded to include neuroanatomical and biochemical proof of the disordered states. Addictions are diseases compounded by genetic predispositions that affect motivational circuitry in the brain. Interrupting the cascading effects of untreated disease on the individual, families, and larger society is an important goal. Medication is a component in treatment. There are multiple textbooks on this subject and this article addresses only a few of the issues [2–4].
The Prescriber, Privacy, and the Court Subpoenas to courts do not provide the authority to release confidential health information that is protected by privacy laws. The prescriber needs to assure that the person who controls protected information has consented to its release or that there has been a judicial determination that privilege does not apply. If uncertain and questioned in court, the prescriber should indicate that the information is privileged and follow the direction of the judge.
Tort Law and the Standard of Care The use of the word prescriber rather than physician is intended to reflect the fact that many jurisdictions allow nonphysicians such as nurse practitioners to prescribe medications. The tort of negligence has been described as “conduct that falls below the standard regarded as normal or desirable in a given community for those who are perceived to be competent in carrying out their profession within the standards of reasonable skill and proficiency” [5]. In prescribing the medications for psychiatric illness, liability for malpractice does not ensue necessarily from a bad outcome but rather from deviation from the accepted use of the medication. In most jurisdictions, the standard of care in assessing negligence is a matter of medical judgment. In making this decision, rarely does the law provide an answer but rather testimony of experts, articles in learned journals and textbooks, guidelines from professional organizations, etc. will be used to advise the decision maker.
Psychopharmacology: Child and Adolescent Lawsuits against prescribers of psychotherapeutic medicine often make claims of negligence in either failing to obtain an informed consent for or in the prescribing, administering, and/or monitoring of medications.
Informed Consent for Psychotheraputic Medications in Children and Adolescents Treatment with psychotherapeutic medication requires informed consent. Applebaum and Gautheil state “Treatment without any consent or over a patient’s objections may constitute a battery, but treatment after an inadequate consent is properly considered as a form of malpractice” [6]. A free person is considered to have a right to control what happens to his or her body. Most jurisdictions give the individual patient and not the prescriber of treatment the right to balance risk versus benefit of the procedure and to consent to it or refuse it. Informed consent involves two essential parts: a document and a process. It is important to document it in the medical record but it is more than a signed piece of paper. Ongoing explanations help the patient make wise decisions about whether it is essential to begin or continue taking a particular treatment or medication. The three elements of informed consent are as follows: 1. the mental competency to make a rational decision; 2. the voluntary nature of the decision; and 3. sufficient information to make a decision. In children and adolescents, the issue of competence and substitute decision making are especially involved.
Competency Statutory rules determine when the age of competence to seek or refuse psychiatric treatment occurs. This often occurs before the age of majority. Emancipated minors have full competence. Statutes and age of consent vary from one jurisdiction to another. Informed assent of the older child or adolescent helps the therapeutic relationship and improves compliance. Research trials are governed by more stringent guidelines in this regard. In the United States, the National
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Commission for Protection of Human Subjects of Biomedical and Behavioral Research has established age 7 as a reasonable minimum age for children involving in some kind of assent or dissent process and “parental permission” rather than “proxy consent” is considered the norm [7]. Sometimes clarification from a court as to who has authority for decision making for a child may be necessary. Divorced or separated parents with shared decision-making powers might disagree with one another’s opinion. Substitute nonparent decision makers who are actively raising the child (grandparents, foster parents, social service agency workers, etc.) may not have the medical decision-making authority to consent.
Voluntary Decision Making Regarding the issue of substitute decision making, one should consider the agency of the prescriber. Children and adolescents rarely seek psychiatric treatment on their own and are usually dependant upon their parents who act as decision makers. Because the parents are so much a part of the child’s decision to be in treatment to some extent, the prescriber should be aware when he or she is acting in their agency as well as the child’s. Other situations of potential for dual agency exist when clinicians are contracted to or are employed by schools or social agencies or treatment facilities. The prescriber should assure that school authorities or others are not coercing decision maker to medicate the child.
Information to Make the Decision To make a submissible case based on negligence in obtaining informed consent, a plaintiff must show nondisclosure, causation, and injury.a To show nondisclosure, a plaintiff must include evidence of the risks involved and what disclosures were made by the prescriber.b Some jurisdictions have a professional standard of disclosure that the sufficiency of information disclosed should be what a “reasonable clinician” would reveal to his or her patient. Expert testimony of what risks a reasonable medical practitioner would disclose under the same or similar circumstances is required.c,d A plaintiff must also establish causation between the inadequate disclosure
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and the injury.e The issue is whether a reasonable person in the plaintiff’s position would have consented to the procedure had the proper disclosure been made.f The plaintiff has the burden of producing evidence from which a jury or other decision maker could determine whether a reasonable person would have consented to the procedure.g Other jurisdictions use a “reasonable person” standard. This would involve disclosing the information sufficient for a reasonable patient or legal decision maker acting on that patient’s behalf to make a rational decision. In those jurisdictions, the clinician should discuss the following matters with the patient and or authorized decision makers: 1. 2. 3.
4.
5.
The nature of the condition for which medication is being proposed. The likely outcome of nontreatment. The proposed medication treatment and how and to what extent that will benefit the patient and condition. The risks and side effects associated with the medication. Risks of medications or other treatments proposed that should be disclosed should include those that a reasonable person would be likely to consider significant. The standard in malpractice case law is that the information not disclosed would have been considered substantial in evaluating the risk. Exceptions to this exist when severe harm could result if disclosure were made (principle of therapeutic privilege). Transparency in self-disclosure is important. The clinician’s biases and skill level should be disclosed as that might also effect a patient’s decision about the risk involved. If a clinician has never treated a certain condition before or never used a certain treatment before, it may be later be judged important to have informed the decision maker of this. Disclosure of potential conflict of interests or even the appearance of such conflict is recommended. Alternative treatments available with their attendant benefits and risks.
Documentation In the defense against a claim of negligence, legible and timely documentation of prescriptions and orders along with details of the informed consent
process, and instructions given to patient and caregivers support the assertion that proper care was given. Prescriptions that are difficult to read pose a hazard to the patient. The prescriber should assure patient and caregivers understand instructions about dosages and interval between doses and potential side effects is important. Warning as to the importance of parental oversight and responsibility to safeguard potentially dangerous medicines should be given. Documentation of all other medications the patient is currently taking and consideration of drug–drug interactions is a part of clinical care. Refills, frequency of follow-up intervals to monitor for effectiveness, appropriate compliance with therapy and side effects is important, particularly in children and adolescents with medicines that have a potential for lethality in overdose, irreversible side effects, or abuse potential. It is important to have permission to communicate with the other individuals involved with the child or adolescent’s care about all medications that are being prescribed and about signs, symptoms of side effects, and positive responses to the medications. When a patient or their decision maker will not allow this, then the prescriber’s ability to treat the patient is compromised.
Law of Agency/Vicarious Liability Multiple professional disciplines interact with individual children and families. Pediatric psychopharmacology is practiced within this greater framework. Given the multidisciplinary nature of the treatment of a child or adolescent with interactions with family, school, and larger society, there might be tensions or disagreement at times of critical decision making regarding issues such as dangerousness to self or others, diagnostic labeling, as well as treatment choice recommendations. The prescriber often does not have input on important treatment decisions. The concept of respondeat superior is affected by these facts. Most others interacting with the child or adolescent are not acting as agents for the prescriber. The prescriber, even a physician, collaborating with a therapist is not responsible for the actions of that therapist unless he or she is directing these activities in a supervisory manner. The nonsupervisory nature of the relationship should be made clear so that false assumptions are not made.
Psychopharmacology: Child and Adolescent
Medication Practices Psychotherapeutic medications for the treatment of mental illness are considered one of the most useful and important forms of treatment available for mental illness in both adults and youth. Millions of prescriptions are written annually. Prescribing medications has become so routine and commonplace; it is easy for prescribers and patients to lose sight of the risks involved. Multiple factors have led to the increased recognition of mental illness in children and adolescents as well as the increase in medication use including the following: 1. The nature versus nurture controversy of the last century yielded an increased emphasis and understanding of the biology of mental illness. Biological psychiatry with primary emphasis on the individual’s biological vulnerabilities interplaying with psychosocial stressors led to popularization of the simplistic concept of “chemical imbalance”. A corollary to this concept was the idea that psychotherapeutic medications righted the imbalance. This notion was applied to youth as well as adults. 2. Large epidemiologic studies such as the 1999 Methodology for Epidemiology of Mental Disorders in Children and Adolescents (MECA) showed significant functional impairment due to mental or addictive disorders in approximately 1 in 10 of the pediatric population, for a total of four million in the United States alone [8]. 4. Successful marketing by the pharmaceutical industry of psychotherapeutic medications had significant impact on both prescribers and the general public in terms of increased expectations of relief from distressing symptoms. Given the awareness of the availability of medications helpful in treating adults, there has been a willingness to treat youth without awaiting regulatory approvals.
Pediatric Psychohamacology in Practice It is a statement of fact that most of the medications, psychiatric or not, used in children and adolescents, with the exception of stimulants, were not extensively studied or approved for use in
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this population. Manufacturers regularly put in disclaimers to that effect in their labeling. Therefore, the use of “off label” (i.e., not regulatory agency approved) prescribing remains the norm rather than the exception. Pharmacodynamics is the branch of pharmacology that studies how medicines work. In general, psychoactive medications alter the biochemical environment in the synaptic space through either the blockade or activation and enhancement (antagonism, partial agonism, and agonism) of nerve cell membrane receptors. This in turn alters the way the nerve cells communicate. In children and adolescents, more than in the midadult period in which most new medications are studied, the brain is developing by growing, and pairing down dopaminergic, serotononergic, and noradrenergic cell networks in areas of the brain, which are important to functions of attention, mood, anxiety, and perceptions. In adult populations these brain systems are relatively stable and the medications have been studied more extensively prior to approval and widespread use. Younger, developing brain systems may be permanently affected by mechanisms that are not well understood. Because of this, children and adolescents have differential risks when administered psychotherapeutic medicines. Examples include different risks of side effects such as extrapyramidal motor side effects and dyskinesias from antipsychotics as well as possibilities of overactivation of mood and attentional systems due to increased sensitivities to antidepressants. Pharmacokinetics studies and informs us as to the absorption, distribution, metabolism, and excretion of medicines. It is important to understand that various people and subpopulations do this differently. In children and adolescents, the phamacokinetic properties of medicines need to be studied thoroughly for the safest administration of medicines that benefit them. Children have a higher gastric and intestinal motility than adults thus favoring more rapid absorption. Prepubescent children and adolescents usually have fewer fat stores compared with adults, which may lead to higher plasma concentration of medicines in part distributed among fat stores. The metabolic breakdown of medications and toxins in the body differs. Excretion of medicines or the metabolites of medicines, usually by the kidneys might also be affected.
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Treatment Because standard of care is determined on all clinical data available for an individual child or adolescent, the following information is intended as informational only and not intended to imply adherence or deviance from the standard. Side effects are fairly common and so management should include regular periodic monitoring and routine reassessment as to the need to continue with the medication.
History Review of history is very important for diagnosis and treatment planning. It is not unusual for psychiatrically ill children to have comorbid medical conditions that can influence their psychiatric symptoms. Developmental history should be reviewed with specific attention to development of gross and fine motor skills, speech and language development, affective relatedness, and attachments. A medical history (allergies, adverse drug reactions, acute and chronic illnesses, hospitalizations, injuries, loss of consciousness and traumatic brain injuries, and treatments) should be obtained. Previous laboratory findings and brain imaging if available should be reviewed. Psychosocial history should include the family of origin, adoption, foster care, exposure to influences of alleged maltreatment, abuse, trauma, and losses. Past psychiatric treatments and results should be reviewed. A recent physical examination by the child or adolescent’s primary care provider should be reviewed. Many psychiatric medications can be teratogenic and most teen pregnancies are unplanned. Sexually active postpubertal girls should have a pregnancy test along with counseling regarding the use of appropriate methods of birth control and methods of preventing sexually transmittable disease. Documentation of the above and appropriate laboratory tests ordered prior to initiation of medication therapies and during ongoing monitoring is important.
Diagnosis Accurate diagnosis in children and adolescents requires clinical assessment often using multiple sources of information including interactions with, observation of, and interview of the child or
adolescent, parents, caregivers, and teachers if possible. Guidelines for assessment and treatment are available from the American Academy of Child and Adolescent Psychiatry, American Academy of Pediatrics and other organizations [9, 10]. Substance Abuse. Drug and alcohol screening with clinical questions augmented by urine toxicology for substances of abuse when indicated should be routine among adolescents and preadolescents. Substanceinduced behavioral effects can mimic psychiatric illness and cause or aggravate other mental illnesses. Substance use disorders and tobacco addiction need treatment along with other mental illnesses. Making appropriate referrals for treatment of addiction and dependence and identification of patients or caregivers who might be misusing medications, altering prescriptions or getting multiple prescriptions from multiple sources (doctor shopping) is important. Examples of Therapeutic Medications. ADHD and the Use of Stimulants and Nonstimulants in its Treatment. Attention deficit hyperactivity disorder (ADHD) is characterized by early childhood onset of an enduring pattern of inattention and/or hyperactivity and impulsive behavior. In total, 4–12% of children are affected by the disorder [11]. Many children can contain their behaviors during office visits and so collecting information about the child’s behavior in multiple settings is most useful. Well-validated and normed behavior rating scales are available and useful in assessing and measuring treatment effects. These would include the Conners’ Rating Scales-Revised; Brown AttentionDeficit Scales; and Swanson, Nolan, and Pelham (SNAP-IV) [12]. Stimulant Medications. In 1937, Bradley reported on the positive effects of amphetamine on children institutionalized for neurobehavioral reasons [13]. Since then, opposing social forces have exerted pressures for either wider acceptance of these medications or for more restrictions on their use. The existence of these pressures has led scientists to explore the issue and, for the most part, demonstrate the efficacy of these medicines [14]. Concerns regarding associations with sudden cardiac death have brought these medications into greater controversy in the recent years.
Psychopharmacology: Child and Adolescent Nonstimulant Medications. Atomoxetine is a selective norepinephrine reuptake inhibitor that is superior to placebo in the treatment of ADHD at appropriate doses [15]. Although the manufacturer recommends once a day dosing, avoiding adverse effects while maintaining adequate therapeutic doses often requires twice a day dosing. Because it shares features with the antidepressants it is associated with an increased risk of suicidality. Guanfacine and clonidine are antihypertensive medications that have found usefulness. They are generally used in children who cannot tolerate or as adjuncts to the other medications. Antidepressant Medications, Mood Disorders, and Suicide. Major depression and bipolar mood disorders are enduring and disabling conditions. Suicide is among the most feared of outcomes in the field of mental health. Ninety percent of suicides occur in the context of psychiatric illness and mood disorders are the most likely illnesses to be associated with the act [16]. Suicide is a major cause of preventable death among youth [17]. The prevalence of mood disorders is relatively low before the onset of puberty and equally distributed among the two sexes. After puberty, however, the prevalence increases to adult levels. Various epidemiologic studies point to a prevalence of 5–10% of teens and young adults suffer from major depression or other disabling depressive disorders such as dysthymia and depressive disorder not otherwise specified [18]. Pharmacotherapy with selective serotonin reuptake inhibitor (SSRI) antidepressants either with cognitive behavioral or interpersonal psychotherapy for children and adolescents with major depressive disorder had been the first line and standard of treatment until 2003 and 2004 [1] when regulators in the United Kingdom, the United States, and the European Common Market, became concerned about possible or even causal links between youth suicidality and antidepressants of all classes. UK regulators went on to advise against the use of almost all antidepressants in persons below 18 years. Black box labeling and letters of warning from manufacturers to prescribers were issued in the United States. These expressed warnings and concerns were based on collective data comparing placebo to active medication in multiple different trials, which showed increased rates of
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suicidality on the active medications and have been extensively reviewed [19]. The stance of regulators was contrary to the opinion of many prescribers who felt the medicines to be very helpful in the real world of clinically complex populations. The warnings had both intended and unintended consequences. Internationally, warnings had the effect of reducing prescriptions to youth by some 20% in 2004 [20]. Coincidental to this decrease in prescribing of antidepressants was a marked increase in actual suicide rates among youth. There exists epidemiologic data showing an inverse correlation between the SSRI prescriptions and suicide rates in multiple population groups in several countries [21, 22]. Antidepressant prescriptions seem to have a protective effect by reducing suicide rates such that strong arguments exist regarding the potential harm resulting from a reduction of SSRI antidepressant use [23]. Indeed, according to the United States Center for Disease Control, after having dropped some 28% from 1990 until 2004, suicide rates for youth in the United States surged 8% leading to 4599 deaths in 2004 following the issuance regulatory letters and black box warning [17]. Prescribers have been left in a conundrum of needing to treat their patients with these medicines despite alarming warnings from regulatory authorities. The best practice to follow is to assure that the diagnosis is correct, the patient makes a full informed consent and to monitor for the development of new onset of suicidal ideations or agitation. The results of the above-noted reviews [19], which used meta-analytic methods, suggest that there is no benefit to the use of tricyclic antidepressants in children and adolescents with depressive disorders and that the risks, given their toxicity in overdose, generally outweigh the benefits of their use in this population. SSRI antidepressant medications remain helpful in the treatment of mood and anxiety disorders [24]. Antipsychotics. Antipsychotics are used in treating hallucinations, delusions, hostility, aggression, and disorganized thinking associated with major mental illness such as bipolar disorder, major depression with psychotic features, and schizophrenia. These diseases often manifest in late adolescence or young adulthood and often go undiagnosed for several years. Antipsychotics are also used in the treatment of children with autism and mental retardation who
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exhibit prominent irritability, aggression, and selfinjurious behavior. It is thought that blockade of D2 receptors in the mesocortical and prefrontal systems is responsible for the antipsychotic effects. With older antipsychotics, the degree of D2 receptor blockade is predictive of the potency of antipsychotic effect on hallucinations, delusions, agitation, hostility, and disorganization. Many side effects are also a function of the medication’s D2 binding properties to receptors in the basal ganglia. Drug-induced Parkinson symptoms such as feeling stiff, shuffling gait, tremor, drooling, and masked facial expression led to the mislabeled term chemical restraint for this group of medicines that helped many people with mental illness to return to more normal lives. The newer second generation antipsychotics (SGAs) (olanzapine, risperidone, paliperidone, ziprasidone, quetiapine, aripirazole, and clozapine) were promoted as having fewer side effects on movement and positive effects on motivational circuitry in the prefrontal cortex. The SGAs seemed to balance out many of the untoward effects of D2 blockade through effects on serotonin 2A receptors, making them agents of first choice. Clozapine, however, because of its potential for causing dangerous agranulocytosis, is reserved for treatment refractory disease. The number of studies supporting their efficacy and safety in children and adolescents is limited. Children, adolescents, and young adults are particularly susceptible to antipsychotic drug-induced movement disorders (Extra-Pyramidal Symptoms (EPS), akithesia, and diskinetic side effects). The newer medicines have proven to have fewer with drug-induced movement disorders in adults but have problematic effects related to weight gain, glucose regulation, lipid regulation, sedation, prolactin levels, and cardiac conduction. It is hypothesized that because of varying proportions of blockage and, in the case of aripiprazole, the partial agonism of the dopamine receptors, as well as the above noted blockade of serotonin receptors, the effectiveness and sensitivities to side effects in children and adolescents varies markedly between one medicine and another. This means caution should be exercised in their use, careful review of improvement of targeted symptoms and monitoring for side effects. Of note, risperidone received approval from the Food and Drug Administration (FDA) for an indication in the treatment of
children with autism and severe problem behaviors [25, 26]. Children and adolescents are generally treated with the lowest possible effective dose of these medications with periodic monitoring for side effects including baseline and follow-up weight measures and laboratory testing for glucose and lipid abnormalities and abnormal involuntary movements all the while examining the benefits and the need for ongoing use. Because of the potential for significant and sometimes irreversible side effects, documentation of the consideration of the risk benefit ratio prior to initiation and while continuing with these medications is important. Mood Stabilizers. Mood stabilizers are used in the treatment of bipolar disorder and schizoaffective disorders. The term mood stabilizer gathered wide use after publication of reports in the late 1980s demonstrating the efficacy of carbamazepine and divalproex in adult patients with bipolar disorder giving more choices than lithium and adjunctive agents [27]. Oxcarbazapine and lamotragine are now also widely used. Use of these medications has migrated into pediatric use. These medicines are associated with potentially serious side effects; some side effects are more prominent in children and adolescents, including hirsuitism and polycystic ovary syndrome in adolescent girls associated with divalproex and increased incidences of severe rashes with lamotragine in children and adolescents. Oxcarbazapine is metabolized more rapidly in preadolescents. Patient, parent, and caregiver education as to side effects is important. Routine laboratory evaluations include complete blood-cell count with differential and platelet counts, metabolic profile including liver function tests, pregnancy tests, thyroid function monitoring, as well as plasma drug levels of lithium, valproate, and carbamazepine.
End Notes a.
Wilkerson, 908 S.W.2d at p. 696. Aiken, 396 S.W.2d at p. 673. c. Aiken, 396 S.W.2d at p. 674–675. d. Wilkerson, 908 S.W.2d at p. 696. e. Aiken, 396 S.W.2d at p. 676. f. Wilkerson, 908 S.W.2d at pp. 696–697 b.
Psychopharmacology: Child and Adolescent g. Wilkerson, at p. 697 (citing Aiken, 396 S.W.2d at p. 676).
[13]
[14]
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March, J., Silva, S., Petrycki, S., Curry, J., Wells, K., Fairbank, J., Burns, B., Domino, M., McNulty, S., Vitiello, B. & Severe, J. (2004). Fluoxetine, cognitivebehavioral therapy, and their combination for adolescents with depression: treatment for adolescents with depression study (TADS). Randomized controlled trial, The Journal of the American Medical Association 292(7), 807–820. [2] Martin, A. & Volkmar, F. (eds) (2007). Lewis’s Child and Adolescent Psychiatry, 4th Edition, Lippincott, Williams & Wilkins, Philadelphia. [3] Coffey, C. & Brumback, R. (eds) (2006). Pediatric Neuropsychiatry, Lippincott, Williams & Wilkins, Philadelphia. [4] Conner, D. & Meltzer, B. (eds) (2006). Pediatric Psychopharmacology Fast Facts, W.W. Norton, New York. [5] Fleming, J. (1992). The Law of Torts, 8th Edition, Law Book, Sidney, p. 102. [6] Applebaum, P. & Gutheil, T. Clinical Handbook of Psychiatry and the Law, 4th Edition, Williams & Wilkins, Baltimore, p. 126. [7] Broome, M.E. (1999). Consent (Assent) for research with pediatric patients, Seminars in Oncological Nursing 15(2), 96–103. [8] (1999). Mental Health: A Report of the Surgeon General, Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Center for Mental Health Services, National Institute of Mental Health, Rockville. [9] Kowatch, R. et al. (2005). Treatment guidelines for children and adolescents with bipolar disorder: child psychiatric workgroup on bipolar disorder, Journal of the American Academy of Child and Adolescent Psychiatry 44, 213–235. [10] American Academy of Pediatrics. Subcommittee on Attention-Deficit/Hyperactivity Disorder and Committee on Quality Improvement (2001). Clinical practice guideline: treatment of the school-aged child with attention-deficit/hyperactivity disorder, Pediatrics 108(4), 1033–1044. [11] Brown, R.T., Freeman, W.S., Perrin, J.M., Stein, M.T., Amler, R.W., Feldman, H.M., Pierce, K. & Wolraich, M.L. (2001). Prevalence and assessment of attentiondeficit/hyperactivity disorder in primary care settings, Pediatrics 107, E43. [12] Swanson, J., Lerner, M., March, J. & Gresham, F.M. (1999). Assessment and intervention for attentiondeficit/hyperactivity disorder in the schools: lessons from the MTA study, Pediatric Clinics of North America 46, 993–1009.
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Bradley, C. (1937). The behavior of children receiving benzedrine, The American Journal of Psychiatry 94, 577–585. Zametkin, A.J. & Rappaport, J.L. (1987). Neurobiology of attention deficit disorder with hyperactivity: where have we come in 50 years? Journal of the American Academy of Child and Adolescent Psychiatry 26, 676–686. Michelson, D., Allen, A.J., Busner, J., Casat, C., Dunn, D., Kratochvil, C., Newcorn, J., Sallee, F.R., Sangal, R.B., Saylor, K., West, S., Kelsey, D., Wernicke, J., Trapp N.J., & Harder, D. (2002). Once-daily atomoxetine treatment for children and adolescents with attention deficit hyperactivity disorder: a randomized, placebocontrolled study, The American Journal of Psychiatry 159(11), 1896–1901. Beautrais A.L., Jopyce P.R., Mulder R.T., Ferguson, D.M., Deavoll, B.J. & Nightingale, S.K. (1996). Prevalence and comorbidity of mental disorders in persons making serious suicide attempts: a case–control study, The American Journal of Psychiatry 153, 1009–1014. Centers for Disease Control and Prevention WISQARS (Web-based Injury Statistics Query and Reporting System). Birmaher, B., Ryan, N.D. & Williamson, D.E., Brent, D.A., Kaufman, J., Dahl, R.E., Perel, J. & Nelson, B. (1996). Childhood and adolescent depression: a review of the past 10 years Part I, Journal of the American Academy of Child and Adolescent Psychiatry 35(11), 1427–1439. U.S. Food and Drug Administration (2006). Clinical Review: Relationship between Antidepressant Drugs and Suicidality in Adults, Food and Drug Administration, Center for drug Evaluation and Research, Rockville. Gibbons, R.D., Brown, C.H., Hur, K., Marcus, S.M., Bhaumik, D.K., Erkens, J.A., Herings, R.M. & Mann, J.J. (2007). Early evidence on the effects of regulators’ suicidality warnings on SSRI prescriptions and suicide in children and adolescents, The American Journal of Psychiatry 164, 1356–1363. Ludwig, J. & Marcotte, D.D. (2005). Anti-depressants, suicide, and drug regulation, Journal of Policy Analysis and Management 24, 249–272. Gibbons, R.D., Hur, K., Bhaumik, D.K. & Mann, J.J. (2006). The relationship between antidepressant prescription rates and rate of early adolescent suicide, The American Journal of Psychiatry 163, 1898–1904. Gibbons, R.D., Hur, K., Bhaumik, D.K. & Mann, J.J. (2006). The relationship between antidepressant prescription rates and rate of early adolescent suicide, The American Journal of Psychiatry 163(11), 1989–10904. Walkup, J. et al. (2002). Treatment of pediatric anxiety disorders: an open-label extension of the research units on pediatric psychopharmacology anxiety study, Journal of Child and Adolescent Psychopharmacology 12(3), 175–188. McCracken, J.T., McGough, J., Shah, B., Cronin, P., Hong, D., Aman, M.G., Arnold, L.E., Lindsay, R., Nash,
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[26]
[27]
Psychopharmacology: Child and Adolescent
P., Hollway, J., McDougle, C.J., Posey, D., Swiezy, N., Kohn, A., Scahill, L., Martin, A., Koenig, K., Volkmar, F., Carroll, D., Lancor, A., Tierney, E., Ghuman, J., Gonzalez, N.M., Grados, M., Vitiello, B., Ritz, L., Davies, M., Robinson, J. & McMahon D. Research Units on Pediatric Psychopharmacology Autism Network (2002). Risperidone in children with autism and serious behavioral problems, The New England Journal of Medicine 347(5), 314–321. Research Units on Pediatric Psychopharmacology Autism Network (2005). Risperidone treatment of autistic disorder: longer-term benefits and blinded discontinuation after 6 months, The American Journal of Psychiatry 162(7), 1361–1369. Emrich, H.M., Dose, M. & von Zerssen, D. (1985). The use of sodium valproate, carbamazepine and oxcarbazepine in patients with affective disorders, Journal of Affective Disorders 8, 243–250.
ROBERT W. LOVELL
Psychosis see Delusions
Psychosis: Puerperal see Postpartum Psychosis
Psychotic Disorder: Shared see Temporary Insanity
Publishing in Forensics and Peer Review see Peer Review as Affecting Opinion Evidence
Pyromania see Firesetting
QiaAmp
Quality Systems: Toxicology
The QIAamp DNA Micro Kit DNA extraction method utilizes a silica-based spin column to separate DNA from other cellular components that are released after cell lysis. DNA binds, specifically, to the silica-gel membrane embedded within the microcentrifuge tube while other cellular components pass through. This process isolates a purified DNA extract as the washing steps remove inhibitory proteins and divalent cations, which are the cofactors for harmful nucleases. DNA is released from the silica column by the addition of an elution buffer. The entire procedure takes approximately 30 min. Lyophilized carrier RNA can be added to the lyzed sample at the beginning of the process to facilitate membrane binding. This is recommended for forensic samples; however, care must be taken to ensure that downstream quantitation methods are DNA specific. QiaAmp microextraction methods have the advantage of being a simple, reliable, flexible, single-tube technique that is highly amenable to automated liquid handling platforms. In many laboratories, QiaAmp is used as a postextraction purification step, particularly for degraded or severely compromised tissue.
Related Articles DNA Extraction SIMON J. WALSH
Introduction Quality management (QM) aims to ensure that the activities necessary to design, develop, and provide a product or service are effective and “fit for purpose”. QM including laboratory accreditation, i.e., inspection and independent certification of laboratories to ensure, as far as possible, the quality and reliability of the work produced, is becoming increasingly important [1]. A prerequisite for laboratory accreditation is to have a documented QM system. It was thought that the likelihood of examination in court was sufficient to ensure the accuracy and reliability of forensic toxicology results, but implementation of QM systems and accreditation of laboratories by regional or national accreditation bodies provide a far more robust method of ensuring quality. Obviously, all this has to be paid for and inspectors themselves have to be trained and accredited. The ISO 9000 family (ISO 9000:2000 and 9001: 2001) form a basis for many QM systems (Box 1) and are maintained by the International Organization for Standardization (ISO, http://www.iso.ch/iso/en/ iso9000-14000/index.html, accessed 27f August 2007). A related set of standards, ISO 14000, is concerned with environmental management. ISO
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Quality Systems: Toxicology
Box 1. Some of the requirements in ISO 9001:2001 • • • • • •
A set of procedures that cover all key processes in the organization being managed Active monitoring of processes to ensure that they are effective Adequate record keeping Monitoring the quality of output, with implementation of appropriate corrective action if necessary Regular review of individual processes and the QM system itself for efficacy Implementation of a culture of continual improvement
works in collaboration with the International Electrotechnical Commission (IEC) and other metrological organizations. ISO/IEC 17025:2005 is the main standard used by testing and reference laboratories to implement a QM system. It replaces ISO/IEC 17025:1999 (formally ISO Guide 25 and EN 45001). There is much in common with ISO 9000/9001, but ISO/IEC 17025 adds the concept of competence. There are two main sections: (i) management requirements that are primarily related to the operation and effectiveness of the laboratory QM system and (ii) technical requirements that address the competence of staff, methodology, and test/calibration equipment. ISO 15189:2007 defines standards for the operation of a medical laboratory, and is consistent with ISO 9000/9001. Laboratory accreditation procedures and conformity assessment bodies (CABs) are assessed against ISO/IEC 17011:2004 (previously ISO/IEC Guide
58). CABs are defined as organizations providing assessment services such as testing, inspection, management system certification, personnel certification, product certification, and calibration.
Laboratory Accreditation The International Laboratory Accreditation Cooperation (ILAC) website (http://www.ilac.org/, accessed 27 August 2007) gives details of accreditation bodies in many countries. Key elements are the Quality Policy, a statement of the quality aims of the organization, and the Quality Manual, which defines the organization’s QM system. The layout of the Quality Manual should follow the outline of ISO 17025:2005. Laboratory operations can be divided into preanalytical, analytical, and postanalytical phases (Box 2). Written procedures, usually known as standard operating procedures (SOP s), should describe all aspects
Box 2. Stages in analytical toxicology laboratory operation •
• •
Preanalytical Procedures must be in place to advise on appropriate sample collection (including sample tubes) and to ensure the safe transport, receipt, and storage of biological samples once in the laboratory, and for arranging the priority for the analysis Analytical Validated (i.e., tried and tested) procedures must be used to perform the requested or appropriate analyses to the required degree of accuracy and reliability in an appropriate timescale Postanalytical A mechanism for reporting results and maintaining confidentiality by telephone, fax, or other electronic means and in writing must be in place. Proper interpretation of results, especially for less-common analytes, must be provided. Full records of the analysis must be kept for at least 5 years (10 or more years in forensic work) unless otherwise determined by statute. Residues of samples must be stored appropriately until disposed of safely in an agreed timeframe
Quality Systems: Toxicology of laboratory operation, including management and health and safety aspects. The Society of Forensic Toxicologists (SOFT) and American Academy of Forensic Sciences (AAFS) have published detailed guidelines for the operation of forensic toxicology laboratories, much of which is also applicable to clinical toxicology laboratories [2]. Implementation and documentation of internal audits, both vertical (when, for example, the documentation concerning the analysis of a particular sample is examined) and horizontal (such as examining operating or quality procedures for internal consistency), are important parts of laboratory accreditation. Clinical or operational audit, i.e., examining the results generated in the light of the purpose for which they were requested, although much more difficult to undertake, is also important in the accreditation process. The results of such audits provide valuable training material. Documentation of “quality queries”, i.e., instances when mistakes or failures in processing have occurred, even if the error or failure was detected and corrected before a result was issued, and implementation and monitoring of corrective action, are also important in the accreditation process.
Method Implementation and Validation Whatever method is used for a given analysis it must be validated, i.e., it must be shown to be “fit for purpose” [3]. Assay validation should conform, as far as possible, with the US Food and Drug Administration (FDA) Center for Drug Evaluation and Research (CDER) guidance for bioanalytical method validation [4]. Data for within-day (repeatability), between-day, and total precision should be calculated according to the protocol proposed by the Clinical and Laboratory Standards Institute [5]. A number of terms important in understanding method validation are given in Table 1. Quantitative methods must have good precision and accuracy. Selectivity (freedom from interference, specificity) is important when a single species is to be measured, but broad specificity may be useful when screening for the presence of a particular class of compounds. The recovery of the analyte, i.e., how much of the compound of interest is recovered from the sample matrix during an extraction, for example, is important if sensitivity is limiting, but need not
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be an issue if the lower limit of quantification (LLoQ), accuracy, and precision of the assay are acceptable. Any quantitative analysis has associated errors, both random and systematic. In chromatographic and other separation methods, the “internal standard” method is often used to reduce the impact of systematic errors such as variations in injection volume, evaporation of extraction solvent, or mass spectrometry (MS) response during the analysis. Thus, a known amount of a second compound that behaves similarly to the analyte during the analysis, but elutes at a different place on the chromatogram or is otherwise detected independently of the analyte (the internal standard) is added at an appropriate stage in the analysis. Subsequently, the detector response of the analyte relative to the response of the internal standard is plotted against analyte concentration when constructing a calibration graph. Requirements for an internal standard for chromatographic assays are summarized in Box 3. Stable isotope-labelled analogues are widely used as internal standards in MS (isotope dilution MS). Isotopic internal standards have virtually identical chemical and physical properties to the analyte and thus extraction, derivatization if needed, chromatography, and fragmentation are often virtually identical. However, the site of isotopic labeling should be chosen such that the bonds linking the isotope are not broken during fragmentation, as bonds involving heavier isotopes are more stable and the fragmentation pattern of the labeled compound could thus differ from that of the analyte. The vibrational frequencies of carbon–deuterium bonds are less than those of the corresponding carbon–hydrogen bonds, for example, so that deuterated compounds tend to be more stable than their unlabeled homologs. That labeled and unlabeled compounds may be partially resolved during the chromatographic analysis (deuterated analogs may elute slightly before the unlabeled analyte in GC-MS, for example) must be borne in mind not only with regard to choosing the correct integration parameters, but also because any ion suppression due to cochromatographed components may differ between the internal standard and the analyte(s). The internal standard may add to the degree of ion suppression in LC-MS, but generally both internal standard and analyte are affected equally by such phenomena [6].
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Quality Systems: Toxicology Table 1
Terms used when reporting method validation
Term Accuracy Calibration range
Coefficient of variation (CV) Higher limit of quantitation (HLoQ) Internal standard
Limit of detection (LoD)
Linearity
Lower limit of quantification (LLoQ) Precision
Relative standard deviation (RSD)
Selectivity Signal-to-noise (S/N ) ratio
Notes The difference between the measured value and the accepted (“true”) value The range of concentrations between the highest and lowest calibration standards. This should encompass the range of concentrations found in the test samples An obsolete term for RSD The highest concentration that can be quantified. Not always quoted, but important in assays with a clear upper “cutoff”, for example, immunoassays and fluorescence assays A second compound, not the analyte, added at an appropriate stage in the assay to correct for systematic errors in the analysis The smallest amount of analyte that can be detected. Usually defined as some multiple (5, for example) of the baseline noise (signal-to-noise ratio = 5) or multiple of the SD of the blank signal A definable and reproducible relationship between a physicochemical measurement (e.g., UV absorption) and the concentration of the analyte, but not necessarily a straight line The lowest concentration that can be measured within defined limits. Usually a concentration for which the precision and accuracy have been set arbitrarily, e.g., RSD 100 Tablets and capsules (licit) (du = dosage unit) 1 − 50 du 51 − 100 101 − 1000 > 1000 Tablets and capsules (illicit) ≤ 10 11 − 27 ≥ 28
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Sample size All 10 √ N
Drugs Methaqualone, cocaine, barbiturates Cannabis, benzodiazepine, psilocybin Opium, morphine, heroin, mescaline
N/2 (up to 20) 20 30 √ N
Methaqualone, barbiturates Benzodiazepine, psilocybin Mescaline
All 3N/4 N/2 21 ≤ N/2 ≤ 50
Methaqualone Lysergide
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Sampling and Estimation of Quantities
•
Proportion of N : advantage – simple; disadvantage – excessive sample sizes for large populations. √ • A function of N : advantage – widely accepted; disadvantage – too small for small populations, excessive sample sizes for large populations. • n = 20 + 10%(N − 20)(N > 20): advantage – heterogeneous populations likely to be discovered before the analysis is complete; disadvantage – excessive sample sizes for large populations. for N < x x≤N ≤y N >y
n=N n=z √ n= N
(where x, y, and z are arbitrary numbers; x < y and x ≤ z < y) advantage: United Nations Drug Control Program recommended method (x = 10, y = 100, z = 10); disadvantage – excessive sample sizes for large populations. • n = 1: advantage – minimum amount of work; disadvantage – least amount of information on the characteristics of the seizure. The Scientific Working Group for the Analysis of Drugs (SWGDRUG) of the US Department of Justice Drug Enforcement Administration recommendations for a sampling plan has several components. • •
The issue of homogeneity. For inhomogeneous bulk material, several samples from different locations may be necessary to ensure that the test results are representative of the bulk material and false negative results are avoided. Statistical approaches are applicable when inferences are to be made about the whole population, as in
•
–
–
the probability that a given percentage of the population contains the drug of interest or is positive for a given characteristic, the total net weight of the population is to be extrapolated from the weight of a sample.
Bayesian Criteria for Determination of a Sample Size A Bayesian approach provides summaries in probabilistic terms such as
“How big a sample should be taken for it to be said that there is a 100p% probability that the proportion of units in the consignment which contains drugs is greater than 100 θ %?”
Or, for a particular case, with p = 0.95 and θ = 0.50, “How big a sample should be taken for it to be said that there is a 95% probability that the proportion of units in the consignment which contains drugs is greater than 50%?”
See the SWGDRUG comments on the applicability of statistical approaches to illustrate the relevance of this approach.
Choice of Sample Size for Discrete Data Large Consignments A consignment of drugs containing N units is considered as a random sample from some superpopulation of units, which contain drugs. Let θ (0 < θ < 1) be the proportion of units in the superpopulation (of which the consignment is a member) that contain drugs. Let m be the number of units sampled from the consignment. The sampling fraction is m/N . Denote the numbers (out of m) that are found to contain drugs by z(≤ m). Then, the probability distribution for z, given m and θ, is the binomial distribution m z θ (1 − θ)m−z ; P r(z|m, θ) = z z = 0, . . . , m
(1)
The purpose of the inspection of the sample is to determine an estimate for θ. A Frequentist Approach. The sample proportion that contains drugs p = z/m provides an estimate of θ. The variance of p is given by Cochran [10] as θ(1 − θ) N − m (2) m N −1 The term θ(1 − θ)/m is the standard deviation of a sample proportion z/m from the binomial distribution in (equation 2). The factor (N − m)/(N − 1) is known as the finite population correction (fpc). Provided the sampling fraction m/N is low, the size of the population has no direct effect on the precision of the estimate of θ. For example, a sample
Sampling and Estimation of Quantities of 500 from a population of 200 000 gives almost as precise an estimate of the population proportion as a sample of 500 from a population of 10 000. The estimated standard deviation of θ in the second case is 0.98 times the estimated standard deviation in the first case. Little is to be gained by increasing the sample size in proportion to the population size. Given a desired magnitude δ for the standard deviation, it is possible to choose the sample size necessary to achieve this. Set δ equal to √ {θ(1 − θ)/m}. Then, m = θ(1 − θ)/δ 2 < 1/(4δ 2 ), the maximum value attained when θ = 1/2. A sample of size m equal to the smallest integer greater than 1/(4δ 2 ) is the smallest sample size that satisfies the requirement that the standard deviation be less than δ. A Bayesian Approach. This approach is based on combining a binomial likelihood for the number z of members of a sample of size m that contain drugs with a beta-distribution, with parameters α and β for the proportion θ of the superpopulation of which the consignment is a subset. The prior distribution for θ is taken to be a beta-distribution with the probability density function given by f (θ|α, β) =
θ α−1 (1 − θ)β−1 , B(α, β)
0 < θ < 1, α > 0, β > 0
(3)
denoted B(α, β), where B(α, β) =
(α)(β) (α + β)
(4)
and is the gamma function, where (t + 1) = t! for integer t > 0
(5)
A scientist who believes that the consignment is either all illicit or all licit with a small probability of something in-between would choose values of α and β close to zero. Then, combining the beta prior (equation 3) with the binomial distribution (equation 1), the posterior distribution for θ given m, z, α, β is Pr(θ|m, z, α, β) =
θ α+z−1 (1 − θ)β+m−z−1 B(α + z, β + m − z)
contains drugs when all units sampled contain drugs (i.e., m = z). Then the criterion may be written mathematically as Pr(θ > 0.5|m, m, α, β) = 0.95
(7)
where m replaces z as the second term to the right of the conditioning bar to show that z = m. This criterion may be written in integral form as 1 m+α−1 θ (1 − θ)β−1 dθ = 0.95 (8) B(m + α, β) 0.5 The general question of Section (3) in which p and θ are specified may be answered by finding the value of m, which solves the equation 1 m+α−1 θ (1 − θ)β−1 dθ =p (9) B(m + α, β) θ Such integrals are easy to evaluate using standard statistical packages, values for m, α, and β being given. Given specified values for θ and p and values for α and β chosen from prior beliefs, the appropriate value of m to solve (equation 9) may be found by trial and error. See Table 2 for examples of values of p for given values of m, α, and β. There may be concerns that it is very difficult for a scientist to formalize his prior beliefs. However, if α and β are small, large differences in the probabilities associated with the prior beliefs do not lead to large differences in the conclusions. This is not the case, however, if there is a probability of a misclassification error [11]. A frequentist approach using the hypergeometric distribution, with an adaptation to allow for false positives and false negatives is described in Faber et al. [12]. The methodology can be extended to allow for units that do not contain drugs. The dependency of the sample size on the values of p and θ is illustrated in Table 3. The prior Table 2 The probability that the proportion of drugs in a large consignment is greater than 50% for various sample sizes m and prior parameters α and β m
(6)
a posterior beta distribution for θ, given the sample size m, the number of illicit units z(≤ m), and prior parameters α and β. Consider the criterion that the scientist wishes to be 95% certain that 50% or more of the consignment
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α
β
2
3
4
5
1 0.5 0.065
1 0.5 0.935
0.92
0.94 0.97 0.90
0.97 0.985 0.95
0.993 0.97
Permission needed from JFS
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Sampling and Estimation of Quantities
Table 3 The sample size required to be 100p% certain that the proportion of units in the consignment that contains drugs is greater than θ , when all the units inspected are found to contain drugs. The prior parameters α = β = 1
1.0 0.8
θ
0.90
0.95
0.99
0.5 0.6 0.7 0.8 0.9 0.95 0.99
3 4 6 10 21 44 229
4 5 8 13 28 58 298
6 9 12 20 43 89 458
1 – F (q )
p 0.6 0.4 0.2 0.0 0.0
0.2
0.4
Permission needed from JFS
parameters α and β are set equal to 1. Consider p = 0.90, 0.95, and 0.99 and consider values of θ = 0.5, 0.6, 0.7, 0.8, 0.9, 0.95, 0.99. The sample size m required to be 100p% certain that θ is greater than the specified value is then given by the value of m that satisfies the equation
0.8
1.0
Figure 1 The prior probability 1 − F (θ ) that the proportion of units in a consignment is greater than θ , for various choices of α and β: α = β = 1(− · −·), α = β = 0.5(−), α = 0.065, β = 0.935(· · ·) [Reproduced with permission from JFS.]
1.0
(10)
a special case of (equation 9). The value of m is thus given by the smallest integer greater than log(1 − p) −1 (11) log(θ0 ) Variation in the prior beliefs, expressed through variation in the values of α and β, may have little influence on the conclusions, once some data have been observed. Figure 1 illustrates the prior probability that the true proportion of illegal units in a consignment is greater than a value θ, for 0 < θ < 1 for three choices of α and β. Figure 2 illustrates the posterior probability that the true proportion of illegal units in a consignment is greater than θ, for these choices of α and β, once four units have been examined and all are found to be illegal.
Small Consignments Suppose now that the consignment size N is small, say N ≤ 50. A sample of m units from the consignment is examined and z(≤ m) units are found to contain drugs. A Frequentist Approach. Consider a frequentist approach based on the hypergeometric distribution.
0.8
1 – F (q )
Pr(θ > θ0 |m, m, 1, 1) = 1 − θ0m+1 = p
0.6 q
0.985 0.970 0.950
0.6 0.4 0.2 0.0 0.0
0.2
0.4
0.6
0.8
1.0
q
Figure 2 The posterior probability 1 − F (θ ) that the proportion of units in a consignment is greater than θ , for various choices of α and β: α = β = 1(− · −·), α = β = 0.5 (−), α = 0.065, β = 0.935(· · ·), after observation of four units all found to be illegal. The corresponding probabilities that at least 50% of the consignment contains illegal units is marked as 0.985(α = β = 0.5), 0.970(α = β = 1), 0.950 (α = 0.065, β = 0.935) [Reproduced with permission from JFS.]
Examples are given in Bates and Lambert [13] and Faber et al. [12]. Let R = Z + Y be the total number of units in the consignment that contains illicit drugs,
Sampling and Estimation of Quantities where Z is the number of units in the sample of size m and Y is the number of units in the remainder (N − m) that contain drugs. Then, the distribution of Z is hypergeometric with R N−R Pr(Z = z) =
z
Nm−z , m
z = 0, 1, . . . , min(R, m)
(12)
The lower limit for θ is R/N , where R is the maximum number of illicit units in the population, which satisfies the following inequality R N−R r m−i i ≤α (13) N i=0
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have not been inspected. Then Y (unknown and ≤n) is the number of units in this remainder that contain drugs. Given θ, the distribution of (Y |n, θ), similar to that of (Z|m, θ), is binomial. However, θ has a β distribution and the distribution of (Y |n, θ) and the distribution of (θ|m, z, α, β) can be combined to give a Bayesian predictive distribution for (Y |m, n, z, α, β), a β-binomial distribution. P r(Y = y|m, n, z, α, β) = (m + α + β) yn (y + z + α) ×(m + n − z − y + β) , (z + α)(m − z + β)(m + n + α + β) (y = 0, 1, . . . , n)
(15)
m
where r is the number of nondrug items in the sample and the confidence level is 100(1 − α)% [7]. When m = z, the inequality is R!(N − m)! ≤α N !(R − m)!
(14)
A Bayesian Approach. A Bayesian approach for small consignments using the hypergeometric distribution is described in Coulson et al. [14]. A discrete prior distribution is chosen for the (N + 1) possible divisions of the consignment into licit and illicit items. The likelihood function is based on the hypergeometric distribution sampling m from N and a posterior distribution obtained. An alternative Bayesian approach for small consignments uses a so-called β-binomial distribution. This distribution provides a probability statement (as distinct from a confidence statement) about the number of units in the consignment that contains drugs. As before, let θ (0 < θ < 1) be the proportion of units in the superpopulation that contains drugs. The probability distribution of z, given m and θ, may be taken to be binomial. For each unit, independently of the others in the consignment, the probability that it contains drugs is taken to be equal to θ. The posterior distribution of θ is another β distribution with parameters (α + z) and (β + m − z). Since the consignment size is small, a better representation of the variability of the number of units Y , which contain drugs in the uninspected section of the consignment, is obtained by considering a probability distribution for Y explicitly. There are n units in the remainder of the consignment (m + n = N ), which
From this distribution, inferences can be made about Y , such as probability intervals or lower bounds for Y .
Quantity The standard of proof is relevant to the estimation of quantity. In state courts in the United States in 2001, the value of Q in a drug trial was defined to be an essential element of the possession charge. As such, the value of Q had to be proved by a jury beyond reasonable doubt. However, in Federal courts, Q was considered an issue of fact and had only to be established on the preponderance of the evidence. This should be borne in mind when interpreting the estimation processes. For further information about procedures in the United States, see the Sentencing Guidelines [15]. The importance of quantity estimation was illustrated in the drug smuggling case of U.S. v. Shonubi. At issue was the estimation of an unknown total amount of heroin that was imported illegally in the digestive tract of the defendant during several trips from Nigeria to the United States. The only quantitative piece of information available was the amount of heroin found in the defendant’s possession on his last trip. This amount was itself the result of a sampling process. Shonubi was found to be carrying internally 103 multicolored balloons, each filled with a white powdery substance. Four of the balloons were selected randomly for testing and inference. The total net weight of the heroin in all 103 balloons was estimated by multiplying the average net weight of the heroin in the four balloons by 103 [16].
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The estimation of the quantity of a drug is treated in two stages. First the proportion of the units in the consignment that contain illicit drugs is modeled. Second, the total weight of the illicit material in those packets that contain anything illicit is estimated. Uncertainty in the prior belief in the proportion of packets that are “illicit” may be represented by a β distribution. It is assumed that there is no prior information for the mean and variance of the distribution of the quantity of drugs in the packages. Details of how such prior information may be considered are given in Aitken et al. [17]. Given the sample size, and thus an estimate of the proportion of a consignment that contains drugs and an estimate of the mean and standard deviation of the weight in the consignment, a confidence interval for the true quantity of drugs may be calculated [7]. A probability interval is appropriate in a Bayesian context. In this context, a probability distribution is associated with a parameter (Q, say) denoting the total quantity of illicit material in the consignment and probability statements of any desired kind may be made. For example, these could include the probability that Q is greater than a certain value, q say, which will be of importance in sentencing hearings; here q may be a borderline between two base offense levels.
Frequentist Approach It is only possible to make a statement about the consignment as a whole with certainty if the whole consignment is analyzed. Once it is accepted that a sample has to be considered, then it is necessary to consider what level of proof is adequate. This is strictly a matter for the court to decide. The method described by Tzidony and Ravreboy [7] considers the consignment as a population and the packages (or units) examined as a sample. The quantities (weights) of drugs in the units are assumed to be random variables that are normally distributed, with population mean µ and population variance σ 2 , say. The mean quantity in a unit in the consignment is estimated by the mean, denoted by x, ¯ of the quantities found in the sample. A confidence interval is determined for µ based on the sample size m, the sample mean x, ¯ the sample standard deviation s of the quantities of drugs in the units examined, and an associated t-distribution. The general expression for
the relevant confidence interval is s (N − m) x¯ − t(m−1) (α/2) √ N m s (N − m) ≤ µ ≤ x¯ + t(m−1) (α/2) √ (16) N m √ where (N − m)/N is the finite population correction factor. The term t(m−1) (α/2) denotes the 100(1 − α )% point of the t-distribution with (m − 1) degrees 2 of freedom, e.g., for the 95% confidence interval, α = 0.05, and t(m−1) (α/2) is the 97.5% point of t(m−1) . The interval is the 100(1 − α)% confidence interval for the mean quantity in a package [7]. The corresponding confidence interval for Q, the total quantity of drugs in the consignment, is obtained by multiplying all entries in the inequalities by N θˆ , where θˆ is an estimate for θ based on the sample of size m. This gives as a 100(1 − α)% confidence interval for Q [7].
s (N − m) ˆ N θ x¯ − t(m−1) (α/2) √ N m
(N − m) s (17) ≤ Q ≤ N θˆ x¯ + t(m−1) (α/2) √ N m A corresponding 100(1 − α)% lower bound for Q, which may be deemed more appropriate in a legal context, is given by the left-hand side of the inequality
(N − m) s N θˆ x¯ − t(m−1) (α) √ ≤ Q (18) N m
Bayesian Approach Consider the consignment as itself a random sample from a larger superpopulation of units or packages, some or all of which contain illegal material. Then, θ (0 < θ < 1) is the proportion of units in the superpopulation, which contains drugs. The variability in θ may be modeled by a β distribution. Let n be the number of packages in the consignment that is not examined. Then, N equals m + n. Let (x1 , . . . , xz ) and (w1 , . . . , wy ) be the weights of the contents of the units examined and not examined respectively, which contain drugs. It is assumed that these weights are normally distributed. The total
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Table 4 Estimates of quantities q g. of drugs, in a consignment of m + n units, according to various possible burdens of proof, expressed as percentages P = 100 × P r(Q > q|m, z, n, x, ¯ s) in 26 packages when six packages are examined (m = 6, n = 20) and z = 6, 5, or 4 are found to contain drugs. The mean (x) ¯ and standard deviation (s) of the quantities found in the packages examined, which contain drugs, are 0.0425 g and 0.0073 g. The parameters for the beta prior are α = β = 1. Numbers in brackets are the corresponding frequentist lower bounds using the finite population correction factor Number of units examined which contain drugs Percentage P 97.5 95 70 50
6 0.689 0.750 0.944 1.015
(0.930) (0.968) (1.067) (1.105)
5 0.501 0.559 0.770 0.862
Possible burden of proof (illustrative)
4
(0.744) (0.785) (0.885) (0.921)
0.345 0.397 0.603 0.704
(0.575) (0.613) (0.704) (0.737)
Beyond reasonable doubt Clear and convincing Balance of probabilities
Permission needed from JFS
q = zx¯ + y w¯ (19) ¯ 2 /(z − 1) be the variAlso, let s 2 = zi=1 (xi − x) ance of the measurements on the units that were examined and found to contain drugs. In the absence of prior information about the mean or variance of the distribution of the weights of drugs in the packages, a uniform prior distribution is used. The distribution and corresponding probability density function of Q may be determined from the relationship Q = zx¯ + y W¯ . Let ft,z−1 (.) denote the probability density function of the t-distribution with (z − 1) degrees of freedom. The probability density function f (q) of Q is then given by [18] n q − (z + y)x¯ ft,z−1 f (q) = 1 1 y=0 sy + z y
−1 1 1 sy P r(Y = y) (20) + z y An example in which a seized drug exhibit contained 26 street doses is given in Tzidony and Ravreboy [7]. A sample of six (m = 6) units was taken and each was analyzed and weighed. Twenty (n = 20) units were not examined. All six of the units examined contained drugs. The average net weight x¯ of the powder in the six units was 0.0425 g. with a standard deviation s of 0.0073 g. A 95% confidence interval for the total quantity Q in the 26 doses is 1.105 ± 0.175 g. Note that this interval incorporates
the finite population correction factor from (equation 2) to allow for the relatively large sample size (m = 6) compared to the consignment size (N = 26). The Bayesian approach described here does not require a finite population correction. The values for Q obtained from the Bayesian argument and corresponding to appropriate percentage points of the distribution may be determined from (equation 20). Some results are given in Table 4, together with corresponding results with the method of Tzidony and Ravreboy, and in Figure 3. 1.0 0.8 Pr(Q > q )
weight, q, of the contents of the units in the consignment is then given by
0.6 0.4 0.2 0.0 0.2
0.4
0.6
0.8 q
1.0
1.2
1.4
Figure 3 The probability that the total quantity Q of drugs (in grams) in a consignment of 26 packages is greater than q, using a Bayesian argument, when six packages are examined and 6(−), 5(− − −), or 4(− · −·) are found to contain drugs. The mean and standard deviation of the quantities found in the packages examined, which contain drugs, are 0.0425 g and 0.0073 g. The parameters for the β prior are α = β = 1 [Reproduced with permission from JFS.]
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Note: A general introduction to sampling techniques is given in Cochran [10]. Reviews of the statistical and legal aspects of the forensic study of illicit drugs are given by Izenman [2, 19]. These includes a discussion of various sampling procedures, various methods of choosing the sample size, a strategy for assessing homogeneity and the relationship between quantity and the possible standards of proof. Further comments on sampling issues are given in various chapters of Gastwirth [20], such as Aitken [21], Gastwirth et al. [22], and Izenman [16, 23, 24], with respect to the Shonubi case.
References [1] [2]
[3]
[4]
[5] [6]
[7]
[8]
[9]
[10] [11]
[12]
Wigmore, J.H. (1979). Evidence in Trials at Common Law, Vol. 2, Little, Brown, Boston. Izenman, A.J. (2003). Sentencing illicit drug traffickers: how do the courts handle random sampling issues, International Statistical Review 71, 535–556. Curran, J.M., Triggs, C.M. & Buckleton, J. (1998). Sampling in forensic comparison problems, Science and Justice 38, 101–107. American Society for Testing and Materials (ASTM) (2001). E 122-00 Standard Practice for Calculating Sample Size to Estimate with a Specified Tolerable Error, the Average for a Characteristic of a Lot or Process. Evett, I.W. & Weir, B.S. (1998). Interpreting DNA Evidence, Sinauer Associates Inc, Sunderland, MA. Frank, R.S., Hinkley, S.W. & Hoffman, C.G. (1991). Representative sampling of drug seizures in multiple containers, Journal of Forensic Sciences 36, 350–357. Tzidony, D. & Ravreboy, M. (1992). A statistical approach to drug sampling: a case study, Journal of Forensic Sciences 37, 1541–1549. United Nations Guidelines: Methaqualone (ST/NAR/15; December, 1998); Lysergide (ST/NAR/17; January, 1989); Cocaine (ST/NAR/7; February, 1986); Benzodiazepine (ST/NAR/16; December, 1988); Cannabis (ST/NAR/8; February, 1987); Psilocybin (ST/NAR/19; December, 1989); Mescaline (ST/NAR/19; December, 1989); Opium, Morphine, Heroin (St/NAR/29/Rev.1; June, 1998). European Network of Forensic Science Institutes Drugs Working Group (2004). Guidelines on Representative Drug Sampling. Cochran, W.G. (1977). Sampling Techniques, 3rd edition., John Wiley & Sons, Chichester. Rahne, E., Joseph, L. & Gyorkos, T.W. (2000). Bayesian sample size determination for estimating binomial parameters from data subject to misclassification, Applied Statistics 49, 119–128. Faber, N.M., Sjerps, M., Leijenhorst, H.A.L. & Maljaars, S.E. (1999). Determining the optimal sample size in
[13]
[14]
[15] [16]
[17]
[18]
[19]
[20] [21]
[22]
[23]
[24]
forensic casework - with application to fibres, Science and Justice 39, 113–122. Bates, J.W. & Lambert, J.A. (1991). Use of the hypergeometric distribution for sampling in forensic glass comparison, Journal of the Forensic Science Society 31, 449–455. Coulson, S.A., Coxon, A. & Buckleton, J.S. (2001). How many samples from a drug seizure need to be analyzed?, Journal of Forensic Sciences 46, 1456–1461. United States Sentencing Commission Guidelines Manual (2007). http://www.ussc.gov/2007guid/GL2007.pdf. Izenman, A.J. (2000c). Assessing the statistical evidence in the Shonubi case, in Statistical Science in the Courtroom, J.L. Gastwirth, eds, Springer-Verlag, New York, pp. 415–433. Aitken, C.G.G., Bring, J., Leonard, T. & Papasouliotis, O. (1997). Estimation of quantities of drugs handled and the burden of proof, Journal of the Royal Statistical Society, Series A 160, 333–350. Aitken, C.G.G. & Lucy, D. (2002). Estimation of the quantity of a drug in a consignment from measurements on a sample, Journal of Forensic Sciences 47, 968–975. Izenman, A.J. (2001). Statistical and legal aspects of the forensic study of illicit drugs, Statistical Science 16, 35–57. Gastwirth, J.L. (ed) (2000). Statistical Science in the Courtroom, Springer-Verlag, New York. Aitken, C.G.G. (2000). Interpretation of evidence and sample size determination, in Statistical Science in the Courtroom, J.L. Gastwirth, eds, Springer-Verlag, New York, p. 1–24. Gastwirth., J.L., Freidlin, B., Miao, W. (2000). The Shonubi case as an example of the legal system’s failure to appreciate statistical evidence, in Statistical Science in the Courtroom, J.L. Gastwirth, ed, Springer-Verlag, New York, p. 405–413. Izenman, A.J. (2000a). Statistical issues in the application of the Federal sentencing guidelines in drug, pornography and fraud cases, in Statistical Science in the Courtroom, J.L. Gastwirth, ed, Springer-Verlag, New York, p. 25–50. Izenman, A.J. (2000b). Introduction to two views on the Shonubi case, in Statistical Science in the Courtroom, J.L. Gastwirth, ed, Springer-Verlag, New York, p. 393–403.
Further Reading American Society for Testing and Materials (ASTM) (2004). E 105-04 Standard Practice for Probability Sampling of Materials. Col´on, M., Rodriguez, G. & Diaz, R.O. (1993). Representative sampling of ‘street’ drug exhibits, Journal of Forensic Sciences 38, 641–648. United States Department of Justice Drug Enforcement Administration (2006). The Scientific Working Group for the Analysis of Drugs (SWGDRUG). Recommendations.
Sampling Trace Evidence U.S. v. Shonubi: Shonubi V : 962 F.Supp.370 (E.D.N.Y. 1997); Shonubi IV : 103 F.3d 1085 (2d Cir. 1997); Shonubi III : 895 F.Supp. 460 (E.D.N.Y. 1995); Shonubi II : 998 F.2d 84 (2d Cir. 1993); Shonubi I : 802 F.Supp. 859 (E.D.N.Y. 1992).
COLIN G. G. AITKEN
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Explosion Debris: Laboratory Analysis of), drugs, and firearms is beyond the scope of this section. The following aspects of trace evidence sampling are covered: 1. 2. 3. 4. 5.
principles of sampling trace evidence; population determination; sampling plans used for trace evidence; sampling questions; and methods of trace evidence sample recovery.
Principles of Sampling Trace Evidence Sampling Trace Evidence at the Crime Scene
Introduction Sampling can be defined as the removal of a part of a substance to assess the materials present in the whole. In a forensic context, sampling has a broader definition as it occurs throughout the forensic process from selection of items at the crime scene to subsampling in the laboratory. Trace evidence by its nature is small in size such that examination commonly requires the use of a microscope [1, 2]. Sampling of trace evidence encompasses the selection, recovery, and removal of material and can include sampling of a single item, similar items, or different items. The reasons for sampling include reducing the number of analytical determinations necessary, time constraints, presentation for instrument analysis, and cost. The first stage in sampling is defining the sampling strategy. The sampling strategy chosen is dependent on the question being asked, the purpose of sampling, the use of results. Therefore, a sampling strategy is necessary, which must satisfy all aspects above including forensic evidential requirements. The second stage is defining the target population for what is being sampled. A sampling plan is established for reasons of effectiveness and efficiency and to ensure the sampling strategy is implemented. The sampling plan forms the third stage. Finally, the sampling methods used ensure the sampling plan is implemented [3]. This section reviews sampling of trace evidence, in particular, paint (see also Paint), glass (see also Glass), fibers (see also Paint), hairs (see also Hair: Animal), soil, and particulates (see also Particles: Form). Sampling of DNA (see DNA), explosives (see Explosions: Scene Investigation;
The Locard exchange principle is quoted as “every contact leaves a trace” [4]. Usually, things are not so simple. When sampling for trace evidence, determining the type(s) of trace evidence one is looking for is crucial in the decision making process. Sampling is based on the case circumstances, the evidence type being looked for, and the items available for analysis. The investigator may be directed by the available case information, although there are occasions when information is scarce, thereby increasing the need for care in the sampling procedure so as not to compromise one evidence type while sampling for another. Sampling processes employed determine what is ultimately examined and the conclusions that can be drawn from the testing results. When sampling for trace evidence, it is necessary to take samples from the area where the transferred trace evidence may have been deposited and take a representative sample from the original source of the trace evidence. Where a house is burgled and the suspect gains entry through a broken window, crime scene investigators seize the articles of clothing worn at the time of the alleged offense by the suspect and take an adequate representative control sample of glass from the window. When a crime scene is examined, it is rarely practical nor is it necessary to examine all of the items available. The initial selection of items to be examined is determined by what is known to have happened (from witness, victim, and suspect statements) and where one is likely to find the evidence type. For example, if one wishes to see if there is evidence that two people were in contact, then selecting the clothing that they were wearing at the time of the alleged contact and looking for evidence of fiber transfer are required.
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Sampling and Subsampling in the Laboratory In the laboratory, the sampling plans and recovery methods chosen depend on the trace evidence type, the case circumstances, and the question being asked. For example, sampling done to determine the presence of paint, glass, particulates, etc., or to determine both the presence and quantity of the substance(s). Some reasons for sampling in the laboratory are as follows: • • •
•
Taking samples to carry out different tests on the population of trace evidence. Taking samples from the population of trace evidence to carry out the same test repeatedly to determine reproducibility of results. Taking a sample from the population to carry out destructive testing (sample is destroyed and no further testing can be carried out on the sample selected). Sampling for practical considerations in relation to presentation for instrument analysis.
Once the decisions have been taken regarding the trace evidence type to sample then one has to decide how that will be done, i.e., what sampling plan will one follow and what recovery method will be used? In essence, sampling at the crime scene and in the laboratory involves risk assessment and risk management. When sampling for trace evidence the operator is always working in a context. No matter how good the sampling process is, it introduces a level of uncertainty. Risk management of sampling involves assessing the level of uncertainty introduced by sampling and adopting sampling plan(s) and methods of recovery such that one has confidence in the sampling decisions taken and the interpretation of the results.
Population Determination One has to decide what to sample before you decide which sampling plan to use. This is the need to define the relevant population. There are two possibilities: (a) a homogenous population where all items look the same e.g., 100 pieces of green glass that look visually similar or (b) a heterogeneous population, for example, 100 pieces of green glass and 100 pieces of clear glass. When one has a heterogeneous population, one would sample from both green and clear glass populations if the case involved a broken
green and clear stained glass window, but would sample only the clear glass population if the case involved a broken clear glass window. Population determination is based on the case circumstances and the trace material sources available [5].
Sampling Plans Used for Trace Evidence In trace evidence analysis, the most common sampling plans used, divide into numerically based and nonnumerically based.
Numerically Based Plans Numerical plans can be statistically based or nonstatistically based. Statistically Based Sampling Plans. Statistically based sampling is used when one is defining a population based on the analysis of the sample taken from that population, for example, defining a population of glass fragments as being from a putative source based on the refractive index of the sample of selected glass fragments. There are two different approaches to statistical sampling, the Frequentist approach and the Bayesian (see also Bayesian Networks) approach [6]. In general, the Frequentist approach is that a fixed but unknown proportion of the population is positive and the proportion of positives in the sample can be used to estimate the proportion of positives in the population. The proportion of positives varies over different samples. This method gives a confidence level that a defined minimum in the population is positive. The most commonly used Frequentist method in trace evidence is the hypergeometric method. The following publications give a good overview of the subject [7–12]. The Bayesian approach assumes that the proportion of positives in the sample is fixed. There is no consideration for repetition of sample testing [11, 13, 14]. The Bayesian approach allows prior information about the population to be taken into account whereas the Frequentist approach does not. Prior information, for example, could be that all the suspect fibers look visually the same and were found on the victim’s jumper. The disadvantage of the Bayesian method is that the values attached to the prior knowledge are subjective. However, using the Bayesian approach is more intuitive and flexible as the results obtained
Sampling Trace Evidence from the evidence can be expressed as probability statements and prior information is taken into account [11, 13]. Nonstatistically Based Sampling Plans. Nonstatistical sampling plans have been documented in relation to drugs analysis [6]. A number of these are also used for trace evidence [12]. Examples of nonstatistical sampling plans used in relation to trace evidence include testing all the samples, testing one, and testing 20. Nonstatistical sampling is simple to apply; however, only limited inferences can be made about the overall properties of the population [6].
Nonnumerically Based Sampling Plans While numerically based sampling plans are well documented, the same cannot be said for nonnumerically based plans. Analysis of trace evidence involves many nonnumerically based sampling plans. Frequently used nonnumerical sampling plans are probability sampling, judgment sampling, and bulk sampling. Probability (Random) Sampling. Probability sampling occurs when every unit in the population has a known probability of being included in the sample and is often referred to as random sampling [15]. For example, if 100 pieces of glass were removed from a suspect’s jacket, randomly picking 10 of them for analysis would constitute random sampling. Depending on the trace evidence type, this may not be practical. In the case of fiber examination, if one had numerous blue fibers on an adhesive lift, one would sample the longest fibers, as long fibers allow destructive testing to be carried out while still allowing retention of some of the original fiber. Judgment Sampling. Judgment sampling involves selecting items based on traits or aspects they have in common with other items in the case. If a pale blue car knocks down and kills a person, one would select pale blue paint found on the victim’s clothes for analysis. The selection is made on the basis of the similarities the sample has with other item(s) in the case. The presence of a dark blue paint on the victim’s clothes may introduce other questions, such as, could a different car have been involved? Bulk Sampling. This type of sampling happens when a sample is taken from a large amount of
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material that does not consist of separate units and is often a feature of subsampling in the laboratory. Bulk sampling occurs when one takes a sample of soil from a field. Considerations include as to where the sample is taken from, how much sample is taken, and whether the sample is representative of the lot. Trace evidence analysis frequently involves the use of many sampling plans used sequentially or at the same time. When a burglar enters a house through the window and the crime scene examiner comes to examine the scene, he uses judgment sampling to target the areas where the intruder may have left trace evidence. When a suspect is caught, judgment sampling is used to select the items of clothing to be taken from the suspect based on what the suspect was seen to have worn at the time. Judgment sampling is used in the laboratory to target paint flakes on the suspects jumper of the same color as that of the paint on the window, and bulk sampling is used to select fibers from the suspect’s jumper to compare with the fibers found on the window. Problems Associated with Sample Plan Selection. While the hypergeometric sampling is used commonly when sampling glass, there is disparity when it comes to deciding what an appropriate sample size is for the other trace evidence types. In the area of fibers, for example, Faber et al. [12] determined that there was a disparity in sample size analyzed between different laboratories. They observed that an objective criterion is needed to determine optimal fiber sample size in casework and suggested the use of the hypergeometric method [12]. Various international forensic organizations have been tackling this problem, e.g., European Network of Forensic Institutes (ENFSI) and European Fibres Group. If an internationally accepted norm were established for different aspects of trace evidence it would greatly enhance sampling norms across different countries. The conclusions drawn from trace evidence are largely influenced by the sampling methods and plans used. It is important that forensic scientists are aware of the methods and plans they are using, and the veracity of the conclusions they reach based on that evidence [16].
Sampling Questions To identify the factors that influence sampling plans and methods, asking questions is helpful. The following are some questions that are relevant when making sampling decisions:
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Sampling Trace Evidence
What background information is available? What question(s) need to be answered? What will the testing results be used for? What type of trace evidence is of interest? Are there any legal requirements? Is identification of material all that is required? What accuracy and precision is required? What is to be sampled and how? Is it necessary to sequence the sampling that is to take place? Should statistical sampling be employed? Is the sampling plan chosen adequate to answer the question asked and does it fulfill the purpose? Is the plan chosen cost effective and efficient? Is there literature to back up the sampling plan chosen? Will it be possible to defend the conclusions drawn from the sampling plan employed?
Finding the answers to some or all of these questions should guide one to appropriate sampling plan(s) and sampling method(s).
Methods of Trace Evidence Sample Recovery While the sampling strategy and sampling plans used influence the testing results so also do the methods of trace evidence sample recovery. Commonly used methods of recovery of trace evidence are removal of the whole item, ‘hand’ picking, taping, brushing, vacuuming, and scraping [4, 17].
Removal of the Whole Item It may not always be possible or appropriate to remove trace evidence at the crime scene. In this situation the whole item is brought to the forensic science laboratory for trace evidence removal.
‘Hand’ picking ‘Hand’ picking of trace evidence is the method of choice when the quantity of evidence, size, and appearance allow. Items are usually collected by hand (gloved) or by using a sharp pointed tweezers using strong light and magnification. This method has the advantage of establishing the position of the material on the item.
Taping The use of adhesive tape is a reliable method of removing very small particles of trace evidence [18, 19]. A short length of adhesive tape is passed repeatedly over the surface of the item ensuring the entire surface under examination is sampled. This is then applied to a sheet of rigid plastic and placed in a clean plastic bag appropriately labeled. Taping is used routinely to remove fibers, hairs, and particulates. This method protects trace evidence from contamination and allows the trace evidence of relevance to be separated from nonrelevant material. The tape-lift is examined under a microscope and the trace evidence removed by circling the evidence on the back of the tape and lifting the tape to remove it, or by circling the evidence and cutting and lifting the section of tape to remove it. The latter method prevents contamination of the lift from elements in the atmosphere.
Brushing Brushing is the method of choice for the removal of paint, glass, and soil. A clean paintbrush or toothbrush is used to brush down the item in question and the resulting debris is collected for examination. It allows retrieval of trace evidence from areas that are difficult to access. Using this method one does not encounter the difficulty of retrieving small fragments of paint, glass, or soil intact from an adhesive lift.
Vacuuming Vacuuming is an efficient way to remove trace evidence. However, its efficiency is a disadvantage in that recently deposited material is mixed with that deposited long ago and the volume of material retrieved lengthens the process of trace evidence retrieval. Vacuuming is performed in a systematic manner and filters changed frequently so that the debris retrieved can be associated with a specific area e.g. sleeves of a jacket. Vacuuming is not recommended for routine use because of the difficulty in interpretation, the rigorous requirements to avoid contamination, and the length of time taken to analyze the contents retrieved.
Scraping Scraping has limited use as a method of sample removal of trace evidence. However, it can be used
Sampling Trace Evidence to collect a control sample of a source of paint. This involves using a clean blade to remove a representative paint sample from the surface (e.g. a painted door) that is collected on clean paper, in a paper envelope, or a tweezer is used to mount the sample on a glass slide. Selection of a suitable method of trace evidence removal is vital to minimize loss of potential evidence, avoid contamination, and to facilitate trace evidence analysis [20].
Conclusion Trace evidence analysis is a valuable tool in crime scene investigation. When sampling for trace evidence, it is important to realize that the methods of sampling and the sampling plans used ultimately affect the evidence obtained and the interpretation of that evidence. It is vital that sampling is carried out correctly and is understood to eliminate loss of potential evidence and to avoid overestimation or underestimation of the significance of the evidence found. Currently sampling of trace evidence is an area that has received little in-depth analysis leading to a lack of uniformity in approach.
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Petraco, N. (1985). The occurrence of trace evidence in one examiner’s casework, Journal of Forensic Sciences 30(2), 485–493. Petraco, N. (1986). Trace evidence – the invisible witness, Journal of Forensic Sciences 31(1), 321–328. Crosby, N.T. & Patel, I. (1995). General Principals of Good Sampling Practice, The Royal Society of Chemistry. Horswell, J. (2004). Collection techniques: present status, in The Practice of Crime Scene Investigation, J. Horswell, ed, CRC Press LLC. Robertson, J. (1999). Protocols for fibre examination and initial preparation, in Forensic Examination of Fibres, 2nd Edition, J. Robertson & M. Grieve, eds, Taylor & Francis, London. European Network of Forensic Science Institutes Drugs Working Group (2003). Guidelines on Representative Drug Sampling, European Network of Forensic Science Institutes Drugs Working Group. Tzidony, D. & Ravreby, M. (1992). A statistical approach to drug sampling: a case study, Journal of Forensic Science 37, 1541–1549. Curran, J.M., Triggs, C.M. & Buckleton, J. (1998). Sampling in forensic comparison problems, Science and Justice 38(2), 101–107.
[20]
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Sandercock, P.L.M. (2000). Sample size considerations for control glass in casework, Canadian journal of Forensic Science 33(4), 173–185. Bates, J.W. & Lambert, J.A. (1991). Use of the hypergeometric distribution for sampling in forensic glass comparison, Journal of Forensic Science Society 31(4), 449–455. Aiken, C.G.G. (1999). Sampling – how big a sample? Journal of Forensic Sciences 44(4), 750–760. Faber, N.M., Sjerps, M., Leijenhorsst, H.A.L. & Maljaars, S.E. (1999). Determining the optimal sample size in forensic casework – with application to fibres, Science and Justice 39(2), 113–122. Causin, V., Schiavone, S., Marigo, A. & Carrisi, P. (2004). Bayesian framework for the evaluation of fibre evidence in a double murder – a case report, Forensic Science International 141, 159–170. Champod, C. & Taroni, F. (1997). Bayesian framework for the evaluation of fibre transfer evidence, Science and Justice 37, 75–83. Houck, M.M. (2005). Forensic fibre examination and analysis, Forensic Science Review 17(1), 17–29. Ramsey, M.H. & Ellison, S.L.R. (ed) (2007). Measurement Uncertainty Arising from Sampling, A Guide to Methods and Approaches, Eurachem /CITAC Guide. Saferstein, R. (ed) (1988). Collection and examination of microtraces: present status, in Forensic Science Handbook, Prentice-Hall. Biermann, T., European Fibres Group (1998). The advantages and disadvantages of 1:1 taping, Proceedings of the Sixth European Fibres Group Meeting. 10–12 June 1998, Dundee, 44–47. Pounds, C.A. (1975). The recovery of fibres from the surface of clothing for forensic examinations, Journal of Forensic Science Society 15, 127–132. SWGMAT SWGoMA (1999). Trace evidence recovery guidelines, Forensic Science Communications 1(3), section 5, http://www.fbi.gov.
MARY GIBLIN
Scalds see Injury: Burns, Scalds, and Chemical
Scanning Electron Microscopy see Microscopy: Scanning Electron Microscopy
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Scientific Method Compared to Legal Method
Scene: Bomb, Management see Bomb Scene Management
Scene: Investigation see Firearms: Scene Investigation
Scene: Crime, Documentation see Crime Scene Documentation
Scene: Shooting see Firearms: Scene Investigation
Scene: Crime, Investigation see Crime Scene Investigation
Scene: Crime, Management see Crime Scene Management
Scene: Explosion see Explosions: Scene Investigation
School Threat Assessment see Threat Assessment: School
School Violence see Threat Assessment: School
Scientific Evidence: Behavioral see Behavioral Science Evidence
Scene: Explosion, Investigation see Explosions: Scene Investigation
Scientific Method Compared to Legal Method
Scene: Fire, Investigation see Fire: Scene Investigation
The acquisition and interpretation of information (data) used by scientists compares, superficially, to the legal method used in determining controversies in a legal forum. Both methods attempt to use a rational approach; both also use an inductive method of solving problems. The differences, therefore, do
Scientific Method Compared to Legal Method not lie in the methodologies chosen to obtain a result, but are rather heavily influenced by the disparate purposes sought to be served [1]. Science seeks to analyze data or information obtained during prior experiments or inquiries in an essentially neutral fashion to obtain the best explanation as to why certain results were manifested, in order that the course of future events may be reliably predicted. Rarely does the scientific method focus on an individual, particular incident. The case to which it is being applied is important only insofar as it permits the scientist to formulate a general hypothesis on how to deal with similar events that are yet to occur. The purpose of the legal method in resolving disputes or controversies is to determine what ought to be, rather than what is. After having considered certain information, the legal system is interested in knowing how findings and conclusions that arise out of the information impact on a specific case that is currently pending before the court. Thus, lawyers are less interested in what the impact of the evidence will be on other cases, but instead are concerned with applying the results to the normative values upon which behavior in our society is conditioned. While it engages in this balancing of values, the legal system may also be creating new norms and values, which will affect future behavior [1]. When differing or opposing values are represented by the parties in a legal controversy, the adversary system, which is the hallmark of the Anglo–Saxon judicial process, casts each participant into an adversary posture. Unlike the neutrality of interpretations with which the scientist seeks to clothe his testimony, the trial lawyer will be interested primarily in advocating the values that favor the party by whom he was retained [2–5]. Failing to recognize the different aims and purpose of science vis-a-vis those at stake in a legal contest has pitted scientists and lawyers against each other in uncomfortable battles. Lawyers often hold experts in disdain because they believe that an expert’s opinion is for sale and that the expert will come to almost any conclusion that is desired by a litigating party. By contrast, scientists may feel estranged from the judicial process because of the intensive crossexamination to which they may be subjected, a process wherein the experts feel that their dignity is impugned and their honesty questioned. The acerbity
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of cross-examination has driven some experts to refusing to testify in court cases. An increased understanding of both sides and the different aims that are the goal of the scientific method, as opposed to those of the legal system, will enhance the effectiveness of experts in offering testimony, and of attorneys seeking to elicit the experts’ opinion testimony [6].
References [1]
[2]
[3] [4] [5]
[6]
Moenssens, A.A., Henderson, C.E. & Portwood S.G. (2007). ScientificEvidence in Civil and Criminal Cases, 5th Edition, Foundation Press, Chapter 1 at § 1.03(2). On the differences between law and science generally, see also, Channels, N.L. (1985). Social Science Methods in the Legal Process. Loevinger, L. (1985). Science, technology, and law in modern society, J urimetrics 26, 1. Patterson, M.R. (1999). Conflicts of interest in scientific expert testimony, William and Mary Law Review 40, 1313. Meyer, C.B. (1997). Science and the law: the quest for the neutral expert witness. a view from the trenches, The Journal of Natural Resources and Environmental Law, 12, 35. For a further illustration of how a scientific process may at times proceed in six different and distinct stages, see Moenssens, A.A., Henderson, C.E. & Portwood S.G. (2007). ScientificEvidence in Civil and Criminal Cases, 5th Edition, Foundation Press, Chapter 1 at § 1.03(2), pp. 14–15.
ANDRE MOENSSENS
Scientific Principles as Evidence in Court see Judicial Notice of Scientific Principles and Facts
Scientific Texts as Evidence in Court see Learned Treatises as Evidence
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Seizures: Behavioral
Search and Seizures see Police Use of Force
Seizures: Behavioral A seizure is a set of behaviors that occurs in association with excessive, aberrant neuronal activity within the brain. Seizures are generally characterized by altered consciousness, motor dysfunction, or sensory dysfunction. Epilepsy is a chronic condition in which the patient experiences recurring seizures.
Definition, Prevalence, and Cumulative Incidence At any given time, approximately 1% of the population manifests epilepsy. There is a total lifetime incidence rate of approximately 4% by age 80. This makes it one of the most common neurological disorders.
Classification of Seizures A classification of seizures is important to facilitate clinical diagnosis and communication, to assess prognosis, and to evaluate whether specific drugs are the most appropriate ones for therapy. Dating back to the 1981 classification proposed by the International League Against Epilepsy (ILAE) [1], seizures are classified first into partial or generalized seizures. Seizures are generally classified as to whether they are partial (seizures that begin in a focal portion of the brain), or whether they are generalized (occurring bilaterally and diffusely without a local onset). Seizures are termed partial if there is either clinical or electroencephalogram (EEG) evidence indicating onset in a focal area of one hemisphere, whereas generalized seizures appear to begin simultaneously in both hemispheres. Partial seizures are divided into three categories: (i) simple partial (not affecting consciousness), (ii) complex partial (involving alteration of consciousness), and (iii) partial seizures evolving into secondarily generalized tonic–clonic (GTC)
convulsions, which could begin as either simple partial or complex partial seizures. Simple partial seizures are marked by no loss of consciousness. They are manifested by behaviors specific to the locale of the seizure origin. Motor seizures involve either an involuntary jerking or stiffening movement or rarely paralysis of a given limb or region of the body. The focal movements can remain localized or involve a progression, for example, beginning in a finger and then spreading to the entire arm and face. The latter is called a Jacksonian seizure. The simple partial motor seizure may also involve versive head turning, postural changes, forced speech or inability to speak, or vocalization. Simple partial somatosensory or special sensory seizures can manifest themselves as tingling, numbness, or as specific visual, auditory (such as buzzing sound), olfactory (such as peculiar smell), or gustatory sensations. Autonomic simple partial seizures are marked by autonomic symptoms, such as nausea, sweating, or goose bumps. Simple partial psychic seizures are manifested by dysphasia (such as trouble with verbal expression), deja-vu (feeling of familiarity), or affective symptomatology (fear, elation). Complex partial seizures are marked by a loss or alteration in consciousness. These can begin as simple partial seizures, and then progress to alterations of consciousness, or can begin with loss or changes of consciousness at the onset. If the complex partial seizure is heralded by a subjective experience, we call this an aura, but the experience actually represents subjective simple partial seizure activity. Clouding of consciousness and automatisms reflect bilateral seizure spread. Automatisms are repetitive, purposeless movements of the extremities (particularly hands) and face, such as lip smacking, chewing, scratching, or rubbing. Less frequently, they can also involve complex behaviors such as reaching for an object, walking, running, or disrobing. Partial seizures can also secondarily generalize into GTC activity. A “postictal” state of confusion, drowsiness, and tiredness often follows the seizure itself. This is least pronounced with simple partial seizures and most pronounced with secondarily generalized seizures. Generalized-onset seizures, seizures that begin bilaterally, can take different forms as well. Generalized seizures are divided into six types: (ii) absence seizures, (ii) myoclonic seizures, (iii) clonic seizures, (iv) tonic seizures, (v) tonic–clonic seizures, and (vi) atonic seizures. Generalized absence seizures
Seizures: Behavioral are characterized by brief (several seconds) loss of awareness or responsiveness and arrest of activity. Absence seizures (also called petit mal ) involve a sudden loss of consciousness that typically only lasts a few seconds. There may or may not be associated minor motor activity, such as automatisms, blinking, slight twitching, decreased tone, or increased tone. GTC seizures are characterized by loss of consciousness at onset, a sudden tonic muscular contraction, and sometimes a movement of air through a closed glottis, producing a “cry”, as well as cyanosis. After the tonic phase, the seizure then evolves into generalized clonic or rhythmic jerking activity from a 4- to 8-s tremor, sometimes accompanied by grunting. The clonic activity is initially fast, and the frequency of the jerks decreases before the seizure stops. GTC seizures are often accompanied by tongue biting and urinary incontinence. Generalized myoclonic seizures are brief, sudden contractions that may be generalized or confined to a group of muscles, or even a single muscle. They can be single and isolated, or occur in a cluster. Consciousness is usually preserved. Some forms of myoclonus are not epileptic and have no associated EEG discharge. Myoclonic seizures usually have a concomitant discharge on the EEG. Generalized clonic seizures are characterized by repetitive clonic jerks, without an initial tonic component. Generalized tonic seizures manifest with a muscular contraction that may vary in duration, severity, and the parts of the body involved. The muscular contractions are more sustained than those of myoclonic seizures. Generalized atonic seizures are characterized by a sudden decrease in muscle tone, which is variable in severity and extent, so that there may simply be a slight head drop, or an abrupt fall to the ground. Status epilepticus is a state of continuous seizure activity or repetitive seizures without recovery in between seizures. When the status epilepticus seizure activity is generalized convulsive, this represents a life-threatening medical emergency due to the potential for damage to the brain. Brain damage is estimated to begin at approximately 20 min after the onset of status, so it is critical to intervene early.
Classification of Epilepsies and Epileptic Syndromes In addition to classifying individual seizures, the epilepsy condition as a whole can be classified. In
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1989, the ILAE has recommended a classification that remains in wide use [2]. It is recognized, however, that advances will necessitate a revision. Most patients with epilepsy will have only partialonset or only generalized-onset seizures. Hence, the classification has two major categories: localizationrelated epilepsies (partial epilepsies is an acceptable synonym) or generalized epilepsies. Each category is further subdivided into idiopathic or symptomatic epilepsies. The idiopathic epilepsies are typically characterized by the absence of acquired brain insult and are widely considered to be of genetic origin. The symptomatic epilepsies have known insults that have caused the epilepsy. In addition, some patients are suspected to have had a brain insult, but one that cannot be definitively identified. These patients are referred to as probably symptomatic (cryptogenic was used as a synonym but has fallen out of favor). Most partial epilepsies are symptomatic or probably symptomatic, while most generalized epilepsies are idiopathic or probably idiopathic. However, it is recognized that many patients have both genetic predisposition to seizures as well as acquired brain insults. Some patients have additional characteristic features that help to group them into recognized epileptic syndromes. The characteristics of syndromes may include specific age at onset, a particular combination of seizure types, a predictable response to treatment, and a variety of other clinical features.
Epidemiology Not all persons who experience seizures have epilepsy. In fact, most do not. Epilepsy is not diagnosed if the seizure is acutely provoked by an insult such as trauma or stroke, or if the seizure accompanies exposure to certain drugs or a derangement in metabolism. Even single unprovoked seizure recurs in less than half of individuals. Of those persons who do have epilepsy, approximately half of them have no known precipitating event or injury. Many factors can provoke seizures. Some reversible alterations that can trigger seizures include metabolic changes, such as low blood sodium, calcium, or magnesium, kidney failure, or liver failure. Many toxins and drugs can trigger seizures. This includes psychoactive prescription drugs such as tricyclic antidepressants, bupropion (Wellbutrin), antipsychotic drugs such as clozapine (Clozaril),
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Seizures: Behavioral
and illicit agents such as cocaine or phencyclidine (PCP). In addition, withdrawal from alcohol, benzodiazepines, or barbiturates can also trigger seizures. In general, seizures do not recur after removing the offending agent or after the withdrawal period has passed. Many factors may contribute to the development of epilepsy. Any disease or condition that injures the cerebral cortex can cause epilepsy. This includes brain infections and inflammations such as encephalitis, head trauma, brain tumors, brain malformations, and degenerative conditions such as Alzheimer’s disease. Chronic alcohol use increases the risk of epilepsy, and this is not due to alcohol withdrawal seizures. Head trauma is a common etiology for epilepsy. The most epileptogenic head trauma is penetrating head injury, with an epilepsy incidence as high as 53% following such injuries. Moderate-to-severe closed head injuries are associated with a significantly increased risk of epilepsy, from 3 to 25 times greater than in the absence of head trauma [3]. Among closed head injury patients, brain contusions and intracranial hemorrhages appear to be strong risk factors for the development of seizures. The presence of skull fractures or prolonged loss of consciousness or posttraumatic amnesia (greater than one day in length) are also risk factors, though not as strongly predictive. Mild head trauma, defined by loss of consciousness or posttraumatic amnesia for less than 30 min, is associated with a slightly greater risk of epilepsy (1.5-fold increase in risk) that is not statistically significant [4]. Other potential causes of seizures or seizurelike episodes should be carefully ruled out in the mild head injury patient presenting with apparent seizures, including withdrawal from alcohol or other substances, hypoglycemia or other metabolic conditions, and psychogenic seizures. The latter are particularly common following mild traumatic brain injury [5]. Even after moderate-to-severe head injury, 33% of patients experiencing seizurelike phenomena were actually experiencing psychogenic seizures [6]. A common legal question is how to prove causality between an injury and epilepsy. Before addressing causality, it is important to first prove the presence of epilepsy. The injury has to be sufficiently severe to cause epilepsy. For example, mild head injury may not stand in court as a cause of epilepsy. Additional requirements are absence of any manifestation of epilepsy before the injury in question and absence
of other known causes of epilepsy. Of course, it is also possible that a preexisting epilepsy can be worsened by an injury [7].
Diagnostic Methods The clinical interview and medical history taken are critical to the assessment of seizures and epilepsy. The history is obtained from both the patient and observers who have witnessed typical attacks. In the description of clinical seizures, evidence for focal seizure onset is sought, for example, the presence of an aura, initial focal sensory symptoms, or motor signs. In addition, the type of aura and the first signs in partial seizures help to localize the seizure onset within the brain. The past history, including prenatal, birth, and early development, and family history may provide insight into the etiology. All of the above may provide the clinician with the opportunity to classify the seizure types and the epileptic syndrome, and identify etiologic factors. The neurological examination is important to identify the focal signs of neurological dysfunction, which would favor partial epilepsy. If the description of the events is strongly suggestive of epileptic seizures, the EEG is an important test to help confirm the presence of a seizure tendency. The EEG is a measure of electrical brain activity, usually recorded from scalp electrodes. Patients with epilepsy frequently have EEG abnormalities in between seizures, called interictal abnormalities. Some of these abnormalities, such as spikes or sharp waves, are fairly specific for epilepsy and are referred to as interictal epileptiform discharges. In partial epilepsies, the interictal epileptiform discharges tend to be focal or regional. These discharges generally have a topographic correlation with the epileptogenic zone, the zone from which seizures are generated. Recordings obtained during seizures will generally show a rhythmic discharge. In generalized epilepsies, epileptiform discharges tend to be generalized and synchronous in the two hemispheres. Approximately 50% of persons with epilepsy will show abnormal electrical activity on their first EEG recording and more than 90% by the fourth recording. There is no apparent benefit to additional EEGs after the fourth recording. The EEG yield can be enhanced with prolonged recording and simultaneous video monitoring, allowing for a direct correlation to be made between
Seizures: Behavioral the behavioral manifestations of the seizure and the changes observed on the EEG. This procedure is usually needed when there is some question about the nature of the seizure, such as whether the spells experienced by the patient might represent psychogenic seizures or pseudoseizures. The psychogenic seizure patient will evidence no EEG changes concomitant to the seizure being videotaped. EEG/video recordings also allow for the localization of seizure onset and evolution. Thus this method is particularly useful for the epilepsy patients considered for surgery. The recording of a seizure on EEG/video can provide a definitive proof of the existence of epilepsy. The recording of interictal epileptiform discharges indicates a seizure tendency and suggests the presence of epilepsy, but cannot prove the presence of epilepsy beyond doubt. It is much harder, almost impossible, to prove the absence of epilepsy. If typical attacks are recorded and are determined to be nonepileptic, and the EEG is always normal in between seizures, then the presence of epilepsy becomes very unlikely. In the patient with seizures, imaging techniques are useful to identify a cause of epilepsy. A structural imaging study of the brain, preferably with magnetic resonance imaging (MRI), should be sought to identify structural abnormalities that may be epileptogenic. In the epilepsy surgery candidate, positron emission tomography (PET), which measures glucose uptake by the brain, is useful to identify functional deficits corresponding to the seizure focus. The epileptogenic focus generally has decreased glucose uptake in between seizures and increased glucose uptake during a seizure.
Differential Diagnosis Several medical conditions can imitate seizures, thus requiring careful differential diagnosis. These conditions can be broadly divided into psychiatric and physiological imitators. Several psychiatric disorders can imitate seizures. Panic disorder is marked by spells of autonomic hyperactivity, including shortness of breath, heart palpitations, sensations of heat or cold, gastric distress, and motor tension. Panic attacks are usually characterized by intact awareness throughout the spell, including fear of having a heart attack or losing one’s mind, and an absence of postictal state or incontinence. Episodic dyscontrol syndrome, intermittent
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explosive disorder, or “rage attacks” also must be differentiated from seizures. The patient with intermittent explosive disorder, though perhaps reporting amnesia for the event, will not evidence altered consciousness or a postictal state. Typically, precipitants for the rage events will be readily identifiable. One of the most common imitators of seizures and epilepsy is the condition of psychogenic nonepileptic seizures (PNES), often called pseudoseizures or pseudoepileptic seizures. PNES are episodes of alteration in movements or responsiveness, which resemble epileptic seizures in some ways, but are purely emotional in nature and lack a concomitant cerebral electrical discharge. They occur most commonly through unconscious “conversion reactions”, but less frequently through voluntary malingering. PNES may account for an estimated 20–30% of patients referred for intractable seizures. PNES are more common in young people, with a relative female predominance. The clinical manifestations of PNES are extremely variable. There may or may not be a reported aura. The onset is often gradual, and always occurs when the patient is awake, even if the patient appears to be asleep. PNES often include motor manifestations, but physical collapse or altered responsiveness may be the only observable manifestations. Many clinical features have been used to diagnose psychogenic attacks and to distinguish them from epileptic seizures. Features that support a diagnosis of PNES include out-of-phase upper and lower extremity movements, side-to-side head movement, and forward pelvic thrusting. Other suggestive clinical features include a gradual onset, “preictal” behavioral changes, “pseudosleep” before seizure onset, discontinuous seizure activity, prolonged duration (“pseudostatus epilepticus” is common), gradual cessation, absence of postictal state, high seizure frequency, excessive variability in ictal manifestations, nonphysiologic progression, eye closure during unresponsiveness, eye fluttering, resistance to eye opening, vocalizations consisting of gagging, retching, gasping, screaming, crying or moaning, retained consciousness and recollection of events with bilateral jerking activity, emotional displays such as crying during events, the presence of an emotional trigger, and the occurrence of events only in the presence of others. If the examiner can suggest the patient into initiating or stopping seizure activity, a psychogenic seizure is suspected. Documented incontinence, tongue biting, and self-injury during attacks
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Seizures: Behavioral
suggest epilepsy, but these features are also reported by patients with PNES. No feature alone is definitive, but a combination of the features noted above can improve the ability to distinguish PNES from epileptic seizures. An elevated serum prolactin level 15–30 min after a seizure also suggests epilepsy, but a normal level does not exclude epilepsy. Prolonged EEG/video monitoring is usually necessary for the definitive diagnosis of PNES. A history of childhood sexual or physical abuse is commonly obtained (approximately 30%). Depression, anxiety, personality disorders, and somatoform disorders are also common and are important to identify and treat. About 10–20% of patients with PNES also have epilepsy. The investigation for coexistent epilepsy is important for treatment, but the exclusion of coexistent epilepsy can be very difficult. An important condition in which seizurelike episodes are consciously generated is Munchausen syndrome or factitious disorder. Patients with this condition have a strong intrapsychic need to fill the patient role. Munchausen’s syndrome by proxy refers to individuals who have a need for another (typically their child) to fill a physically ill patient role. Affected individuals are often very knowledgeable through study of medical works and accounts of seizure symptoms. Other patients may malinger seizurelike events in order to obtain personal injury or worker’s compensation benefits, or to obtain antiepileptic medication. It is possible that malingering patients choose an episodic disorder to simulate in order to avoid direct scrutiny of their symptoms in the examination room. Among physiological disorders imitating epilepsy, syncope is a common symptom related to a transient global reduction in cerebral blood flow. A cardiac origin, such as an arrhythmia, is more of a concern in older individuals, whereas in adolescents and young adults, syncope is most often neurally mediated. Neurally mediated syncope usually features a prodrome of nausea, lightheadedness, and dimming of vision. An observer may witness pallor. This prodrome is usually longer than the aura preceding an epileptic seizure. Up to 90% of syncope is associated with motor activity, predominantly brief multifocal myoclonus that lasts for a few seconds. This is to be distinguished from epileptic tonic–clonic activity, which is longer in duration and synchronous on the two sides. Recovery is usually much faster with syncope than with a seizure, without a “postictal state”. Syncope is usually not associated with tongue biting
or incontinence. In neurally mediated syncope, the patient usually has enough warning to sit down or at least break his or her fall, whereas patients with epileptic seizures may collapse suddenly, without any warning. If there is doubt, an EEG can be helpful. Other medical disorders that can be confused with seizures include migraine headaches, which can have a prodromal period marked by visual or somatosensory symptoms, vertigo, or confusion. The characteristic headache and nausea that follow the prodrome usually make the diagnosis clear, but they are not always present. Migraine symptoms tend to have a more gradual onset and a longer duration than those of seizures. Transient ischemic attacks (TIAs) are usually characterized by negative symptoms and signs, such as numbness, visual loss, or weakness, whereas seizures most often produce positive phenomena, such as paresthesias, hallucinations, or involuntary motor activity. Other conditions that can be confused with seizures are transient global amnesia, a transient amnestic state that may mimic a temporal lobe seizure, and “drop attacks of the elderly”, a syndrome of sudden falling without self-described loss of consciousness or postictal state. Hypoglycemia can cause lightheadedness, a sense of hunger, and an alteration of consciousness, which can lead to syncope or in some instances seizure activity, if the patient does not ingest glucose. Movement disorders such as hemiballismus, dystonia, and myoclonus can occasionally be confused with seizures. A few sleep disorders such as parasomnias and REM behavior disorder occasionally masquerade as seizures. Parasomnias such as sleep walking, sleep talking, or night terror arise from deep, slow wave sleep, whereas seizures more often arise in light sleep. REM behavior disorder arises from an abnormal REM sleep in which inhibition of motor activity is impaired. Narcolepsy includes sleep attacks, cataplexy, or loss of tone with emotion or startle, visual hallucinations upon falling asleep or waking up, and sleep paralysis, an inability to move upon waking up.
Adverse Consequences of Seizures and Epilepsy There is an increased risk for epileptic patients to suffer from injuries, primarily due to falls and other accidents caused by the seizures themselves. Burns due to seizures are very common and account for
Seizures: Behavioral 0.8–3.7% of burn center admissions [8, 9]. There is an increased risk of fractures, concussions, and spinal cord injuries as well. There is likewise an increased risk of mortality among seizure patients, including those caused by drowning and other accidents. Sudden unexplained death in epilepsy (SUDEP) is one of the leading causes of epilepsy mortality. Death occurs most often in association with a seizure, and disproportionately during sleep. There is no apparent structural cause, and the most likely cause of death is either respiratory depression or cardiac arrhythmia, or a combination of both. Seizure control is the most important measure for reducing mortality due to SUDEP. Occupational impairment and disability are conditions complicating the lives of many persons with epilepsy. A large proportion of individuals with epilepsy lose their jobs upon acquiring the illness. For many others, the threat of seizures occurring while at work is a significant burden. The Social Security Administration identifies epilepsy as a “listed impairment” for which disability benefits are awarded, though many individuals even with intractable seizures often have difficulty obtaining their benefits through the Social Security disability determination system. Driving restrictions due to epilepsy account for a considerable portion of the impairment in daily activities encountered by epilepsy patients, and is a factor that figures heavily into epilepsy patients’ ratings of their quality of life. In the United States, in 28 states patients must be seizure-free for a specific period, ranging from 3 to 12 months, before they are allowed to drive. In other states, medical advisory boards and/or the patient’s physician play a role in determining fitness to drive. Many states do not shield the physician from legal liability for their decision. Factors that reduce the likelihood of accidents include the presence of a 6- to 12month seizure-free interval, and, in the individual patient, the presence of reliable auras, monitoring and adjustment of antiepileptic drugs (AEDs), and the absence of previous accidents. Patients with an established pattern (more than six months) of seizures occurring exclusively in sleep or seizures without change in awareness or responsiveness do not need to be restricted from driving [10]. Discrimination against persons with epilepsy is a serious obstacle to employment and the maintenance of normal social relationships. The stigma
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perceived by epilepsy patients, and internalization of shame about their condition, are factors in their perceived quality of life. The appearance of stories about seizures in the print media have been shown to often exaggerate the risk of dying during a seizure, to overestimate the curative powers of anticonvulsant medications, and to use demonic imagery in stories about seizures. The use of the term epileptic, discouraged by epilepsy associations, is often used in the print media. The American with Disabilities Act provides guidelines and regulations to employers and employees in the workplace regarding seizures and the management of and responsibilities of employees with epilepsy.
Treatment There is general agreement that treatment has to be initiated after two seizures, because the risk of recurrence is very high. However, it is not clear if treatment is necessary after a single seizure. A number of factors predict a higher risk of seizure recurrence and encourage initiation of therapy after a single seizure. These factors include the presence of a known cause of epilepsy and the presence of epileptiform discharges on the EEG. Patients with a low risk of seizure recurrence have to be involved in the treatment decision and have to balance the risk of seizures and the risks and inconvenience of medication therapy. The initial treatment of epilepsy is with one AED, chosen based on efficacy for the specific seizure type, and taking into account the specifics of each patient. Approximately 50% of patients will become seizure-free with the first AED. For those who are resistant to the first AED, a second AED is substituted or added. Other treatment methods for treatmentresistant patients include the ketogenic diet, particularly in some forms of pediatric epilepsy. The patient is put on a restricted high fat and low carbohydrate diet, which causes ketones to accumulate in the body, with resultant anticonvulsant effects. The vagal nerve stimulator is the only device that is currently approved for epilepsy therapy. An electrode is implanted in the neck and wrapped around the left vagus nerve and a pulse generator and battery are implanted over the chest and connected to the electrode. The optimal stimulation parameters are identified through gradual titration. Approximately
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two-thirds of patients with epilepsy are resistant to treatment. If the epilepsy is focal, surgical resection of the epileptogenic zone is considered and can be highly effective. AEDs can have a problematic impact on patient behavior and cognition. Many of these agents have side effects of sedation, impaired attention, irritability, and impaired memory. Adverse effects that are of potential legal relevance include suppression of intelligence and learning ability in children taking AEDs, as well as the potential for impaired intelligence and overall neuropsychological functioning in children born to mothers taking AEDs during pregnancy. Evidence-based practice parameters promulgated by the American Academy of Neurology conclude that AEDs in general are implicated in teratogenic effects during pregnancy. The risk may be greatest for mothers taking valproic acid and carbamazepine, or for those taking multiple medications. The risk of major malformations (structural abnormalities requiring surgery to prevent death or dysfunction) is approximately doubled in children exposed to AEDs in utero, from 2–3% to 4–6%. For patients who become seizure-free on seizure medications, treatment is continued for at least two years. The decision to stop the seizure medications has to take into consideration factors that predict a higher recurrence rate. These factors include an abnormal EEG and the presence of brain damage. The patient also has to understand the potential consequences of seizure recurrence. There is a small risk that recurrent seizures may not be as easy to control as the initial seizures.
Seizures, Aggression, and the Law In criminal trials, the contention that violent behavior has occurred as a result of a seizure disorder is sometimes offered as a criminal defense. In such cases, the question is whether the defendant possessed a culpable mental state at the time of the alleged events, or whether the act was an automatic, nonvolitional one caused by a seizure or its after effects. Technically, such a defense is not an insanity defense (see Insanity: Defense), but is a defense based upon alleged automatism. The law views acts carried out in a seizure as automatic, with no volitional component, hence there is no criminal culpability (see Automatism as a Defense to Crime).
Ictal aggression, the commission of a violent act during a seizure itself, is thought to be very rare. Presumably, such an action would be part of an often-repeated, stereotyped automatism typically manifested by the person with the seizure disorder. Such aggression is rare, and would be accompanied by a confused mental state in which the person attacks another in a haphazard, involuntary fashion without a triggering event. The attack is usually limited to pushing, clutching, or shoving. According to Treiman, all documented cases of possible ictal aggression reviewed by him showed that the behavior was either (i) nonaggressive violent automatisms that were stereotyped and repetitive from seizure to seizure, (ii) reactive automatisms manifested by directed aggression after the onset of a clearly identifiable complex partial seizure, or (iii) resistive violence at the end of a complex partial or GTC seizure occurring while the individual was being restrained while still in a postictal, confused state [11]. In the case of aggressive automatisms, the patient’s behavior before the episode would be normal, and no specific triggers for the aggression will be present. The onset is quite sudden, with normal behavior one moment and the next displaying inappropriate behavior. Observers will typically report that the patient suddenly stopped, began to stare, and began to show evidence of confusion and automatisms. The aggression will be poorly defined and inappropriate, with attacks on those who happen to be physically nearby, rather than on those with a psychological connection to the patient. Following the conclusion of the episode, consciousness will return. The patient will likely not recall the incident. Treiman has described guidelines for determining whether there is a relationship between a violent event and epilepsy prior to proffering an expert legal opinion [11]. These include that the diagnosis of epilepsy should be established by a neurologist with a special competence in epilepsy, the presence of epileptic automatisms should be documented by the history and EEG/video monitoring, the presence of aggression during epileptic automatisms should be verified in a video-recorded seizure, the aggressive act should be characteristic of the patient’s habitual seizures as shown in the history and should be of short duration and not in response to any external stimulus except restraint, and that the neurologist should judge whether the act followed the known sequence of behavioral changes in complex partial
Seizures: Behavioral seizures or whether it was too complex a behavior to have been carried out as part of an epileptic automatism. The presence of interictal violence is also sometimes in question in cases in which an individual with a seizure disorder commits a violent act, but not during a seizure itself. There does not seem to be an association between epilepsy and violence, other than perhaps beyond the known association between mild brain dysfunction and impulsivity. There is no evidence that seizure disorder itself predisposes individuals to violent acts. Thus, there is no reason to question criminal responsibility in cases of alleged interictal violence, though Fenwick has attributed some cases of mild aggressiveness to prodromal irritability occurring prior to seizure activity [12]. Such irritability is not likely to contribute to an insanity defense, though it may lead to an argument of decreased culpability for a given act of aggression (see Mitigation Testimony).
References [1]
[2]
[3]
[4]
[5]
[6]
[7]
[8]
Commission on Classification and Terminology of the International League Against Epilepsy (1981). Proposal for revised clinical and electroencephalographic classification of epileptic seizures, Epilepsia 22(4), 489–501. Commission on Classification and Terminology of the International League Against Epilepsy (1989). Proposal for revised classification of epilepsies and epileptic syndromes, Epilepsia 30(4), 389–399. Annegers, J.F. & Coan, S.P. (2000). The risks of epilepsy after traumatic brain injury, Seizure 9(7), 453–457. Annegers, J.F., Hauser, W.A., Coan, S.P. & Rocca, W.A. (1998). A population-based study of seizures after traumatic brain injuries, The New England Journal of Medicine 338(1), 20–24. Barry, E., Krumholz, A., Bergey, G.K., Chatha, H., Alemayehu, S. & Grattan, L. (1998). Nonepileptic posttraumatic seizures, Epilepsia 39(4), 427–431. Hudak, A.M., Trivedi, K., Harper, C., Booker, K., Caesar, R.R. & Agostini, M.A., Van Ness, P.C., DiazArrastia, R. (2004). Evaluation of seizure-like episodes in survivors of moderate and severe traumatic brain injury, The Journal of Head Trauma Rehabilitation 19(4), 200–295. Tai, P.C. & Gross, D.W. (2004). Exacerbation of preexisting epilepsy by mild head injury: a five patient series, The Canadian Journal of Neurological Sciences 31(3), 394–397. Rimmer, R.B., Bay, R.C., Foster, K.N., Jones, M.A., Wadsworth, M. & Lessard, C., Mathieson, K., Caruso, D.M. (2007). Thermal injury in patients with seizure
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disorders: an opportunity for prevention, Journal of Burn Care and Research 28(2), 318–323. [9] Wirrell, E.C. (2006). Epilepsy-related injuries, Epilepsia 47(Suppl 1), 79–86. [10] Krauss, G.L., Ampaw, L. & Krumholz, A. (2001). Individual state driving restrictions for people with epilepsy in the US, Neurology 57(10), 1780–1785. [11] Treiman, D.M. (1999). Violence and the epilepsy defense, Neurologic Clinics 17(2), 245–255. [12] Fenwick, P. (1989). The nature and management of aggression in epilepsy, The Journal of Neuropsychiatry and Clinical Neurosciences 1(4), 418–425.
JAMES S. WALKER AND BASSEL ABOU-KHALIL
Self-Incrimination: Capacity to Waive see Capacity to Waive Miranda Rights
SEM see Microscopy: Scanning Electron Microscopy
Semen: Differential Extraction see Differential Extraction
Semen: Test for see Acid Phosphatase
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Sentencing: Demographic Factors in
Sentencing: Demographic Factors in A jury trial is a complex process that includes many factors for jurors to consider when trying to render a judgment of guilt or determine sentencing length for a guilty defendant.a Evidence shows that jurors try to make good decisions by considering the case at hand, the strength of the evidence, and other appropriate factors; but there is also ample research to show that jurors’ decisions are also affected by extralegal factors. In particular, demographic factors of the defendant such as race, age, and gender have also been shown to affect decisions. These factors can make expert testimony appropriate to the extent that knowledge of their impact may assist the trier of fact (see Mitigation Testimony).
Race of the Defendant Although racial inequalities are not as prevalent as they were a century ago, subtle inequalities continue to exist in the American courtroom. Most of the research, focused on the racial disparity between Caucasians and African-Americans, reports prejudiced decisions from white jurors when the defendant is of African-American decent [1–4]. White jurors are also more likely to convict and impose harsher sentences on a member of another race than on a member of their own race. However, Caucasians are not the only ones displaying racial bias; juries predominantly made up of African-Americans are less likely to convict a black defendant compared to a white defendant who commits the same crime [2, 5, 6] and individual jurors of African-American decent are also more likely to convict a Caucasian defendant than they are to convict a fellow African-American [3, 7]. Although these studies suggest that racial bias is still an important part of the American legal system, other studies have failed to detect a racial bias in verdict decisions [e.g., [8]] and sentencing judgments [e.g., [9]]. Two relevant theories can explain these disparate findings and help explain why some studies have found an effect of racial bias while others have not. The phenomenon of ingroup/outgroup bias is a robust finding in the psychological literature [3] and
is one explanation for why jurors of one race are more lenient with members of their own race and harsher when defendants represent a different racial group. According to this explanation, individuals display a strong preference for members of their own group (e.g., race) and have negative attitudes towards outgroup members [e.g., [10, 11]]. The ingroup/outgroup bias has been found in a variety of studies and across many different contexts [e.g., [12, 13]]. For example, Pettigrew [13] found that positive behavior of ingroup members is attributed to an inherent disposition, whereas positive outgroup member behaviors are attributed to situational factors. The opposite would be true for negative behaviors. This theoretical perspective would explain why juror bias could be exhibited when the defendant is of another race than the juror. However, the ingroup/outgroup bias phenomenon cannot explain why some studies have failed to detect racial bias in juror sentencing and verdict decisions. Gaertner and Dovidio [14] postulated a second explanation for the research findings. They suggest that a new form of racism, namely modern racism or aversive racism, can explain the failure to detect juror bias in several studies [9, 15]. According to Gaertner and Dovidio, the fact that there has been a decline in the display of overt prejudice and explicit racist beliefs does not mean that racism does not exist any more, it simply means that individuals censor their public display of racism, because society does not condone most forms of racism today and Caucasians have moved toward an egalitarian value system [4]. This implicit racism is more likely to manifest itself in public policies (e.g., affirmative action) and is usually not blatantly displayed. Gaertner and Dovidio [14] suggest that Caucasians make a conscious effort to appear egalitarian as long as they are aware that a racial issue is relevant. Thus, it is only when Caucasians interact with members of another race, and no explicit racial issue is presented, they will show prejudice. When a motivation to appear egalitarian is “not” activated individuals will display racial bias. Taken to the jury level, verdict and sentencing decisions should be most impacted by race when racial prejudices are not made salient to jurors [3, 4, 14, 16, 17]. If race is made salient in a case, white jurors are less likely to act prejudicial when making sentencing recommendations [3] than when it is not particularly mentioned or weighted as important [3].
Sentencing: Demographic Factors in Finally, it should be mentioned that under certain circumstances jurors might be “more” likely to impose harsher sentences on members of their own race. When ingroup members perceive a member of their group negatively and as threatening to the positive image of the ingroup, they are more likely to evaluate this member in a negative way [18]. This phenomenon is known as the black sheep effect (BSE) and was first introduced by Marques and colleagues [19–22]. Kerr et al. [23] applied the BSE to a mock juror paradigm and found support for the notion that negatively perceived ingroup members would be punished more harshly and be given longer sentences than outgroup members. This however, was only the case when the evidence against a negatively perceived ingroup member was strong. When the evidence was weak, white jurors displayed the typical ingroup bias in their judgments.
Age of the Defendant A defendant’s age can be construed as either a mitigating or extralegal factor. On the one hand, the court system makes allowances for youthful offenders. Defendants under the age of 18 are often separated from adults, seen in courts designed specifically for youthful offenders, and court outcomes often focus on rehabilitation instead of punishment. In this way, age serves as a mitigator. The age of the defendant is also an extralegal factor because once jurisdictional decisions are made age should not affect jurors’ judgments in a particular case. However, numerous studies have shown that age does influence jurors’ judgments. As with race, jurors should not be influenced by the age of a defendant. The adult court system imposes a justdesserts rationale for sentencing, meaning harsher offenses should receive harsher punishments [24, 25]. Age should not be a factor in such decision making. However, numerous studies show that this not the case [e.g., [26, 27]]. Young defendants (those under the age of 13) are often treated more leniently than older defendants and some studies have found that older adolescents who are tried as adults may be treated more harshly than adults who commit the same crime [27]. Several researchers have suggested that jurors’ decisions may follow a utilitarian (rather than a just-desserts) approach [24, 25, 28], meaning that
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factors such as perceived deterrence, incapacitation, and rehabilitation will influence jurors sentencing recommendations. For example, the utilitarian approach would predict that younger offenders would be treated with more leniency than adult offenders because jurors may believe that a young offender has a better chance of being rehabilitated and being harmed more by prison than a middle-aged adult offender [29]. Also, an elderly offender could be perceived as less dangerous and blameworthy than a middle-aged adult offender and therefore, sentenced more leniently [25]. Both archival [30, 31] and experimental [28, 29] studies have supported the utilitarian perspective during sentencing.
Elderly Offenders Wilbanks [31] examined secondary records for elderly (60 years old and up) and nonelderly (25–59 years old) offenders throughout the criminal justice process. Wilbanks found that nonelderly offenders were more likely to be incarcerated and sentenced to longer prison time than elderly offenders, whereas the elderly were slightly more likely to be convicted, but not necessarily sentenced to serve time in prison. This archival data illustrates that elderly offenders may be treated more leniently than middle-aged adults during sentencing, supporting the utilitarian perspective. Evidence toward this leniency during sentencing of the elderly has also been found in empirical studies. Bergeron and McKelvie [29] presented mock jurors with either a murder or theft vignette in which the defendant was a 20-, 40-, or 60-year-old man. In the murder case, the 20- and 60-year-old defendants were treated with more leniency than the 40-year-old defendant. The 40-year-old defendant was sentenced to serve more prison time and was not recommended for parole as quickly as the 20or 60-year-old defendants. These data are congruent with the utilitarian perspective and suggest that age is an important factor during sentencing that jurors consider, even if only unconsciously when rendering their decisions.
Juvenile Offenders The other end of the age spectrum that is of importance during sentencing is that of adolescent, or juvenile offenders. As with elderly offenders, the age of juvenile offenders influences juror’s judgments
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of guilt. Several studies [27, 32, 33] have found a positive relationship between age and perceptions of guilt, meaning, the younger the juvenile defendant is, the less culpable he or she is perceived. Furthermore, younger defendants are also less likely to be convicted [33]. These findings are congruent with research on adolescent development [e.g., [34–36]] that postulates that adolescence is a period of poor decision making skills because of significant cognitive and social developmental changes, resulting in a decrease of blameworthiness of the adolescent for his or her behavior. Though most young offenders are seen in juvenile courts, many states in the mid 1980s and early 1990s passed laws that would ease the prosecution of juveniles as adults [37, 38] allowing harsher punishments compared to the rehabilitative juvenile system [39, 40]. For example, some states passed laws that allowed the juvenile system to be bypassed entirely for children who reached certain ages and who committed specific crimes. However, to date only three field studies exist that compared the differential outcomes for adults and juveniles tried as adults [41–43]. Eigen [41] found that juveniles who were charged with nonfelony killings in Philadelphia were more likely to be convicted than adults and more likely to receive a verdict of first- or second-degree murder (68%) than adults (38%). Strom et al. [43] obtained similar results when they compiled crime statistics in 75 counties in the United States. The authors found that juveniles tried as adults who were charged with violent crimes were more likely to be convicted compared to adult defendants. The most recent field study by Rainville and Smith [42] however found no difference between juveniles and adults who were prosecuted in an adult criminal court. The above-mentioned field studies illustrate that juveniles who are charged with violent offenses and tried as adults often receive the same punishment as adults and sometimes even harsher punishments. Experimental research that has examined how juveniles are sentenced in an adult criminal court compared to adults has obtained similar findings [e.g., [26, 27]]. Tang and Nunez [27] examined undergraduate mock jurors who were either prosecution-biased (PB) or defense-biased (DB). These mock jurors read a murder trial involving a 19-year-old adult offender, a 16-year-old juvenile offender who was tried as
an adult, or a 13-year juvenile offender who was tried as an adult. The authors found that PB jurors were more likely to convict the 16-year-old juvenile offender and had higher confidence in their verdicts. These results illustrate that juvenile offenders who are tried as adults and charged with a serious offense can be at a disadvantage compared to adult offenders. Other studies of younger defendants have found that the harsh treatment of juveniles may not extend to juveniles younger than 13. In fact several studies have found that children younger than 13 are treated more leniently by mock jurors [26, 44]. This suggests that a certain cutoff age exists that would predict when juvenile offenders will or will not be treated more harshly than adult defendants.
Gender of the Defendant Gender of the defendant has received less research attention; however, several consistent findings have emerged. Early work on gender differences in sentencing decisions found that women were at an advantage compared to men [45, 46] during sentencing. Since then not much has changed with regard to the differential treatment of women and men during sentencing. The finding that women receive lighter sentences than men has become a robust one in the literature [e.g., [47]]. Extensive literature reviews [48, 49] emphasize the strength of the association between gender and sentencing and some scholars [48–50] even argue that the gender of the defendant is the strongest demographic predictor during sentencing, even more so than race or age. The gender disparity becomes most profound at the point in the judicial process when a defendant is either sentenced to jail time or receives a nonincarcerative sanction such as probation [47]. Women are typically 12–23% less likely to spend time in jail compared to men [e.g., [25, 49, 51]]. However, if a defendant is sentenced to jail, the research is mixed and the disparity between men and women is not as profound. Some studies have found an effect of gender that suggests that women are sentenced with more leniency [25, 51–56] while others found no differences between men and women during sentencing [49, 56–59]. Some other studies have even found women to be at a disadvantage during sentencing [e.g., [44, 60]], but these studies involved cases with juvenile defendants.
Sentencing: Demographic Factors in Only a few studies have examined how various crime types affect this gender bias during sentencing. Rodriguez et al. [e.g., [47]] found in a large sample of convicted offenders in Texas that for minor offenses, such as property or drug offenses, women were sentenced less harshly than men. For violent offenses, women are just as likely as men to be sentenced to jail, however, if sentenced to jail, women received substantially shorter sentences than men. There are two theoretical explanations that aid in explaining the differential treatment for men and women during sentencing, namely the chivalry thesis and the focal concerns theory. The chivalry thesis postulates that women are generally stereotyped as childish and not as blameworthy as men and therefore should not be punished the same way as men are [51, 57]. However, much of the current research fails to completely support this thesis. A more recent theory, the focal concerns theory, which is similar to the utilitarian approach mentioned above, stipulates that judges or other criminal justice investigators do not have enough time to adequately evaluate all the information for a given case and that their judgments often incorporate some form of human error. They therefore rely on shortcuts that will help them make the best decision at hand. Three focal points that will typically aid them in their decision making are blameworthiness, dangerousness of the defendant, and practical constraints [47]. Men may be perceived as more likely to survive prison than women [25] or may be perceived as more dangerous than women [56]. Focal concerns theory is at the core of explaining why women receive milder sentences and if sentenced to jail they may receive shorter sentences than men.
Conclusion On the basis of the literature reviewed here, it appears that extralegal factors still play an important role in the way defendants are treated by the criminal justice system and especially during sentencing decisions [25]. However, a jury trial is far too complex to reduce jurors’ decisions down to a few variables and it still remains difficult to determine with absolute certainty what factors will ultimately influence jurors’ decisions. Another level of complexity that this article did not address is that of jury deliberations [e.g., [61, 62]] and how decisions after deliberations often vary
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greatly from that of individual jurors. Furthermore, several demographic characteristics have not been discussed in this article, such as socioeconomic status or relationship status of the defendants, which can also impact jurors’ judgments in a case. Nevertheless, it can be said that demographic factors continue to influence jurors’ decisions and should not be ignored by judges or lawyers during trial proceedings.
End Notes a.
In most states jurors do not make sentencing decisions in felony cases. Only Arkansas, Kentucky, Missouri, Oklahoma, Texas, and Virginia allow jurors to sentence defendants in felony cases.
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sexual assault allegations, Law and Human Behavior 24, 421–437. [61] London, K. & Nunez, N. (2000). The effect of jury deliberations on jurors’ propensity to disregard inadmissible evidence, Journal of Applied Psychology 85, 932–939. [62] McCoy, M.L., Nunez, N. & Dammeyer, M.M. (1999). The effect of jury deliberations on jurors’ reasoning skills, Law and Human Behavior 23, 557–575.
Further Reading Ulmer, J.T. (2000). The rules have changed – So proceed with caution: a comment on Engen and Gainey’s method for modeling sentencing outcomes under guidelines, Criminology 38, 1231–1244.
ANDRE KEHN
AND
NARINA L. NUNEZ
Serial Homicide Introduction The term serial murder (and serial killer) was not even a part of the forensic lexicon until the 1970s, when it was popularized by one of the authors (RR), then an investigator with the Behavioral Science Unit of the US Federal Bureau of Investigation (FBI) [1]. The precise definition of serial murder has been the subject of some debate, which has somewhat hampered research efforts. However, most proposed definitions share the following elements common: (i) there have been at least two victims (some definitions require three victims), (ii) victims are killed in a noncontinuous manner (i.e., there is an emotional “cooling off” period between murders), and (iii) the murders usually involve a sexual component [2–4]. Serial murder may be a universally terrifying concept, but it is an extraordinarily rare event. In a study of the frequency of serial sexual homicide, it was found to account for only 0.5% of all homicides over a 10-year period in Virginia [5]. In contrast to the sensationalized perception that serial murder is a growing “epidemic”, there does not appear to be solid evidence that this is the case. An analysis of homicide victims from 1960 to 1998 indicates that the percentages of female homicide victims have actually decreased [6]. Because the victims of serial murderers
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are overwhelmingly female, it has been argued that this data supports the notion that serial murder is not increasing in frequency. However, this data does not address the rate of serial murder in which victims are men or children. Other research has challenged prior beliefs about serial murder. For example, it had previously been widely accepted that a disproportionate number of serial murderers are Caucasian. Yet researchers have demonstrated that the number of African-American serial murderers closely corresponds to the overall proportion of African-American males in the United States [7]. When a serial murderer begins to commit homicides, the local community is often dramatically impacted. Media coverage is unrelenting, and residents generally live in fear until the perpetrator is apprehended. Residents living in a community exposed to serial murder may even experience posttraumatic stress disorder symptoms for varying periods of time [8]. Yet, despite the high level of interest, there is no universally accepted theory that adequately explains the etiology of serial murder [9]. This may be partly reflective of the fact that serial murder is an event with an extremely low base rate, and therefore difficult to study via rigorous scientific methods [5]. Once the concept of serial murder gained widespread recognition, one expert noted that the “tendency of the press, public, and public officials to regard such individuals as mad solely on the basis of their crimes reflects the widespread need to attribute such behavior to alien forces” [10]. This tendency may be understood as the desire to disavow the notion that another human being could commit such atrocities. Could serial murder “simply be part of the spectrum of human possibility, a brutal dark side of man, not representing demons or disease”[11]? Or, do we have reliable evidence of biopsychosocial deficits in certain cases? This article provides a broad overview of the literature and research in an attempt to address these questions.
History While the term serial murder may be relatively new [12], its occurrence is not. It is quite possible that serial murderers have always been among us. Perhaps the first documented serial killer was a first
century Roman woman named Locusta. She was a “professional poisoner” who lived in the time of Nero (54 AD), and was ultimately executed [13]. In the fifteenth century, Gilles de Rais, a wealthy French aristocrat, raped and killed some 100 young boys because it brought him “pleasure” [14]. In sixteenth century France, it is likely that myths such as “werewolves” were used to explain the deeds of serial murderers that were too horrifying to attribute to human beings [14]. In the United States, there have been documented cases of serial murder as far back as the 1800s. In 1886, psychiatry professor Richard von Krafft Ebing wrote the classic Psychopathia Sexualis, in which he described the characteristics of individuals who appeared to obtain sexual gratification from acts of sadistic domination. The next major contribution to the understanding of serial murderers was in 1970, when forensic psychiatrist Robert Brittain produced detailed clinical descriptions of sadistic murderers he had encountered over his career [15]. Beginning in the early 1970s, media coverage of notorious cases such as Ted Bundy and the Hillside Stranglers produced a sense of urgency to study and explain the phenomenon. In the 1980s, experts working in the FBI’s Behavioral Science Unit began the pioneering study that ultimately established the foundation for scholarly research of serial murder. To emphasize the sexual nature of the crimes, and to distinguish these offenders from others who murder serially for other reasons (e.g., contract killers), the term sexual homicide was adopted [4]. In a sexual homicide, the perpetrator engages in some form of sexual activity before, during, or after the murder. For each individual serial sexual homicide offender, the performance and meaning of the sexual element may vary.
Typology FBI researchers gathered data from exhaustive interviews of 36 convicted serial murderers. From this data, they were able to extract and analyze core personality and behavioral characteristics [16]. The traits and behaviors identified allowed distinctions to be made between different types of serial murderers. For ease of conceptualization and communication, offenders were categorized into either “organized” or “disorganized” types. These terms
Serial Homicide Table 1
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Serial murder organized – disorganized typology
Organized offender traits Good verbal skills, socially adept May live with spouse Reasonably intelligent Usually employed Planning of crime Ruse or con to gain control of victim Targeted victim Crime scene: suggests control, order Crime scene and death scene not the same Movement of body Attempts to conceal evidence
were initially meant to help law enforcement interpret crime scenes, and are best understood as generalized distinctions occurring on a continuum. The organized–disorganized typology provided illustrative descriptors of personality and behavior, and had the advantage of being easily grasped by both law enforcement and mental health professionals. The major organized–disorganized typology traits are listed in Table 1. The term mixed sexual homicide was used to describe the offender, whose crime scene reflected aspects of both the organized and disorganized types, thus lying on the continuum between them. Finally, the term sadistic murderer describes the offender who is primarily a sexual sadist, and derives the greatest satisfaction from the victim’s response to torture [4]. Since the original organized–disorganized typology was advanced, a number of other typologies have been proposed. A clinically based typology has been advanced that categorizes perpetrators as either “compulsive” or “catathymic” [17]. The compulsive perpetrators are similar to the FBI’s organized killers. They leave organized crime scenes, and can be diagnosed with sexual sadism, as well as antisocial/narcissistic personality disorders. The catathymic perpetrators leave disorganized crime scenes, and may be diagnosed with a mood disorder and varying personality traits. While the compulsive type displays emotional detachment and autonomic hyporeactivity, the catathymic type are less psychopathic. In contrast, the catathymic types are autonomically hyperreactive, and may have histories of abuse. Like the organized–disorganized typology, these types are
Disorganized offender traits Poor verbal and social skills Loner or lives with parents Low intelligence Under or unemployed Little-to-no planning of crime Blitz or surprise attack of victim Victim of opportunity Crime scene: disarray Crime scene and death scene often the same Body left at death scene Little-to-no attempts to conceal evidence
generalized concepts, and any individual case is likely to fall on a continuum between the two. A number of researchers have pointed out that nearly all serial murderers demonstrate a core of organized features, and that it is the degree of disorganization that most differentiates them [18]. Along a similar line of reasoning, a statistical analysis of 85 sexual murderers yielded a “five-cluster” model [19]. It was noted that most offenders shared core characteristics such as preparatory behavior, precautionary behavior, and some degree of sophistication. This core of behaviors was referred to as the undifferentiated pattern, and the other four patterns (predator, fury, rape, and perversion) were differentiated from it. The predator pattern is similar to the organized or sadistic offender as described by the FBI. This offender was characterized as older, more mobile, Caucasian and likely to be living with a partner. They tend to be well groomed, collectors of crime literature and sexual materials. This group may also operate with an accomplice. The fury pattern represents an unfocused, explosive obliteration of the victim, and is most similar to the FBI’s disorganized type. The murder is characterized by excessive violence and overall disorganization. The chances of this offender having or not having a mental disorder are roughly equal. The rape pattern consists of offenders whose primary goal is sexual intercourse. They use that amount of force that is necessary to carry out the rape. Application of force is typically minimal, and there is no indication of sexual dysfunction in the offender. Thus, this pattern may be conceptualized as a sexual assault that ultimately resulted in murder. The crime scene
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will not reflect any great degree of perversion, but a relatively straightforward violent sexual attack. These offenders may have some prior peripheral acquaintance with the victim, such as living in the same apartment complex. The assault usually occurs in a single indoor location, such as the victim’s home. The offense is usually unplanned, and characteristic of a younger offender who attacks a victim of opportunity. Thus, the scene may reflect elements of the FBI’s disorganized type. The perversion pattern offender engages the victim in conversation by offering reassurances. Offenders tend to be older with bisexual or homosexual orientations, while their victims tend to be younger and male. The offense usually involves some type of pedophilic assault that culminates in murder. In general, serial murderers do appear to share some core characteristics. However, research has begun to focus on the differences that distinguish various subgroups of serial murderers. The following descriptions represent a sampling of some serial murder subgroups that have been studied, and should not be considered exhaustive.
Female Serial Murderers Relatively little has been written about female serial murderers as compared to their male counterparts. In a review of published literature on female serial murder, the most common motive identified was material gain [20]. Sexual or sadistic motives are believed to be extremely rare in female serial murderers. Psychopathic traits and histories of childhood abuse have been consistently reported in these women [20]. In a study of 105 female serial killers, the preferred method of killing was poisoning [21]. An analysis of 86 female serial killers from the United States found that the victims tended to be spouses, children, or the elderly [22]. Sometimes referred to as black widow killers, these women tend to be geographically stable and live in the same area where their offenses occurred. Their victims are not strangers, and the methods they use are covert or “low profile” [21]. On rare occasions, women may be involved with a male serial killer as a part of a serial killing “team” [23]. Perhaps one of the more high profile female serial killers in the United States was Aileen Wuornos, who was convicted of killing seven men in separate incidents. Wuornos had claimed that all of the men had raped her (or attempted to) while she was working as
a prostitute. Thus, she did not fit the typical profile of a female serial killer. Her case received remarkable media and Hollywood attention. In a detailed case study analysis, it was theorized that Wuornos was biologically predisposed to psychopathy, and her abusive childhood resulted in serious attachment deficiencies [24]. Finally, her aggressive narcissism and antisocial lifestyle predisposed her to situations in which she was able to commit acts of predatory murder. Wuornos was executed by lethal injection in 2002 in Florida.
Juvenile Serial Murderers Serial murder by children and adolescents is exceedingly rare, and little scientific information is available. In a study of six cases, juvenile serial murderers were found to exhibit signs of sexual sadism, predatory violence and the use of “hands on” methods of killing [25]. The average age of the juveniles when they committed their first murder was 14. There is somewhat more data on juvenile sexual homicide, and it is hypothesized that youths who go on to commit serial murder would have originated from this group [24]. In a study of 16 juvenile sexual homicides, 10 factors were commonly found in the perpetrators [26]. These factors are listed in Table 2. Three of these factors (impaired capacity to feel guilt, neuropsychiatric vulnerabilities, and serious school problems) were found in 100% of the offenders. Owing to increasing law enforcement sophistication, it is possible that juvenile sexual murderers will be apprehended after their first offense, making juvenile serial murder even rarer [25]. Nevertheless, professionals working with juveniles should be sensitive Table 2 “Big 10” factors in 16 juvenile sexual murderers [26] 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Impaired capacity to feel guilt Neuropsychiatric vulnerabilities Serious school problems Child abuse Family dysfunction History of interpersonal violence Prior arrests Sadistic fantasy Psychopathic personality traits Personality disorder diagnosis (especially schizoid or schizotypal)
Serial Homicide to the fact that violent fantasies can develop early in the life of a sexual murderer [27].
Physician Serial Murderers The study of medical serial killers has gone overlooked until relatively recently. This may be due to an unwillingness to perceive sworn “healers” as potential murderers. However, research has revealed that medical killers may actually be the most prolific of all serial killers. Doctors who serially murder their patients are considered to belong to a larger group of “career-assisted killers.” The term clinicide has been used to describe “the unnatural death of multiple patients in the course of treatment by a doctor” [28]. Such murders may be difficult to detect, since they often occur in settings where death is expected to happen. Doctors accused of clinicide will be likely to put forth the defense that they were relieving suffering or providing euthanasia. Clinicidal doctors may have extreme narcissistic personalities, and may obtain pleasure by “determining” when a person will die. One of the most deadly doctor serial killers may also hold the dubious distinction of being one of the most prolific serial murderers to date. Dr Harold Shipman, a UK physician, was convicted of killing 15 patients with lethal injections of narcotics. In a posttrial investigation, it was concluded that Shipman was responsible for 218 known victims [29]. Other estimates have suggested that the number is closer to 450 [30]. Most of Shipman’s victims were not terminally ill, nor did they have an immediate lifethreatening illness. Shipman refused to speak to anyone, and no complete psychological assessment was ever performed on him [29]. He committed suicide in prison in 2004. Other healthcare professionals have been implicated in serial murder. In a study of 90 healthcare killers, 86% were nurses and 12% were doctors [31]. Injection was the most common method used, followed by suffocation, poisoning, and tampering with equipment. Fifty-four of the 90 cases were ultimately convicted. A total of 2113 deaths could be attributed to these 54 convicted healthcare killers.
Other Subgroups As research has progressed, specific subgroups have been singled out for more detailed analyses. For
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example, sexual murderers of children have been singled out for separate study and comparison. It has been found that sexual murderers of children are more often victims of childhood sexual abuse, and have more deviant sexual fantasies than sexual murders of women [32]. In addition, sexual murderers of children are more likely than sexual murders of women to: use pornography prior to the offense, have contact with the victim, premeditate the offense, use strangulation, hide and dismember the body. Another body of research indicates that sexual murderers of elderly women present a particularly distinct profile [33, 34]. It has been suggested that sexual murderers of men may differ in certain respects from those who murder women. An initial typology has been proposed, although it was based on a study of only 10 cases [35]. The avenger type is usually involved in prostitution, and has a history of childhood abuse. A triggering event during a sexual exchange may elicit memories of abuse, which leads to severe expressive violence and murder. The sexual predator type premeditates his offense, and is motivated by deviant sexual fantasy. Victims of the sexual predator type are often adolescents or young men. The offense involves abduction, confinement, and sadistic acts. The nonsexual predator type sets out to rob a vulnerable, often older homosexual man. The victim may be seduced, and substance use by both victim and offender occurs prior to the offense. Usually, the victim is not sexually assaulted, and the murder may have resulted from an escalation of violence during the robbery.
Motivations Most research on the motivations of serial murderers has focused on sexual fantasies and/or a need for control and domination. Indeed, one of the most reliable psychological findings in the mental lives of serial murderers is the presence of violent sexualized fantasy. Convicted serial murderers have consistently described a high frequency of violent fantasies that are both persistent and arousing [15, 36, 37]. In a comparison of 25 serial sexual murderers with 17 single sexual murderers, it was found that the serial murder group had a higher prevalence of paraphilias and violent sexual fantasies [38]. It was theorized that serial murderers’ deviant fantasies may
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be reinforced via repeated pairing with compulsive masturbation. This has led to the speculation that deviant sexual fantasy may serve as a rehearsal of sorts for eventual murder [39]. In fact, many cases of serial murder have involved strong components of sexual fantasy, use of pornography, or other media with sexually sadistic themes [40]. Internet and digital technology may provide a new and abundant source of deviant fantasy material for the sexual murderer [41]. A study of 28 sexual murderers suggested that they may be driven by certain “implicit theories” or cognitive schemas they had about life [42]. It was found that the offenders had commonly held beliefs such as “the male sex drive is uncontrollable”, and the world is generally hostile and dangerous. Other guiding cognitions included anger and resentment toward women, and a sense of entitlement. Related findings came from a study comparing 19 sexual murderers to 16 nonmurdering rapists [43]. The sexual murderers, compared to rapists, reported higher levels of grievance toward females in childhood, higher levels of loneliness in adolescence and were more likely to portray themselves as victims, as adults. Because a number of well-known serial murderers have served in the military, a social learning theory has been hypothesized, whereby the military may provide the associations and reinforcements to enable efficient killing [44]. Military training is seen as helping the offender objectify victims, and reinforcing the tendency to use lethal aggression. Hostility and aggression, in general, have been proposed as possible motives. This theory suggests that either anger, or anger fused with sexual arousal, drives serial murder [45]. This fusion theory was proffered to explain the murders committed by Jeffrey Dahmer [46]. Here, it is important to make the distinction between rapists who murder to silence their victims, versus the socalled lust-murderer who derives sexual satisfaction from the act of rape–murder [27]. Finally, a convincing argument has been put forth that anger is not causative in sexual homicide. This hypothesis stresses that the physiology of anger and sexual arousal are usually mutually incompatible. True anger, as opposed to aggression, has an inhibitory effect on erectile and sexual functioning. This reasoning holds that sexual motivation is the primary motive in sexual murders, whereas anger and/or control over victims are secondary [3].
Offense Behavior The study of serial murderers’ offense behavior provides important data for homicide investigators. Serial murderers often leave confusing and violent crime scenes, which must be carefully analyzed for behavioral evidence. A study that compared single and serial homicide offenses found that serial offenders targeted more women, and killed more strangers [47]. While single homicide offenders killed out of anger, serial offenders appeared to be sexually motivated. The serial offenders were significantly more likely to use strangulation, move the body from the death scene and dispose of the body in a remote location. Some commonly observed serial sexual murder offense behaviors are listed in Table 3. Serial murderers may clean the victim’s genital area to remove evidence, and may take personal items from the victim as souvenirs [48]. Prostitutes may represent a common victim pool for serial killers [49]. In the analysis of serial murder crime scenes, the concepts of staging and posing may play important roles. Staging is a purposeful alteration of the crime scene by an offender to throw off investigators [52]. The offender may be concerned about being a likely suspect, and wish to direct the investigation away from him or her. Three types of staging have been described: (i) staging to appear like a suicide or accident, (ii) staging to appear like a sexual homicide, and (iii) arson to destroy evidence [53]. In contrast, posing is the positioning of the victim’s body by the offender. Posing, a very rare offense behavior, often involves leaving the victim in a sexually degrading position. This may either be to shock police, or simply for the offenders own gratification [52]. Serial murderers who leave posed victims may also leave evidence of binding, stabbing, or bludgeoning. Table 3 Serial sexual murder offense behaviors [16, 50, 51] Binding, torture Stabbing, biting Attempted or completed sexual intercourse (oral, anal, vaginal) Victim left nude or seminude Sexual positioning of victim’s body Insertion of foreign objects into victim’s body cavities Semen on or near victim’s body Victim’s personal items taken
Serial Homicide It has been found that the geographic locations of serial murderers’ offenses are critically important. The geographic sites of 155 serial killer disposal sites were analyzed, and a strong relationship was found between the location of the offender’s home and the disposal site [54]. The vast majority (89%) of offenders lived within a circle defined by the disposal sites that were furthest from each other. The finding that serial murderers appear to operate in a certain spatial location around their home has been called the circle hypothesis [54].
Psychiatric Findings Most data on psychiatric diagnoses of serial murderers comes from individual case studies and retrospective analyses. The majority of these studies have suggested a common constellation of diagnoses: psychopathy, antisocial personality, sexual sadism, and other paraphilias (especially voyeurism, fetishism, transvestism, and sometimes necrophilia). More recent and well-designed comparison studies have yielded similar findings. For example, a study comparing sexual murderers to other general sex offenders found that the sexual murderers had greater levels of psychopathy, sadism, fetishism, and transvestism [55]. In addition, the sexual murderers began their criminal careers earlier, and had stronger histories of fire setting and cruelty to animals. The sexual sadism seen in serial murderers must be distinguished from sexual sadism between consenting adults that would not be considered criminal. The variant of sexual sadism seen in serial murderers is at the extreme end of the spectrum, as it ultimately involves killing for sexual excitement. Such individuals may engage in torturing victims to the point of death to obtain the “pleasure in complete domination” over them [56]. To better capture this distinction, the diagnosis “sexual sadism, homicidal type” has been proposed for serial sexual murderers [3]. It is noteworthy that a higher level of gratuitous and sadistic violence was found in the homicides committed by psychopathic sexual murderers when compared to nonpsychopathic sexual murderers [57]. There is considerable overlap between the construct of psychopathy, and another diagnostic construct described in serial murderers called malignant narcissism. Malignant narcissism has been defined as an extreme variant of narcissistic personality disorder, antisocial personality, sadism, and a tendency
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to paranoid reactions [58]. This clinical construct has been proposed by a number of theorists studying serial murder [59]. It is suggested that malignant narcissism is best viewed as an aspect of personality structure, as opposed to a formal mental disease. This theoretical concept has been used to explain the chronic sadistic arrogance and lack of empathy observed in most serial murderers.
Paraphilias Paraphilias, particularly voyeurism and fetishism, have been described in many serial murderers. Over 70% of sexual murderers had these paraphilias in the early FBI studies [16]. Some individuals with voyeurism and fetishism may engage in burglaries that actually serve the purpose of gratifying these two paraphilias [60]. Offenders may steal sexually related items during a burglary, such as female undergarments. Such offenses may, in fact, be part of a progression to an eventual sexual homicide. In a descriptive review, it was found that serial murder was associated with multiple paraphilias [61]. It was speculated that multiple paraphilias served to enhance and reinforce the overall sexual experience of the offender.
Obsessive–Compulsive Traits Focusing on the seemingly compulsive nature of the offenses, researchers have speculated about the significance of the obsessive qualities of the serial murderer, particularly the organized type. These individuals demonstrate a tendency toward orderliness, obsessive, fantasy, and ritualistic behavior (posing the body, biting, inserting objects, etc.) during their murders that suggest compulsive qualities. A study finding high rates of compulsive masturbation in sexually sadistic serial murderers may support the hypothesis of underlying obsessive–compulsive traits [62]. Other support comes from Rorschach studies of sexual murderers who evidenced high levels of obsessional thinking [63, 64]. Experts believe that these obsessive and compulsive traits, combined with higher than average intelligence, permit the organized offender to avoid apprehension.
Other Disorders There appears to be a very low rate of psychosis among serial murderers, and approximately half
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Table 4 Psychiatric disorders found in serial murderers Psychopathy “Malignant” narcissism Antisocial personality disorder Borderline personality disorder Schizoid and Schizotypal personality disorders Substance use disorders Paraphilias (sexual sadism, voyeurism, fetishism, transvestism, and necrophilia) Asperger’s disorder
of perpetrators report substance use prior to their offenses [16]. At the present time, there is no conclusive evidence that specific organic factors play a causal role in the creation of a serial murderer. However, studies have found right temporal lobe abnormalities [65], as well as subtle neurological abnormalities in sexual sadists [66]. Neurodevelopmental deficits have been hypothesized as a possible contributing factor to serial murder (Table 4), most notably in the case of Jeffrey Dahmer [67, 68]. Investigators have described an association between autism spectrum disorders and a subgroup of serial murders, and propose that Dahmer may have suffered from Asperger’s disorder. Along these lines, it is interesting to note that after exhaustive interviews with Dahmer, one author (RR) was impressed by the “peculiar” nature of Dahmer’s presentation [69]. A possible neuropsychiatry genetic defect has been found in a few cases of sexual homicide. The sex chromosome abnormality XYY had previously been associated with criminal behavior [70]. More recently, researchers found three men with the XYY chromosome abnormality in a sample of sexual homicide offenders [71]. The rate was found to be higher than what would be expected among prisoners or the general population. All three men were diagnosed with sexual sadism and psychopathy.
Developmental Theories A number of different psychosocial theories have been put forth regarding the developmental etiology of serial murder. Investigators have speculated that the behavior may result from a deadly convergence of (i) early childhood attachment disruptions, (ii) psychopathy, and (iii) early traumatogenic abuse [72]. However, there is conflicting evidence on the presence of child abuse in the development of serial
murderers. When the FBI studied 36 serial murderers, many of them had a history of either abuse or neglect [16]. Forty-three percent reported a history of childhood sexual abuse, and 74% reported a history of psychological abuse, which typically involved humiliation. A study of 48 homicidal sex offenders found high rates of childhood abuse and removal from the family home [73]. In contrast, others have found that a majority of sexually sadistic murderers had no evidence of childhood abuse [56, 74]. One possibility accounting for these differences may be due to heterogeneity in the populations studied. When sexual murderers with a history of sexual abuse were compared to murderers without such a history, significant differences were found [75]. Sexual murderers with a history of early sexual abuse were more likely to begin fantasizing about rape earlier. In addition, they developed more severe sexual deviancy. Besides sexual abuse, the family histories of many sexual murderers reveal unstable environments, which may predispose them to disordered early life attachments. Approximately 70% of sexual murderers’ families had histories of alcohol abuse, and about 50% had family members with criminal histories [76]. It has been hypothesized that parental neglect, from either absence or preoccupation with their own life problems, may have further impaired these men’s ability to form healthy attachments. Animal cruelty has been a common finding in the childhood and adolescent developmental stages of many serial murderers. The link between animal cruelty during childhood and subsequent physical violence during adulthood has been demonstrated in a number of studies [77, 78], resulting in the addition of animal cruelty to the diagnostic and statistical manual of mental disorders, 3rd edition, revised (DSM III-R) as a symptom under the diagnosis of conduct disorder in 1987. In keeping with the developmental theme of conduct disorder symptoms, researchers have also commented on a possible link between childhood fire setting and adult serial murder [79]. The association between serial murder and enuresis has not been as strongly born out in the research to date. Obviously, all children who are diagnosed with conduct disorder and/or engage in animal cruelty do not go on to become serial murderers. Nevertheless, it is thought that in the cases of those who do, an early “practicing” of violent and sadistic behavior on a living creature may play a role in desensitizing the individual to violence against humans. This notion
Serial Homicide has been termed the graduation hypothesis to denote the progression or “graduation” from animal cruelty to sadistic acts against humans [80]. Thus, some individuals may progress past mere desensitization, toward intense pleasure from acts of cruelty and ultimately murder. Psychodynamically oriented investigators have theorized that a sexually provocative mother may contribute to the formation of a serial murderer [17, 81]. It is important to note that this premise is far from another “blaming” of the mother theory. Rather, investigators point to documented instances of strikingly inappropriate sexual behavior on the part of the mother that would easily qualify as sexual abuse. Evaluations of some convicted serial murderers suggest that a displacement of aggression from their mothers onto to their female victims was present during their offenses. Upon review of the developmental theories and individual case studies, the following traits are frequently observed in serial murderers: deviant sexual interests, a strong need for control of a victim, a very active deviant fantasy life, and psychopathic traits allowing for the objectification of victims. When these traits are synthesized into a gestalt, the clinical picture that emerges is one of an individual who spends excessive time in a reverie of deviant fantasy, has a tendency toward isolation, a need for totally submissive partners, and a preference for autoerotic pleasure [82]. As can be imagined, such an individual will be unlikely to have healthy relationships, and subsequently must depend on fantasy for gratification. However, at some point, mere fantasy becomes an insufficient source of pleasure for the potential serial murderer. It is theorized that what follows is a gradually progressive series of “try outs,” where he attempts to turn his fantasies into reality. For example, an offender may begin by simply following a potential victim. This may next progress to voyeurism or breaking into victim’s homes [60]. During a burglary, the offender may steal fetishistic items for sexual pleasure. When this fails to provide sufficient satisfaction, the offender may progress to rape and ultimately murder. The behavior is positively reinforced over time through paired association with masturbation, making the deviant fantasies extremely refractory to extinction[38]. Each time the offender murders a victim, there is further stimulation of fantasy and an overall reinforcement of the cycle.
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Assessment and Prevention Evaluations of serial murderers may occur for a number of different purposes. Interviews may be conducted by law enforcement upon apprehension, by forensic mental health in the event that a mental disease defense is raised by the defendant, and after conviction for research purposes. Forensic assessments of suspected serial murderers are best done by those with experience evaluating psychopathic and serial sexual offenders. Dishonesty and underreporting of deviant fantasies and offenses are commonplace, and a meticulous review of collateral data prior to the evaluation is necessary. Individuals who have already confessed to murders may still be unwilling to discuss the sexual nature of their offenses for a variety of reasons, the most common being the fact that sex offenders are severely harassed by other inmates in prison. In the authors’ experience, many such individuals will want to focus on the aggressive aspects of their crimes, and downplay the sexually deviant aspects.
Interviewing Strategies Interviewing strategies and approaches will need to be tailored to both the purpose of the interview and the individual nuances of the case. Regardless of the purpose of the interview, it is essential to gather and review all relevant collateral data prior to interviewing the offender. This will not only lend important perspective but will also better allow the interviewer to realize when the offender is giving false or misleading information [27]. The use of a cointerviewer has been suggested both for safety purposes, as well as to provide added objectivity and oversight [83]. Very often, the quality of data obtained during an interview will only be as good as the rapport that the interviewer is able to establish. In studies of interviews of sex offenders, a “humanistic” style of interview has been found to yield the best results [84]. This style requires the interviewer to assume a sympathetic, nonjudgmental stance, as opposed to a “dominant” interrogation style of interview. In a study of interview styles of murderers and sex offenders, it was found that interviews marked by dominance were associated with a higher proportion of denials [85]. In contrast, a humanistic style was associated with greater admissions. Because many serial
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murderers will be discerning, intelligent individuals, they will likely perceive even subtle critical or judgmental attitudes in the interviewer. Thus, verbal or nonverbal communication relating bias or disrespect should be avoided. Rather, a humanistic interview style that relies on an understanding and respectful approach is recommended. While open-ended types of questions are recommended, the interviewer should consider using some type of interview protocol as a general guide for consistency and reliability. The interviewer should not assume that the offender’s sexually related crimes are limited to those for which he has been charged or convicted. The interviewer should inquire about concurrent assaultive behavior or deviant fantasies that may have occurred during other, seemingly unrelated criminal acts such as burglary or breaking and entering. Finally, it has been observed that sexual offenders, for a variety of reasons, may be slow to reveal incriminating details [86]. Thus, repeated interviews may be a helpful consideration. Table 5 lists generally recommended strategies for interviewing serial murderers. When serial murderers are interviewed for research purposes, it has been suggested that interviews should be conducted postconviction, as well as after the possibility of all appeals by the offender are exhausted [47]. In addition, researchers should consider offering some form of written assurance of confidentiality. These precautions have the aim of reducing the offender’s motivation for giving deceptive or otherwise self-serving answers.
Prevention Most experts believe that the prognosis for individuals who have committed serial murder is extremely poor [87, 88]. At the present time, a preventive approach has received the widest endorsement. It has Table 5
Recommended interviewing strategies
Gather all relevant supplemental data Thoroughly review data prior to interview Consider a cointerviewer Establish good rapport Attempt to “understand” subject’s perspective Use “humanistic” interview style Avoid “dominance” or interrogation interview style Avoid a judgmental or critical approach Consider repeated interviews
been suggested that more attention be paid to prevention in child and adolescent sex offenders, given that future adult serial murderers may come from this population. Children and adolescents who demonstrate sexually sadistic fantasies, or other early warning signs should be followed closely by mental health professionals who are in a position to direct efforts toward extinguishing the reinforcing cycle, and conducting periodic risk assessments [37]. The field of juvenile sex offender treatment has been gaining increasing attention; however, it remains in its very early stages. Current reviews of treatment efficacy support the use of cognitive behavioral methods, residential treatment programs, supervision, family therapy, and psychosocial interventions [89, 90]. Pharmacotherapy remains understudied, but various psychotropic agents have been utilized, including testosterone lowering agents [91]. In a study of 21 adolescent sex offenders, the use of Naltrexone, a medication used to treat some obsessional and impulsive disorders, was associated with decreased masturbation and sexual fantasies [91]. Much more research in the area of juvenile sex offender treatment is needed to be able to establish a greater degree of confidence in treatment efficacy [92].
Possible Early Warning Signs In an effort to help guide forensic risk assessments, a list of “10 ominous signs” has been suggested [93]. The list consists of traits, characteristics, and behaviors frequently found in the backgrounds of perpetrators of sexual homicides. It is suggested that when these signs are seen in combination, the juvenile may be predisposed to committing sexual homicides when older. The 10 ominous signs are listed in Table 6. Table 6
Ominous signs [93] (when seen in combination)
Childhood abuse Inappropriate maternal sexual conduct Pathological lying and manipulation Sadistic fantasy with a compulsion to act Animal cruelty Need to control and dominate others Repetitive firesetting Voyeurism, fetishism and sexual burglary Unprovoked attacks on females and generalized misogynous emotions Ritualistic behavior
Serial Homicide
Conclusions Serial murderers have been described as representing an exceedingly small, yet “freakish side show in the circus of American punishment” [94]. Despite this very reasonable assertion, serial murderers captivate a disproportionately large amount of society’s attention, study, and fears. In the case of serial murderers, we apparently have a substantial desire to know the face of evil. Perhaps this is driven by our fear that these “moral monsters”, unbranded by physical stigmata, will be able to commit atrocities undetected. Indeed, a journalist covering the Jeffrey Dahmer trial was unable to fathom how ordinary Dahmer appeared, remarking that “there was nothing to him” [95]. Yet another reason may be that it is the tension between the killer’s outer normalcy and inner deviance that elicits our tireless fascination [96]. Whatever the case, serial murderers’ offenses represent the extreme pole on the continuum of human cruelty and selfishness. In this article, some of the biological and psychological theories on serial murder have been discussed. However, it is important to recognize how limited our present understanding remains in terms of the etiology and development of serial murder, so that erroneous conclusions are not drawn. While researchers have identified traits and abnormalities common to serial murderers, there are many who possess these traits and do not go on to become serial murderers. What is it that leads some to act on their deviant fantasies while others do not? Until future research can help clarify this question, we must satisfy ourselves with the notion that “the leap from fantasy to action has much to do with character and the vicissitudes of life . . .” [97]
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Related Articles Aggression Assault: Sexually Motivated Profiles: Psychological and Behavioral Psychopathy JAMES L. KNOLL, IV, ROBERT K. RESSLER, ROBERT R. HAZELWOOD AND ANN W. BURGESS
or stamping. A range of restoration techniques are available, which makes it possible to restore the original alphanumeric marking in sufficient detail to be able to read it. Most firearms are marked by their manufacturers with a serial number or a combination of numbers and letters in at least one location. On some firearms, the complete serial number may be repeated on all the major components, i.e., the frame, cylinder, and barrel of a revolver. In other instances, the last few digits of the main alphanumeric mark is repeated upon even relatively small components. These can appear in obvious exposed exterior areas or, in some cases, in locations that can only be revealed by stripping the firearm. It is common practice for criminals to obliterate the identifying marks on illegally owned firearms to make the tracing of them more difficult. Forensic firearms examiners are frequently tasked with restoring these obliterated marks or finding a secondary location where the marking is repeated.
Principles
Serial Killer see Homicide: Multiple (Behavior)
Serial Murder see Serial Homicide
Serial Number Restoration: Firearm Introduction Many manufactured objects bear a serial number or other identifying numbers, letters or codes, which may be removed, altered, or obliterated. These markings are produced in various ways during the manufacturing process, such as etching, casting, engraving,
In many cases, identifying numbers, letters, or marks, are produced using procedures that involve compression such as stamping. This process induces changes in the structure underlying the impressions. If the marking is then removed by filing or grinding so that it is no longer visible, the area of the altered structure remains. By applying etching solutions, with or without heat, the area of the altered structure can be made visible, as that the area will react in a different manner to the base metal. Close examination of an object is required to verify that a marking should be present in a particular location and that it has been obliterated. The examination should indicate the method by which the numbers, letters, or mark were originally recorded and the method of obliteration. These assessments will dictate the available restoration options. The following are some of the common methods used to place identification marks on firearms.
Etching and Electrical Discharge Machining (EDM) Etching and electrical discharge machining (EDM) refer to the production of identifying numbers, letters,
Serial Number Restoration: Firearm or marks by eroding the base material. The process involves discharges of electrical spark to erode conductive materials such as carbon or stainless steel. Little or no deformation of the underlying material occurs with this process and, as a result, completely obliterated serial numbers are almost impossible to restore.
Casting As with etching and electrical discharge machining, casting involves little or no deformation of the underlying material. Therefore, when the markings are thoroughly obliterated, they are almost impossible to restore, especially if there has been neither ‘cold working’ nor the addition of any foreign material to the parent metal.
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for this purpose. The metal surface is generally removed until all visible traces of the serial number, letters, or marks are removed. Restoration using acid etching or magnetic particle processes have a high success rate.
Center Punching or Over-Stamping A line of holes is center punched into the serial number, letters, or marks using a hammer and punch. If deep enough, these alter the underlying structure of the metal and destructive restoration techniques are unlikely to be successful. Other number or letter stamps are sometimes used to over-stamp existing ones in an attempt to alter the original digits. Nondestructive visual examination methods can be useful in identifying the remaining key areas of the original marking.
Engraving There are two general methods of engraving, namely, rotating burrs and vibrating impact tools. Rotating burrs gouge the surface but do not deform the underlying material, whereas vibrating engraving tools have various shaped tips, generally rounded or chisel pointed, and they deform the underlying material while impacting it.
Milling or Drilling Milling or drilling has a similar effect on the underlying structure of metal as filing or grinding, but this often removes more material. Visual examination can be useful on drilled areas to identify any remaining key areas of the original digits, but if the milling or drilling is deep enough, destructive techniques are unlikely to be successful.
Stamping Stamping is one of the most common methods of adding serial numbers, letters, or other markings to firearms. It is also known as punching and usually involves forcing a shaped tool into the base material. All variations of this method involve compression (cold working) of the base material, which provides the potential for restoration of the original identifying marks.
Welding Welding essentially remelts part of the base material, adding new material from the filler rod or wire. This produces gross changes in the underlying material, and acid etching techniques are generally unsuccessful in identifying the original markings.
Nondestructive Restoration Techniques Obliteration
Visual Inspection
Different techniques are used in the attempt to obliterate numbers, letters, or marks. The most common methods of obliteration are described below.
In many instances, when a drill or a punch has been used to obliterate the original serial number, it is possible to identify individual digits from the remaining fragments that are still visible, provided these fragments contain a key portion of the digit. A low-powered stereo microscope is generally required to aid recognition of the fragments; contrast techniques can also be useful. The most common are
Filing/Grinding Mill Bastard or Bastard (1/2 round) metal files and grinding wheels are the tools most commonly used
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rubbing chalk over the erased area or using a filtered light source (e.g., a Polilight lamp) to create ultraviolet or other light frequencies that may enhance the marking.
lacquer can be applied to provide contrast and then Ardrox black magnetic ink can be sprayed over the treated area. The restoration usually appears almost immediately.
Wood
Acid Etching (Stainless Steel, Mild Steel, and Iron)
Some firearms have identification marks in their wooden stocks or grips. If the mark is burnt in or made by cutting with a chisel or a knife, it cannot be restored once obliterated. However, if the mark has been punched in, for example, the serial number or military marks on a Lee Enfield caliber. 303 British rifle, then the same considerations apply as with metals. The simplest and most effective method of restoration is to run a jet of steam onto the erased surface. The steam softens the wood and causes the bent fibers to spring back and the broken fibers to swell. As a result, the wood will project the marking above the surface and it can be read.
Before using this technique, it is important to identify what type of metal is to be worked on. This will determine the type of chemical solution to be used. When acid etching stainless steel, mild steel or iron, the surface area must be cleaned with acetone to ensure it is free from oil or grease. The area to be treated is then polished with a fine grade of wet and dry abrasive paper (400 Grade) to make restoration easier to see. Badly scratched or scored areas should be lightly polished with a fine abrasive pad on the dermal tool. This simply reduces the amount of labor required to achieve a smooth surface. There is debate over whether the use of heat is a necessary step in the restoration process. The principle surrounding the use of heat is that it will anneal the metal if a temperature of approximately 300 ° C is reached. An indicator of this temperature is when the metal assumes a straw color. It is essential that the metal is not heated too strongly. The reason for annealing is to enable the compressed and distorted metal to adjust itself to the conditions. If the metal is heated to red heat, the temperature is sufficiently high to soften the metal and on cooling, the metal becomes homogeneous and can no longer be differentiated. A Bunsen burner or blowlamp is all that is needed to achieve the desired result. Once the metal has been allowed to cool, Fry’s reagent, which consists of a mixture of hydrochloric acid, cupric chloride, ethanol, and water, can be used to acid etch the metal. Modified Fry’s reagent can also be used; this mixture consists of the same ingredients except ethanol, but in a different proportion. At the completion of the etching process, it is recommended that a lacquer is used to seal the restored numbers, letters, or marks. Alternatively, light oil should be applied to the treated area to protect it from corrosion.
Destructive Restoration Techniques On occasions an examiner can polish the defaced area flat with wet and dry abrasive paper to find the original markings are still visible under the correct lighting conditions, without the need for further treatment. If further treatment is required, then it is important to determine the metal type before commencing treatment.
Magnetic Particle The concept of magnetic particle restoration was developed in 1957 in the United States of America. It relies on the principle that any change in density or of molecular structure causes a change of the magnetic flow lines from the north to the south poles. Therefore the magnetic particles tend to congregate around the obliterated number, letter, or marking, making it visible. This process requires the surface area to be smooth and polished to achieve the best results. Once prepared, the object should be placed on an AC or DC powered magnet. Industrial magnetic crack testing devices have proved particularly successful using AC or direct DC power sources. Once the object has been charged, Ardrox white background
Acid Etching (Aluminum and Aluminum Alloys) The most common and effective solution is a 10% sodium hydroxide and water. Preparation of the
Serial Number Restoration: Firearm surface metal is the same as that described for Fry’s reagent. Fry’s solution can still be used on aluminum or aluminum alloys, but it reacts very quickly. Therefore it should only be used when a result cannot be achieved with 10% sodium hydroxide. Hume-Rothery solution is an alternative to modified Fry’s reagent; it contains cupric chloride, hydrochloric acid, and water in different proportions. This reagent reacts very energetically with aluminum alloys and deposits a layer of loose brown copper, which must be wiped off. The procedure for using Hume-Rothery solution is basically the same as for mild steel, stainless steel, and iron, except that the aluminum surface should not be cleaned with abrasives. Instead, any paint or grease can be removed with acetone before commencing the acid etching process. Vinella’s solution is also an effective reagent on aluminum or aluminum alloys. It contains glycerine, hydrofluoric acid and nitric acid. However, hydrofluoric acid is extremely corrosive and a dangerous substance to work with. Therefore this reagent is not recommended for Occupational Health Safety and Wellbeing (OHS&W) reasons.
Heat The use of heat has already been mentioned in combination with acid etching techniques on stainless steel, mild steel, and iron. It can also be used by itself on these metals after the surface area has been smoothed and polished. The process is commonly used on engine blocks to restore engine numbers, but greater care needs to be exercised on gun metals because they are far more fragile.
Further Reading ATF National Tracing Center (1999). ATF Guide to Illegal Firearms Trafficking Investigations, Section 2, Serial Number Removal Definitions and Codes, ATF National Tracing Center Publication, pp. 11–19. Barabash, T. & Fahey, R.T. (1977). Non-destructive methods of restoring defaced serial numbers, AFTE Journal 9(1), 23. Brown, E.W. (2001). Serial number restoration on ruger p series aluminum alloy frames, AFTE Journal 33(1), Winter, 57. Chisum, W.J. (1966). A catalytic process for restoration of serial numbers in aluminum, Journal of the Forensic Science Society 6, 89.
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Collins, J.M. (1999). Modern marking and serial numbering methods, AFTE Journal 31(3), Summer, 309. Cook, C.W. (1989). Obliterated serial numbers, AFTE Journal 21(2), 166. Dragan, P. (1996). Abrasive wheels for serial number restoration preparation, AFTE Journal 28(1), 21. Du Preez, D.T. (1997). Manual to Ballistic and Related Identification Methods, UNISA, Pretoria, pp. 204–210, 216–224. Finor, J.M. & Rone, C. (1998). Serial number restoration of obliterated welded on type characters, AFTE Journal 30(4), Fall, 649. Heard, B.J., (1997). Handbook of Firearms and Ballistics: Examining and Interpreting Forensic Evidence, John Wiley & Sons, West Sussex, pp. 213–221. Heflin, T.M. (1984). Overstamp, AFTE Journal 16(3), 12. Kennington, R.H. (1997). One swab serial number restoration, AFTE Journal 29(3), Summer, 288. Klees, G.S. (2002). The restoration of obliterated laser-etched firearm identifiers by conventional and alternative decryption methods, AFTE Journal 34(3), Summer, 264. Knowles, M. (1985). Instant recovery of obliterated serial numbers, AFTE Journal 17(3), 63. Massiah, E.E. (1976). Techniques and formula, AFTE Journal 8(2), 26. Miller, K.E. (1972). Current assist for die stamp impression restoration, AFTE Journal 4(3), 38. Nickolls, L.C. (1956). The Scientific Investigation of Crime, Erased Identification Marks, Butterworth & Co, London, 150–164. O’Reilly, W.E. (1970). Magnetic restoration of serial number, AFTE Newsletter 2(3), 26. Polk, D.E. & Giessen, B.C. (1989). Metallurgical aspects of serial number recovery, AFTE Journal 21(2), 174. Polk, D.E. & Giessen, B.C. (1975). Metallurgical aspects, AFTE Journal 17(2), 38. Sherlock, W.E. & Keating, D.M. (1995). Obliterated serial number tracking program, AFTE Journal 27(4), 264. Shoshani, E. & Klain, A. (2001). Altering a serial number, AFTE Journal 33(2), Spring, 133. Thornton, J.I. & Cashman, P.J. (1976). The mechanism of the restoration of obliterated serial numbers by acid etching, Journal of the Forensic Science Society 16(1), 69–71. Treptow, R.S. (1978). Handbook of Methods for the Restoration of Obliterated Serial Numbers, NASA. Wagoner, A. (1999). Griffin’s reagent for serial number restoration in stainless steel, AFTE Journal 31(4), Fall, 497.
Related Articles Firearms: Overview Toolmarks NICHOLAS R. MAIDEN
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Sex Determination of Remains
Sex Determination of Remains Once one has verified that the remains are human and recent, the anthropologist must proceed to reconstruct the biological profile. This entails the collection of all possible information from the skeletal remains, which may lead to identification. This goes from sex, age, stature, and ancestry, to all dental (hence the strong link with forensic odontology) and osseous features (deformations, pathologies, nonmetric traits), and, finally, to facial reconstruction. In an ideal system, the biological profile should be compared with descriptions of missing persons in order to find the best possible matches. Then one should proceed to perform a comparison between antemortem and postmortem data by odontological, anthropological, or genetic analyses (sometimes fingerprints may also exist on the degraded remains, which are not completely skeletonized, but this is more the domain of the fingerprint expert or the forensic pathologist). Concerning the biological profile (sexing, aging, etc.), odontological aspects also will be taken into account in this Forensic Anthropology section (see Anthropology: Age Determination of Remains; Odontology), leaving the specific identification aspects mainly to the Forensic Odontology chapter. Sexing is the first step in the completion of the biological profile. Determination of sex of human remains is frequently immediate even in severely decomposed cadavers, thanks to the fact that genital organs are among the last soft tissues to disappear. In skeletonized remains, however, such tissues are not present and thus one must rely on the dental and skeletal structure. In the past decade, DNA testing has started to prevail. However, although it is extremely sensitive as a technique, one must deal with the problem of extraction, degradation, contamination, and costs. Conservation of DNA depends on various environmental variables, still not completely known, even if sporadic DNA has been used for sexing even ancient remains. Anthropological criteria are quicker and cheaper for sexing; however, they too have their limits. On one hand, they are dependant on the integrity of the skeleton. Extremely fragmented remains may be impossible to sex (if crucial parts have been lost). On the other hand, they do not always give accurate and absolute results. Another
limit to the skeletal analysis is subadults. Skeletons of children and adolescents cannot be sexed due to the incompleteness of morphological characteristics. Some authors have advanced the hypothesis concerning different dental dimensions and particularly the conformation of the auricular surface of the ilium, which, in infant ilia, is elevated when the sex is female and flat when it is male. However, extreme caution should be applied with such methods whose authors indeed warrant an error rate of 50–60%. Other hints on sex of a subadult can be given by the difference in maturation between the dentition and the skeleton. Girls usually have similar maturation stages for the skeleton and the teeth; boys seem to have a slower dental development. Thus a discrepancy between dental and skeletal development in a subadult may indicate a male sex. However, even this method may be full of pitfalls. Determination of sex on adult complete skeletons, on the other hand, is quite reliable and has two main approaches: a morphological and a metric one. Both approaches are complementary and reflect sexual dimorphism in the shape and dimension in almost all bones, but particularly and more significantly, the cranium and the skull. Metric parameters reflect, on the other hand, different sizes between males and females, in particular, as concerns the diameter of articular extremities. There is, however, an intermediate zone of superimposition and only individuals whose dimensions fall below and above it can be safely classified as male or female [1–43]. The most reliable anatomical site for sexing is the hip. Female bones reflect the tendency to adapt to pregnancy and childbirth. The female pelvis is relatively lower and larger compared to the male one. Generally speaking, in front of an entire pelvis (left and right innominate and sacrum) this appearance can be quite diagnostic, as shown in Figures 1 and 2. It is, however, less intuitive that there are other parts of the pelvis that may be, per se, indicative of sex. The most important bones remain the pubic ones, particularly that area constituting Phenice’s triad, a series of three characters, which are very reliable sex indicators. These consist of (i) the ventral arc: this is an elevated bony crest, which extends across the ventral surface of the pubic body laterally from the center of the body until it reaches the ischiopubic ramus (Figures 3 and 4).(ii) the subpubic concavity, which is a small medial concavity at the medial extremity of the subpubic angle, present in females;
Sex Determination of Remains
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A
Figure 1 Female pelvis. The letter A is situated in the subpubic angle, which is very wide in the female
Figure 3 Pubis seen from the front. The arrow points to the ventral arc in the female pubis
B
Figure 2 Male pelvis. The letter B is under a very narrow subpubic angle, typical of males. Also notice the much more narrow nature of the anterior pubic region with respect to the pelvis in Figure 1
(iii) the shape of the ischiopubic ramus (or presence of the ischiopubic crest). The female ischiopubic ramus has a crest along the ramus and is narrower. The value of these parameters has been confirmed by several authors and this triad remains a fundamental sex indicator. Other important sex markers of the pelvis are the shape of the sciatic notch: it is narrow in males and forms an obtuse angle in females (Figures 5 and 6). The preauricular sulcus is an evident concavity (notch) beneath the auricular surface, which articulates the ilium with the sacrum. This is more commonly present in females than in males. Most authors will agree that the entire pelvis will reach a degree of accuracy in sexing between 95 and 98%. However,
Figure 4 tral arc
Isolated typical male pubic bone with no ven-
as all biological markers, a margin of overlapping of the two sexes must be taken into account. Finally, the sacrum is also usually taken into account. A flat sacrum is generally female, while a concave one is male. The cranium is the next best sex indicator, although reliability slides down to 80–85%. The male cranium is, in general, larger and rougher with more marked muscular insertions. Males tend to develop prominent crests near the muscle insertions, which move the head and mandible. These include the temporal lines, where temporal muscles insert, and the mastoid processes, which project inferiorly behind the auditory meatus.
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Sex Determination of Remains
1
2
3 4 6
7
Figure 5 Female right innominate bone (medial view): the arrow indicates a large sciatic notch
Figure 7 Female skull, where one can appreciate (1) flat glabella; (2) thin orbital margin; (3) a zygomatic arch that stops in length at the external auditory meatus; (4) small and medially inclined mastoid process; (5) (posterior) small nuchal crest; (6) no gonial eversion and delicate mandibular angle; and (7) round mandibular symphysis
1
2
3 4
6
Figure 6 Male right innominate bone (medial view): the sciatic notch is much narrower
However, such insertions may be marked even in women who have occupational stress in these areas. Ethnological studies show the development of such characters in women who prepare hides with their teeth or who carry weights on their heads. In general, main sexual differences in the cranium can be seen in the anatomical areas shown in Figures 7 and 8. As regards the anthropometric approach, numerous publications exist on metrical differences between sexes of almost every single bone. One can observe the diameters of the heads of humeri and femurs, and/or measure the ratios of pelvic structures, such as the ischiopubic index. An alternative is the
7
Figure 8 Male skull, where one can appreciate (1) pronounced glabella; (2) thick and rounded orbital margin; (3) a zygomatic arch that proceeds beyond the external auditory meatus; (4) large and vertical mastoid process; (5) (posterior) large nuchal crest; (6) gonial eversion and rough ridges on the mandibular angle; and (7) squared mandibular symphysis
discriminant function analysis. However, the single most commonly used parameters are the head of the femur, of the humerus and of the radius. Generally, if the diameter of a humeral head is greater than 47 mm, the person is a male and less than 43 mm it is a female; a female radial head is 21 mm or less and in males it is usually over 23 mm. The vertical diameter
Sex Determination of Remains of the femoral head is usually over 48 mm in males and less than 43 mm in females. There is then a vast literature on the metric analysis of various anatomical districts such as heads, diaphyses, and epicondyles of long bones and lengths and widths of tali, calcanei, sacrum, metatarsals, and metacarpals [25–43]. One advantage of metrical analysis is that it will entail a smaller error within nonexpert observers. Discriminant function analysis is also a valid, although more complex, support to sexing. It allows the combination of numerous measures in a single mathematical function in order to discriminate between two groups: male and female, based obviously on data taken from two known sample groups. With the combination of different measurements, discriminant functions give more weight to variables, which are more efficient in sexing and in distinguishing between two groups, namely, male and female. Discriminant functions have already been calculated and published for cranial, mandibular, pelvic, and other regions of the skeleton. All these methods, however, both metric and morphological, are subject to variations within populations. It is therefore crucial, when sexing, to use morphological or metric parameters or discriminant functions tared on populations similar to the one that is being studied. A final remark on sex should be made concerning signs of pregnancy. Some authors have indicated that notches on the dorsal surface of the pubis indicate that the woman underwent pregnancy. More marked ones even indicate several pregnancies. These theories, however, should not be taken too seriously as they have, in part, been revealed wrong by the presence of such notches in the bones of women known to have been nulliparous.
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Case, D.T. & Ross, A.H. (2007). Sex determination from hand and foot bone lengths, Journal of Forensic Sciences 52(2), 264–270. Dayal, M.R. & Bidmos, M.A. (2005). Discriminating sex in South African blacks using patella dimensions, Journal of Forensic Sciences 50(6), 1294–1297. Dar, G. & Hershkovitz, I. (2006). Sacroiliac joint bridging: simple and reliable criteria for sexing the skeleton, Journal of Forensic Sciences 51(3), 480–483. Patriquin, M.L., Steyn, M. & Loth, S.R. (2005). Metric analysis of sex differences in South African black and white pelves, Forensic Science International 147(2–3), 119–127. Ubelaker, D.H. & Volk, C.G. (2002). A test of the Phenice method for the estimation of sex, Journal of Forensic Sciences 47(1), 19–24. Asala, S.A. (2001). Sex determination from the head of the femur of South African whites and blacks, Forensic Science International 117(1–2), 15–22. Franklin, D., Oxnard, C.E., O’Higgins, P. & Dadour, I. (2007). Sexual dimorphism in the subadult mandible: quantification using geometric morphometrics, Journal of Forensic Sciences 52(1), 6–10. Gentry Steele, D. (1979). The estimation of sex on the basis of the talus and calcaneus, American Journal of Physical Anthropology 45(3 pt 2), 581–588. Giles, E. & Elliot, O. (1963). Sex determination by discriminant function analysis of crania, American Journal of Physical Anthropology 21, 53–68. Gualdi-Russo, E. (2006). Sex determination from the talus and calcaneus measurements, Forensic Science International 171(2–3), 151–156. Holcomb, S.M.C. & Konigsberg, L.W. (1995). Statistical study of sexual dimorphism in the human fetal sciatic notch, American Journal of Physical Anthropology 97(2), 113–125. Hu, K.S., Koh, K.S., Han, S.H., Shin, K.J. & Kim, H.J. (2006). Sex determination using nonmetric characteristics of the mandible in Koreans, Journal of Forensic Sciences 51(6), 1376–1382. Kalmey, J.K. & Rathbun, T.A. (1996). Sex determination by discriminant function analysis of the petrous portion of the temporal bone, Journal of Forensic Sciences 41(5), 865–867. Introna, F., Di Vella, G. & Campobasso, C.P. (1998). Sex determination by discriminant analysis of patella measurements, Forensic Science International 95(1), 39–45. Iscan, M.Y., Loth, S.R., King, C.A., Shihai, D. & Yoshino, M. (1998). Sexual dimorphism in the humerus: a comparative analysis of Chinese, Japanese and Thais, Forensic Science International 98(1–2), 17–29. Kemkes, A. & G¨obel, T. (2006). Metric assessment of the “mastoid triangle” for sex determination: a validation study, Journal of Forensic Sciences 51(5), 985–989. Kim, D.I., Lee, U.Y., Park, D.K., Kim, Y.S., Han, K.H., Kim, K.H. & Han, S.H. (2006). Morphometrics of the hyoid bone for human sex determination from
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digital photographs, Journal of Forensic Sciences 51(5), 979–984. King, C.A., Iscan, M.Y. & Loth, S.R. (1998). Metric and comparative analysis of sexual dimorphism in the Thai femur, Journal of Forensic Sciences 43(5), 954–958. Listi, G.A. & Bassett, H.E. (2006). Test of an alternative method for determining sex from the os coxae: applications for modern Americans, Journal of Forensic Sciences 51(2), 248–252. McCormick, W.F., Stewart, J.H. & Greene, H. (1991). Sexing of human clavicles using length and circumference measurements, The American Journal of Forensic Medicine and Pathology 12(2), 175–181. Mac Laughlin, S.M. & Bruce, M.F. (1990). The accuracy of sex identification in European skeletal remains using the Phenice characters, Journal of Forensic Sciences 35(6), 1384–1392. Mahfouz, M., Badawi, A., Merkl, B., Fatah, E.E., Pritchard, E., Kesler, K., Moore, M., Jantz, R. & Jantz, L. (2007). Patella sex determination by 3D statistical shape models and nonlinear classifiers, Forensic Science International 173(2–3), 161–170. Mall, G., Graw, M., Gehring, K. & Hubig, M. (2000). Determination of sex from femora, Forensic Science International 113(1–3), 315–321. Mall, G., Hubig, M., Kuznik, J., Penning, R. & Graw, M. (2001). Sex determination and estimation of stature from long bones of the arm, Forensic Science International 117(1–2), 23–30. Marino, E.A. (1995). Sex estimation using the first cervical vertebra, American Journal of Physical Anthropology 97(2), 127–133. Phenice, T.W. (1969). A newly developed visual method of sexing the os pubis, American Journal of Physical Anthropology 30(2), 297–201. Purkait, R. (2001). Measurements of ulna – a new method for determination of sex, Journal of Forensic Sciences 46(4), 924–927. Robling, A.G. & Ubelaker, D.H. (1997). Sex estimation from the metatarsal, Journal of Forensic Sciences 42(6), 1062–1069. Rogers, T.L. (1999). A visual method of determining the sex of skeletal remains using the distal humerus, Journal of Forensic Sciences 44(1), 57–60. Rogers, N.L., Flournoy, L.E. & McCormick, W.F. (2000). The rhomboid fossa of the clavicle as a sex and age estimator, Journal of Forensic Sciences 45(1), 61–67. Rogers, T.L. (2005). Determining the sex of human remains through cranial morphology, Journal of Forensic Sciences 50(3), 493–500. Steyn, M. & Iscan, M.Y. (1999). Osteometric variation in the humerus: sexual dimorphism in South Africans, Forensic Science International 106(2), 77–85. Steyn, M. & Iscan, M.Y. (1998). Sexual dimorphism in the crania and mandibles of South Africans whites, Forensic Science International 98(1–2), 9–16.
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Sutherland, L.D. & Suchey, J.M. (1991). Uses of the ventral arc in pubic sex determination, Journal of Forensic Sciences 36(2), 501–511. Tanaka, H., Lestrel, P.E., Uetake, T., Kato, S. & Ohtsuki, F. (2000). Sex differences in proximal humeral outline shape: elliptical Fourier functions, Journal of Forensic Sciences 45(2), 292–302. Ukelaker, D.H. & Volk, C.G. (2002). A test of the Phenice method for the estimation of sex, Journal of Forensic Sciences 47(1), 19–24. Wahl, J. & Graw, M. (2001). Metric sex differentiation of the pars petrosa ossis temporalis, International Journal of Legal Medicine 114(4–5), 215–223. Wescott, D.J. (2000). Sex variation in the second cervical vertebra, Journal of Forensic Sciences 45(2), 462–466. Williams, B.A. & Rogers, T. (2006). Evaluating the accuracy and precision of cranial morphological traits for sex determination, Journal of Forensic Sciences 51(4), 729–735. Wiredu, E.K., Kumoji, R., Seshadri, R. & Biritwum, R.B. (1999). Osteometric analysis of sexual dimorphism in the sternal end of the rib in a West African population, Journal of Forensic Sciences 44(5), 921–925.
Related Articles Anthropology DNA: Degraded Samples CRISTINA CATTANEO
AND
DAVIDE PORTA
Sex of Deceased see Species Determination of Osseous Remains
Sex Offenders: Treatment of The term paraphilia, as defined by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), is used to refer to recurrent sexual fantasies, urges, or behaviors involving nonhuman objects, suffering or humiliation, children or
Sex Offenders: Treatment of other nonconsenting persons. Paraphilic interests are fairly common in men and include a wide variety of behaviors typically seen in clinical populations seeking evaluation and treatment for paraphilias [1]. Those who most frequently seek psychiatric treatment for sex offenses are those accused of or involved in child molestation, voyeurism, exhibitionism, fetishism, frottage, and public masturbation [2]. The term sex offender is used to refer to an individual who has been legally convicted of a sex offense. The terminology “sex offender” does not provide any information regarding the offender’s reason for committing the sexual offense nor does it indicate the presence or absence of a paraphilia. The psychiatric treatment of sex offenders is distinct from other clinical populations. Recent changes in sex offender legislation have mandated treatment for offenders deemed “sexually dangerous” or “sexually violent” in psychiatric hospitals as civil committees. Such legislation has fueled long-standing debates on the diagnosis of paraphilias, the nature of mental illness, and the treatability of sex offenders [3].
Background The efficacy of sex offender treatment is unknown. Although studies comparing treated and untreated sex offenders have been done, measurement of outcome is flawed, with recidivism rates underestimating the actual recurrence of the pathological behavior [4]. Methodological challenges such as sample selection, study design, and assessment of outcome represent significant problems in the treatment efficacy studies. The majority of treatment efficacy studies are conducted on incarcerated or civilly committed offenders. Those individuals who are incarcerated or civilly committed represent a unique population with treatment outcomes, which may not generalize to the nonincarcerated or community-residing sex offender. Many studies do not differentiate between types of offenders. For example, a study that evaluates child molesters may not differentiate between intrafamilial and extrafamilial offenders. Research suggests that incest offenders recidivate at approximately half the rate of extrafamilial child molesters [5]. A well-designed study of treatment efficacy in sex offenders would compare treated offenders with a matched, randomly assigned control group. However, the ethical and public safety implications of such a
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study impede its design. Sex offenders are extremely heterogeneous and when this is not recognized it is very difficult to make comparisons among treatment efficacy studies [2]. The determination of treatment success in sex offenders is arbitrarily defined. Investigators have not agreed upon a standardized measurement of improvement. Although all treatment studies report sex offender recidivism, recidivism is measured in various ways. Some studies measure recidivism based on an offender’s self-report, whereas other studies define recidivism based on an offender’s arrest records. Studies measuring sexual arousal by penile plethysmography define improvement as a reduction in deviant sexual arousal. In a meta-analysis by Hanson and Bussiere [6], erections to children (as measured by penile plethysmography) was the factor most highly correlated to recidivism in over 28 000 sex offenders. However, the use of penile plethysmography has not been generally accepted by the scientific community due to a lack of reliability between the different types and models of plethysmographs in addition to debate over the validity and appropriate use of penile plethysmography [7].
Biological Treatment The scientific basis of biological treatment in sex offenders is the reduction of sexual behaviors by decreasing testosterone levels. Testosterone is a steroid hormone produced by the testes and responsible for the development of secondary sex characteristics in men. Testosterone helps maintain sex drive, the production of sperm cells, male hair patterns, muscle mass, and bone mass. Testosterone strongly influences both male and female sexual drive and the resultant sexual behavior [8]. Animal studies show that male copulatory behavior is almost entirely dependent on circulating levels of plasma testosterone [9]. The production of testosterone is mediated by follicle-stimulating hormone (FSH) and luteinizing hormone (LH), both of which are produced by the pituitary gland. LH signals the testes to produce testosterone. The hypothalamus senses whether the production of testosterone is too much or too little. If the testes are producing too little testosterone, the hypothalamus secrets a hormone called
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Sex Offenders: Treatment of
gonadotropin-releasing hormone (GnRH) that signals the pituitary to increase production of LH, which results in an increase in testosterone production. If the testes are producing too much testosterone, the hypothalamus secretion of GnRH is inhibited. This process whereby the hypothalamus modulates the production of testosterone is called negative inhibition.
Surgical Treatment Surgical treatment for sex offenders consists of two types: neurosurgery and castration. The neurosurgical procedure involves stereotaxic removal of parts of the hypothalamus to disrupt production of male hormones and decrease sexual arousal and impulsive behaviors [4]. This procedure had significant adverse effects and was considered largely ineffective. Surgical castration is the removal of the testes. The effect of surgical castration is to globally reduce available androgen by the removal of the testes [2]. Sturup [10] followed 107 castrated sex offenders and compared them with 58 sex offenders who were not castrated over a period of 18 years. The castrated individuals recidivated at a 4.3% rate. The 58 uncastrated individuals recidivated at a 43% rate. Postcastration follow-up studies provide the most comprehensive outcome data on the effect of reducing plasma testosterone and the resultant suppression of the sexual drive and deviant sexual behavior [11]. These studies have reported recidivism rates of less than 5% with follow-up periods of up to 20 years in a large sample size [11]. The introduction of antiandrogen and hormonal medications has rendered surgical castration nearly obsolete. The effects of surgical castration can be achieved through chemical castration, i.e., the use of medications to decrease testosterone production, without the invasiveness and irreversibility of surgery. Some states in the United States, such as Texas and California, mandate chemical or surgical treatment of dangerous sexual offenders. Controversy exists as to whether surgical castration should be offered as a treatment as chemical castration achieves the same results and spares the procedure.
Pharmacologic Treatment Antiandrogens. Androgens are male sex hormones that promote the development and maintenance of
male sex characteristics. Testosterone is the most common androgen in man. Antiandrogen treatment refers to treatment with drugs used to block production or interfere with the action of male sex hormones. Cyproterone acetate (CPA) and medroxyprogesterone (MPA) are the two most commonly used antiandrogen medications. CPA is not available in the United States but is widely available in Canada and Europe. Both CPA and MPA are synthetic progesterones that reduce the serum level of testosterone. Reduction of testosterone has been shown to reduce libido, erections, ejaculations, and spermatogenesis [12]. A meta-analysis of antiandrogen studies completed by Grossman et al. [4] suggests that recidivism rates in antiandrogen-treated offenders are less than that in untreated offenders. The studies report a spectrum of differences between patients treated with antiandrogens and those not treated, with recidivism rates as low as 1% for treated patients and as high as 68% for untreated patients [4]. In 1992, Copper et al. [13] performed the first direct comparison of CPA and MPA. The results suggested that MPA and CPA performed equally in decreasing sexual thoughts and fantasies, frequency of masturbation, and erection. The risks associated with the use of antiandrogen agents include side effects such as weight gain, hyperglycemia, hot and cold flashes, liver dysfunction, hypertension, muscle cramps, phlebitis, gastrointestinal complaints, and feminization [4]. In addition there is little known about the long-term sequelae of antiandrogen treatment. The majority of antiandrogen studies follow patients for eight years or less. The patient who agrees to antiandrogen treatment should be educated about the absence of long-term data. Hormonal Agents. Leuprolide and Triptorelin are hormonal agents referred to as long-acting GnRH agonists. These agents inhibit the secretion of LH with a resulting decrease in plasma testosterone levels and libido [14]. They produce a chemical castration in that the hypothalamic-pituitary axis is exhausted and there is a potent inhibition of gonadotropin [15]. Rosler and Witztum treated 30 men with severe long-standing paraphilias with triptorelin [16]. Treatment was associated with suppression of serum testosterone. A meta-analysis of pharmacotherapy of paraphilias with long-acting agonists of luteinizing hormone-releasing hormone was
Sex Offenders: Treatment of conducted by Briken et al. [17]. In total, the studies reported on a sample of 118 treated patients. Patients previously treated with other agents like CPA, MPA, or selective-serotonin-reuptake inhibitors (SSRIs) reported better effects when taking luteinizing hormone-releasing hormone (LHRH) agonists. None of the treated patients had a relapse. The results indicated that all men showed a decrease in deviant sexual fantasies, desires, and abnormal sexual behavior. In an observational study, Krueger and Kaplan [18] treated 12 patients with various diagnosed paraphilias and comorbid psychiatric disorders with leuprolide. All patients reported a significant reduction or even cessation of deviant sexual arousal and/or interests. The side effects associated with GnRH agonists include decreased bone mineral density or osteopenia, weight gain, hyperglycemia, diabetes, hypertension, and insomnia. The most commonly reported side effects are erectile/ejaculatory problems and gynecomastia [18]. In general, patients reported fewer side effects on GnRH agonists when compared to antiandrogens. The preliminary studies of GnRH agonist suggest that leuprolide and triptorelin may be more effective, better tolerated alternatives to antiandrogen treatment. Selective-Serotonin-Reuptake Inhibitors (SSRIs). Although the pharmacologic mechanism is poorly understood, SSRIs have been shown to be effective in reducing paraphilic symptoms. Kafka [19] treated 21 subjects with paraphilic disorders or paraphilicrelated disorders with SSRI monotherapy. A total of seventeen subjects showed a decrease in symptoms while being treated with an SSRI without significant side effects. Greenberg et al. [20] demonstrated that sertraline, fluvoxamine, and fluoxetine were equally effective in reducing paraphilic symptoms. Although data exists to suggest that SSRIs are effective in the treatment of paraphilias, presently there is insufficient data to conclude that SSRIs are equally efficacious as antiandrogens or hormonal agents.
Psychological and Behavioral Treatment Psychological approaches to the treatment of sex offenders focus on direct treatment approaches to modify offenders’ cognitions and attitudes. Cognitive approaches described the concept of cognitive
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distortions (minimizations, excuses, justifications) as one factor that may maintain offender behavior [21]. Relapse prevention and the sexual assault cycle are theoretical models purporting to describe the cognitions and behaviors of sex offenders before, during, and after their abusive acts [22]. An offender prevents relapse by the identification and arrest of the thoughts and actions, which lead to sexual offending. The majority of sex offender treatment programs offer a combination of cognitive-behavioral and relapse prevention therapies. The rationale for the implementation of behavioral techniques to control sexual arousal is based on the clinical observation that abusive sexual fantasy is linked with abusive sexual behavior. The factor that most consistently distinguishes male sex offenders from other males is sexual arousal disorder profiles as measured by phallomteric assessment [23]. The modification of an individual’s behavior is achieved by altering individual reactions to stimuli through positive and negative reinforcements. These reinforcements condition an individual by reinforcing positive behaviors and extinguishing negative behaviors. More specifically, the behavioral techniques used to control sexual arousal employ olfactory aversion conditioning, covert sensitization, and masturbatory satiation to extinguish deviant sexual arousal and reinforce appropriate sexual arousal. Recidivism rates from cognitive and behavioral treatment programs range from 3% to 31% depending on the study [4]. In a meta-analysis by Hall [24], it was found that cognitive-behavioral treatment and antiandrogen treatment were comparable in their treatment effects and significantly more effective than behavioral treatment alone.
Models of Treatment The treatment of individuals with paraphilias and sex offenders has primarily focused on two areas: cognitive-behavior group treatment and pharmacologic treatment. Treatment programs are based on recent research that reveals that victim empathy, remorse, responsibility training, and relapse prevention are integral components of a treatment program. A survey conducted by the Safer Society in 1994 asked sex offender treatment providers to identify the treatment modalities delivered in their program. The results revealed
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Sex Offenders: Treatment of
that greater than 90% of programs utilized the following treatment modalities: victim empathy, anger management, and cognitive distortions; 75% of programs provided social skills/assertiveness training, approximately 42% prescribed SSRIs, and 19% prescribed antiandrogens [25]. Langevin et al. [26] queried the sex offenders in treatment about acceptable types of treatment. The preferred therapies were individual psychotherapy, social skills training, and group therapy, whereas aversion conditioning, castration, and sex drive–reducing drug therapy were the least acceptable forms of treatment.
Ethical and Legal Considerations The legal and ethical issues that arise in the course of sex offender treatment are unique to this population. As such, the traditional codes of ethics employed in medical treatment are not applicable to the treatment of sex offenders. A significant percentage of sex offenders receiving treatment have been mandated by the courts as part of incarceration or to be released into the community. The concept of mandated or involuntary treatment raises the issue of whether informed consent is possible in sex offender treatment. A condition of informed consent for medical treatment is that the consent must be voluntary. Obviously, court-ordered sex offender treatment is not voluntary. Individuals who reject treatment are subject to punishment imposed by the courts. Individuals who have been ordered by the court to receive treatment do not have a choice regarding the type of treatment or the treatment provider. Sex offenders are required to complete particular programs, irrespective of any other treatment that they might be receiving, in order to gain community release or avoid imprisonment [27]. In the medical model, patients have a right to refuse various types of treatment. The right to refuse treatment is based on an individual’s constitutional right to privacy. The court views sex offenders as incompetent patients, and as such the court becomes the decision maker regarding treatment.
Confidentiality and Privilege Confidentiality refers to the physician’s obligation to keep information learned in a professional
relationship private from other parties. Privilege refers to the patient’s right to prevent a physician from providing testimony about personal medical information. Both confidentiality and privilege are routinely breached in sex offender treatment. When individuals enter treatment, they are required to give permission for their cases to be discussed with both clinical and nonclinical personnel, correctional officers, members of their family, past and potential victims, and those associated with them and fellow offenders [27]. In response to the deviations from traditional ethical codes inherent in sex offender treatment, ethical and practice guidelines were developed by the Association for the Treatment of Sexual Abusers (ATSA). ATSA’s code of ethics endorses standards of professional conduct that promote competent practice, and as such, they represent a public commitment to clients and society toward the goal of preventing sexual violence. The ATSA guidelines state that the ethical care of sex offenders is achieved by encouraging individuals to take responsibility for their behavior, that is, admission of guilt. ATSA maintains that the identification and collaborative management of risk and safety factors are indeed in the best interests of both sex offender patients and potential victims owing to the grave consequences incurred by sexual offender recidivism [28].
Castration of Sex Offenders In 1996, California became the first state to authorize the use of either chemical or surgical castration for certain sex offenders who were being released from prison into the community. To date, additional nine states have authorized surgical or chemical castration for sex offenders, including Georgia, Montana, Oregon, Wisconsin, Florida, Iowa, Louisiana, and Texas. The American Psychiatric Association stated “these laws, which predicate release from prison on chemical castration by surgery or antiandrogenic agents, are objectionable because they are not based on adequate diagnostic and treatment considerations. They also improperly link medical treatment with punishment and social control” [2]. In some states informed consent for the procedure is not required, while in other states informed consent requires only that the offender be informed regarding the side effects [29].
Sex Offenders: Treatment of
Conclusion and Future Directions Further Research Although studies have demonstrated the effectiveness of some modalities of sex offender treatment, the scientific literature does not identify a definitive effective treatment. The literature suggests that both cognitive-behavioral therapies and antiandrogen medication decrease sex offender recidivism. However, the current sex offender legislation in the United States is not based on the literature. Rather, the legislation focuses on the preventive detention of sex offenders without concurrent evidence-based sex offender treatment. The future of research in the treatment of sex offenders lies in the development of evidence-based knowledge that will inform both clinical decisions and public policy. This effort may be afforded by interdisciplinary collaboration between the scientific community, correctional professionals, and policy makers.
the public and the courts. In order to implement an evidence-based treatment, the offender must be afforded the opportunity for treatment. The opportunity for treatment is created by an informed society that legislates treatment that is informed by scientific evidence. The education of the public is integral in the successful treatment of sex offenders.
References [1] [2]
[3] [4]
[5]
Specialized Training Many psychiatrists are unfamiliar with the fundamentals of the assessment and treatment of individuals with paraphilias. The advent of laws for the civil commitment of sex offenders has resulted in the need for psychiatrists trained in paraphilias. As a result of sex offender legislature, the treatment and release decisions regarding sex offenders have become a focus of attention for psychiatry [30]. Forensic psychiatrists or psychologists must render an opinion as to whether the sex offender has a diagnosed mental disorder and, as such, represents a risk to public safety if released from custody into the community [31]. In order to provide competent care to individuals with paraphilias, psychiatrists should be educated about the evidence-based approach to the treatment and evaluation of this population.
[6]
[7]
[8]
[9] [10]
[11]
Education of the Public [12]
The general public perceives sex offenders as a homogenous group of offenders who are not treatable. However, recent meta-analysis has demonstrated that sex offenders are a highly heterogeneous population with different rates of reoffending and responsiveness to treatment. The successful treatment of sex offenders is dependent, in part, on the support of
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[13]
[14]
Crepault, C. & Coulture, M. (1980). Men’s erotic fantasies, Archives of Sexual Behavior 9, 565–580. The American Psychiatric Association Task Force on Sexually Dangerous Offenders (1999). Dangerous Sex Offenders: A Task Force Report of the American Psychiatric Association, American Psychiatric Association, Washington, D.C. Zonana, H. (1997). The civil commitment of sex offenders, Science 278, 1248–1249. Grossman Linda, S., Martis, B. & Fichtner, C.G. (1999). Are sex offenders treatable? A research overview, Psychiatric Services 50(3), 349–361. Marshall, W.L. & Barbaree, H.E. (1988). The long-term evaluation of a behavioral treatment program for child molesters, Behavior Research and Therapy 26, 499–511. Hanson, R.K. & Bussiere, M.T. (1996). Predictors of Sexual Offender Recidivism: A Meta-analysis, User Report No 1966-04, Department of the Solicitor General of Canada, Ottawa. Ferrall, W.R. & Card, R.D. (1988). Advancements in physiological evaluation of assessment and treatment in the sexual aggressor, in Sexual Aggression: Current Perspectives, R. Prentky & V.L. Quinsey, eds, New York Academy of Sciences, New York. Davidson, J.M., Smith, E.R. & Damassa, D.A. (1977). Comparative analysis of the roles of androgen in the feedback mechanisms and sexual behavior, in Androgens and Antiandrogens, L. Martini & M. Motta, eds, Raven, New York, pp. 137–149. Bancroft, J. (1989). Human Sexuality and Its Problems, Churchill Livingstone, Edinburgh. Sturup, G.K. (1953). Sexual offenders and their treatment in Denmark and other Scandinavian countries, International Review of Criminal Policy 4, 1–19. Ortmann, J. (1980). The treatment of sexual offenders, castration and antihormone therapy, International Journal of Law and Psychiatry 3, 443–451. Donovan, B.T. (1984). Hormones and Human Behavior, Cambridge University Press, London. Cooper, A.J., Sandhu, S., Losztyn, S. & Cernovsky, Z. (1992). A double-blind placebo controlled trial of medroxyprogesterone acetate and cyproterone acetate with seven pedophiles, Canadian Journal of Psychiatry 37, 687–693. Bradford, J.M. (1983). Research on sex offenders: recent trends, Psychiatric Clinics of North America 6, 715–731.
2338 [15] [16]
[17]
[18]
[19]
[20]
[21]
[22]
[23]
[24]
[25]
[26] [27]
[28]
[29]
[30]
Sex Offenders: Treatment of
Bradford, J.M.W. (1983). Research in sex offenders, The Psychiatric Clinics of North America 6(4), 715–733. Rosler, A. & Witztum, E. (1998). Treatment of men with paraphilia with a long-acting analogue of gonadotropinreleasing hormone, New England Journal of Medicine 338, 416–465. Briken, P., Hill, A. & Berner, W. (2003). Pharmacotherapy of paraphilias with long-acting agonists of luteinizing hormone-releasing hormone: a systematic review, The Journal of Clinical Psychiatry 64(8), 890–897. Krueger, R.B. & Kaplan, M.S. (2001). Depot-leuprolide acetate for treatment of paraphilias: a report of twelve cases, Archives of Sexual Behavior 30, 409–422. Kafka, M.P. (1994). Sertraline pharmacotherapy for paraphilias and paraphilia-related disorders an open trial, Annals of Clinical Psychiatry: Official Journal of the American Academy of Clinical Psychiatrists 6, 189–195. Greenberg, D.M., Bradford, J.M.W., Curry, S. & O’ Rourke, A. (1996). A comparison of treatment of paraphilias with three serotonin reuptake inhibitors: a retrospective study, The Bulletin of the American Academy of Psychiatry and the Law 24, 525–532. Murphy, W.D. (1990). Assessment and modification of cognitive distortions in sex offenders, in Handbook of Sexual Assault: Issues, Theories, and Treatment of the Offender, W.L. Marshall, D.R. Laws & H.E. Barbaree, eds, Plenum Press, New York, pp. 331–342. Carich, M.S., Gray, A., Rombouts, S., Stone, S., Pithers, M. & William, D. (2003). Relapse prevention and the sexual assault cycle, in Handbook for Sexual Abuser Assessment and Treatment, Safer Society Press, Vermont, pp. 77–104. Murphy, W.D. & Barbaree, H.E. (1994). Assessments of Sex Offenders by Measures of Erectile Response: PsychoMetric Properties and Decision Making, Safer Society Press, Brandon. Hall, G.C.N. (1995). Sexual offender recidivism revisited: a meta-analysis of recent treatment studies, Journal of Consulting and Clinical Psychology 63, 802–809. Freeman-Longo, R.E., Bird, S., Stevenson, W.F. & Fiske, J. (1994). Nationwide Survey of Treatment Programs and Models, Safer Press, Brandon, pp. 19–20. Langevin, R., Wright, P. & Handy, L. (1988). Sexual Abuse: A Journal of Research and Treatment 1(3). Glaser, B. (2003). Therapeutic jurisprudence: an ethical paradigm for therapists in sex offender treatment programs, Western Criminology Review 4(2), 143–154. Levenson, J.S. & D’Amora, D.A. (2003). An ethical paradigm for sex offender treatment: response to glaser, Western Criminology Review 4(2), 143–154. Scott, C.L. & Holmberg, T. (2003). Castration of sex offenders: prisoners’ rights versus public safety, The Journal of the American Academy of Psychiatry and the Law 31, 502–509. Lieb, R., Quinsey, V. & Berliner, L. (1998). Sexual predators and social policy, Crime and Justice 23, 43–114.
[31]
Screenivasan, S., Weinberger, L.E. & Garrick, T. (2003). Expert testimony in sexually violent predator commitments: conceptualizing legal standards of “mental disorder” and “likely to reoffend”, The Journal of the American Academy of Psychiatry and the Law 31(4), 471–485.
RENEE SORRENTINO
Sexual Abuse see Child Sexual Abuse Accommodation
Sexual Abuse: Child see Child Sexual Abuse
Sexual Abuse Accommodation Syndrome see Child Sexual Abuse Accommodation
Sexual Assault see Assault: Sexually Motivated
Sexual Assault: Child see Child Sexual Abuse
Sexual Assault: Drugs see Drug-Facilitated Sexual Assault
Sexual Fatalities see Autoerotic Deaths
Shaken Baby Syndrome
Sexual Homicide see Homicide: Multiple (Behavior)
Sexual Misadventure see Autoerotic Deaths
Sexually Transmitted Infections see Northwest Juvenile Project
Sexually Violent Predator see Dangerousness: Risk of
Shaken Baby see Battered Child Syndrome
Shaken Baby Syndrome
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survive with greater or lesser degrees of neurological damage [1]. The term non-accidental head injury (NAHI) has been preferred as it has no implications for mechanism of injury. Other features often associated include a sole carer at the time of collapse and a clinical history that is incompatible with the severity of the injuries. The diagnosis of inflicted injury becomes less problematic if there is objective evidence of violence, such as bruises, fractures, or burns, but objective evidence of trauma has not always been necessary in making the diagnosis. Central to the assessment of these cases is whether the triad of findings can be regarded as diagnostic of abuse with any degree of certainty. This review examines the evidence base for each element of the triad and the current biomechanical evidence regarding mechanisms of infant head injury and its pathological investigation.
History SDH has been associated with child abuse since the mid-19th century [2]. Kempe described SDH with multiple skeletal injuries and bruises as the battered child syndrome and Caffey described long bone fractures and SDH [3–5], but it is Guthkelch [6] who developed the hypothesis that the whiplash–like movements during shaking cause the characteristic bilateral thin film SDH of the syndrome. He based his hypothesis, that shaking causes tearing of the cerebral bridging veins leading to SDH, on the biomechanical studies of Ommaya [7] who was researching adult head injury in road traffic accidents. Following Guthkelch’s paper, the “shaken baby syndrome” has become widely accepted as a form of child abuse [1].
Introduction The Triad of Injuries The diagnosis “shaken baby syndrome” (SBS) has been widely accepted for over 30 years, but recent evidence from biomechanical and clinical observational studies questions the validity of the syndrome.
The three elements of the triad are encephalopathy, RH, and SDH.
Retinal Hemorrhages (RHs)
Definition The diagnosis of SBS is based on the clinical triad of encephalopathy, retinal hemorrhage (RH), and subdural hemorrhage (SDH) in infants, usually under six months of age, who may die unexpectedly or
RHs have been regarded as an important indicator of inflicted injury, but many other causes of retinal bleeding are recognized in infants, for example after normal birth, raised intracranial pressure, blood dyscrasias, hemoglobinopathies, extracorporeal membrane oxygenation, cataract surgery, and accidental
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trauma [8]. Postmortem indirect ophthalmoscopy has shown RHs to be more common after natural disease and accidental injury than after inflicted injury [9]. These authors also noted that infants suspected to have been abused were more likely to have ophthalmological examination in life than infants with accidental injuries or natural diseases. This bias readily distorts the true incidence of RH in non-accidental injury. Indeed Vinchon [10] noted in his study of infant head injury that “In the construct of our study we could not obviate the circularity bias, and the evaluation of the incidence of RH in child abuse remains a self-fulfilling prophecy”. These authors did, however, suggest that the extent and nature of retinal bleeds may be more important as indicators of inflicted head injury than their existence per se [10]. The main hypotheses for genesis of RH are that it is the result of venous obstruction, which in turn may result from compression of the optic nerve by raised intracranial or intravascular pressure, even transiently, or that the tissues of the retina are torn during the act of shaking. This latter hypothesis does not withstand biomechanical scrutiny [11].
Encephalopathy This term may be widely interpreted to include a range of clinical manifestations from feeding difficulties, vomiting, and sleepiness to seizures and fulminating cerebral edema. The specific neuropathological features of traumatic brain injury are contusions and traumatic axonal injury. Hypoxic-ischemic injury and brain
(a)
swelling are frequently seen but are not specific for trauma. Contusions are very uncommon in infant brain trauma in the absence of skull fractures. Identification of axonal injury now depends on the immunocytochemical demonstration of beta amyloid precursor protein (BAPP). This is a very sensitive marker of interruption of normal axonal flow but may be upregulated after hypoxic–ischemic injury and metabolic disruption as well as trauma (Figure 1). Distinction of traumatic axonal expression of BAPP from other causes is fraught with difficulty, and depends in part on its distribution [12], [13], [14]. Neuropathological studies have shown that in babies who die following NAHI, the underlying brain pathology is widespread hypoxic-ischemic injury and not diffuse traumatic axonal injury as previously believed [12, 13]. In this series axonal injury was seen in a limited distribution in the lower brainstem and in only a minority of cases. Radiological studies have confirmed these pathological observations [15]. This observation is important as traumatic axonal injury will lead to immediate loss of function causing clinical symptoms from the time of trauma. In contrast, hypoxic-ischemic injury and ensuing brain swelling take variable periods of time to develop and a baby so damaged may not show immediate symptoms. Even fatal brain trauma may present with a lucid interval between injury and clinical collapse [16, 17]. Lucid intervals are more frequently seen in infants less than two years of age [18], reflecting the very different responses of the infant brain to injury due to the specific intracranial pathophysiology before the skull bones fuse [19].
(b)
Figure 1 (a) Acute axonal injury. Bands of BAPP expression in an infarcted area of brain in acute hypoxic-ischemic injury. (b) Axonal swellings expressing BAPP restricted to the pontine cortico-spinal tracts, considered to indicate traumatic damage
Shaken Baby Syndrome Damage to the cervical nerve roots has been documented as part of the pathology of shaking injury [14]. It has not been established that this is the result of shaking, as cervical cord displacement resulting from brain swelling may also cause traction on nerve roots in the region. Autopsy studies in man and primates have shown that the spinal cord is displaced during extension and flexion of the neck [20, 21] and it remains a possibility that hyperextension and flexion could cause traction damage to nerve roots throughout the length of the spinal cord, but this has not been documented in living infants.
Subdural Hemorrhage (SDH) SDH is perhaps the most important and consistent component of the triad. In the acutely sick infant, it is frequently the first clinical sign, identified on brain scan, to raise the question of abuse. There are no specific imaging patterns that can distinguish inflicted from accidental intracranial injury [22, 23]. Autopsy and imaging studies show that infant SDH is usually a thin bilateral film and not a thick, unilateral space occupying clot as seen in traumatic SDH in older children and adults [12, 13, 24]. This raises the question of whether the two forms have the same etiology and anatomical source. Causes of Subdural Hemorrhage. The commonest cause of SDH in infants is said to be trauma [25] although a recent study has shown a significant incidence (26%) of birth-related SDH [26]. Other causes in infants include benign enlargement of the extracerebral spaces (BEECS), clotting disorders, hemorrhagic disease of the newborn, rare metabolic diseases, vascular malformations, and neurosurgical procedures [25, 27]. Traumatic SDH Proposed traumatic causes of infant SDH are inflicted injury such as shaking and/or impact and accidental injuries such as falls. Impact includes blunt impact of an object on the head and that resulting from a fall or striking the moving head on a rigid surface. The biomechanical aspects of these injuries are discussed below. The vast majority of cases described as SBS have evidence of impact [28]. While the pathologist may be able to determine features indicative of impact, it is not, of course, possible to distinguish accidental from non-accidental injuries by pathology.
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Low-Level Falls Low-level falls have the potential, albeit only rarely, to cause SDH in infants and young children. Absolute height is not as important a criterion for injury as the exact nature of the fall for a particular infant, in a particular circumstance [29]. The effects of twisting, rotation, or crushing of the structures of the neck are crucial in terms of outcome. Biomechanical studies show that falls even from low levels of 3–4 ft can generate far greater forces in the head than shaking [11]. There are a number of case series demonstrating that infants and children may suffer intracranial damage including retinal and intracranial hemorrhage after falls from levels as low as 3 ft [10, 17, 30–33]. While most babies may suffer little from an apparently trivial fall, this is clearly not always the case. Birth-Related SDH Three studies, using magnetic resonance imaging (MRI), have shown a surprisingly high incidence of SDH after birth in asymptomatic infants. Whitby identified SDH in the first two days of life in 9% [32], while SDH was seen in up to 46% of otherwise normal neonates using higher resolution MRI scanning [26, 34]. With regard to method of delivery, ventouse or instrumental deliveries have been associated with a higher incidence of intracranial injury [35, 36]. Towner [37] found an increased incidence of intracranial hemorrhage after instrumental delivery with ventouse or forceps and emergency caesarean section, but the incidence was lower after caesarean section before labor had begun. However, it should be noted that all of Looney’s cases followed normal vaginal delivery [26]. While neonates with SDH may be asymptomatic [26, 35] they may also have signs in the neonatal period including unexplained apnoea, dusky episodes, hypotonia, seizures, and lethargy [38]. Sources of SDH. Traditional belief is that in SBS the SDH results from tearing of the superficial bridging veins as they cross from the brain to the dural sinuses [6] (Figure 2). This has never been proved. Indeed it is very difficult to find documented evidence of torn bridging veins at surgery or at autopsy. Cushing, who operated on neonates with SDH and subsequently performed the autopsies wrote “In two of the cases I have examined I have satisfied myself
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Shaken Baby Syndrome
Figure 2 Infant bridging veins may be visualized by opening the skull very carefully, but they are readily torn in normal autopsy procedures. (Picture courtesy of Dr P. Lantz)
that such ruptures were present. A positive statement, however, cannot be given even for these cases, since the dissection and exposure, difficult enough under any circumstances, owing to the delicacy of the vessels is the more so when they are obscured by extravasated blood” [39]. More recently Maxeiner [40] addressed the problem by injecting radio-opaque dye into the veins at autopsy to assess their integrity after removing the top of the head in one piece, hard-boiled egg style. This approach is not widely used as it destroys much of the brain and injection pressures need to be carefully monitored if the veins are not to be ruptured artifactually.
Figure 3
Volpe [41] said that SDH was by no means always traumatic and suggested that in neonates without tentorial tears the bleeding may arise from the tributary veins of the dural sinuses. Autopsy studies from the older literature show bridging vein rupture is uncommon, Craig described 62 neonatal SDH, of which only 3 had torn bridging veins, all of those with overriding sutures [42]. Larroche described 700 autopsies 18% with SDH. [43] She noted an association with hypoxic-ischemic injury (Figure 3). She did not identify torn veins. If SDH does not arise from torn bridging veins, what other sources may there be? Two obvious
Fresh subdural blood seen after birth asphyxia. (Picture courtesy of Dr I. Scheimberg)
Shaken Baby Syndrome Arachnoid granulation
Superior sagittal sinus
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Intradural fluid channel Lateral lacuna of sagittal sinus
Dura
Inner dural plexus Subarachnoid space Arachnoid barrier membrane
Cortical draining vein Falx
Figure 4 Diagram representing a coronal slice through the brain and dura indicating the intradural sinuses and their relationship to cortical surface veins, arachnoid granulations, and intradural fluid channels
alternative sites of origin exist, the dura itself and the old subdural membranes (Figure 4). Dural Hemorrhage The dura is composed of two leaflets, the periosteal and the meningeal dura, separated by a thin vascular channel, which widens to form the large dural sinuses [44]. There are particularly extensive venous sinuses in the posterior falx, [45] a frequent site of high signal on brain scans in asphyxiated infants. Bleeding into the falx is well recognized in asphyxiated infants [46]. It has long been acknowledged that optic nerve sheath hemorrhage arises from the dura [47] and more recently the dura was proposed as the source of intracranial SDH in infants [48] (Figure 5). Careful microscopic examination of the dura confirms that intradural bleeding is common in asphyxiated infants, particularly in the dural folds of the falx and tentorium close to the large venous sinuses [49]. In some cases intradural bleeding leaks out on to the subdural surface leading to macroscopically evident subdural haematoma [50].
Healing Subdural Membranes Healing of SDH is by formation of a thin, vascular membrane consisting of fibroblasts, macrophages, which often contain altered blood products, and wide thin-walled capillaries with a potential to rebleed [51] (Figure 6). It is uncommon in infants to see a double layered membrane around a localized mass of resolving clot, as seen in the elderly, probably because the infant SDH usually forms as a thin film rather than as a mass lesion. Contrast injection is required to identify the membranes radiologically [52]. In some cases, acute SDH leads to accumulation of fluid in the subdural space. The reasons for this are unknown. Fluid collections may result from immaturity of the arachnoid granulations and impaired cerebrospinal fluid (CSF) absorption [22], and be influenced by the method of treatment of the acute hematoma. Surgical evacuation or tapping may prevent later reaccumulation of fluid [53, 54]. The period of time for redevelopment of subdural fluid collections may be long, between 15 and 111 days [55]. It is likely that an important
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Shaken Baby Syndrome
(a)
(b)
Figure 5 (a) The dura is thickened and congested and there is patchy subarachnoid and subdural blood. Autopsy 44 h after collapse following choking episode. (Courtesy of Dr I. Sheimberg.) (b) H & E stained section of falx showing it to be destroyed by massive acute bleeding
(a)
(b)
(c)
Figure 6 (a) Dural surface showing a very thin yellow-brown membrane, which has partly lifted during removal of the brain. Head injury four weeks prior to death. (b) H & E stained section of acute bleed overlying a chronic membrane, which consists of some six layers of fibroblasts between which are macrophages and new capillaries (three days after collapse with acute SDH) (c) Same section stained with CD34 to show endothelial cells. Note capillaries growing into the fresh clot
Shaken Baby Syndrome
(a)
2345
(b)
Figure 7 (a) A collection of fresh subdural blood at the dorsal aspect of the sacral spinal cord. Baby died within hours of inflicted abdominal injury with acute and chronic subdural hemorrhage. (b) Microscope section showing an elliptical collection of fresh blood dorsal to the spinal cord. The blood is within a chronic subdural membrane indicated by the iron pigment, stained here by Perl’s stain. Baby died three weeks after traumatic subdural hemorrhage
contribution to chronic subdural fluid accumulation is repeated rebleeding and oozing from a chronic subdural membrane [56, 57]. There is little information regarding the potential for birth-related SDH to evolve into chronic fluid collections. Whitby followed nine cases with a repeat scan at one month; none had developed a chronic collection [35]. Rooks followed 18 cases for up to 3 months, one developed a further subdural bleed [34]. However these studies could not identify membranes as contrast was not used. Chronic membranes have been seen at autopsy in up to 31% of infants dying unexpectedly without previous clinical evidence of chronic SDH [58]. In view of the potential for acute accidental SDH to evolve into a chronic collection several months later [55], it would appear likely that the same pattern would follow birth-related SDH. At this time, we simply have insufficient information. Distribution. In the first few days after bleeding, subdural blood sediments under the influence of gravity and undergoes secondary redistribution to the most dependent part, the posterior falx and tentorium [59]. Radiological studies show that subdural blood tracks down around the spinal cord [60] and, if the spine of babies with intracranial SDH is examined at autopsy, blood is regularly seen in the subdural space and around sacral nerve roots in the most dependent parts of the dural sac (Figure 7).
Differential Diagnosis of SBS The most common causes of the triad are impact, birth-related SDH, BEECS, coagulopathies, apnoea, asphyxia and choking, acute life-threatening events (ALTEs), osteogenesis imperfecta, osteopenia of prematurity, and metabolic diseases [14, 28, 61, 62, 63].
Choking/Asphyxia In a considerable number of cases, vomiting and/or reflux are described at the time of collapse, and in some there is a history of feeding difficulties, gastroesophageal reflux, and choking or apnoeic episodes [14, 62]. SBS is commonly diagnosed in the first three months of life, the age of peak incidence of sudden infant death syndrome. Inhalation of feed or vomit may play a part in sudden infant death [64] and awake apnoea is associated with gastroesophageal reflux [65]. The physiological response to aspiration may be dramatic; foreign material on the larynx causes laryngospasm, which is associated with startle, cessation of respiration, hypoxaemia, bradycardia, and a doubling of blood flow to the brain [66]. These circumstances, with or even without vigorous resuscitation, may cause reperfusion injury and a preexisting healing subdural membrane may bleed. The dura itself may become hemorrhagic and ooze blood into the subdural space (Figure 8). As long ago as 1905, Cushing suggested that coughing, choking, and
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Shaken Baby Syndrome
(a)
(b)
Figure 8 (a) Cortical vein thrombosis. Infant died 10 days after collapse following two choking episodes. Several surface veins are thrombosed (arrows). (b) Section of thrombosed vein shows a network of new capillaries growing into the periphery of the thrombus (CD31)
Peak head acceleration (g)
Bed – mattress
25.4 cm
50
50.8 cm
75
Inflicted slamming style impacts onto surfaces noted
Leather sofa
76.2 cm
100
From adult male’s arms
125
25
0
Free fall impacts onto carpeted stairs (fall heights noted)
Figure 9 Comparative forces generated by dropping or shaking and slamming a dummy representing a six-month-old infant (C Van Ee, personal communication 2007)
venous congestion may explain some forms of infant SDH [39], a hypothesis recently revived by Geddes, [48, 67].
Biomechanics Biomechanics is the application of principles of physics to biological systems and has been the mainstay of research into motor vehicle safety for six decades. It was just such research into noncontact head injury from rear-end shunts that stimulated Guthkelch to formulate his hypothesis for SBS in
1971 [6]. Ommaya [7] had caused concussion, SDH, and white matter shearing injury (diffuse axonal injury) in primates by whiplash. Guthkelch suggested that the rotational forces of shaking would cause tearing of bridging veins and bilateral subdural bleeding, although Ommaya himself warned that “It is improbable that the high speed and severity of the single whiplash produced in our animal model could be achieved by a single manual shake or even a short series of manual shaking of an infant in one episode”. More recent studies using “crash test dummies” indicate that impact generates far more force than
Shaken Baby Syndrome shaking (Figure 9) and that impact is required to produce SDH [68]. Cory and Jones [69] generated forces that exceeded the injury threshold for concussion, but not for SDH or axonal injury. Their adult shaker volunteers fatigued after 10 seconds. While they concluded that “It cannot be categorically stated, from a biomechanical perspective, that pure shaking cannot cause fatal head injuries in an infant ”, they noted that in their experiments there were chin and occipital contacts at the extremes of the shaking motion that could have caused impact. These authors expressed their concerns regarding the difficulties in extrapolating to human infants the findings in both dummy and animal models. Biomechanical studies have shown that falls and impact to the head produce significant rotational forces when the impacting forces are not aligned through the center of gravity of the head, due to hinging of the head on the neck. Shaking is not necessary to cause rotational acceleration. Neck injuries may be underreported in babies dying after severe abuse [70]. In Ommaya’s study, 11 of 19 primates had neck injuries; these were adult animals with mature neck structure and musculature. It is likely that the forces required to cause intracranial injury will also damage the weak infant neck [71]. In road traffic accidents, infants who suffer single severe hyperextension forces have cervical fractures, dislocations, spinal cord injury, and torn nerve roots, not SDH [72–74].
Investigation of Shaken Baby Syndrome SBS or NAHI is most likely to occur in an infant dying suddenly under the age of six months. Autopsy should be performed with careful consideration of this diagnosis and appropriate steps taken to support or exclude it. The records of pregnancy and delivery must be carefully studied to look for any evidence of complications that could mimic NAHI. These include pregnancy disorders such as oligohydramnios, fetal hypokinesia, and prematurity, which lead to osteopenia and predispose to fractures. The birth history and method of delivery are important as SDH may arise at this time while being entirely asymptomatic in the neonatal period. Head circumference charts are important; head circumference measurements taken at birth and in the subsequent weeks may reflect abnormal head growth, which can indicate an accumulating subdural fluid collection and a propensity to rebleed.
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The clinical history may give clues to other problems in the early weeks of life. Vomiting, feeding problems, and apnoeic episodes and ALTEs may indicate difficulties with coordination of breathing, sucking and swallowing, and vulnerability to choking. Any event that threatens life may also potentially end it. The history of the baby’s terminal collapse must also be carefully examined. Parents may describe events that reveal a cause for collapse. In any other field of medicine, the clinical history is regarded as the cornerstone of diagnosis and it should not be disregarded without serious critical evaluation. The autopsy can reveal evidence of trauma such as deep bruises and fractures not seen in clinical examination. The examination of the intracranial contents is paramount. The scalp and skull require careful examination for evidence of bruising and fractures. Suture separation due to raised intracranial pressure and wormian bones can be mistaken for fractures. When the cranium is opened, the presence of any intracranial bleeding must be noted. Unclotted blood may escape from the subdural space as the skull is opened and be mistaken for bleeding from the dural sinuses. It is important to note the volume and nature of blood and the presence of xanthochromia, indicating older bleeding. As the cranium is opened, the bridging veins should be visualized and their integrity assessed. If there is a question of bridging vein rupture, histological examination may assist in establishing this. The dural sinuses and draining veins should be examined for evidence of thrombosis. The dura must be carefully examined for evidence of older bleeding. A chronic subdural membrane may be thin and patchy and represented only by patches of light brown discoloration. Multiple samples should be taken from the dura, including the falx and tentorium, for histological examination to look for evidence of intradural bleeding and rupture onto the subdural surface. This may be the source of significant subdural blood. The brain must be fixed for detailed histological examination. In all of these cases, the time between collapse and death may play a significant part in the final pathology. A baby who has collapsed and becomes apnoeic with subsequent cardiopulmonary rescuscitation (CPR) and ventilation will be shocked and suffer multiorgan failure with altered clotting, loss
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Shaken Baby Syndrome
of integrity of vessels and membranes, oozing of blood into intracranial compartments, including the subarachnoid and subdural spaces, and development of the “respirator brain”. Review of the brain imaging in life is essential in assessing, as far as possible, just how much hemorrhage occurred at the time of collapse and how much may be the result of subsequent secondary changes. It is recognized that SDH may continue to bleed after initial onset [75] especially if a baby is very sick. Finding a large clot at autopsy may suggest traumatic rupture of a large vessel, but comparison with early brain scans may indicate that the bleed was only minor at the outset, indicating a slower oozing process with different implications for causation. It is becoming increasingly obvious that not all SDH arises from traumatic rupture of blood vessels.
[9]
[10]
[11]
[12]
[13]
[14]
Acknowledgment
[15]
I would like to thank Dr Irene Scheimberg and Dr Pat Lantz for providing pictures and Dr Chris Van Ee for valuable discussion and for preparing Figure 8.
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Hwang, S.K. & Kim, S.L. (2000). Infantile head injury, with special reference to the development of chronic subdural hematoma. Child’s Nervous System 16(9), 590–594. [56] Ito, H., Yamamoto, S., Komai, T. & Mizukoshi, H. (1976). Role of local hyperfibrinolysis in the etiology of chronic subdural hematoma. Journal of Neurosurgery 45(1), 26–31. [57] Markwalder, T.M. (1981). Chronic subdural hematomas: a review. Journal of Neurosurgery 54(5), 637–645. [58] Rogers, C.B., Itabashi, H.H., Tomiyasu, U. & Heuser, E.T. (1998). Subdural neomembranes and sudden infant death syndrome. Journal of Forensic Sciences 43(2), 375–376. [59] Vinchon, M., Noule, N., Tchofo, P.J., Soto-Ares, G., Fourier, C. & Dhellemmes, P. (2004). Imaging of head injuries in infants: temporal correlates and forensic implications for the diagnosis of child abuse. Journal of Neurosurgery 101(1 Suppl), 44–52. [60] Yamaguchi, S., Hida, K., Akino, M., Yano, S. & Iwasaki, Y. (2003). Spinal subdural hematoma: a sequela of a ruptured intracranial aneurysm? Surgical Neurology 59(5), 408–412. [61] McNeely, P.D., Atkinson, J.D., Saigal, G., O’Gorman, A.M. & Farmer, J.P. (2006). Subdural hematomas in infants with benign enlargement of the subarachnoid spaces are not pathognomonic for child abuse. AJNR. American Journal of Neuroradiology 27(8), 1725–1728. [62] Hylton, C. & Goldberg, M.F. (2004). Images in clinical medicine. Circumpapillary retinal ridge in the shakenbaby syndrome. New England Journal of Medicine 351(2), 170. [63] Paterson, C.R. (2003). Clinical Review Radiological features of the brittle bone diseases. Journal of Diagnostic Radiography and Imaging 5(1), 39–45. [64] Thach, B.T. (2000). Sudden infant death syndrome: can gastroesophageal reflux cause sudden infant death? American Journal of Medicine 108(Suppl 4a), 144S–148S. [65] Spitzer, A.R., Boyle, J.T., Tuchman, D.N. & Fox, W.W. (1984). Awake apnea associated with gastroesophageal reflux: a specific clinical syndrome. Journal of Pediatrics 104(2), 200–205. [66] Miller, M.J. & Kiatchoosakun, P. (2004). Relationship between respiratory control and feeding in the developing infant. Seminars in Neonatology 9(3), 221–227. [67] Geddes, J.F. & Talbert, D.G. (2006). Paroxysmal coughing, subdural and retinal bleeding: a computer modelling approach. Neuropathology and Applied Neurobiology 32(6), 625–634. [68] Prange, M.T., Coats, B., Duhaime, A.C. & Margulies, S.S. (2003). Anthropomorphic simulations of falls, shakes, and inflicted impacts in infants. Journal of Neurosurgery 99(1), 143–150. [69] Cory, C.Z. & Jones, B.M. (2003). Can shaking alone cause fatal brain injury? A biomechanical assessment of the Duhaime shaken baby syndrome model. Medicine Science and the Law 43(4), 317–333.
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Related Articles Autopsy Battered Child Syndrome WANEY SQUIER
Shoe Impressions: Comparison of see Footwear and Foot Impressions: Foot Impressions and Linking Foot to Shoe
Shooting Distance: Determination see Shooting Distance: Estimation of
Shooting Distance: Estimation of
Shooting Distance: Estimation of Introduction The range from which a weapon has been fired is an important component in the reconstruction of firearmrelated cases (see also Firearms: Scene Investigation). The firing-distance estimation is based on the examination of the appearance of the bullet entrance hole and the examination of the firearm discharge residue (FDR) patterns around the hole using various techniques. In casework the patterns obtained in a case are compared to those obtained in test firings. Although many authors in the field use the term shooting-distance determination, many forensic examiners around the world, including the Israel Police, prefer to use the term estimation instead of determination because of the intrinsic inaccuracy of the examination. The reason for this is a high variability of the FDR patterns from shot to shot when using the same weapon and ammunition. To increase the accuracy of the examination, the forensic examiner should use, for test firings, the weapon and ammunition used in the case whenever possible. In most of the shooting cases in which there is a need for a firing-distance estimation, the victim or the victim’s clothing have to be examined. In many cases, bullets hit surfaces of various parts of the human body directly without passage through any intermediate medium. In some instances other exhibits which happened to be targets of shooting have to be examined. Such exhibits may be cars, walls, doors, windows, furniture, etc. Many of these cannot be processed in the laboratory. FDR is projected from the muzzle of a firearm in a roughly conical pattern: the larger particles travel higher distances than the smaller ones before they are stopped by the air resistance [1]. Four ranges for shooting distance as described in the literature [2–5] are based on the appearance of the bullet holes on the human body: contact range, near contact range, intermediate range and distant range. In contact wounds, the muzzle of the firearm is held against the surface of the body at the time of discharge. The appearance of tearing, scorching, soot, or the imprint of muzzle, characterizes contact wounds. Virtually, no FDR is seen around the bullet hole. In near
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contact wounds, the muzzle of the weapon is a few centimeters away from the body. In this range, a wide zone of powder soot overlaying seared blackened skin surrounds the wound. An intermediate range gunshot wound is one in which the muzzle of the firearm is held a few tens of centimeters away from the body, producing “powder tattooing” of the skin. In distant range no damage effects or FDR particle patterns are observed around the gunshot wound. With most handguns and ammunitions, visually detectable FDR is not found in the case of shots fired at ranges greater than 30–45 cm [1]. In this text a review of the methods for visual/ microscopic, color tests and instrumental analysis of the entrance bullet holes and FDR patterns around them for shooting-distance estimation is provided. Comprehensive reviews on the subject have been published over the years [2–5]. The aspect of shooting-distance estimation for targets shot by pellet loads from shotguns may be found elsewhere [1, 2] and is not discussed here.
Visual/ Microscopic and Color Tests Clothing Targets FDR patterns around the entrance bullet holes consist of propellant residues and metallic residues from the bullet, e.g., lead and copper, as well as gunshot residues (GSR) (primer residues). These residues may be detected visually/microscopically if the target cloth is of a bright enough color. However in most of the cases there is need for color chemical tests or instrumental analysis in order to assess the FDR patterns around the entrance bullet holes. Walker [6] proposed to use Griess reaction to visualize free nitrite ions (on the shot target), originating from the combustion of ester nitrates (e.g., nitrocellulose (NC) and nitroglycerine (NG) in the gunpowder. In this test, the Griess reagent consisting of sulfanilic acid and α-naphthyl amine in acetic acid aqueous solution is used. The detection of nitrite ions is based on the formation of diazonium ion from sulfanilic acid and nitrite. The diazonium ion couples with α-naphthyl amine to form an orange azo dye. In a series of three papers [7–9], Dillon reports on the modified Griess test (MGT) as a color test for nitrites and recommends a protocol for FDR examinations in muzzle to target distance estimations. In the modified test, Dillon proposes to use
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Shooting Distance: Estimation of
α-naphthol instead of α-naphthyl amine (the Walker test) or N -(1-naphthyl)-ethylenediamine dihydrochloride. According to him both the replaced reagents are carcinogenic. However, in the literature on chemical safety data [10], N -(1-naphthyl)-ethylenediamine dihydrochloride is not reported as being carcinogenic. In fact, in Israel this reagent is used with sulfanilamide routinely for “the local” MGT [11]. The term MGT does not refer to one specific defined test. In fact, it appears that every author who introduces any modification to the original Griess test calls it an MGT. The proposed protocol [7] includes visual, microscopic and chemical (lead and nitrites) tests. It recommends to conduct first the MGT and then the sodium rhodizonate test (SRT) for lead. The reason for this sequence is because the rhodizonate is applied directly on the target. Dillon contends that particulate lead is a random nonreproducible phenomenon, whereas the presence of vaporous lead is quite significant in that it is found principally at closer ranges. Glattstein et al. reported on an improved method for shooting-distance estimation on clothing [11]. The novel part of the method includes transfer of total nitrite (nitrite ions and unburned smokeless powder residues) from the target to an adhesive lifter. After the transfer, lead and copper deposits around the bullet entrance hole are partially extracted consecutively to the Benchkote (Whatman) filter papers moistened with dilute acetic acid and ammonia solutions respectively. Their patterns are visualized by rhodizonate for lead (red color) and rubeanic acid for copper (dark green color). The MGT is carried out after alkaline hydrolysis of the smokeless powder residues on the adhesive lifter. The purpose of lifting gunpowder residues from the shot cloth target is to eliminate interferences caused by conducting MGT directly on the target, with or without the hydrolysis step. It was found that almost a complete transfer of gunpowder residues to the adhesive lifter was obtained and the vaporous lead and copper are not transferred to the adhesive lifter. The widely used MGT detects only free nitrite ions formed from the combustion of smokeless powder. The unburned smokeless powder particles cannot be detected by this method. Alkaline hydrolysis prior to the MGT has been proposed to increase the sensitivity of the test for gunpowder residues. The purpose of the alkaline hydrolysis is to cause disproportionation of the unburned NC and NG to carbonyl compounds and
free nitrite ion, thus increasing the available amount of nitrite ions for MGT. Before starting the estimation of the shooting distance it is desirable to determine that the hole is a bullet entrance hole. This can be done by applying methods for chemical visualization of lead (rhodizonate) and copper (rubeanic acid) at the perimeter of the hole [12]. From the accumulated experience in the Israel Police it has been observed that, the color tests did not give positive results on all bullet holes in clothing, although it was known that a lead bullet or a full metal jacket (FMJ, brass) bullet were used.
Persistence of FDR on Clothing Targets Several studies dealt with possible effects of various factors on clothing items after shooting with regards to the shooting-distance estimation [7, 13–16]. Most of these found that mechanical handling of clothing or soaking them in blood, in still or running water, considerably decreases the amount of FDR around the bullet entrance holes. Emonet et al. [16] reported that the medical manipulations of clothing lead to an increase of the loss of visible and nitrated FDR of about 30–40%. Even et al. [13], on the other hand did not find a significant effect of soaking in still water on the obtained FDR patterns. Sometimes casework requests are received to estimate shooting distance on clothing items that underwent machine washing. Vinokurov et al. [17] conducted a study to assess the effect of machine washing or brushing of clothing items on FDR patterns around bullet entrance holes. Results show that those treatments considerably decrease the amount and density of FDR (machine washing more than brushing).
Exhibits that Cannot be Processed in the Laboratory Glattstein et al. [18] examined the feasibility of the method developed for clothing [11] as described above, for additional materials such as galvanized steel, glass, plywood, and high pressure laminated plastic sheets of melamine and phenolic materials (Formica). It was found that for the above tested target materials and shooting distances the amounts and densities of the FDR detected visually (without any treatment) were considerably smaller than those obtained after chemical treatments. Total nitrite
Shooting Distance: Estimation of patterns visualized on the lifters applied on the various targets were similar to those obtained on the lifters from the cotton cloth at relatively short shooting distances, i.e., up to about 25 cm. As shooting distances become greater, the number and density of nitrite spots on the lifters from all the tested materials targets decreases considerably in comparison to the lifters from the cotton cloth for the same distance; the plywood target showed the most similar results to the cotton cloth. If there is no possibility to conduct test firing at a material similar to the evidence, then test firings may be carried out on cotton cloth. In such a case the visualized pattern of the total nitrite will be sufficient to state that the shooting distance on the evidence was equal or below the shooting distance at which similar visualized patterns of the total nitrite are obtained on the cotton cloth.
Instrumental Methods
The Human Body as a Target
References
In many shooting cases, bullets hit surfaces of various parts of the human body (mostly the head) directly, without passage through any intermediate medium. For the purpose of assessing the shooting distance, most of the forensic literature describes only visual/microscopic methods for the examination of appearance of the wound and FDR patterns around it [2, 4, 19]. Nonetheless, sodium rhodizonate and rubeanic acid reagents were proposed for the visualization of lead and copper patterns around the gunshot wounds [20, 21]. As in cases of clothing and other objects, implementing color tests (in addition to visual/microscopic visualization) might increase the accuracy of shooting-distance estimation. An additional unique problem pertaining only to the human body is that there is no possibility to conduct test firing on the same material as in the case of other exhibits. The proposed solution for test firings was to use various simulant materials. Recommendations for those materials were based on the studies comparing those materials to the skin of some animals, like rabbits or pigs. Glattstein et al. [22] examined the feasibility of applying an adhesive lifter to the entrance bullet wound in human body surfaces to visualize the total nitrite patterns, as was reported for clothing and other exhibits above. Stahling and Karlsson [23] reported a similar method for lifting and visualizing gunpowder residues from skin.
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FDR patterns around the bullet hole may be visualized by infrared (IR) photography [24] and IR imaging devices [25] due to the considerably higher absorbance of IR radiation by the soot than by other materials like fabric. X-ray radiography may also be used for that purpose because of the much higher absorbance of X-radiation by metallic deposits of the FDR than by clothing. X-ray fluorescence (XRF), atomic absorption spectroscopy (AAS) and neutron activation analysis (NAA) have also been used by some laboratories to estimate the range of shooting [3]. Recently, with the advent of the Micro-XRF technology and its increasing use in forensic science for the elemental analysis of trace evidence, some laboratories examined its feasibility for shootingdistance estimation [26].
[1]
Rowe, W.F. (2005). Firearms identification, in Forensic Science Handbook, 2nd Edition, R. Saferstein, ed., Pearson Prentice Hall, Vol. 2. [2] Sellier, K. (1991). Shot Range Determination, Forensic Science Progress 6, Springer-Verlag, Berlin, Heidelberg. [3] Lichtenberg, W. (1990). Method for the determination of shooting distance, Forensic Science Review 2, 38–62. [4] Zeichner, A. & Glattstein, B. (2002). Recent developments in methods of estimating shooting distance, The Scientific World Journal 2, 573–585. [5] Di Maio, V.G.M. (1999). Gunshot Wounds: Practical Aspects of Firearms, Ballistics and Forensic Techniques, CRC Press. [6] Walker, J.T. (1940). Bullet holes and chemical residues in shooting cases, Journal of Criminal Law and Criminology 31, 497. [7] Dillon, J.H. (1990). The modified Griess test: a chemically specific chromophoric test for nitrite compounds in gunshot residues, AFTE Journal 22, 243–250. [8] Dillon, J.H. (1990). The sodium rhodizonate test: a chemically specific chromophoric test for lead in Gunshot Residues, AFTE Journal 22, 251–256. [9] Dillon, J.H. (1990). A protocol for gunshot examination in muzzle to target distance determination, AFTE Journal 22, 257–274. [10] (1985). The Sigma-Aldrich Chemical Company, Inc., Material Safety Data Sheet for N-(1-Naphthyl) ethylenediamine dihydrochloride, November 2001–January 2002. [11] Glattstein, B., Vinokurov, A., Levin, N. & Zeichner, A. (2000). Improved method for shooting distance estimation. Part I. Bullet holes in clothing items, Journal of Forensic Sciences 45, 801–806.
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[13]
[14]
[15]
[16]
[17]
[18]
[19]
[20]
[21]
[22]
[23]
[24]
[25]
[26]
Short Tandem Repeats
Steinberg, M., Leyst, Y. & Tassa, M. (1984). A new field kit for bullet hole identification, Journal of Forensic Sciences 29, 169–176. Even, H., Bergman, P., Springer, E. & Klein, A. (1988). The effects of water-soaking on firing distance estimations, Journal of Forensic Sciences 32, 319–327. Haag, L.C. (1991). A method for improving the Griess and sodium rhodizonate tests for GSR patterns on bloody garments, AFTE Journal 23, 808–815. Bonfanti, M. & Gallusser, A. (1995). Problems encountered in the detection of gunshot residues, AFTE Journal 27, 105–122. Emonet, F., Bonfanti, M. & Gallusser, A. (1999). Etude des phenomes physique affectant les residues de tir et engenders lors de la manipulation des habits par le personnel medical, Canadian Society of Forensic Science Journal 32, 1–13. Vinokurov, A., Zeichner, A., Glattstein, B., Levin, N., Koffman, A. & Rozengaten, A. (2001). Machine washing or brushing of clothing and the influence on shooting distance estimation, Journal of Forensic Sciences 46, 928–933. Glattstein, B., Zeichner, A., Vinokurov, A. & Shoshani, E. (2000). Improved method for shooting distance estimation. Part II. Bullet holes in objects that cannot be processed in the laboratory, Journal of Forensic Sciences 45, 1000–1008. Heard, B.J. (1997). Handbook of Firearms and Ballistics: Examining and Interpreting Forensic Evidence, John Wiley & Sons, Chicester, West Sussex, England. Stone, I.C. & Petty, C.S. (1991). Interpretation of unusual wounds caused by firearm, Journal of Forensic Sciences 36, 736–740. Molchanov, V.I., Popov, V.L. & Kalmykov, K.N. (1990). Gunshot Wounds and their Forensic Medicine Examination (in Russian), Meditzina, Leningrad. Glattstein, B., Zeichner, A., Vinokurov, A., Levin, N., Kugel, C. & Hiss, Y. (2000). Improved method for shooting distance estimation. Part III. Bullet holes in cadavers, Journal of Forensic Sciences 45, 1243–1249. Stahling, S. & Karlsson, T. (2000). A method for collection of gunshot residues from skin and other surfaces, Journal of Forensic Sciences 45, 1299–1302. Eastman Kodak Company (1972). Applied Infrared Photography, Kodak Publication No. M-28, Eastman Kodak Co., Rochester, NY. Abrink, A., Andersson, C. & Maehly, A.C. (1984). A video system for the visualization of gunpowder patterns, Journal of Forensic Sciences 29, 1223–1224. Flynn, J., Stoilovic, M., Lennard, C., Prior, I. & Kobus, H. (1998). Evaluation of X-ray microfluorescence spectrometry for the elemental analysis of firearm discharge residues, Forensic Science International 97, 21–36.
ARIE ZEICHNER
Short Tandem Repeats Introduction Short tandem repeats (STRs) or microsatellites are discrete sequences of DNA that are repeated end on end. STR repeats in the human genome are analogous to carriages on a train. They can be repeated up to 100 times in tandem in the genome and have fragment lengths of between 100 and 400 bp [1]. Figure 1 shows the basic structure of a simple repeat STR. The repeated DNA sequence of an STR consists of 2–5 nucleotides as di-, tri-, tetra-, and pentanucleotide repeats. More than 23 000 tetranucleotide STR loci alone have been characterized since the completion of the human genome project [2]. Tetranucleotide repeats are the most common STRs used by forensic laboratories throughout the world. Trinucleotide and pentanucleotide loci are less common. Dinucleotide loci are the most common in the human genome; however, as they are more prone to artifacts that affect interpretation, they are not used for forensic purposes [3]. STRs used for human identity testing are located in the noncoding regions of the DNA, either within genes (introns) or between genes. They have been adopted universally by forensic biology laboratories as they are short and highly polymorphic, distributed throughout the genome, and are amenable to polymerase chain reaction (PCR) and automation. STRs are analyzed using the PCR. Primers of known sequence bind to either side of the target STR sequence (see Figure 1). Using PCR, STR profiles may be generated from as little as 0.2 ng of input DNA.
Examples of Common STRs Used for Forensic Applications The selection criteria for STRs in forensic use are based on their robustness, size, variability between individuals (polymorphic), and ability to be combined in a single test for ease of analysis (known as multiplexing). Table 1 contains a list of STRs commonly used by the forensic community for DNA analysis. This list is not intended to be exhaustive. Table 1 also includes core loci for the combined DNA index
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Short Tandem Repeats Primer
Flanking region
STR
Flanking region
Primer
TCAT TCAT TCAT TCAT TCAT
Figure 1
Table 1
Diagram of an STR sequence TCAT containing five repeats
A list of commonly used forensic STR loci and those included in the Interpol core set of loci and CODIS Applied Biosystems profiling kits
STR loci CSF1PO D2S1338 D3S1358 D5S818 D7S820 D8S1179 D13S317 D16S539 D18S51 D19S433 D21S511 FGA TH01 TPOX vWA Penta D Penta E ACTBP2 (SE33) Amelogenin
CODIS Interpol Identifiler E E E E E E E E
E
E E E E E
E E E
E
E
E
E E E E E E E E E E E E E E E
Profiler Plus
Promega Corp
SGMPlus
Sefiler
E E
E E
E
E
E E E E E E
E E E E E E
E
E
PowerPlex 16 PowerPlex ES E
E E E E E E E E
E
E E E E E E E
E
E E E E E E E
E E E
E E
E
system (CODIS) and Interpol databases (discussed later). Although not an STR, amelogenin is discussed in this work as it is routinely added to commercial STR assays for gender determination. Amelogenin is a gene that occurs on the X and Y chromosomes of the human genome [4]. The PCR primer set targets a 6 bp deletion that occurs on the X chromosome. This enables the X and Y chromosomes to be distinguished after electrophoresis. Female individuals are designated XX and males XY (see Figure 2). Amelogenin can also be useful for determining the ratio of male-to-female DNA in a mixed DNA profile. There are several genetic variations at amelogenin that may cause difficulties in interpretation. In one, the Y chromosome fails to amplify, making the individual genotypically female [5]. Other amelogenin abnormalities that may impede interpretation include
E
E
E
E
E
E E
E
trisomic states (XXY, XYY, and XXX) and rare genetic disorders that may lead to differences of genotype and phenotype [6].
Nomenclature Designation of Loci An internationally accepted nomenclature for the designation of STRs is vital for interlaboratory comparison and databasing [7, 8]. STR sites analyzed on the DNA are designated on the basis of their position within the genome. Markers that are part of a gene have its name within the designation. For example, STR marker TH01 is located within intron 1 of the tyrosine hydroxylase gene. STR markers that are not part of a gene are designated by the following pattern:
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Short Tandem Repeats 100
110
100
X 103.46
110
X 103.52
Y 109.22
X 103.46
Figure 2
Amelogenin loci of a female (XX) and male (XY) individual
DxSy where D is DNA, x is the chromosome number, S indicates that the sequence only occurs once in the genome (single), and y is a counter for when the site was identified. For example, D21S11 describes the 11th site discovered on chromosome 21. STR loci can also be preceded by the letters HUM, which indicate their human origin. The repeat motif for each STR is defined according to the International Society of Forensic Genetics (ISFG) recommendations for nomenclature as being the first 5 nucleotides on the GenBanka forward strand [9].
Designation of Alleles Simply, STR alleles are designated by the number of repeats they contain. Repeats are designated on the basis of comparison with allelic ladders that incorporate all common alleles. STRs can be categorized by the length of their repeat unit (di-, tri-, tetra-, and pentanucleotide) and also by the type of repeat pattern they conform to. Different classes of STRs have been identified, depending on their repeat structure. Simple repeats contain core sequences identical in sequence and length (for example, TH01). Compound repeats contain two or more adjacent simple repeats (for example, VWFA31). Complex repeats may contain several repeat blocks of variable repeat length with variable intervening sequences (for example, D21S11) [10]. Common examples of simple, compound, and complex STRs and their repeat structures are given below. The numbers outside the brackets surrounding
the repeat unit sequence give an indication of the number of times the sequence may repeat. Simple repeat, for example, TH01: (AATG)5 – 11 Compound repeat, for example, VWFA31: (ATCT)2 (GTCT)3 – 4 (ATCT)9 – 13 Complex repeat, for example, D21S11: (TCTA)4−6 (TCTG)5−6 (TCTA)3 TA(TCTA)6 TCA(TCTA)2 TCC ATA(TCAT)8−16 Complex hypervariable repeats are another, more complex, type of STR. A well-known example is ACTBP2 (also referred to as SE33 ). The common tetranucleotide repeat motif is (AAAG)n ; however, variants mono, di-, tri-, and tetranucleotides are also scattered through the locus. This makes ACTBP2 very polymorphic and for this reason it is a required STR for the German national DNA databank. However, the designation of alleles within this locus is problematic if based on solely counting repeats. For this reason, the size of the STR is measured and it is recommended that alleles be labeled “type-” to reflect this [7].
Microvariants Where alleles at an STR locus do not contain complete repeat units, these are termed microvariants. The microvariants are designated by the number of complete units and the number of additional base pairs of the partial repeat. The most common microvariant is allele 9.3 at TH01. TH01 9.3 is actually 10 repeat units with the loss of a single adenine in the seventh unit [11]. The repeat motif for TH01 9.3 is (AATG)6 ATG(AATG)3 .
Short Tandem Repeats
STR Analysis in Practise Visualization of STRs STRs are amplified using the polymerase chain reaction, which exponentially amplifies the target STR by a series of heating and cooling reactions. The size of the STR products is measured after PCR amplification by electrophoresis. Early STR analysis involved separating the PCR product on polyacrylamide gels followed by visualization using silver staining. Now, PCR products are labeled with fluorescent markers, which then undergo gel electrophoresis or, more commonly, capillary electrophoresis. The PCR product is loaded on the gel or capillary and subjected to an electrical charge. The negatively charged DNA travels through the medium dependent on its size. Smaller fragments of DNA travel faster through the gel or capillary. The actual size of the STR fragments is measured against two standard markers: an internal size standard that is injected with the sample and an allelic ladder that comprises common alleles with the STR loci. The DNA fragments are labeled with fluorescent probes. As the DNA travels through the gel or capillary, the probes are excited by a laser and the fluorescence is measured by a camera. The use of different color dyes enables multiple, overlapping loci to be analyzed concurrently, which is important for multiplexed STR assays. STR profiles result in a string of numbers (the allele counts or number of repeat units for STR analyzed) associated with the loci analyzed. For this reason, the data can be easily stored and compared within databases.
Multiplexes and Commercial STR Assays The primers targeting several STRs may be combined into one PCR reaction and amplified simultaneously. This is called multiplex PCR and is a rapid and convenient way to profile many STRs, thus generating a DNA profile. STRs present in multiplexed assays are chosen on the basis of their discriminating power, low levels of stutter, and compatibility with other loci. The choice of STR in commercial multiplexed assays can also be heavily influenced by demand from customers who must adhere to core loci, for example, CODIS and Interpol (discussed later). Several different STR assays or multiplexes are commercially available for use in forensic DNA analysis and paternity or identity testing. These are used
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widely by the forensic community as they have been extensively validated and scrutinized in the courts of numerous countries, making them universally accepted. The use of commercial STR assays also promotes uniformity and enables database conformity. Not all laboratories, however, use commercial STR assays. Some have developed in-house assays that may or may not have loci in common with commercial assays [12]. Indeed, even the commercially available kits do not share all loci in common with other laboratories. Two major suppliers of forensic DNA profiling kits and technology are Applied Biosystems, Foster City, California and Promega Corporation, Madison, Wisconsin. Both companies have developed several STR assays for forensic STR analysis (Table 1). The development and optimization of STR multiplexes can be very demanding and both labor intensive and time consuming [13]. For this reason, many laboratories have opted to use commercial assays where validation papers and population databases are freely available. The quality assurance requirements for developmental validation are rightly very stringent. Both Promega and Applied Biosystems have developed 15 loci STR multiplexes with amelogenin. Both kits incorporate all 13 CODIS loci and Interpol’s standard set of loci. Initially, two STR assays were required to test all 13 CODIS loci: Promega’s PowerPlex 1.1 and PowerPlex 2.1 or Applied Biosystem’s Profiler Plus and COfiler . See Figure 3 for an example of a male DNA profile generated using the 15 STR multiplex Identifiler . Identifiler uses four different dyes to label the loci. The internal size standard is labeled with a fifth color.
Core Loci and Databasing (Interpol and CODIS) STRs were first described as being potentially useful markers for forensic DNA analysis in the early 1990s [1]. The first national DNA database using STR profile data was started in the United Kingdom in 1995. This was followed by the establishment of the New Zealand National DNA Database in 1996 [14]. Several other European countries followed suit in the late 1990s. Many countries were analyzing different loci. To aid criminal investigation across the relatively open European borders, an Interpol working group proposed a European standard set of
Figure 3
0
1600
1600 0
0
1600
0
1600
9 267.63
28 200.30 Identifiler_v1
9 267.63
28 200.30
D21S511
D7S820
11 324.56
10 320.49
CSF1PO
7 175.11
6 171.12
TH01
Identifiler_v1
11 228.96
9 220.86
D13S317
13 284.54
11 276.50
D16S539 19 322.94
22 335.07
D2S1338
17 178.79
15 170.82
vWA
Identifiler_v1
11 242.06
9 234.06
TPOX
16 299.03
15 294.86
D18S51
12 155.55
10 146.96
D5S818
An Identifiler profile of a male individual
Y 112.25
X 106.59
Amelogenin
26 251.19
25 247.13
FGA
100 110 120 130 140 150 160 170 180 190 200 210 220 230 240 250 260 270 280 290 300 310 320 330 340 350 360
14.2 123.25
13.2 119.28
D19S433
100 110 120 130 140 150 160 170 180 190 200 210 220 230 240 250 260 270 280 290 300 310 320 330 340 350 360
18 135.90
17 131.93
D3S1358
100 110 120 130 140 150 160 170 180 190 200 210 220 230 240 250 260 270 280 290 300 310 320 330 340 350 360
16 157.35
14 148.68
D8S1179
100 110 120 130 140 150 160 170 180 190 200 210 220 230 240 250 260 270 280 290 300 310 320 330 340 350 360
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Short Tandem Repeats four loci in 1998. In 1999, this was expanded to seven loci (see Table 1) [15]. In 1997, the United States agreed to 13 core STR loci for their national DNA database, known as CODIS (see section “Core Loci and Databasing Interpol and CODIS”). Common sets of STR loci are required for collaboration between different testing laboratories within the same country or between different countries. Comparison of DNA profiles within national or international databases can be used to link individuals to crimes and to generate crime-to-crime links indicating recidivist offending patterns. The more core loci compared, the less likely adventitious links will be generated.
Linkage to Genetic Diseases The number of repeats at STR loci is highly variable between individuals as they undergo no selective pressure and are thought to be noncoding. There have been reports, however, of several core STR loci being linked to genetic diseases, including certain TH01 alleles indicating susceptibility to schizophrenia [16]. To date, all claims have been disputed by further studies [17], and no STRs have been removed from the core sets of forensic loci examined.
Mutations and Rare Alleles Mutation STR loci are prone to mutation; the reason is their variability amongst individuals and therefore their usefulness in forensic DNA and identity testing. The high mutation rate of STRs is not problematic for routine forensic work. Generally, DNA profiles generated from crime samples are compared directly with reference profiles generated using the same DNA STR assays. More problematic is parentage testing (paternity or maternity investigations). Mutation rates of STRs can be measured by analyzing many paternity trios (father, mother, and child) and comparing STR alleles. A child must inherit one allele from their father and one from their mother at each locus. This is demonstrated in Figure 4 with an example of two parent/child pedigrees at one STR locus. The first shows
Example (i) 12,13
Example (ii)
13,14
12,13
12,14
13,14
12,15
Figure 4 Two pedigrees of mother, father, and child at one loci. In example (i) the child must have inherited the “12” allele from the mother and the “14” from the father. In example (ii) a mutation has occurred most likely due to an insertion one repeat in length and the child has inherited a “15” allele
an expected pedigree and the second, a pedigree with mutation in the male germ line. Brinkmann et al. investigated 10 844 parent/child sets at nine STRs used for paternity testing and reported a mutation rate of between 0 and 7 × 10−3 for the loci tested. The number of mutations in the male germ line is 5–6 times higher than the maternal germ line. Generally, the more polymorphic (variable) and complex STRs exhibit the most mutation [18]. All mutations observed in this study were due to either whole repeat loses or repeat gains (22 involving single unit repeats and 1 example of a double repeat). The stepwise mutation model has been theorized to explain how STR alleles mutate by an increase or decrease on one repeat unit [19]. The likelihood of mutation must be taken into account when investigating paternity cases as false exclusions may be possible on account of differences of only one or two alleles. Mutation rates and their mechanisms are discussed in more detail in [20] and [21]. Other types of genetic mutations that give rise to microvariants are insertions and deletions of single nucleotides. The resulting allele often differs from full repeat units present in the allelic ladder by only a few nucleotides. These alleles are therefore sized as being “off-ladder” and many laboratories refer to them as being “rare” alleles. One example at the FGA locus is given in Figure 5.
Primer Binding Site Mutations Discordant genotype profiles may result from the differences in primer sequences used between STR
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Short Tandem Repeats 240
250
24 243.06
26.1R 252.22
Identifiler_v1 240
22 235.06
23 239.09
250
24 243.13
25 247.18
26 251.24
27 255.32
28 25
26.2 253.24
Figure 5
Rare allele at the FGA locus seen after amplification using AmpFlSTR Identifiler
assays produced by different manufacturers and different STR assays produced by the same manufacturer. The PCR amplification of STR alleles with mutations at primer binding sites may result in little or no extension during amplification. Total dropout of one allele at a locus leads to false homozygosity and the missing allele is called a null allele. A well-characterized primer binding site mutation is at the D8S1179 locus in the Chamorro (indigenous people of the Marianas Islands) and Filipino
populations [22], caused by a single point mutation (G to A transition) in the reverse primer binding sequence. The high frequency of homozygotes at D8S1179 in the Chamorro and Filipino populations was detected after performing a concordance study between Promega’s PowerPlex 16 assay and Applied Biosystem’s Profiler Plus . In their Identifiler STR assay, Applied Biosystems includes an additional D8S1179 reverse primer specific for the variant
Short Tandem Repeats 140
150
2361
160
14 149.31
16 158.12
SGM_plus_v1 140
12 140.37
150
13 145.00
14 149.48
160
15 153.86
16 158.19
17 162.40
18 166.54
Figure 6 An example of a primer binding site mutation at D8S1179 using AmpFlSTR SGMPlus . This individual was subsequently typed as a D8S1179 14,16 using AmpFlSTR Identifiler
that results in recovery of the null alleles not previously amplified [23]. In Figure 6, a primer binding site mutation in the reverse primer of D8S1179 has resulted in only partial amplification of the second (16) allele after amplification with SGMPlus . The amplification of this sample using Identifiler resulted in two alleles of equal height. Another reported example of discordant genotypes between different commercial STR assays was at FGA where a heterozygote profile was observed using the PowerPlex 16 primers and a single homozygote allele was observed using the Profiler Plus primers [24]. When comparing profiles generated using different assays, for example between different national DNA databases or old crime profiles and reference samples subsequently typed using more recent STR assays, these discordant profiles may become problematic. Database searching can be flexible regarding the stringency with which STR profiles are compared. By incorporating one or more allowed allele mismatches between different profiles, mutations causing discordant profiles due to differing primers within assays can be investigated.
Triallelic Patterns Triallelic patterns may be observed at individual STR loci. These can arise from trisomy (triplicated chromosomes), somatic mutation, or localized chromosomal rearrangement. There are only three known autosomal trisomies that are thought to be nonfatal; chromosome 21 resulting in Down’s syndrome, 13 giving rise to Patau syndrome, and 18 giving rise to Edwards syndrome. All three result in individuals with birth defects, mental retardation, and reduced life expectancy. The other types of triallelic patterns have been classified into two types: type 1 resulting from somatic mutations in one cell line giving rise to cells with two different genotypes and type 2 resulting from localized chromosomal rearrangement and appearing as three bands of equal height [25]. A high frequency of somatic mutations has been discovered in buccal cells of patients with oral cancer. In one study of 100 patients, 25 allelic nonconcordant profiles were detected following DNA typing of nine STR loci when compared with blood samples taken from the same individuals [26]. As for primer binding site mutations, somatic mutations and
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Short Tandem Repeats
localized chromosomal rearrangements do not complicate forensic investigations when directly comparing crime samples to reference samples. They may, however, make the interpretation of mixed DNA profiles more difficult by confusing the analyst when determining the number of individuals whose DNA may be present in a sample.
Nonstandard STRs X-Chromosomal STRs The application of X-chromosomal STRs (ChrX STRs) to forensic DNA analysis is not widely undertaken. Females possess two X chromosomes that recombine similar to autosomes (non sex chromosomes). Males inherit one X chromosome wholly from their mother and females share their paternal X chromosome with their father. ChrX STR analysis is not as powerful as autosomal STR analysis for forensic identity testing; however, it may be useful for cases where traces of female DNA are present in stains of high male DNA content, for example, vaginal epithelial cells on a penis [27]. ChrX STR analysis is more useful in cases of complex parentage testing where DNA from close family members or the putative parents is not available. One example would be for investigating body remains from mass disaster cases. ChrX STRs are also useful for paternity testing of female offspring (see Case Study 1).
Case Study 1 ChrX STR typing was employed in a case of questioned paternity of a female where reference samples were unavailable for the putative father and paternal grandparents. Samples were available for two paternal “uncles” (putative father’s brothers) and the child’s mother. Using the ChrX STR types of the “uncles”, the grandmaternal genotype was reconstructed. Using this, the putative father was excluded as being the true father as he did not carry some of the necessary paternal ChrX STR alleles [28].
Many ChrX STR loci have been identified and have been shown to be suited for forensic use due
to their high variability. A commercial ChrX STR assay with eight ChrX STRs is available (Mentype ArgusX-8 from Biotype AG) as is a website containing current research, nomenclature, and mutation rates [29].
Y STRs Y STRs are located on the Y chromosome and are therefore only suited to profiling male DNA (see Y-Chromosome Short Tandem Repeats). Y STRs are useful in the presence of large amounts of female DNA that would have otherwise masked the male DNA, for example, male epithelial cells on vaginal swabs after digital penetration. A Y STR haplotype is also useful for determining familial relationships. As with ChrX STR analysis, Y STRs are useful in determining deficiency paternity cases, although with male offspring. Y STR profiles are haplotypes as they are noncombining and may be shared by many individuals. Commercial Y STR assays are available from both Promega Corporation and Applied Biosystems, which test up to 12 and 17 Y STR loci, respectively [30].
miniSTRs The Identifiler and PowerPlex 16 STR assays both have loci with total lengths of over 350 bp. While STRs are relatively small, which contributes to their success in the analysis of forensic samples, most of their lengths can be regions of DNA flanking the repeat units (see Figure 1). This flanking DNA increases the STR length, allowing more loci to fit into commercial STR assays. By removing the flanking sequences and moving the primers to immediately flank the repeat units, miniSTRs are created (see Mini-STRs). miniSTRs are advantageous as they allow more degraded and lower amounts of DNA to be successfully amplified by the PCR and analyzed. Lengths of miniSTRs can be up to 300 bp smaller than their counterpart PCR products in commercial standard STR assays. Generally, miniSTRs also maintain database compatibility as they target the same STR loci. However, because the primers are redesigned, some discordance is to be expected (see earlier discussion). Another disadvantage is due to the restriction in size of the miniSTR amplification product as this means that less miniSTRs can be squeezed into commercial assays [31].
Short Tandem Repeats The European (ENSFI and EDNAP) groups have already recognized the importance and usefulness of miniSTRs. They have recommended that European laboratories maintain their seven core loci and reengineer the primers to convert them to miniSTRs. They also recommend the adoption of three new European core loci, which are miniSTRs that have not been previously seen in major standard commercial STR assays: D10S1248, D2S441, and D22S1045 [32, 33].
can link an animal to an individual where the animal is the perpetrator (for example, in dog attacks; see Case Study 3) or an individual to an animal where the link places the individual at the scene of a crime (see Case Study 4). Case Study 3 In Budapest, in 2001, DNA was analyzed from possible saliva stains extracted from the clothing from two deceased infants thought to be killed by the family dog. DNA profiling analysis using a commercially available canine STR multiplex assay (StockMark Kit Canine I Ver.3 from Applied Biosystems) indicated that the DNA profile generated from the possible saliva stains was consistent with the DNA profile from a reference sample collected from the dog [36].
Nonhuman STRs for Forensic Investigations Plant STRs The most common application of forensic DNA profiling to plant material is for Cannabis sativa. Cannabis is widely used as a recreational drug. The cultivation and possession of cannabis is illegal in many countries. However, in some countries its cultivation for fiber and seed oil may be legal. The DNA testing of Cannabis can be useful for forensic investigations in species identification, identifying drug versus fiber strains, linking hydroponic seizures, and, more recently, determining the source of origin (whether nationally or internationally) [34]. STR analysis of other plant material, however, has also been reported (see Case Study 2). This case highlights the potential of other plant material in forensic cases.
Case Study 2 STR analysis was undertaken on two Quercus geminata (sand live oak) leaves located in a murder suspect’s vehicle. A DNA profile was generated at four STR loci for both of the leaves. This profile was compared with “reference” DNA profiles from several trees located near the burial site of the deceased. The STR profiles from the leaves located in the vehicle were different from samples collected from the trees [35].
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Case Study 4 In a now-famous case, an estranged husband was implicated in the murder of his wife on Prince Edward Island, Canada. Ten dinucleotide STRs were used to test snowy white cat hair found on a jacket located near the scene of the crime. The STR profile obtained corresponded to that of reference hair recovered from Snowball, the cat belonging to the estranged husband’s parents [37]. Since this case, Menotti-Raymond et al. have published details for a 11 tetranucleotide STR multiplex intended for the genetic individualization of domestic cats [38].
Animal STRs are chosen and analyzed in the same fashion as human STRs. Many polymorphic STR loci have been identified for a wide variety of animals including dogs, cats, pigs, and badgers. Animal STR analysis can also be important for investigations into illegal trade, poaching, or endangered species where species identification is important.
Animal STRs
End Notes
The forensic analysis of animal STRs has become more common in recent years. STR analysis of biological material from animals domestic or otherwise
a.
http://www.ncbi.nlm.nih.gov/Genbank/. GenBank is an annotated collection of all publicly available nucleotide sequences.
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References [1]
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Edwards, A., Civitello, A., Hammond, H.A. & Caskey, C.T. (1991). DNA typing and genetic mapping with trimeric and tetrameric tandem repeats, American Journal of Human Genetics 49, 746–756. Collins, J.R., Stephens, R.M., Gold, B., Long, B., Dean, M. & Burt, S.K. (2003). An exhaustive DNA micro-satellite map of the human genome using high performance computing, Genomics 82, 10–19. Hauge, X.Y. & Litt, M. (1993). A study of the origin of ’shadow bands’ seen when typing dinucleotide repeat polymorphisms by the PCR, Human Molecular Genetics 2(4), 411–415. Sullivan, K.M., Mannucci, A., Kimpton, C.P. & Gill, P. (1993). A rapid and quantitative DNA sex test: Fluorescence-based PCR analysis of X-Y homologous gene amelogenin, BioTechniques 15(4), 637–641. Santos, F.R., Pandya, A. & Tyler-Smith, C. (1998). Reliability of DNA-based sex tests, Nature Genetics 18(2), 103. von Wurmb-Schwark, N., Bosinski, H. & Ritz-Timme, S. (2007). What do the X and Y chromosomes tell us about sex and gender in forensic case analysis? Journal of Forensic and Legal Medicine 14(1), 27–30. Gill, P., Brinkmann, B., d’Aloja, E., Andersen, J., Bar, W., Carracedo, A., Dupuy, B., Eriksen, B., Jangblad, M., Johnsson, V., Kloosterman, A.D., Lincoln, P., Morling, N., Rand, S., Sabatier, M., Scheithauer, R., Schneider, P. & Vide, M.C. (1997). Considerations from the European DNA profiling group (EDNAP) concerning STR nomenclature, Forensic Science International 87(3), 185–192. DNA Commission of the International Society of Forensic Haemogenetics (1994). DNA recommendations – 1994 report concerning further recommendations of the DNA Commission of the ISFH regarding PCR-based polymorphisms in STR (short tandem repeat) systems, Forensic Science International 69(2), 103–104. Benson, D.A., Karsch-Mizrachi, I., Lipman, D.J., Ostell, J., Rapp, B.A. & Wheeler, D.L. (2002). GenBank, Nucleic Acids Research 30(1), 17–20. Urquhart, A., Kimpton, C.P., Downes, T.J. & Gill, P. (1994). Variation in short tandem repeat sequences – a survey of twelve microsatellite loci for use as forensic identification markers, International Journal of Legal Medicine 107, 13–20. Puers, C., Hammond, H.A., Jin, L., Caskey, C.T. & Schumm, J.W. (1993). Identification of repeat sequence heterogeneity at the polymorphic short tandem repeat locus HUMTH01[AATG]n and reassignment of alleles in population analysis by using a locus-specific allelic ladder, American Journal of Human Genetics 53(4), 953–958. Grubwieser, P., Zimmermann, B., Niederstatter, H., Pavlic, M. & Parson, W. (2006). Validation study and population data of 15 “new” STR loci: a highly
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discriminating set for paternity and kinship analysis, International Congress Series 1288, 447–449. Butler, J.M. (2005). Constructing STR multiplex assays, in From Methods in Molecular Biology Vol 297: Forensic DNA Typing Protocols, A. Carracedo, ed, Humana Press Inc, Totowa, NJ. Harbison, S.A., Hamilton, J.F. & Walsh, S.J. (2001). The New Zealand DNA databank: its development and significance as a crime solving tool, Science and Justice – Journal of the Forensic Science Society 41(1), 33–37. Martin, P.D., Schmitter, H. & Schneider, P.M. (2001). A brief history of the formation of DNA databases in forensic science within Europe, Forensic Science International 119(2), 225–231. Thibaut, F., Ribeyre, J.M., Dourmap, N., Meloni, R., Laurent, C., Campion, D., Menard, J.F., Dollfus, S., Mallet, J. & Petit, M. (1997). Association of DNA polymorphism in the first intron of the tyrosine hydroxylase gene with disturbances of the catecholaminergic system in schizophrenia, Schizophrenia Research 23(3), 259–264. Burgert, E., Crocq, M.A., Bausch, E., Macher, J.P. & Morris-Rosendahl, D.J. (1998). No association between the tyrosine hydroxylase microsatellite marker HUMTH01 and schizophrenia or bipolar I disorder, Psychiatric Genetics 8(2), 45–48. Brinkmann, B., Klintschar, M., Neuhuber, F., Huhne, J. & Rolf, B. (1998). Mutation rate in human microsatellites: influences of the structure and length of the tandem repeat, American Journal of Human Genetics 62, 1408–1415. Xu, H. & Fu, Y.X. (2004). Estimating effective population size or mutation rate with microsatellites, Genetics 166(1), 555–563. Buckleton, J., Triggs, C.M. & Walsh, S.J. (2005). Forensic DNA Evidence Interpretation, CRC Press, Boco Raton. Butler, J.M. (2005). Forensic DNA Typing, Elsevier, Burlington. Leibelt, C., Budowle, B., Collins, P., Daoudi, Y., Moretti, T., Nunn, G., Reeder, D. & Roby, R. (2003). Identification of a D8S1179 primer binding site mutation and the validation of a primer designed to recover null alleles, Forensic Science International 133(3), 220–227. Collins, P.J., Hennessy, L.K., Leibelt, C.S., Roby, R.K., Reeder, D.J. & Foxall, P.A. (2004). Developmental validation of a single-tube amplification of the 13 CODIS STR loci, D2S1338, D19S433, and amelogenin: the AmpFSTR identifiler PCR amplification kit, Journal of Forensic Sciences 49(6), 1265–1277. Budowle, B. & Sprecher, C.J. (2001). Concordance study on population database samples using the PowerPlex 16 kit and AmpFSTR Profiler Plus kit and AmpFSTR COfiler kit, Journal of Forensic Sciences 46(3), 637–641. Clayton, T.M., Guest, J.L., Urquhart, A.J. & Gill, P.D. (2004). A genetic basis for anomalous band patterns
Short Tandem Repeats: Interpretation
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encountered during DNA STR profiling, Journal of Forensic Sciences 49(6), 1207–1214. Yang, C.H., Hsieh, L.L., Tsai, C.W., Chiou, F.S., Chou, S.L., Hsu, B.D. & Pai, C.Y. (2003). Evaluation of the DNA stability of forensic markers used in betelquid chewers’ oral swab samples and oral cancerous specimens: implications for forensic application, Journal of Forensic Sciences 48(1), 88–92. Szibor, R. (2007). X-chromosomal markers: past, present and future, Forensic Science International: Genetics 1, 93–99. Szibor, R., Krawczak, M., Hering, S., Edelmann, J., Kuhlisch, E. & Krause, D. (2003). Use of X-linked markers for forensic purposes, International Journal of Legal Medicine 117(2), 67–74. Szibor, R., Hering, S. & Edelmann, J. (2006). A new web site compiling forensic chromosome X research is now online, International Journal of Legal Medicine 120(4), 252–254. Johns, L.M., Burton, R.E. & Thomson, J.A. (2006). Study to compare three commercial Y-STR testing kits, International Congress Series 1288, 192–194. Hill, C.R., Kline, M.C., Mulero, J.J., Lagace’, R.E., Chang, C.-W., Hennessy, L.K. & Butler, J.M. (2007). Concordance study between the AmpFSTR MiniFiler PCR amplification kit and conventional STR typing kits, Journal of Forensic Sciences 52(4), 870–873. Gill, P., Fereday, L., Morling, N. & Schneider, P.M. (2006). The evolution of DNA databases – recommendations for new European STR loci, Forensic Science International 156(2–3), 242–244. Gill, P., Fereday, L., Morling, N. & Scheeider, P.M. (2006). Letter to the editor. New multiplexes for Europe – Amendments and clarification of strategic development, Forensic Science International 163, 155–157. Gilmore, S., Peakall, R. & Robertson, J. (2003). Short tandem repeat (STR) DNA markers are hypervariable and informative in Cannabis sativa: implications for forensic investigations, Forensic Science International 131, 65–74. Craft, K.J., Owens, J.D. & Ashley, M.V. (2007). Application of plant DNA markers in forensic botany: genetic comparison of Quercus evidence leaves to crime scene tress using microsatellites, Forensic Science International 165, 64–70. Padar, Z., Egyed, B., Kontadakis, K., Furedi, S., Woller, J., Zoldag, L. & Fekete, S. (2003). Importance of canine identification in the Hungarian forensic practise, International Congress Series 1239, 897–900. Menotti-Raymond, M.A., David, V.A. & O’Brien, S.J. (1997). Pet cat hair implicates murder suspect, Nature 386, 774. Menotti-Raymond, M.A., David, V.A., Wachter, L.L., Butler, J.M. & O’Brien, S.J. (2005). An STR forensic typing system for genetic individualization of domestic
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cat (Felis catus) samples, Journal of Forensic Sciences 50(5), 1061–1070.
Further Reading Butler, J.M. (2006). Genetics and genomics of core short tandem repeat loci used in human identity testing, Journal of Forensic Sciences, 51(2), 253–265. Ruitberg, C.M. & Reeder, D.J., Butler, J.M. (2001). STRBase: a short tandem repeat DNA database for the human identity testing community, Nucleic Acids Research 29(1), 320–322.
JO-ANNE BRIGHT
Short Tandem Repeats: Interpretation STR Profiles Since around the mid-1990s, short tandem repeat (STR) profiles have been the most widely used form of DNA profile evidence, in both criminal and civil cases. They are used both to help establish the identity of the source(s) of a biological sample, and to evaluate claims of relatedness, for example, of a child with a putative father or a missing person with a parent or sibling. For further details of the biology and technology underling STR profiles, see [1]. Here, we give only brief details essential for appreciation of interpretation issues. Broadly speaking, these issues are similar for STR profiles as for other DNA profiles; for an introduction, (see Evidence Interpretation: a Logical Approach). There are some aspects that are specific for STR profiles, for example, the impact of population genetics issues, and analyses of paternity and other relationships, depend on details of the STR mutation process. Also stutter artifacts that arise in STR profiling have an important role in the analyses of unbalanced mixture profiles (for details, see Mixture Interpretation: DNA). At STR loci, DNA sequence motifs (typically in forensic applications of length four base pairs) are repeated in tandem. The number of repeats tends to vary because of the relatively high mutation rate, around one mutation per STR locus every
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500 generations, compared with about one mutation every 50 million generations at a typical genomic site. This variation can be captured cost-effectively by measuring the length of a chromosome fragment that includes the STR locus. Actually, this length is measured indirectly, inferred from the speed of the fragment under an electric field. The lengths of any flanking regions can be subtracted from the inferred length to deduce the number of repeat units. Thus, an individual’s genotype at an STR locus can be reported as an unordered pair of integers, giving the number of repeats of the STR motif on each chromosome. For example, the pair (7,9) indicates seven copies of the repeat motif on one chromosome and nine on the other. Partial repeats sometimes occur: an allele designated as 9.3 has nine full repeats and one imperfect repeat having only three base pairs.
Single-Source Identification Using Likelihood Ratios
P(C = s|Ed ) =
Suppose that we have a DNA sample from a crime scene, contributed by a single individual C who will be assumed here to be the offender. We also have a matching STR profile from a defendant s. Let Ed denote the two matching STR profiles. All the probabilities reported below are conditional on relevant background information, but this will be suppressed in the notation. The probability that C = s, given the evidence, can be written as P(C = s|Ed ) =
1+
1 i∈P
wi Ri
(1)
where P is the population of alternative possible culprits, and Ri denotes the likelihood ratio (LR) comparing the hypothesis C = s, with the alternative that C is some other individual, i: Ri =
P(Ed |C = i) P(Ed |C = s)
(2)
The other evidence (or prior) ratio wi is the ratio of the probabilities that C = i and that C = s, both evaluated in the light of the evidence other than Ed ; that is, wi =
P(C = i) P(C = s)
simplifies many formulas, and has the advantage that Ri can often be interpreted as a match probability. For us, small LRs indicate strong evidence against s. Equation (1) is not directly useful to a forensic DNA expert in court, because the wi lie beyond the domain of his/her expertise. Thus the expert is normally limited to advising on values for the Ri for various alternative possible suspects. However, familiarity with equation (1) is crucial for a clear understanding of evidential weight. For example, it is possible to reformulate the hypotheses so that the Ri and wi change in value yet P(C = s|Ed ) remains unchanged. This arises in the debate about the effect of database searches ([2], Sec 6.1). Thus, the LR is not an absolute measure of weight of evidence, but depends on the formulation of the hypotheses. In the simplest scenario in which Ri = r and wi = 1 for all i ∈ P, equation (1) simplifies to
(3)
Most forensic authors define the LR with numerator and denominator interchanged. Our definition
1 1 + Nr
(4)
where N is the size of P. This unrealistic scenario illustrates the crucial point that a value for Ri does not measure the overall strength of the STR evidence against s. Here, N and r play equally important roles. More generally, the overall strength involves the sum of the wi Ri over all other individuals i. The population P is assumed to include all the possible sources of the crime stain other than s. Note, in particular, that there is no need to invoke any “random man”, which concept can cause confusion in the interpretation of DNA profile evidence ([2], Sec 8.2). Although P should include all realistic alternative suspects, there is some flexibility as to how many extra individuals are included. Often, it might be appropriate to include in P all men aged, say, between 16 and 65 living within, say, 1 h driving time of the crime scene. However, P could include everyone on earth except s, if desired. The value of wi will typically be extremely small for i that reside far from the crime scene, and so it makes very little difference to equation (1) whether they are included in P. Since P can be large, it may seem impractical to compute a separate Ri for every member of P. However, individuals with the same degree of relatedness with s will have the same value of Ri and hence can be grouped together to simplify equation (1). For example, the population P of alternative culprits may be partitioned into various categories
Short Tandem Repeats: Interpretation of direct relatives, such as siblings and cousins, while individuals apparently unrelated to s might be classified into three groups: • • •
same population, same subpopulation same population, different subpopulation different population.
To avoid overstating the evidence against s, if the value of Ri varies within a group then the largest value should be applied for all members of the group. Because of migrations and intermarriages, the population and subpopulation are difficult to define precisely. Nevertheless, such concepts often correspond to natural groupings, and they are useful in formulating population genetics models that can allow for the principle effects of population genetic structure on DNA profile match probabilities.
case, using θ we can, nevertheless, still calculate the required match probabilities in terms of the degree of variation of subpopulation allele proportions about p. In some simple models, θ can also be interpreted as the probability that two alleles are descended identically from a common ancestor. Hence θ is also called a coancestry coefficient or kinship coefficient. Then θ can be thought of informally as the amount of shared ancestry within a population, and so is large for small, isolated populations with little immigration.
The Sampling Formula Suppose that n alleles have been sampled in the subpopulation, of which m are green. Then the probability that the next allele sampled is also green can be expressed as mθ + (1 − θ)pG 1 + (n − 1)θ
The Population Genetics Parameter θ , or FST Suppose that the population is “UK Caucasians”, and the subpopulations relevant to a particular crime might include regional subpopulations, or migrant or religious groups such as people of Polish or Jewish ancestry. STR allele frequency estimates are available from a database of individuals classified as UK Caucasians. The accuracy of the estimates will be affected both by the size of the database and the fact that it is not scientific random sample but a “convenience sample” of available individuals. Nevertheless, we can be reassured by the observation that different databases of Caucasian individuals give similar allele proportions at the STR loci in widespread forensic use. For subpopulations, however, direct frequency estimates are often not available: in practice this is always the case because the relevant subpopulation is not strictly defined. The similarity of allele frequencies in broadly defined Caucasian populations does not provide reassurance that narrowly defined subpopulations will also have similar allele proportions: their smaller sizes and distinct histories can make them more variable than large, well-mixed populations. To deal with the problem of unknown subpopulation allele proportions, we make use of the coefficient FST [3], also called θ, which can be interpreted in terms of the variation of subpopulation allele proportions about a given reference value, which here would be taken to be the allele proportion, say p, in the UK Caucasian population. Although we cannot estimate the STR allele proportion directly relevant to the
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(5)
(see [2], Chap 5 for justification.) When m = n = 0, we obtain probability pG that the first allele drawn is green. The probability that the first two alleles drawn are both green is pG (θ + (1 − θ)pG ) = pG2 + θpG (1 − pG )
(6)
Increasing θ raises the probability of observing two green alleles, because the second allele may be identical with the first through descent from a recent common ancestor. Conversely, increasing θ decreases the probability of a green allele followed by a blue, which is (1 − θ)pG pB
(7)
Successive use of expression (5) can be used to build up joint probabilities for any ordered sequence of alleles.
Likelihood Ratios and Match Probabilities Introducing the notation x ≡ D to denote “x has profile D”, Ed can be written succinctly as C ≡ D, s ≡ D, and the LR, equation (2), becomes Ri =
P(C ≡ D, s ≡ D | C = i) P(C ≡ D, s ≡ D | C = s)
(8)
Here, we initially ignore the possibility of error, so that if C = s then crime scene and defendant profiles
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are certain to match. Assuming also that the fact that an individual committed the crime does not of itself alter the probability that they have a particular profile, equation (8) can be simplified further to Ri =
P(i ≡ D, s ≡ D) = P(i ≡ D | s ≡ D) (9) P(s ≡ D)
Thus, under these conditions, Ri reduces to the conditional probability, called the match probability, that i has the profile given that s has it: population genetic effects arise, and can be dealt with, via this conditioning. Other evidence such as eyewitness reports and alibis are typically irrelevant to DNA profile match probabilities, but the background information to a case can include •
information about the relatedness of s with some other individuals; allele proportion information from population databases of DNA profiles; other relevant population genetics data and theory.
• •
and these can be important for match probabilities. An essential feature of the match probability is that it takes account of both the observed profiles that form the match. Some authors, for example [4], misleadingly refer to the population proportion of the profile as a match probability which is inappropriate since the concept of “match” involves two profiles, not one. Equation (9) indicates that the question relevant to forensic identification is not “what is the probability of observing a particular profile?”
but “given that I have observed an individual with this profile, what is the probability that another (unprofiled) individual will also have it?”.
The parameter θ appears in our answer to this question, to take into account possible shared ancestry between the two individuals. Ignoring a defendant’s coancestry with other possible sources of the crime stain is systematically unfair to him. Human population genetics is complicated, and inevitably, θ is an imperfect measure, but by choosing a suitable value defendants will not be systematically disfavored, while match probabilities remain small enough to form the basis of satisfactory prosecutions in most cases.
Single-Locus Match Probabilities Consider the case that both i and s are homozygous for allele A. If we assume that they are unrelated, both come from the same subpopulation, and neither is inbred, then equation (9) corresponds to the conditional probability that two further alleles are both A, given a sample of two alleles that are both A. This is obtained as the product of two instances of expression (5), with m = n = 2 and m = n = 3: Ri =
(2θ + (1 − θ)pA )(3θ + (1 − θ)pA ) (10) (1 + θ)(1 + 2θ)
In the heterozygous case, under the same assumptions, we need the probability that two further alleles are A and B, given that two observed alleles are A and B. Taking two times expression (5) with m = 1, n = 2 times expression (5) with m = 1, n = 3, gives Ri = 2
(θ + (1 − θ)pA )(θ + (1 − θ)pB ) (11) (1 + θ)(1 + 2θ)
See Figure 1 for a graph showing how equations (10) and (11) vary with θ for some particular values of the pj for j ∈ {A,B}. Note that increasing θ does not always increase Ri . Table 1 gives numerical values of single-locus Ri for hypothetical genotypes and pj values at four STR loci, for four values of θ that span the range used in practice. These match probability formulas are conditional on the values of θ and the pj . Thus, strictly, they only apply if these parameters are known exactly, which is never the case in practice. In a fully Bayesian approach, equations (10) and (11) should be integrated out with respect to probability distributions for the unknown values of θ and the pj , based on the available background information, for example from forensic DNA profile databases and population genetics theory and data. A simpler and more interpretable approach is preferred, in which this background information is used to obtain estimates for θ and the pj , which are then “plugged in” to the conditional formulas. Care is required to choose the most appropriate “plug-in” values for the parameters, as these need not satisfy the usual criteria for statistical estimators (see below). Use of equations (10) and (11) implies an assumption of Hardy–Weinberg Equilibrium (HWE) within subpopulations, but not in the broader population from which the forensic database is drawn. Thus tests of deviations from HWE applied to
Short Tandem Repeats: Interpretation
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1.2
p = 0.2, het p = 0.2, hom p = 0.5, het p = 0.5, hom
1.0 0.8 0.6 0.4 0.2 0.0 0.0
0.2
0.4
0.6
0.8
1.0
Fst
Figure 1 Single-locus match probabilities calculated using equations (10) and (11) for θ (= FST ) ranging from 0 to 1. In the heterozygote case, the proportions of the two alleles are both equal to p Table 1 Single-locus match probabilities assuming i unrelated to s, for four STR loci and various values of θ , for the alleles specified in column 2 and assuming the population proportions given in column 3 Match probability (×103 ) STR locus D18 D21 THO1 D8
Genotype 14, 28, 9·3, 10,
16 31 9·3 13
Population proportions 0·16, 0·23, 0·30, 0·09,
0·14 0·07 0·30 0·33
forensic databases are not directly relevant to match probability calculations. Deviations from HWE do directly affect the probability of observing a particular genotype, but not the conditional match probability given by expression (9). Match probability formulas that take into account inbreeding within subpopulations, are more complicated than equations (10) and (11), but, nevertheless, relatively easy to apply [5]. The match probabilities are slightly increased for homozygotes, and decreased for heterozygotes; the overall effect on profile match probabilities is usually very small, but may be worth taking into account when highly inbred populations are relevant to a case.
Multiple Loci: The “Product Rule” There has been much debate in the forensic science literature about the validity of the “product rule”
θ =0
θ = 1%
θ = 2%
θ = 5%
45 32 90 59
49 37 101 65
52 41 112 70
64 54 145 85
for combining DNA match probabilities across loci. Combining probabilities via multiplication implies an assumption of statistical independence, and so the debate is equivalent to a debate about the independence of STR genotypes at different loci. This question can be rephrased: For two distinct individuals i and s, does the event that their genotypes match at one or more STR loci affect the probability that they will match at the next locus?
If i and s are directly related through one or more known common ancestors (e.g., grandparents), then matches at distinct loci are not independent, but an appropriate adjustment for the relationship can restore approximate independence. All humans are related at some level, and if i and s are apparently unrelated, this only means that the relationship between them
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Table 2 Match probabilities for the four-locus STR profile of Table 1 under some possible relationships of s and i, and for various values of θ Match probability Relationship Identical twin Sibling (×10−3 ) Parent/child (×10−4 ) Half-sib (×10−5 ) Cousin (×10−5 ) Unrelated (×10−6 )
θ = 0 θ = 1% θ = 2% θ = 5% 1 17 14 23 6 8
1 19 17 29 8 12
1 20 19 35 10 17
1 23 29 61 20 43
is unknown and presumed to be distant. However, it is not necessarily distant enough to be negligible for the purposes of calculating match probabilities. Thus, use of the product rule based on an assumption of no relatedness at any level is unfair to defendants. However, the match probabilities given by equations (10) and (11) are conditional on a level of coancestry between apparently unrelated individuals measured by θ. Although match probabilities at many loci cannot readily be checked, the available population genetics theory and data support the view that, given a suitable value of θ, match probabilities obtained as products of the probabilities in equations (10) and (11) will not be systematically unfavorable to defendants. Whole-profile match probabilities using the θadjusted product rule applied to the four STR loci of Table 1, and using various values of θ, are given in the final row of Table 2. Assuming θ = 5% increases the four-locus match probability more than fivefold relative to the θ = 0 case, and this extrapolates to more than a 50-fold increase for 10 loci, and about 200-fold for a 13-locus profile match.
Relatives of s So far we have been considering alternative possible culprits i that are unrelated to s. Here we consider the possibility that i and s are directly related through one or more specified common ancestors. We continue to assume that the DNA profile of i is not available to the court: it would in principle be desirable to exclude close relatives of s from suspicion by examining their DNA profiles, but this is rarely possible in practice. Considering first a single locus, let Z denote the number of alleles at the locus that i and s share
Table 3 Distribution of ibd status and coefficient of relatedness for some possible relationships of s and i. The value of κj is the probability that i and s share j alleles at a locus identical by descent (ibd) from a recent common ancestor, and κ is half the expected number of alleles shared ibd. The values for aunt, uncle, niece, nephew, grandparent, and grandchild are the same as for half-sib Relationship Identical twin Sibling Parent/child Half-sib First cousin Double first cousin Unrelated
κ0
κ1
0 1/4 0 1/2 3/4 9/16 1
0 1/2 1 1/2 1/4 6/16 0
κ2
κ
1 1/4 0 0 0 1/16 0
1 1/2 1/2 1/4 1/8 1/4 0
identical by descent (ibd) from a known, recent, common ancestor (e.g., parent or grandparent), and let κj = P(Z = j )
(12)
for j = 0, 1, 2. The values of κj under some regular (i.e., no inbreeding) relationships are shown in the first three columns of Table 3. If Z = 0, then it is the same as if s and i were unrelated and we write M2 for the appropriate match probability, either from equation (10) or (11). If Z = 2, a match is certain. For Z = 1, consider first the case that s ≡ AA. Since one allele of i is ibd with an observed allele of s, we require the probability of observing a further A allele, given that two alleles have been observed to be both A. Using expression (5) with m = n = 2 we obtain M1 = P(A | AA) =
2θ + (1 − θ)pA 1+θ
(13)
If s ≡ AB, the allele shared ibd by i and s is equally likely to be A or B. The match probability is then equivalent to the probability of observing the non-ibd allele, given that A and B have been observed: P(A | AB) + P(B | AB) 2 θ + (1 − θ)(pA + pB )/2 = 1+θ
M1 =
(14)
The overall single-locus match probability for relatives is then κ2 + κ1 M1 + κ0 M2
(15)
Short Tandem Repeats: Interpretation Four-locus match probabilities based on (14) and the product rule are shown in Table 2 for the four STR loci of Table 1. Notice that the value of θ still affects the match probability even when i and s are assumed to be closely related. This is because, as well as matches arising via alleles shared ibd from the recent known ancestor(s) of i and s, alleles can also be shared ibd from more distant common ancestors. However, the relative importance of θ declines as the known relationship between i and s becomes closer [6].
Values for the pj The population database to be used to estimate the pj should be that most appropriate for i, the alternative possible culprit under consideration. The error arising from the database population not being exactly appropriate can be addressed using θ. Here we consider only the issue of accounting for the effects of sampling uncertainty in observed allele proportions. One way to address this issue is to estimate pj at a heterozygous locus by pj =
xj + 2 n+4
(16)
where xj is the frequency of allele j in the database, and n is the total number of alleles [6, 7]. In the homozygous case, an analogous estimate is pj =
xj + 4 n+4
(17)
These estimates can be thought of as adding both the crime-scene and defendant profiles to the database; such estimation methods are sometimes called pseudocount methods. They can be justified as approximations to the posterior mean given the sample allele counts and a uniform prior distribution for the allele proportions.
The value of θ Published estimates of θ at STR loci, for subpopulations within the major human “racial” groups are often small, and typically less than 1%. See, for example, [8, 9] for estimates in some European Caucasian populations. Many other authors have estimated θ at forensic STR loci in various populations
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and using different methodologies; see [10] for a brief review. Typically, they report very small values. There are several arguments for using larger values in forensic practice than suggested by these estimates. Recall that our goal is not to estimate a “best” value for θ, but to choose “plug-in” values that give a match probability similar to that which would be obtained from using the full Bayesian approach. Because of the skewness of appropriate distributions for θ, the “plugin” value that mimics the effect of integration over θ may be much larger than, say, a maximum-likelihood estimate of θ. Moreover, published estimates of θ usually relate to the variation of allele proportions around the observed mean of the subpopulations studied, whereas in forensic applications, the reference value is the forensic database value. The θ estimate can vary substantially according to the choice of reference value, and is often much larger than when the reference value is estimated from the data. Broadly speaking, the less appropriate is the database for the genetic background of a possible culprit, the greater is the appropriate value of θ. For these reasons (see [2], Sec 6.3, for a fuller discussion), it is suggested that a relatively large value, such as 2%, be used when both defendant and alternative possible culprit are drawn from a relatively well-mixed, large population, and perhaps 3% could be used if both are drawn from one of the large minority groups. In some small minority groups, θ = 5% may be appropriate. These suggested values are based on informal judgements, and should not be regarded as prescriptive. If i is not from the same racial group as s, then they have little coancestry and so a small value of θ can be justified. However, since the problem of representativeness of any database remains, as well as possibilities for some coancestry even across apparent racial groups, the use of a nonzero value of θ in every case, perhaps setting 1% as the minimum, is advocated.
Laboratory, Handling errors, and Evidence Tampering There are at least two ways in which an observed STR profile match could have arisen even though C = s: 1. defendant and culprit happen to have matching DNA profiles and no typing error occurred (“chance match”);
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Short Tandem Repeats: Interpretation
defendant and culprit have distinct DNA profiles, and the observation of matching profiles is due to an error in one or both recorded profiles (“false match”).
Both (1) and (2) are typically unlikely, but (2) may not be negligible in comparison to (1), yet (2) is typically not explicitly considered in conjunction with (1). An argument that is often advanced for this is that error probabilities are difficult to assess. Even if error rates from external, blind trials are available, there will usually be specific details of the case at hand that differ from the circumstances under which the trials were conducted, and which make it more or less likely that an error has occurred. Some critics of DNA profile evidence have argued that the match probabilities reported in court are irrelevant and potentially misleading because they relate to (1) only, whereas (2) is likely to be more important in practice. This argument has some force, and proponents of DNA profiling have been prone to mistakes and exaggeration in their attempts to discount it [11]. The chance of a false inclusion error due to genotyping anomalies is so remote as to be negligible, even relative to the match probability, because it is not the probability of any error that is relevant, but an error that causes a false match. Contamination is a distinct possibility in some settings, but because evidence and crime samples are routinely typed by different staff in different laboratories, sometimes with a substantial time gap, in many cases this possibility can also reasonably be ruled out. This leaves the possibility of false inclusion due to handling or labeling error, or evidence tampering. A conspiracy theory, such as that police and/or judicial authorities colluded to manufacture evidence falsely linking the defendant with the crime scene, may be regarded by a reasonable juror as substantially more plausible than a 1 in a billion chance match, even when there are no particular reasons to suggest a conspiracy. For this juror, the probability of such a conspiracy based on all the other evidence, is more important than the chance match probability. There seems no role for a forensic scientist to predict whether a juror might pursue such a line of reasoning, and hence the only reasonable option is to supply the juror with a match probability based on (1), but also to try convey an understanding of the possibilities for a false match and how these affect evidential weight.
Partial Profiles So far we have assumed good quality crime-scene DNA samples and no profiling errors, so that a perfect match of crime-scene and defendant profiles is expected if s is the source of the crime-scene DNA. However, if the crime-scene sample is very small and/or degraded, the crime-scene profile may be subject to stochastic phenomena such as drop-out, drop-in, imbalanced peak heights and exaggerated stutter. Under these circumstances, a prosecution may proceed against s even though his profile does not exactly match the crime-scene profile. When all the crime-scene profile alleles are evident in the profile of s, but the converse does not hold, the crime-scene profile is sometimes referred to as partial and the prosecution case requires that drop-out has occurred. Strictly, we can only be sure that alleles have dropped out if there is a locus with no observed alleles: no conclusion about drop-out should refer to the profile of s. The analysis of profiles in the presence of drop-out and related phenomena is a major current challenge for the forensic DNA community, and completely satisfactory solutions are not yet available. One unsatisfactory approach [12] that is often used in practice involves using the standard LR when two alleles are observed in the crime-scene profile, 2p when one allele is observed, and 1 when no alleles are observed. For a more advanced attempt at formulating appropriate LRs, see [13], but the software described there is not widely available. Note that a “partial” profile that arises because some loci are not profiled does not raise any problem of interpretation: the fact that additional loci might have been profiled but were not, is irrelevant to the assessment of the loci that were profiled.
Database Searches Many countries maintain national databases of the STR profiles of named individuals for criminal intelligence purposes. The question thus arises as to the appropriate method for assessing the DNA profile evidence when the defendant was identified following a search through a database. The number of individuals involved in such a search, and even the fact that there was a search, may not be reported to the court (see also DNA Databases and Evidentiary Issues). Many commentators, including [4], have wrongly claimed that the fact that a DNA profile match is
Short Tandem Repeats: Interpretation
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more likely when it results from a search means that the evidence is weakened by the search. An analysis that focuses on the relevant question–is s the source of the crime-scene DNA profile?–shows that DNA evidence is usually slightly stronger in the database search setting than when no search has occurred. To see this, imagine an enormous database that records the STR profiles of everyone on earth. If the defendant’s profile were the only one in this database to match the crime-scene profile, then the evidence against him would be overwhelming. Although the DNA evidence may be (slightly) stronger in the context of a database search, the overall case against the defendant may be weaker because there is little or no non-DNA evidence against the defendant, see [14, 15].
to the consequences of historic Mongol conquests, possibly even to Genghis Khan himself [17]. Similar historical events on a smaller scale may have led to an unrecognized, local elevation of the concentration of a specific Y haplotype that is otherwise rare. For example, substantial microgeographical variation in forensic Y-chromosome haplotypes has been reported in the Cantabria region of Spain [18]. Although selection is thought likely to influence the distribution of Y haplotypes, because no assumption of either HWE or linkage equilibrium is made, it seems reasonable to assume that selection will not adversely affect the validity of equation (17).
Match Probability for Y Chromosome STR Profiles
Uniqueness
Because the Y chromosome is paternally inherited, and for the most part does not undergo recombination, a Y-STR profile can be treated as a single allele, or “haplotype”, characterized by the repeat counts at STR sites along the chromosome. The match probability involves the probability that a particular man has a certain haplotype given that another man has it. This is conceptually simpler than for autosomal loci because there is no need for multiplication of frequencies either within or across loci. Using an approach analogous to that used to derive (10) and (11), the match probability for a Y haplotype with population frequency p is
The current generation of STR profiling technology uses 10 or more loci, so that match probabilities for individuals unrelated to the defendant are typically extremely small, often less than 1 in a billion even with a generous allowance for θ. It thus seems reasonable to consider the possibility that the STR profile is unique, and if this could be established, then the need for calculating and reporting LRs could be avoided. Although this idea is attractive, it encounters a number of difficulties, such as the choice of threshold for declaring a profile to be unique. Perhaps more importantly, the non-DNA evidence in a case also has a bearing on the question of uniqueness, but lies outside the domain of a DNA expert. Under some simplifying assumptions on the numbers of individuals with different degrees of relatedness to the defendant, and assuming no evidence other than the STR profiles, 10 STR loci usually suffice to establish a probability greater than 99.9% that the STR of s is not shared by any individual in P [19].
Ri = θ + (1 − θ)p
(18)
Since p is typically unknown, a “pseudocount” estimator, analogous to equations (15) and (16) for autosomal loci, can be used: = p
x+2 N +2
(19)
where x denotes the database count of the observed Y haplotype. Population structure is particularly important for Y haplotypes: values of θ are typically high, reflecting geographical clustering of males with common paternal ancestry [16]. There are only a few studies on the appropriate fine geographical scale. A specific Y haplotype that is frequent in many parts of Asia, and largely unobserved elsewhere, has been attributed
Other Approaches to Assessing STR Evidence
Random Man Not Excluded (RMNE) Another approach to the evaluation of STR profiles that avoids computing LRs is to report the inclusion probability of a crime-scene profile, or the probability that a “random man” would not be excluded as the contributor. In the case of a single-source crime-scene profile, the random man not excluded (RMNE) probability is the probability that a randomly chosen alternative possible culprit would match the crime scene
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DNA profile. In this setting, the exclusion probability is numerically equivalent to the LR for i unrelated to s (but typically assumes θ = 0). However, the two approaches are conceptually very different. The rationale underlying the RMNE probability cannot adequately cope with relatives of the defendant among the alternative culprits, and can be highly misleading in the presence of drop-out (partial profiles). The idea of a random alternative suspect can lead jurors to ignore the role of the number of possible culprits in evidential assessments, and clear thinking about laboratory and other errors, and the effect of searches, can also be undermined. All of these aspects are readily dealt with in the LR framework. One specific difficulty that “random man” can cause in this setting concerns the argument over which population the man is supposed to have been randomly drawn from [20]. Since “random man” is a fictional character, these arguments can never be resolved. The issue is important, since too broad a definition of the population leads to overstatement of the evidence, because a large population must contain many people sharing little ancestry with s. If we try to avoid this overstatement by specifying the narrowest possible population, we are led to the population consisting of s only, in which the match probability is one. Numerical differences arise between RMNE and LR values for paternity, since the former makes no distinction between a homozygous and a heterozygous nonexcluded alleged father, whereas the LR correctly recognizes that the DNA evidence at this locus is about twice as strong against the homozygote. Even more important differences arise in the setting of crime-scene DNA profiles with two or more unknown contributors (see Mixture Interpretation: DNA). Here, the RMNE probability is usually taken to be the probability that a random unknown individual would have both alleles at each locus included among the alleles of the mixed crime-scene profile. This probability does not take account of the profile of the defendant, other than noting that it falls within a (usually large) class of profiles. In the case of two codefendants alleged to be contributors to the mixed crime-scene profile, the evidence can weigh more heavily against one defendant than the other, whereas the RMNE probability will be the same for both defendants. The advantages of the RMNE probability include its being relatively easy to calculate and explain,
and that it does not require any assumption about the number of contributors to a mixture. Because it ignores relevant information, the RMNE probability is usually larger than the LR, often considerably so. This statistical inefficiency is sometimes seen as a virtue, in that use of the RMNE probability is regarded as “conservative”. However, conservativeness is not guaranteed, and by using an appropriate θ-value we can make the LR conservative while still relatively efficient.
Paternity The principles of combining LRs to evaluate a probability of paternity are similar to those underpinning equation (1). However, in practice DNA evidence is often assessed differently when paternity rather than identification is at issue. Many forensic scientists, lawyers, and academic commentators seem reluctant to consider in the paternity setting the very low prior probabilities that are now often accepted for identification. Indeed, there is a shamefully high prevalence of an unjustified assumption that both s, and an unrelated “random man” i, have a prior probability 1/2 of being the father [21]. This “even prior” assumption is convenient, since in the absence of relatives of s it implies that the likelihood ratio Ri is also the posterior probability that s is not the father. It may often be based on the assumption that equal prior weight should be assigned to the, typically conflicting, claims of s and the mother m. However this ignores, for example, additional background evidence, and multiple alternative fathers.
Likelihood Ratios for Paternity Typically, the STR evidence consists of the profiles of the mother m, alleged father s, and child c, in which case Ri =
P(profiles of c, s, and m | father is i) (20) P(profiles of c, s, and m | father is s)
Here, the fact that m is the mother of c is regarded as background information in both probabilities, but is not explicit in the notation. It is usually reasonable to assume that the probabilities that s and m have particular profiles is unaffected by whether s is the father of c, and it follows that we can rewrite equation
Short Tandem Repeats: Interpretation (20) as a ratio of conditional probabilities for the child’s profile: P(profile of c | profiles of s and m, father is i) Ri = (21) P(profile of c | profiles of s and m, father is s) in which the profile probabilities for s and m have cancelled. The denominator is easily evaluated using Mendelian transmission probabilities, and is, for example, equal to one if m ≡ AB, s ≡ CC, and c ≡ AC. For the numerator, we require the conditional probability of c’s paternal allele, given the profiles of s and m and the hypothesis that i is the father. First, suppose that the coancestry of i and s is specified by θ, but m has no coancestry with either (for example, she is from a different racial group). Then the profile of m is uninformative about the profile of i, and the paternal allele of c may be regarded as a third allele drawn from the subpopulation of i and s, given that two observed alleles (from s) are both C. Invoking the sampling formula (5) with m = n = 2 we obtain Ri = P(C | CC) =
2θ + (1 − θ)pC 1+θ
(22)
Reasoning similarly in the heterozygous case s ≡ CX, the denominator is 1/2 and Ri = 2P(C | CX) = 2
θ + (1 − θ)pC 1+θ
(23)
If i, s, and m are all assumed to have the same level of coancestry, then the sampling formula (5) can be used again but now with n = 4 because of the four alleles observed in s and m (see Missing Persons and Paternity: DNA and [2], Chap 7). for examples and further details.
Mutation If an STR profile consists of around ten loci, there is very roughly a 2% probability that there will be a mutation in transmission from father to child, in which case ignoring the possibility of mutations could lead to a false exclusion. If the profiles are consistent with s being the father of c at many loci, but there is an apparent exclusion at just one or perhaps two loci (Table 4), it may still be the case that the STR evidence overall supports the claim that
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Table 4 Three examples of scenarios in which a mutation is required to sustain the the hypothesis that m and s are the parents of c Scenario Child c Mother m Alleged father s
≡ ≡ ≡
(i)
(ii)
(iii)
AB AC CD
AB AC AD
AB DD AC
s is the father. A systematic treatment of this question when the mother’s profile is available, but ignoring coancestry is given by Dawid et al. [22]. The latter omission is rectified by Ayres [23], who treats the case that any two of m, s, and i have the same level of coancestry, θ, correcting formulas given in [24] that neglected the possibility of maternal transmission. Perhaps the most common theoretical model for STR mutation is the stepwise mutation model (SMM) in which a mutant allele has either k − 1 or k + 1 repeat units, each with probability 1/2, where k is the current repeat number. The SMM has no stationary distribution, so that two similar populations isolated from each other do not converge under the SMM to the same allele frequency distribution. Thus, substantial between-population diversity is expected under the SMM for populations that exchange few migrants. By contrast, there is typically little between-population variation at human STR loci, suggesting high migration rates and/or the invalidity of the SMM. In fact, the strict SMM is known to be false, for example, because the mutation rate increases with allele length and occasional two-step mutations occur, although it may provide an adequate approximation for some purposes. The SMM can easily be modified, for example, by hypothesizing a bias toward contraction mutations in long alleles, to obtain STR mutation models that do have a stationary distribution [25]. Such models can provide a better fit to observed data than the SMM, and are consistent with the observed between-population homogeneity of allele proportions at many STR loci.
Conclusion The theory based on likelihood ratios outlined above does not provide a formulaic answer to the problem
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Short Tandem Repeats: Interpretation
of how to convey complex STR profile evidence to a nonscientific court. It does, however, provide a solid theoretical framework for the forensic scientist to think clearly about weight-of-evidence issues, and hence to draw well-informed conclusions about what a rational judge or juror needs to be informed of in order for them to carry out their tasks of evaluating the evidence. For further details of STR interpretation beyond those given here, see and also Statistical Evidence in Court [2, 10, 26, 27, 28]
[15] [16]
[17]
[18]
References [1]
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[6]
[7]
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[14]
Butler, J.M. (2005). Forensic DNA Typing: Biology, Technology and Genetics of DNA Markers, 2nd Ed, Elsevier. Balding, D.J. (2005). Weight of Evidence for Forensic DNA Profiles, John Wiley & Sons. Wright, S. (1951). The genetical structure of populations, Annals of Eugenics 15, 323–354. National Research Council (1996). The Evaluation of Forensic DNA Evidence, National Academy Press. Ayres, K.L. & Overall, A.D.J. (1999). Allowing for within-subpopulation inbreeding in forensic match probabilities, Forensic Science International 103, 207–216. Balding, D.J. & Nichols, R.A. (1994). DNA profile match probability calculation: how to allow for population stratification, relatedness, database selection, and single bands, Forensic Science International 64, 125–140. Balding, D.J. (1995). Estimating products in forensic identification using DNA profiles, Journal of American Statistical Association 90, 839–844. Balding, D.J., Greenhalgh, M. & Nichols, R.A. (1996). Population genetics of STR loci in Caucasians, International Journal of Legal Medicine 108, 300–305. Balding, D.J. & Nichols, R.A. (1997). Significant genetic correlations among Caucasians at forensic DNA loci, Heredity 78, 583–589. Buckleton J.S., Triggs C.M. & Walsh, S.J. (eds) (2005). Forensic DNA Evidence Interpretation, CRC Press. Koehler, J.J. (1996). On conveying the probative value of DNA evidence: frequencies, LRs, and error rates, University of Colorado Law Review 67(4), 859–886. Buckleton, J. & Triggs, C.M. (2006). Is the 2p rule always conservative? Forensic Science 159, 206–209. Gill, P., Kirkham, A. & Curran, J. (2007). LoComatioN: a software tool for the analysis of low copy number DNA profiles, Forensic Science International 166, 128–138. Balding, D.J. & Donnelly, P. (1996). Evaluating DNA profile evidence when the suspect is identified through a database search, Journal of Forensic Science 41, 603–607.
[19] [20] [21]
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[24]
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[26]
[27] [28]
Balding, D.J. (2002). The DNA database controversy, Biometrics 58, 241–244. Jobling, M.A., Pandya, A. & Tyler-Smith, C. (1996). The Y chromosome in forensic analysis and paternity testing, International Journal of Legal Medicine 110(3), 118–124. Zerjal, T., Xue, Y.L., Bertorelle, G., Wells, R.S., Bao, W.D., Zhu, S.L., Qamar, R., Ayub, Q., Mohyuddin, A., Fu, S., Li, P., Yuldasheva, N., Ruzibakiev, R., Xu, J., Shu, Q., Du, R., Yang, H., Hurles, M.E., Robinson, E., Gerelsaikhan, T., Dashnyam, B., Mehdi, S.Q. & TylerSmith, C. (2003). The genetic legacy of the Mongols, American Journal of Human Genetics 72(3), 717–721. Zarrabeitia, M.T., Riancho, J.A., Lareu, M.V., LeyvaCobiaan, F. & Carracedo, A. (2003). Significance of micro-geographical population structure in forensic cases: a Bayesian exploration, International Journal of Legal Medicine 117(5), 302–305. Balding, D.J. (1999). When can a DNA profile be regarded as unique? Science and Justice 39, 257–260. Roeder, K. (1994). DNA fingerprinting: a review of the controversy, Statistical Science 9, 222–278. Koehler, J.J. (1993). DNA matches and statistics: important questions, surprising answers, Judicature 76(5), 222–229. Dawid, A.P., Mortera, J. & Pascali, V.L. (1996). Nonfatherhood or mutation? A probabilistic approach to parental exclusion in paternity testing, Forensic Science International 124(1), 55–61. Ayres, K.L. (2002). Paternal exclusion in the presence of substructure, Forensic Science International 129, 142–144. Ayres, K.L. (2000). Relatedness testing in subdivided populations, Forensic Science International 114, 107–115. Whittaker, J.C., Harbord, R.M., Boxall, N., Mackay, I., Dawson, G. & Sibly, R.M. (2003). Likelihood-based estimation of microsatellite mutation rates, Genetics 164(2), 781–787. Robertson, B. & Vignaux, G.A. (1995). Interpreting Evidence – Evaluating Forensic Science in the Courtroom, John Wiley & Sons. Evett, I.W. & Weir, B.S. (1998). Interpreting DNA evidence, Sinauer Associates. Rudin, N. & Inman, K. (2002). An Introduction to Forensic DNA Analysis, 2nd Edition, CRC Press.
DAVID BALDING
Signature Comparison see Handwriting and Signatures, Comparison of
Soil: Forensic Analysis
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Signatures see Handwriting and Signatures, Interpretation of Comparison Results
Social Influence: Affect and Decision Making see Crime Victims’ Decision to Report Crime
Simulations: Computer, as Evidence see Computer Animation and Simulation Evidence
Social Isolation as Risk Factor in Elder Abuse see Elder Abuse: Risk
Skeletal Remains: Identification of see Human Remains and Identity; Species Determination of Osseous Remains
Skeletal remains: Identity see Trauma Analysis of Skeletal Remains
Skeleton: Trauma see Trauma Analysis of Skeletal Remains
Sleepwalking see Automatism as a Defense to Crime
Sociopathic Personality Disorder see Psychopathy
Sociopathy see Psychopathy
Soil: Forensic Analysis Introduction Forensic soil science is the science or study of soil that involves the application of soil science, especially studies that involve soil morphology, soil mapping (assisted by existing soil maps and spatially held soil data), mineralogy, chemistry, geophysics, biology, and molecular biology to answer legal questions, problems, or hypotheses. Soil science is the term commonly used to study soil as a natural body in the landscape and as a resource to be managed for agricultural production, environmental waste disposal, and construction. Soils mean different things to different people. Soil scientists (pedologists) view soils as being made up of different size mineral particles (sand, silt, and clay) and organic matter. Soils have complex
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Soil: Forensic Analysis
biological, chemical, physical, mineralogical, and hydrological properties that are always changing with time. Hence, soil is dynamic, teeming with organisms, and is an integral part of the environment. Agronomists, farmers, and gardeners, on the other hand, see soil as a medium for growing crops, pastures, and plants – primarily in the top 50 cm of the Earth’s surface. Engineers regard soil as material to build on and excavate, and are usually concerned primarily with moisture conditions and the capacity for soil to become compacted and support structures. However, some people regard soil as “dirt” or “mud” because it makes them “dirty” when they make contact with it. Pedology (from the Greek pedon = soil), is the soil science discipline concerned primarily with understanding the variety of soils and their distribution, and is most directly concerned with the key questions concerning sampling, descriptions, processes of soil formation including the quality, extent, distribution, spatial variability, and interpretation of soils from microscopic to megascopic scales [1]. This description and interpretation of soils can be used in addressing the questions ‘What is the soil like?’ and ‘Where does it come from?’ (i.e., provenance determination) in studies relating to characterizing and locating the sources of soils to make forensic comparisons. Forensic soil scientists are more specifically concerned with soils that have been disturbed or moved (usually by human activity), sometimes comparing them to natural soils, or matching them with soil databases, to help locate the scene of crimes. Forensic soil scientists usually obtain soil samples from crime scenes and suspected control sites from which soil may have been transported by shoes, a vehicle, or a shovel. Soil properties are diverse and it is this diversity, which may enable forensic soil scientists to use soils with a degree of certainty as evidence in criminal and environmental investigations [2, 3]. Forensic soil science is a relatively new activity that is strongly “method orientated” because it is mostly a technique-driven activity in the multidisciplinary soil areas of pedology, soil survey, soil mineralogy, soil chemistry, soil molecular biology, soil geophysics, and forensic science. There are few reviews of the specific application of one soil science discipline to criminalistics at the time of writing (i.e., apart from a recent series of publications by Fitzpatrick [2], Fitzpatrick et al. [3], Dawson et al. [4],
and Ritz et al. [5]). Conversely, there are several wider-ranging and soil-related reviews, which provide comprehensive reviews of (i) “forensic geology” [6–12] and, (ii) “geoforensics”, which focuses more on the geoscience techniques such as forensic geophysics, forensic remote sensing and geological trace evidence [13–15], and (iii) archaeology [16]. Soil materials are routinely encountered as evidence by police, crime scene investigators, and forensic staff. However, most forensic and physical evidence laboratories either do not accept or are unable to adequately characterize soil materials. The main reason for this is that the morphological, mineralogical, and spectroscopic analytical knowledge required to examine and interpret such soil evidence needs a large amount of training and expertise that is not yet available in most forensic science facilities. In recent years, soil science technology has advanced dramatically and become very specialized and, for this reason, scientists and police investigation units are not using soil information as much as they did previously (e.g., application mainly of petrographic microscope data). Currently, soil analyses are generally only performed in investigations of serious crime and usually where human DNA analyses or analyses of other more commonly used types of trace evidence were not possible. Consequently, there is an opportunity for the application of soil analysis in the forensic examination of soil from a wider spectrum of routine forensic investigations. This review outlines traditional and new soil methods, as well as systematic approaches for the forensic examination of soils.
Soil as a Powerful Contact Trace Theory of Transfer of Soil Materials from One Surface to Another as a Result of Contact The transfer of trace evidence is governed by what has become known as the Locard Exchange Principle [17], which states that when two surfaces come into physical contact there is a mutual exchange of trace evidence between them. For example, the exchange can take the form of soil material from a location transferring to the shoes of a person who walked through that location. These types of transfers are referred to as primary transfers (e.g., evidence is transferred from the soil surface to the shoe and later recovered from the shoe, such as in the treads of
Soil: Forensic Analysis the sole or within the shoe). Once a trace material has transferred, any subsequent movements of that material, in this case from shoes (e.g., from the shoe to the carpet in a vehicles foot well), are referred to as secondary transfers. These secondary transfer materials can also be significant in evaluating the nature and source(s) of contact. Hence, the surface of soils can provide information linking persons to crime scenes. Higher order transfers (tertiary transfers) of trace evidence can also occur, which can present interpretative problems for forensic soil scientists because the ultimate source of trace evidence may be extremely difficult to identify. Aardahl [18] lists the properties of the ideal trace evidence: (i) it is highly individualistic; (ii) it has a high probability of transfer and retention; (iii) it is nearly invisible; (iv) it can quickly be collected, separated, and concentrated; (v) the merest traces are easily characterized; and (vi) it is able to have computerized database capacity. In this context, glitter (i.e., entirely manmade tiny pieces of Al foil or plastic with vapor-deposited Al layer) has been considered to be the ideal contact trace [19]. Soil materials may be considered as approaching the ideal “contact trace”, and the following brief discussion considers how closely they fulfill the criteria of Aardahl.
Soil is Highly Individualistic Diversity of Natural Soils. It is important to understand and know the different kinds of soils and how they form because this helps in making accurate forensic comparisons. To determine the wide variety of soils that occur in the world, it is necessary to understand soil classification systems used to illustrate this. Soil classifications help to organize knowledge about soils, especially in conducting soil surveys. The two international soil classification systems, which are widely used, are the World Reference Base (WRB) [20] and Soil Taxonomy [21]. Many countries also have national and specialized technical classifications [22]. Soil surveys enable the depiction of soils across a landscape and soil maps are made to show the patterns of soils that exist and provide information on the properties of soils. Soil maps are produced at different scales to depict soils over (i) large areas such as the world, countries, and regions (1 : 100 000 or smaller scale), and (ii) detailed areas such as farms (1 : 10 000 or larger scale). A wide diversity of natural soils exists and
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each has its own characteristics (e.g., morphology, mineralogy, and organic matter composition). For example, according to the United States Department of Agriculture (USDA), which collects soil data at many different scales, there are over 50 000 different varieties of soil in the United States alone. Parent material, climate, organisms, and the amount of time it takes for these properties to interact vary worldwide. Anthropogenic Soils. Urban soils is a class of anthropogenic or anthropic soils, a term used in several soil classification systems [20] to indicate soils that are essentially under strong human influence in urban and suburban areas. They are characterized by a strong spatial heterogeneity, which results from the various inputs of exogenous materials (e.g., compost, minerals, technological compounds, and inert, organic, or toxic wastes) and the mixing of the original (natural) soil material (e.g., parks, gardens, landscaping, and cemeteries). Mine or quarry soils are another class of anthropic soils, which are also strongly influenced soils, but found away from cities. Anthropic soils are characterized by a great ecological heterogeneity, and show special distinctness of soil properties. These specific soils also contain a large array of historical information, which has been proved very useful in understanding and quantifying soil differences in forensic soil comparisons. The major question posed is how can soils be used to make accurate forensic comparisons when we know that both natural and anthropic soils are highly complex and that there are thousands upon thousands of different soil types in existence? The following key issues are especially important in forensic soil examination because the diversity of soil strongly depends on topography and climate, together with anthropogenic contaminants: •
•
Forensic soil examination can be complex because of the strong diversity and heterogeneity of soil samples. However, such diversity, heterogeneity, and complexity enables forensic examiners to distinguish between soil samples, which may appear similar to the untrained observer. A major problem in forensic soil examination is the limitation in the discrimination power of the standard and nonstandard procedures and methods.
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Soil: Forensic Analysis
No standard forensic soil examination method exists. The main reasons for this are that examination of soil is concerned with detection of both (i) naturally occurring soils (e.g., minerals, organic matter, soil animals, and included rock fragments) and (ii) anthropogenic soils that contain manufactured materials such as ions and fragments from different environments whose presence may impart soil with characteristics that will make it unique to a particular location [e.g., material from quarries, asphalt, brick fragments, cinders, objects containing lead from glass (see Examination of Fibers and Textiles), hydrocarbons, paint chips (see Paint: Interpretation), and synthetic fertilizers with nitrate, phosphate, and sulfate]. In spite of the increasing impact of human activities on soil and the likelihood that all of Earth’s ecosystems have been influenced to some extent by humans, many soils still retain their basic morphology imparted by natural soil-forming processes. These anthropogenic properties make the naturally occurring soils even more individualistic.
Soil is Easy to Characterize: Large and Trace Amounts Historical Analysis Methods for Forensic Soil Samples: 1856–1904. Soil materials are generally easy to characterize, especially by way of the following published historical examples, which demonstrate how large amounts of soil materials have been characterized using quick morphological and light optical methods to solve crime cases. On a Prussian railroad, in April 1856, a barrel which contained silver coins was found on arrival at its destination to have been emptied and refilled with sand. Prof Ehrenburg of Berlin acquired samples of sand from stations along railway lines and used a light microscope to match the sand to the station from which the sand must have come [22]. This is arguably the very first documented case where a forensic comparison of soils was used to help police solve a crime [2]. Then, in 1887, Sir Arthur Conan Doyle published several fictional cases involving Sherlock Holmes such as “A Study in Scarlet” in Beeton’s Christmas Annual of London where Holmes can “Tell at a glance different soils from each other . . . has shown me splashes upon his trousers, and told me by their colour and consistence in what part of London he had received them”. In 1891, in “The Five Orange Pips”, Holmes observed “chalk-rich soil” on boots. This clearly indicates that Conan Doyle was well aware of the key soil
morphological properties (color and consistence) and soil mineralogy (chalk) in forensic soil comparisons. Further, as documented by Murray and Tedrow [9, 10], “October 1904, a forensic scientist in Frankfurt, Germany named George Popp was asked to examine the evidence in a murder case where a seamstress had been strangled in a bean field with her own scarf. George Popp successfully examined soil and dust from clothes for identification to solve this real criminalistic case”. Standard/Traditional Analysis Methods for Forensic Soil Samples. The methods of soil analysis used in forensic science are predicated on the size of the sample and the use to which the analytical results will be put. The aim of forensic soil analysis is to associate a soil sample taken from an item (e.g., shoes, clothing, shovel, or vehicle) by police with a specific location. To achieve this aim, the methods of analyses chosen must be able to discriminate between soil samples from different locations. Importantly, the methods used for comparing the samples must be practical (use of standard methods), inexpensive, accurate, and applicable to small and large samples. The methodology for describing soils has been developed and refined by soil scientists for more than a century [23]. Soils from crime scenes and control sites can be investigated at least in part with traditional soil survey descriptive approaches/techniques; however, these methods must be properly adapted and new methodology must still be developed [3]. Soil morphological descriptors such as color [24], consistency, structure, texture, segregations/coarse fragments (charcoal, ironstone, or carbonates), and abundance of roots/pores are the most useful properties to aid the identification of soil materials (e.g., [23, 25]) and to assess practical soil conditions (e.g., [26]). These soil morphological descriptions follow strict conventions whereby a standard array of data is described in a sequence, and each term is defined according to both the USDA Field book for describing and sampling soils, Version 2.0 [25] and National standard systems (e.g., Australian Soil and Land Survey Field Handbook by McDonald et al. [27].
Soil has a High Probability of Transfer and Retention In general, soil usually has a strong capacity to transfer and stick, especially the fine fractions in soils
Soil: Forensic Analysis (clay and silt size fractions) and organic matter. The larger quartz particles (e.g., >2-mm size fractions) have poor retention on clothes and shoes and carpets. Fine soil material (e.g., their 3 >1
3 X >2 >1 >3
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