s e c t
. I
o n
The Profession
Chapter 1
Who are Physical Therapists,
and What Do They Do?
Definition of Physic...
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s e c t
. I
o n
The Profession
Chapter 1
Who are Physical Therapists,
and What Do They Do?
Definition of Physical Therapy Scope of Practice Education and Qualifications Practice Settings Hospital
Home Health Care
School System
Private Practice
Clinical Education of Students Models of Disablement The Five Elements of Patient/ Client Management Examination Patient History Observation Systems Review Tests and Measures Pain
Evaluation
Diagnosis
Prognosis
Plan of Care (POC) Coordination of Care
Progression of Care
Discharge Plan
Intervention
Coordination/Communication/ Documentation Documentation APTA Guidelines for Documentation
Basic Principles of Clinical
Documentation
Patient/Client-Related Instruction Procedural Interventions Choosing an Intervention Strategy
Outcomes Discharge/Discontinuation of Intervention Prevention and Promotion of Health, Wellness, and Fitness Members of the Health Care Team Physical Therapy Director
Staff Physical Therapist
Physical Therapist Assistant
Physical Therapy/Occupational
Therapy Aide
1
2
SECTION I. THE PROFESSION
Physical Therapy and Physical Therapist Assistant Student Physical Therapy Volunteer Home Health Aide OccupauonalTherap~t
Certified Occupational Therapist Assistant Speech-Language Pathologist (Speech Therapist) Certified Orthotist Certified Prosthetist Respiratory Therapist Respiratory Therapy Technician Certified (CRRT) Primary Care Physician (PCP) Physician's Assistant (PA) Physiatrist Chiropractor Registered Nurse Rehabilitation (Vocational) Counselor Audiologist Athletic Trainer (ATC) Social Worker Massage Therapist Acupuncturist
Risk Management Measurement and Assessment Strategies
Program Development
Professional Standards
Guide for Professional Conduct of the Physical Therapist Interpreting Ethical Principles Principle Principle Principle Principle Principle Principle Principle Principle Principle Principle Principle
1 2 3 4 5 6 7 8 9 1I) 11
Standards of Practice for Physical Therapy and the Criteria Preamble Legal/Ethical Considerations Administration of the Physical Therapy Service Patient/Client Management
Chapter 2 Administration The United States Health Care System Overview Cost Containment Increased Requirements and Justification The Funding of Health Care Publicly Funded Plans
Quality of Care Current Concerns About Quality of Care
Budgets-Fiscal Responsibilities Budget The Operating Budget The Capital Budget Budget Calendar Zero-Base Budget
Expenses/Costs
Accounts Payable
Accounts Receivable
Health Care Regulations Fiscal Regulations Certificate of Need (CON) Regulations Patient Self-Determination Act of 1990
Quality Assurance/Quality
Improvement
Quality Assurance (QA) Continuous Quality Improvement (CQI) Utilization Review Quality Regulations Health Professionals Regulation Health Insurance Regulation Access-Related Insurance Regulations Americans with Disabilities Act
Cost-Related Insurance
Regulations
Voluntary Accreditation Voluntary Accrediting Agencies Joint Commission on Accreditation of Healthcare Organizations UCAHO) Accreditation Council for Services for Mentally Retarded and Other Developmentally Disabled Persons (AC-MRDD) Commission on Accreditation of Rehabi Iitation Faci Iities (CARF)
SECTION I. THE PROFESSION
Comprehensive Outpatient Rehabilitation Facility (CORF)
The Typical JCAHO Accreditation Process Health Care Insurance: Reimbursement Private Health Insurance Industry Private Health Insurance Managed Health Care Systems Health Maintenance Organizations (HMOs) Point-of-Service (POS) Plans Preferred Provider Organizations (PPOs) Point-of-Purchase Plans Primary Care Networks
Government Health Insurance Medicare Medicaid Balanced Budget Act of 1997 (BBA) Health Care Financing Administration (HCFA)
Worker's Compensation Personal Payment and Free Care Consumer-Driven Health Care Programs Health Insurance and Portability Accountability Act (HIPAA) HIPAA Privacy Rule
HIPAA Terminology
Medical Records Threats to Medical Record Privacy Current Protections
Personnel Supervision/ Management of the Department Management and Leadership Theories Bass Theory of Leadership
Four-Framework Approach
Managerial Grid
Management Styles Managers Versus Leaders
Meetings Job Descriptions Performance Appraisal Rating Systems
Completing a Performance
Appraisal
Staff Motivation Professional Growth Policy and Procedure Manuals Material Safety Data Sheet (MSDS)
Incident/Occurrence Reporting Sentinel Event Reporting Illegal Practice and Malpractice Malpractice
Informed Consent
Statutory Laws
Licensure laws
Workers' Compensation Acts
Unions
Chapter 3 Research Statistics Populations and Samples Variables and Types of Data Data Collection and Sampling Techniques Graphical Representation of Organized Data Data Description Measures of Central Tendency Measures of Variation Measures of Position
Probability
The Normal Distribution
Confidence Intervals
Confidence Intervals for the Mean Confidence Intervals for Variances and Standard Deviations
Hypothesis Testing Type I Errors Type II Errors Significance Level Probability (p) Value The Power of a Hypothesis Test z-Test t-Test
Chi-Square and Analysis of Variance (ANOVA) Chi-Square
Analysis of Variance (ANOVA)
Analysis of Covariance (ANCOVA)
Intraclass Correlation Coefficient
Choosing the Correct Statistical Test
Research Design Control
Control Group
Experimental Group
Placebo Effect
Random Assignment
Definitions
3
4
SECTION I. THE PROFESSION
Use of Evidence-Based Practice (EBP) Scientific Rigor by Type of Research Design Instrumentation-Gold Standard Sensitivity and Specificity Validity Construct Val idity Face Validity Content Validity External Validity Internal Validity Criterion-Referenced Validity Prediction Value Likelihood Ratio
Reliability Threats to Validity and Reliability Chapter 4 Education Motivation
Maslow's Hierarchy of Needs
Learning Theories
Domains of Learning Educational Activities Decision-Making Problem-Solving Sensory Motor Learn ing
Learning Styles Analytical Learner Intuitive/Global Learner Inductive Versus Reasoning: Deductive Reasonings Initiative: Active Versus Passive Learning
Improving Compliance with Learning and Participation Community and Staff Education Using Visual Aids Cultural Influences
Chapter 5 Fundamentals and Core Concepts Tissues of the Body Epithelial tissue
Nervous Tissue
Connective Tissue
Connective Tissue Proper Tendons and Ligaments Bone Cartilage Tissue Bursae Connective Tissue Disorders
i
i
_L
Muscle Tissue Muscle Function Pathology of Muscle Joint Classification Arthrokinematics Osteoki nematics Degrees of Freedom Close-Packed and Open-Packed Positions of the Joint Capsular and Noncapsular Patterns of Restriction End-Feels Arc of Pain Measuring Range of Motion Grading Accessory Movements Hypomobility, Hypermobility, and Instabi Iity
Kinesiology General Principles of Biomechanics Directional Terms Movements of the Body Segments Planes of the Body
Axes of the Body
Levers
Flexibility
Physiology Physiology of Exercise Energy Systems Measures of Energy Expenditure
Body Mass Index (BM/) Bioelectrical Impedance Analysis The Metabolic Equivalent (MET) Nutrients Carbohydrates
Fats
Proteins
Vitamins and Minerals
Nerve and Muscle Physiology Resting Membrane Potential (RMP) Action Potential The Synapse Neurotransmitters The Neuromuscular Junction
Thermoregu lation Conservation and Production
of Body Heat
The Immune System T-Lymphocytes
Organs of the Immune System
Immunodeficiency
The Healing Process Wound Healing
Muscle Healing
SECTION I. THE PROFESSION
Tomography
Destruction Phase
Repair Phase
Remodeling Phase
Positron (PET)
Ligament and Tendon Healing Phase I: Hemorrhagic Phase II: Inflammatory Phase III: Proliferation Phase IV: Remodeling Maturation
and
Articular Cartilage Healing
Meniscal Healing
Extrinsic Pathway
Intrinsic Pathway
Bone Healing Imaging Studies Radiography Conventional Radiography Stress Radiograph Contrast-Enhanced Radiography
Emission Tomography
Magnetic Resonance Imaging Diagnostic Ultrasound Radionucleotide Scanning Fluoroscopy Transcranial Magnetic Stimulation (TMS) Magnetoencephalography (MEG) Miscellaneous Information Standard and Transmission-Based Precautions The Intensive Care Unit Environment Airways Lines Miscellaneous Equipment
5
Who are Physical Therapists, and What Do They Do?
The Guide to Physical Therapist Practice referred to hereafter as The Guide was developed by tlle American Physical Ther"py Association (APTA) "to encourage a uniform approach to physical therapist practice and to explain Lo the world the nature of thaL prnctice."l 'Ibe Guide is
divided into two parts: ~ ~
Part 1 delineates the physical therapist's scope of practice and
describes patient management by physical therapist. (PTs).
Part 2 describes each of the di>lgnostic preferred practice pat
terns of patients typically treated by PTs.
DEFINITION OF PHYSICAL THERAPY The Guide defines physical therapy as follows: Physical therapy includes diagnosis and management qf movement dys
function and enhancement q(physical andfunctiona/ abilities; restora
tion, maintenance, and promotion ofoptimal physicalfuncttotl, ('PUmal
fitness and weI/ness, and optimal quality of life as it relates 10 movement
and health: and pret!(mtion of the onset, symptoms, and pTORression of
impairments, fi~nctional limitations, and disabilities that may result
/rum dil>eases, disorders, conditif.J1/s, or injuries,
SCOPE OF PRACTICE Physical therapy is defmed as the care and services provided by or under the direction and snpervi'iion of a physical therapist.:l ~ ~
Physical therapbts are the only professionals who provide
physical therapy.
Physical fuerapist assistmt. (PTAs)-unUcr tlle direaion and super
vision of the physical therapi....,t-are the only pamprofessionaL.,
who assL~ in the provision of physical theiJ.py interventions.
7
8
SECTION I. THE PROFESSION
EDUCATION AND QUALIFICATIONS PTs are professionally educated at the college or university level and are required to be licensed in the state (or states) in which they prac tice. Education programs for the preparation of physical therapists have been recognized in some manner ~ince 1928, when the APTA Brst published a list of approved programs'> ~ ~
--------------------,
Study Pearl CAPTEonly
and PTA education
sitional£IDd.:,r ~PhYsic;rl Jh
Graduates from 1926 to 1959 completed physical therapy cur ricula approved by appropriate accreditation bodies. Graduates from 19(";0 to the present have successfully com pleted professional physical therapist education programs accredited by the CommL.,sion on Accreditation in Physical Therdpy Education CCAPTE). CAPTE also makes autonomous decisions concerning the accreditation status of continuing education programs for the physical therapists and physical therapist assistants.
:programs, which arE! consi.
profeSsional Pro~aI]K. ••
The APTA house of delegates first authorized the education of physical therapist assistants at the 1%7 Annual Conference.
PRACTICE SETTINGS Physical therapists praCTice in a broad range of inpatient, outpatient, and conununity-based settings, including those described in the next sections and listed in Table 1-1.
HOSPITAL Hospitals may be classified in a number of ways, including by, ~
~
~
~
Length of stay (short-term or long-term) Acute-<eare (short-term hospital): An acute-care hospital can be defined as a facility that provides hospital care to patients who generally require a stay of up to 7 days, and whose focus is on a physical or mental condition requiring immediate intervention and constant medical attention, equipment, and personnel. Following a stay in the acute-ing nursing home patients. .. The MDS for nursing facility residents is a comprehensive resideD[ assessment iru;uumenl (RAT) that measures functional scatus~ mental health status, and beilltvioml stalUS 10 identify chronic care patient needs and fomlaJize a care plan in response to 18 re'llident assessment protocols (RAPs). .. Under federal regulation, assessments arc conducted at a time of aJmjssion into a nursing facility, upon reUlm. from a 72-hollf hospital admission, whenever there is a significant change in status, 4uarterly, and annually. Physical therapist involved in the c-oordiruued services of medical, social, educational, vocational, and the other rehabilitative services (OT, speech). (Continued)
10
SEGION I. THE PROFESSION
TABLE 1-1. PRACTICE SETTINGS (Continued) SETTING
Chronic care facility
Comprehensive outpatient rehahilitation facility (CORF)
Custodial care facility
Hospice cut:'
Pl'csuna) care
Ambulatory care (outpatient care)
~
CHARACTERISTICS
... Primary emphasis is to provide intensive physiCll and cognitive restorative services in the early months to disabled persons to facilitate their return to maximum functional capacity. ... Typical stay is .'i to 4 months (short term). ... Long-tem1 care facility that is facility or commullit~r' based. ... Sometimes refcncd to 3-90
Poor to moderate agreement Good agreement Reasonable agreement for clinical measurements
Data from Portney L, Watkins MP. Foundations of Clinical Research: Applications to Practice. Norwalk, Cf: Appleton & Lange; 1993.
random error. If the null hypothesis is rejected, there is a dif ference in the outcome of the different treatment levels at a sig nificance a and it remains to be determined between which treatment levels the actual differences lie. The two-way analysis of variance is an extension to the one-way analysis of variance, in which comparisons can be made between two or more population means with two or more inde pendent variables (hence the name two-way) called factors.
Analysis of Covariance (ANCOVA). ANCOVA is a test used to compare means of a continuous outcome variable among two or more treatment groups or conditions after controlling for the effects of intervening variables (covariates). For example, two groups of subjects are compared on the basis of diet parameters using two different types of exercises; the subjects in one group are male and the subjects in the second group are female; sex then becomes the covariate that must be controlled during statistical analysis. Intraclass Correlation Coefficient. The intraclass correlation coefficient (ICC) is a reliability coefficient calculated with variance esti mates obtained through an analysis of variance (ANOVA) (Table 3-5).11 The ICC has been advocated as a statistic for assessing agreement or consistency between two methods of measurement, in conjunction with a significance test of the difference between means obtained by the two methods. The advantage of the ICC over correlation coeffi cients is that it does not require the same number of raters per subject, and it can be used for two or more raters or ratings. I 1 CHOOSING THE CORRECT STATISTICAL TEST
Study Pearl
The choice of which statistical test to use depends on the question being asked. I ~
~
~
~
~
If the design is to learn about the association between two vari ables (e.g., what is the relationship between arm girth and elbow flexor strength?), a correlation coefficient should be calculated. If the question deals with prediction (e.g., if the patient has a knee range of motion of 10 to 50 degrees on the second post operative day, how many days will the patient likely remain in the hospital?), a regression analysis is appropriate. If the question is whether a treatment has an effect, or shows a difference (e.g., does spinal traction reduce the signs and symptoms of a cervical root compression?), a chi-square, analy sis of variance (ANOVA), or t-test is appropriate. For a correlation study to determine the degree of association, a Spearman rho is used for ordinal data, whereas a Pearson cor relation coefficient is calculated for interval data. If the question is whether two groups differ on the dependent variable, and the data are normally distributed with equal vari ances, a t-test is appropriate.
RESEARCH DESIGN There are a number of primary types of research designs (Table 3-6).
CHAPTER 3. RESEARCH
117
TABLE 3-6. RESEARCH DESIGNS
Controlled trials Uncontrolled trials Single-blind study Double-blind study
These require the experimental procedure to be compared with a placebo or another previously accepted procedure. Controlled studies are more likely than uncontrolled studies to determine whether differences are due to the experimental treatment or to some of the extraneous factors. These involve the investigators describing their experience with an experimental procedure; however, the experimental procedure is not formerly compared with a placebo or another previously accepted procedure A study in which the investigator does not know if the subject is in the treatment or the control group. A study in which neither the investigator nor the subject knows if the subject is in the treatment or the control group.
CONTROL Ideally, the researcher should attempt to remove the influence of any variable other than the independent variable in order to evaluate its effect on the dependent variable. An experimental design has the pur pose of minimizing or contolling the effects on extraneous variables so that the relationship between the independent variable(s) and the dependent variable(s) can be ascertained.
CONTROL GROUP The control group is used as a standard for comparison with experi mental groups in terms of age, abilities, race, and so on. For example, a particular study may divide participants into two groups-an "experi mental group" and a "control group." The experimental group is given the experimental treatment under study, while the control group may be given either the standard treatment for the illness or a placebo. At the end of the study, the results of the two groups are compared.
EXPERIMENTAL GROUP Study participants in the experimental group receive the drug, device, treatment, or intervention under study. In some studies, all participants are in the experimental group. In "controlled studies," participants will be assigned either to an experimental group or to a control group.
PLACEBO EFFECT The placebo effect is the measurable, observable, or felt improve ment in health not attributable to treatment. Experimental research uses placebos (usually sugar or starch pills) to test the effect of a medication-an inactive substance that looks like medicine but con tains no medicine and has no treatment value (a placebo) is adminis tered to the patient. While participants in the control group are given the placebo, the other members of the study are given the actual medication.
RANDOM ASSIGNMENT Random assignment is assignment by chance, like flipping a coin or pulling numbers out of a hat. This method is sometimes used to deter mine who is in the experimental group and who is in the control group.
118
SECTION I. THE PROFESSION
For example, in a study with random assignment to one of two groups, participants have a 50% chance of being assigned to either group.
Study Pearl
DEFINITIONS A number of statistical terms and defmitions are outlined in Table 3-7.
USE OF EVIDENCE-BASED PRACTICE (EBP) Evidence-based practice (EBP) is the integration of three key elements: best research evidence, clinical expertise, and patient values. It is hav ing an increasing impact on the profession of physical therapy. When integrating evidence into clinical decision-making, an understanding of how to appraise the quality of the evidence offered by clinical studies is important. Judging the strength of the evidence becomes an important part of the decision-making process.
SCIENTIFIC RIGOR BY TYPE OF RESEARCH DESIGN Unfortunately, many of the experimental studies that deal with physical therapy topics are not well-designed trials. Awareness of the distinction between efficacy and effectiveness is important for therapists attempt ing to translate evidence to practice. ~
Efficacy: refers to outcomes of interventions provided in a con trolled setting under experimental conditions. When attempt ing to apply the results of an efficacy study, a therapist must
TABLE 3-7. STATISTICAL TERMS AND DEFINITIONS DEFINITION
TERM
Abstract
A summary of the paper, usually between 100 and 500 words, that describes the most important aspects of the study, including: ~ ~ ~ ~
Conclusion Empirical methods Hawthorne effect Parameter Peer review
Population
The The The The
problem investigated. subjects and instruments involved. design and procedures. major findingslconclusions.
The conclusion responds to the original research question and hypothesis to describe what the study showed. It should bring coherence to the study. Research methods and data-gathering techniques supported by measurable evidence, not opinion or speculation. An untreated subject experiences a change simply from participating in a research study. Similar to the placebo effect. Numerical measurements describing some characteristic of the population. A process by which research studies are examined by an independent panel of researchers for review. The purpose of such is to open the study to examination, criticism, review, and replication by peer investigators and ultimately incorporate the new knowledge into the field The population of a study refers to the group of people represented in a study. For example, if a researcher took a nationally representative sample of 1500 fourth-grade students, the sample is the 1500 fourth-grade students, but the population of the study would be fourth graders in general.
CHAPTER 3. RESEARCH
119
TABLE 3-8. A HIERARCHY OF EVIDENCE GRADING LEVEL OF EVIDENCE GRADING = A
Type of Study
Randomized controlled trial
LEVEL OF EVIDENCE GRADING = C
LEVEL OF EVIDENCE GRADING = B
Cohort study
~
~ ~
~
Nonrandomized trial with concurrent or historical controls Case study Study of sensitivity and specificity of a diagnostic test Population-based descriptive study
LEVEL OF EVIDENCE GRADING = D ~ ~ ~
Cross-sectional study Case series Case report
LEVEL OF EVIDENCE GRADING = E ~
~
Expert consensus Clinical experience
Data from Sackett DL. Rules of evidence and clinical recommendations on the use of antithrombotic agents. Chest. 1986;89:2S-3S.
~
consider whether subject characteristics and the manner in which intervention was provided generalize to patients on their caseloads and how to adapt the intervention to constraints within their practice settings. 14 Effectiveness: refers to outcomes of interventions provided within the scope of clinical practice.
Sackett15 proposed a five-level system that relates the experimental design to levels of evidence and grades of recommendation (Table 3-8). A grade A recommendation (the randomized controlled trial, Table 3-9), indicates that outcomes are supported by at least one level I study. A grade B recommendation indicates outcomes are supported by at least one level II study. A grade C recommendation indicates that outcomes are supported by level III, IV, or V studies. The Oxford Center for Evidence-Based Medicine has elaborated on Sackett's levels of evidence (Table 3-10).
Study Pearl
TABLE 3-9. THE RANDOMIZED CONTROLLED TRIAL (RCI) An experimental design in which subjects are randomly aSSigned to an experimental or control group permitting the strongest
inferences about cause and effect. Typically volunteers agreed to be randomly allocated to groups receiving one of the following: ~ ~ ~
Treatment and no treatment. Standard treatment and standard treatment plus a new treatment. Two alternate treatments.
The common feature is that the experimental group receives the treatment of interest and the control group does not. At the end of the trial, outcomes of subjects in each group are determined-the difference in outcomes between groups provides an estimate of the size of the treatment effect. ~ ~ ~
Less exposed to bias.
Ensures comparability of groups.
Provides evidence of efficacy
Data from Maher CG, Herbert RD, Moseley AM, et al. Critical appraisal of randomized trials, systematic reviews of radomized trials and clinical prac tice guidelines. In: Boyling ]0, ]ull GA, eds. Grieve's Modern Manual Therapy: The Vertebral Column. Philadelphia: Churchill Livingstone; 2004:603--614; Petticrew M. Systematic reviews from astronomy to zoology: myths and misconceptions. BM]. 2001;322:98-101; Palisano R], Campbell SK, Harris SR. Evidence-based decision-making in pediatric physical therapy. In: Campbell SK, Vander Linden OW, Palisano R], eds. Physical Therapy for Children. St. Louis: W.B. Saunders; 2006:3-32.
120
SECTION I. THE PROFESSION
TABLE 3-10. OXFORD CENTER FOR EVIDENCE-BASED MEDICINE LEVELS OF EVIDENCE
LEVEL Ia
Ib
Ic
2a
2b
2c 3a
3b
THERAPY/ PREVENTION, ETIOLOGY/HARM
PROGNOSIS
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS/ SYMPTOM PREVALENCE STUDY
ECONOMIC AND DECISION ANALYSES
SR (with homogeneity") SR (with homogeneity") SR (with homogeneity") SR (with homogeneity") SR (with of level I diagnostic of RCTs of inception cohort of prospective cohort homogeneity") studies; CDRt studies; CDRt with Ib studies of level I validated in different studies from different economic studies populations clinical centers Individual RCT (with Individual inception Validating·· cohort study Prospective cohort Analysis based on cohort study with with goodm reference study with good narrow confidence clinically sensible interval*) >80% follow-up; standards; or CDRt follow-up···· costs or CDRt validated in a tested within one alternatives; single population clinical center systematic review(s) of the evidence; and including multiway sensitivity analyses Allor none! Allor none case-series Absolute SpPins and Allor none Absolute SnNouts (see text) case-series better-value or worse-value analyses tm SR (with homogeneity") SR (with homogeneity") SR (with homogeneity·) SR (with homogeneity") SR (with of either retrospective of level >2 diagnostic of 2b and better homogeneity") of cohort studies studies studies of level >2 cohort studies or untreated control economic studies groups in RCTs Analysis based on Retrospective cohort Exploratory"· cohort Individual cohort Retrospective cohort study (including study or follow-up clinically sensible study with goodm study, or poor low quality RCT; of untreated control reference standards; follow-up costs or alternatives; limited review(s) patients in an RCT; CDRt after derivation, e.g., < 80% follow-up) derivation of CDRt or validated only on of the evidence, split-sample!!! or or validated on or single studies; split-sample!!! only and including databases multiway sensitiv ity analyses "Outcomes" research; "Outcomes" Research Ecologic studies Audit or outcomes ecological studies research SR (with homogeneity") SR (with homogeneity") SR (with homogeneity") SR (with of case-control homogeneity") of of 3b and better of 3b and better studies studies studies 3b and better studies Individual Nonconsecutive study; or Nonconsecutive Analysis based case-control study without consistently cohort study, or on limited very limited alternatives or applied reference standards population costs, poor quality estimates of data, but including sen sitivity analyses incorporating clinically sensible variations.
(Continued)
CHAPTER 3 RESEARCH
121
TABLE 3-10. OXFORD CENTER FOR EVIDENCE-BASED MEDICINE LEVELS OF EVIDENCE (Continued)
LEVEL
4
THERAPY/ PREVENTION, ETIOLOGY/HARM Case-series (and poor quality cohort and case-control studies!! ) Expert opinion without explicit critical appraisal, or based on physiology, bench research, or "tlrst principles"
5
PROGNOSIS Case-series (and poor quality prognostic cohort studies''') Expert opinion without explicit critical appraisal, or based on physiology, bench research or "first principles"
DIAGNOSIS Case-control study, poor or nonindependent reference standard Expert opinion without explicit critical appraisal, or based on physiology, bench research or "first principles"
DIFFERENTIAL DIAGNOSIS/ SYMPTOM PREVALENCE SruDY
ECONOMIC AND DECISION ANALYSES
Case-series or superseded reference standards
Analysis with no sensitivity analysis
Expert opinion without explicit critical appraisal, or based on physiology, bench research or "tlrst principles"
Expert opinion without explicit critical appraisal, or based on economic theory or "first principles"
Users can add a minus-sign to denote the level of that fails to provide a conclusive answer because of: ~ ~
~
EITHER a single result with a wide confidence interval (such that, for example, an ARR in an Ref is not statistically significant but whose confidence intervals fail to exclude clinically important benefit or harm). OR a systematic review with troublesome (and statistically significant) heterogeneity. Such evidence is inconclusive, and therefore can only generate grade D recommendations.
·By homogeneity we mean a systematic review that is free of worrisome variations (heterogeneity) in the directions and degrees of results between
individual studies. Not all systematic reviews with statistically significant heterogeneity need be worrisome, and not all worrisome heterogeneity need
be statistically significant. As noted above, studies displaying worrisome heterogeneity should be tagged with a minus sign at the end of their designated
level.
tClinical decision rule. (These are algorithms or scoring systems which lead to a prognostic estimation or a diagnostic category.)
IMet when all patients died before the Rx became available, but some now survive on it; or when some patients died before the Rx became avail
able, but none now die on it.
IIBy poor quality cohort study we mean one that failed to clearly define comparison groups and/or failed to measure exposures and outcomes in the
same (preferably blinded), objective way in both exposed and nonexposed individuals and/or failed to identify or appropriately control known con
founders and/or failed to carry out a sufficiently long and complete follow-up of patients. By poor quality case-control study we mean one that failed to
clearly define comparison groups and/or failed to measure exposures and outcomes in the same (preferably blinded), objective way in both cases and
controls and/or failed to identify or appropriately control known confounders.
lllSplit-sample validation is achieved by collecting all the information in a single tranche, then artificially dividing this into "derivation" and "validation"
samples.
ttAn "absolute SpPin" is a diagnostic finding whose specificity is so high that a positive result rules in the diagnOSiS. An "absolute SnNout" is a diag
nostic finding whose sensitivity is so high that a negative result rules out the diagnosis.
flGood, better, bad, and worse refer to the comparisons between treatments in terms of their clinical risks and benefits.
tttGood reference standards are independent of the test, and applied blindly or objectively applied to all patients. Poor reference standards are hap
hazardlyapplied, but still independent of the test. Use of a nonindependent reference standard (where the "test" is included in the "reference," or
where the "testing" affects the"reference") implies a level 4 study.
ttt!Better-value treatments are clearly as good but cheaper, or better at the same or reduced cost. Worse-value treatments are as good and more expen
sive, or worse and equally or more expensive.
··Validating studies test the quality of a specific diagnostic test, based on prior evidence. An exploratory study collects information and trawls the
data (e.g., using a regression analysis) to find which factors are "significant."
···By poor quality prognostic cohort study we mean one in which sampling was biased in favor of patients who already had the target outcome, or the
measurement of outcomes was accomplished in 80%, with adequate time for alternative diagnoses to emerge (e.g., 1---6 months acute, 1-5
years chronic).
Grades A B C D
of Recommendation Consistent level 1 studies Consistent level 2 or 3 studies or extrapolations from level 1 studies Level 4 studies or extrapolations from level 2 or 3 studies Level 5 evidence or troublingly inconsistent or inconclusive studies of any level
Data produced by Phillips B, Ball C, Sackett D., et al. from Oxford Center for Evidence-Based Medicine Levels of Evidence. www.cebm.net/ index.aspx?0=1025, November 1998.
122
SECTION I. THE PROFESSION
TABLE 3-11. SYSTEMATIC REVIEWS
Systematic reviews
Meta-analysis
Reviews of the literature conducted in a way that is designed to minimize bias--"a study of studies." Recently published reviews can be used to assess the effects of health interventions, the accuracy of diag nostic tests, or the prognosis for a particular condition. Usually involve criteria to determine which studies will be considered, the search strategy used to locate studies, the methods for assessing the quality of the studies, and the process used to synthesize the find ings of individual studies. Particularly useful for busy clinicians who may be unable to access alI the relevant trials in an area and may otherwise need to rely upon their own incomplete surveys of relevant trials. NB: A systematic review is only as good as the quality of each study. A mathematical synthesis of the results of two or more research reports. A meta-analysis can be performed on studies that used reliable and valid measures and report some type of inferential statistic (e.g., t-test, ANOVA)
Data from Maher CG, Herbert RD, Moseley AM, et al. Critical appraisal of randomized trials, systematic reviews of radomized trials and clinical prac tice guidelines. In: Boyling JD, Jull GA, eds. Grieve's Modern Manual Therapy: The vertebral Column. Philadelphia: Churchill Livingstone; 2004:603---D14; Petticrew M. Systematic reviews from astronomy to zoology: myths and misconceptions. EM]. 2001;322:98-101; Palisano RJ, Campbell SK, Harris SR. Evidence-based decision-making in pediatric physical therapy. In: Campbell SK. Vander Linden DW, Palisano RJ, eds. Physical Therapy for Children. St. Louis: W.E. Saunders; 2006:3-32.
Study Pearl The
critically app provides a form summarize the from a literature s, part of clinical appraised mary of' clinical
Evidence-based practice is a four-step process: 1. A clinical problem is identified and an answerable research question is formulated. 2. A systematic literature review is conducted and evidence is collected. 3. The research evidence is summarized and critically analyzed. 4. The research evidence is synthesized and applied to clinical practice. Practice guidelines are systematically developed statements to assist patient and practitioner decisions about management of a health condition (Table 3-12).14 In general, practice guidelines include rec ommendations for the following: 14 ~ ~
~ ~ ~
~ ~
Who should receive the intervention? Expected outcomes. Documentation including selection of reliable and valid tests and measures. Utilization of services (frequency and duration, number of visits). Procedural interventions. Coordination of care. Discharge planning.
TABLE 3-12. CLINICAL PRACTICE GUIDELINES
Recommendations for management of a particular clinical condition. Intended to provide current standards for quality practice in order to improve effectiveness and efficiency of health care. Involve compilation of evidence concerning needs and expectations of recipients of care, the accuracy of diagnostic tests, effects of therapy, and prognosis. Usually necessitate the conduct of one, or sometimes several, systematic reviews. May be presented as clinical decision algorithms. Can provide a useful framework upon which clinicians can build clinical practice. Data from Maher CG, Herbert RD, Moseley AM, et al. Critical appraisal of randomized trials, systematic reviews of radomized trials and clinical prac tice guidelines. In: Boyling JD, Jull GA, eds. Grieve's Modern Manual Therapy: The Vertebral Column. Philadelphia: Churchill Livingstone; 2004:603-ti14.
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In 1998 an international group of researchers and policymakers formed the AGREE (Appraisal of Guidelines for Research and Evaluation) collaboration in order to improve the quality and effec tiveness of clinical practice guidelines. 14
INSTRUMENTATION-GOLD STANDARD The instrumentation-gold standard can be defined as an instrument with established validity that can be used as a standard for assessing or comparing other instruments.
SENSITIVITY AND SPECIFICITY Sensitivity represents the proportion of a population with the target dis order, which has a positive result with the diagnostic test. A test that can correctly identify every person who has the target disorder has a sensi tivity of 1.0. SnNout is an acronym for when Sensitivity of a symptom or sign is high, a negative response rules out the target disorder. Thus, a "high" sensitive test helps rule out a disorder. Specificity represents the proportion of the study population with out the target disorder, in whom the test result is negative (Table 3-13). 8 A test that can correctly identify every person who does not have the tar get disorder has a specificity of 1.0. SpPin is an acronym for when specificity is extremely high, a positive test result rules in the target dis order. Thus, a 'high' specific test helps rule in a disorder or condition. A test with a very high sensitivity, but low specificity, and vice versa, is of little value, and the acceptable levels are generally set at between 50% (unacceptable test) and 100% (perfect test), with an arbi trary cutoff of about 80%.8 There are several types of validity, including construct validity, face validity, content validity, external validity, con current validity, and criterion-referenced validity.
VALIDITY Validity is defined as the degree to which a test measures what it pur ports to be measuring, and how well it correctly classifies individuals with or without a particular diseaseY-19 Validity is directly related to the notion of sensitivity and specificity.
Construct Validity. Construct validity refers to the ability of a test to represent the underlying construct (the theory developed to organ ize and explain some aspects of existing knowledge and observations). Construct validity refers to overall validity.
TABLE 3-13. CONCEPTS AND DEFINITIONS OF SENSITIVIlY, SPECIFICIlY, AND PREDICTIVE VALUES CONCEPT Sensitivity Specificity Positive predictive value (PPV) Negative predictive value
DEFINITION Proportion of patients with a disease who test positive. Proportion of patients without the disease who test negative. Proportion of patients who actually have the disease who test positive. If the target disease is uncommon, there are many more false-positive results and the PPV goes down. Proportion of patients who do not actually have the disease and who test negative.
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Face Validity. Face validity refers to the degree to which the ques tions or procedures incorporated within a test make sense to the users. The assessment of face validity is generally informal and nonquantita tive and is the lowest standard of assessing validity-it is based on the notion that the finding is valid "on the face of it." For example, if a weighing scale indicates that a normal-sized person weighs 2000 pounds, that scale does not have face validity. Content Validity. Content validity refers to the assessment by experts that the content of the measure is consistent with what is to be measured. Content validity is concerned with sample-population representativeness-that is, the knowledge and skills covered by the test items should be representative to the larger domain of knowledge and skills. In many instances, it is difficult if not impossible to administer a test covering all aspects of knowledge or skills. Therefore, only sev eral tasks are sampled from the population of knowledge or skills. In these circumstances, the proportion of the score attributable to a par ticular component should be proportional to the importance of that component to total performance. In content validity, evidence is obtained by looking for agreement in judgments by judges. In short, one person can determine face validity, but a panel should confirm content validity.
External Validity. External validity deals with the degree to which study results can be generalized to different subjects, settings, and times. n ,2o Internal Validity. Internal validity can be defmed as the degree to which the reported outcomes of the research study are a consequence of the relationship between the independent and dependent variables and not the result of extraneous factors. Criterion-Referenced Validity. Criterion validity is determined by comparing the results of a test to those of a test that is accepted as a "gold-standard" test (a test that is accepted as being close to 1000A! valid).8 There are three types of criterion-referenced validity: concurrent, predic tive, and discriminant. Concurrent Validity. The degree to which the measurement being validated agrees with an established measurement standard adminis tered at approximately the same time. Concurrent validity is a form of criterion validity. Predictive Validity. Predictive validity is the extent to which test scores are associated with future behavior or performance. Discriminant Validity. Discriminant validity is the ability of a test to distinguish between two different constructs, and is evidenced by a low correlation between the results of the test and those of tests of a different construct. Diagnostic tests are used for the purpose of discovery, confirma tion, and exclusion. 21 Tests for discovery and exclusion must have high sensitivity for detection, whereas confirmation tests require high speci ficity (Table 3-13).22 The sensitivity and specificity of any physical test
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to discriminate relevant dysfunction must be appreciated to make mean ingful decisions. 23 Other points used in testing include the prediction value, confidence interval, and likelihood ratio.
Prediction Value. The prediction value of a positive test indicates that those members of the study population who have a positive test outcome will have the condition under investigation (Table 3-13).8 The diagnostic power of the negative test outcome relates to those of the study population with a negative test outcome who do not suffer from the condition under investigation. 8 Likelihood Ratio. The likelihood ratio is the index measurement that is considered to combine the best characteristics of sensitivity, specificity, positive predictive value, and negative predictive value. Likelihood ratios are expressed as odds and are calculated from values used to calculate sensitivity and specificity. The likelihood ratio indi cates how much a given diagnostic test result will lower or raise the pretest probability of the target disorder. 8,9 RELIABILITY
Reliability is defined as the extent to which repeated measurements of a relatively stable phenomenon are close to each other. 24 Test retest reliability is the consistency of repeated measurements that are separated in time when there is no change in what is being meas ured. Any difference between the two sets of scores represents measurement error, which can arise from a number of factors includ ing intrarater variability, interrater reliability, or a lack of consistency of results. Reliability may be measured as repeatability between measurements performed by the same examiner (intrarater reliabil ity), or between measurements by different examiners (interrater reliability). Instrument reliability deals with the tool used to obtain a measurement. Reliability is quantitatively expressed by way of an index of agree ment, with the simplest index being the percentage agreement value. 'The percentage agreement value is defmed as the ratio of the number of agreements to the total number of ratings made. 25 However, because this value does not correct for chance agreement, it can provide a mis leadingly high estimate of reliability.18,25-27 The results of an examination are of limited value if they are not consistently repeatable.17,18 The kappa statistic (K) is a chance-corrected index of agreement that overcomes the problem of chance agreement when used with nominal and ordinal data (Table 3-14).28 However, with higher-scale data such as ordinal and parametric data, it tends to underestimate reliability, in which case a weight kappa (ranked) or ICC (parametric) should be usedY 'Theoretically K can be negative if agree ment is worse than chance. Practically in clinical reliability studies, K usually varies between 0.00 and 1.00.12 The K statistic does not differ entiate among disagreements; it assumes that all disagreements are of equal significance. 12 A number of calculations, including the Pearson product moment correlation coefficient and the intraclass correlation coefficient, can be used to assess reliability.
TABLE 3-14. KAPPA (K) BENCHMARK VALUES VALUE (0/0)
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100
DESCRIPTION
Poor to fair agreement Moderate agreement Substantial agreement Excellent agreement Perfect agreement
Data from Portney L, Watkins MP. Foundations ofClinical Research: Applications to Practice. Norwalk, Cf: Appleton & Lange; 1993.
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THREATS TO VALIDITY AND RELIABILITY
The most common threats to validity and reliability are: ~
~
~ ~ ~ ~ ~
~ ~ ~ ~
Ambiguity: when correlation is taken for causation.
Errors of measurement: random errors or systematic errors.
History: when some critical event occurs between pretest and
posttest. Instrumentation: when the researcher changes the measuring device. Maturation: when people change or mature over the research period. Mortality: when people die or drop out of the research. Regression to the mean: a tendency toward middle scores. The John Henry effect: when groups compete to score well. Sampling bias: the tendency of a sample to exclude some members of the sampling universe and over-represent others. Setting: something about the setting or context contaminates the study. The Hawthorne effect: a tendency of research subjects to act atyp ically as a result of their awareness of being studied.
REFERENCES 1. Underwood FB. Clinical research and data analysis. In: Placzek JD, Boyce DA, eds. Orthopaedic Physical Therapy Secrets. Philadelphia: Hanley & Belfus; 2001: 130-139. 2. Bluman AG. The nature of probability and statistics. In: Bluman AG, ed. Elementary Statistics: A Step by Step Approach. 4th ed. New York: McGraw-Hill; 2008: 1-32. 3. Bluman AG. Organizing data. In: Bluman AG, ed. Elementary Statistics: A Step by Step Approach. 4th ed. New York: McGraw Hill; 2008: 33-100. 4. Bluman AG. Measures of central tendency. In: Bluman AG, ed. Elementary Statistics: A Step by Step Approach. 4th ed. New York: McGraw-Hill; 2008: 101-176. 5. Bluman AG. Probability and counting rules. In: Bluman AG, ed. Elementary Statistics: A Step by Step Approach. 4th ed. New York: McGraw-Hill; 2008: 177-242. 6. Bluman AG. The normal distribution. In: Bluman AG, ed. Elementary Statistics: A Step by Step Approach. 4th ed. New York: McGraw-Hill; 2008: 281-341. 7. Bluman AG. Confidence intervals and sample size. In: Bluman AG, ed. Elementary Statistics: A Step by Step Approach. 4th ed. New York: McGraw-Hill; 2008: 343-385. 8. Van der Wurff P, Meyne W, Hagmeijer RHM. Clinical tests of the sacroiliac joint, a systematic methodological review. Part 2: validity. Man Ther. 2000;5: 89-96. 9. Jaeschke R, Guyatt G, Sackett DL. Users guides to the medical lit erature. III. How to use an article about a diagnostic test. B. What are the results and will they help me in caring for my patients? lAMA. 1994;27:703-707.
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10. Bluman AG. Hypothesis testing. In: Bluman AG, ed. Elementary Statistics: A Step by Step Approach. 4th ed. New York: McGraw-Hill; 2008: 387-455. 11. Huijbregts PA. Spinal motion palpation: a review of reliability studies. j Man Manip Ther. 2002;10: 24-39. 12. Portney L, Watkins MP. Foundations ojClinicalResearch: Applications to Practice. Norwalk, CT: Appleton & Lange; 1993. 13. Sackett DL, Strauss SE, Richardson WS, et al. Evidence Based Medicine: How to Practice and Teach EBM. 2nd ed. Edinburgh: Churchill Livingstone; 2000. 14. Palisano RJ, Campbell SK, Harris SR. Evidence-based decision making in pediatric physical therapy. In: Campbell SK, Vander Linden DW, Palisano RJ, eds. Physical Therapy jor Children. St. Louis: Saunders; 2006: 3-32. 15. Sackett DL. Rules of evidence and clinical recommendations on the use of antithrombotic agents. Chest. 1986;89:25-3S. 16. Fetters L, Figueiredo EM, Keane-Miller D, et al. Critically appraised topics. Pediatr Phys Ther. 2004;16:19-21. 17. Feinstein AR. Clinimetrics. Westford, MA: Murray Printing Company; 1987. 18. Marx RG, Bombardier C, Wright JG. What do we know about the reliability and validity of physical examination tests used to exam ine the upper extremity? j Hand Surg. 1999;24A:185-193. 19. Roach KE, Brown MD, Albin RD, et al. The sensitivity and speci ficity of pain response to activity and position in categorizing patients with low back pain. Phys Ther. 1997;77:730--738. 20. Domholdt E. Physical Therapy Research: Principles and Applications. Philadelphia: Saunders; 1993. 21. Feinstein AR. Clinical biostatistics XXXI: on the sensitivity, speci ficity & discrimination of diagnostic tests. Clin Pharmacol Ther. 1975;17:104-116. 22. Anderson MA, Foreman n. Return to competition: functional rehabilitation. In: Zachazewski JE, Magee DJ, Quillen WS, eds. Athletic Injuries and Rehabilitation. Philadelphia: Saunders; 1996: 229-261. 23. Jull GA. Physiotherapy management of neck pain of mechanical origin. In: Giles LGF, Singer KP, eds. Clinical Anatomy and Management oj Ceroical Spine Pain. The Clinical Anatomy oj Back Pain. London: Butterworth-Heinemann; 1998: 168--191. 24. Wright JG, Feinstein AR. Improving the reliability of orthopaedic measurements. j Bone joint Surg. 1992;74B:287-291. 25. Haas M. Statistical methodology for reliability studies. j Manip Physiol Ther. 1991;14:119-132. 26. Cooperman JM, Riddle DL, Rothstein JM. Reliability and validity of judgments of the integrity of the anterior cruciate ligament of the knee using the Lachman's test. Phys Ther. 1990;70:225-233. 27. Shields RK, Enloe LJ, Evans RE, et al. Reliability, validity, and respon siveness of functional tests in patients with total joint replacement. Phys Ther. 1995;75:169. 28. Laslett M, Williams M. The reliability of selected pain provocation tests for sacroiliac joint pathology. Spine. 1994;19:1243-1249.
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Comprehension Questions
1. Explain the differences between a sample and a population. 2. In the following statement, determine whether adescriptive or inferential statistic has been used. In the year 2010,148 million Americans will be enrolled in an HMO. 3. In the following statement, determine whether adescriptive or inferential statistic has been used. The national average annual medicine expenditure per person is $1058.
4. Classify each of the following as nominal-level, ordinal-level, interval-level, or ratio level measurements: pages in the city of Pittsburgh telephone book, weights of air humidifiers, ages of students in a classroom.
5. Which of the following variables is qualitative? A. Number of cars sold in one year by a local dealer. B. limes it takes to perform an ultrasound. C. Colors of theraband in a PT department. D. Capacity in cubic feet of Hubbard tank. 6. Which of the following variables is continuous? A. Water temperatures of three whirlpools in the PT department. B. Number of ultrasound treatments provided each day by the physical therapy department. C. The number of staff members in the department. D. Whether the members of staff are male or female.
7. Name the four basic sampling methods. 8. In the following example, name the type of sampling that is being used: every seventh patient entering a physical therapy department. 9. True or false: Probability is used as a basis for inferential statistics. A. True. B. False. 10. The number of absences per year that a worker has is an example of what type of data? 11. A researcher divided subjects into two groups according to gender and then selected members from each group for his sample. What sampling method was the researcher using? 12. What is the name of the graph that is used to investigate whether or not two variables are related? 13. True or false: Frequency distributions can aid the researcher in drawing charts and graphs. A. True. B. False.
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14. True or false: Data collected over a period of time can be graphed by using a pie graph. A. True. B. False. 15. What is another name for the ogive? 16. What graph should be used to show the relationship between the parts and the whole? 17. Data such as blood types can be organized into what type of frequency distribution? 18. For the situation where the most typical case is desired, which measure of central tendency-meaning, median, or mode-should be used? 19. If the mean of five values is 64, find the sum of the values. 20. Find the mean of 10, 20, 30, 40, and 50. 21. What is the relationship between variance and standard deviation? 22. True or false: In a data set, the mode will always be unique. A. True. B. False. 23. Why is the standard normal distribution important in statistical analysis? 24. What is the total area under the standard normal distribution curve? 25. What percentage of the area falls below the mean? Above the mean? 26. About what percentage of the area under the normal distribution curve falls within one standard deviation above and below the mean? 27. You decide to use agroup of healthy college student volunteers to study the effects of BAPS board exercises on ankle ROM and balance scores. Twenty volunteers partici pate in the 20-minute exercise sessions 3 times a week for 6 weeks. Measurements are taken at the beginning and end of the sessions. At the conclusion of the study, significant differences were found in both sets of scores. Based on this research design, you conclude that: A. The validity of the study was threatened with the introduction of sampling bias. B. BAPS board exercises are an effective intervention to improve ankle stability fol lowing chronic ankle sprain. C. The reliability of the study was threatened with the introduction of systematic error of measurement. D. The Hawthorne effect may have influenced the outcome of the study. 28. A valid informed consent for research purposes must include all of the following ele ments except: A. A statement ensuring the subject's commitment to participate for the duration of the study. B. An understandable explanation of the purpose and procedures to be used. C. All reasonable and foreseeable risks and discomforts. D. All potential benefits of participation.
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29. A study of the local population was necessary to determine the need for a new phys ical therapy center in the area. The researchers performing the study divided the pop ulation by sex and selected a random sample from each group. This is an example of what type of random sample? A. Systematic random sample. B. Random cluster sample. C. One-stage cluster sample. D. Stratified random sample. 30. You read a clinical study investigating the relationship between ratings of perceived exertion (RPE) and type of exercise: arm isokinetics versus leg isokinetics. The study reports a correlation of 0.55 with the arm isokinetics and a correlation of 0.80 with the leg isokinetics. From these findings, you could determine: A. Leg isokinetic exercises are highly correlated with RPE while arm isokinetic exer cises are only moderately correlated. B. Both arm and leg isokinetic exercises are only moderately correlated with RPE. C. Both arm and leg isokinetic exercises are highly correlated with RPE. D. The common variance of both types of testing is only 25%.
Answers 1. A population is the totality of all subjects possessing certain common characteristics that are being studied. A sample is a group of subjects selected from apopulation. 2. Inferential.
3. Descriptive. 4. All are ratio-level measurements-they are measured relative to atrue zero point, as opposed to an arbitrary zero point. 5. The answer is C. 6. The answer is A.
7. Random, systematic, stratified, and cluster. 8. Systematic.
9. The answer is A. This statement is true. 10. Discrete. 11. Nominal. 12. Scatter plot or scatter diagram.
13. The answer is A. This statement is true. 14. The answer is B. This statement is false. 15. Cumulative frequency graph. 16. Pie graph.
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17. 18. 19. 20. 21.
25.
Categorical. Mode. 320. 30. The square root of the variance is the standard deviation. The answer is B. This statement is false. Many variables are normally distributed, and the distribution can be used to describe these variables. 1, or 100%. 50% of the area lies below the mean, and 50% of the area lies above the mean.
26. 27. 28. 29. 30.
68%. The answer is A. The answer is A. The answer is D. The answer is A.
22.
23.
24.
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Education
There are probably as many ways to teach as there are to learn. Learning refers to the ways people acquire, process, store, and apply new infor mation. To identify realistic goals, instructors must be skilled in assessing a patient's readiness or a patient's progress toward goals.
MOTIVATION One of the most important basic learning principles to understand is that motivation plays a critical role, and that success is more predictably motivating than failure (Table 4-1). Basic principles of motivation exist that are applicable to learning in any situation. ~ ~
~
~
~
The environment can be used to focus the patient's attention on what needs to be learned. Interesting visual aids, such as booklets, posters, or practice equip ment, motivate learners by capturing their attention and curiosity. Incentives, including privileges and receiving praise from the educator, motivate learning. Both affiliation and approval are strong motivators. Internal motivation is longer lasting and more self-directive than is external motivation, which must be repeatedly reinforced by praise or concrete rewards. However, some individuals have lit tle capacity for internal motivation and must be guided and reinforced constantly. Learning is most effective when an individual is ready to learn, that is, when one wants to know something.
MASLOW'S HIERARCHY OF NEEDS Maslow's hierarchy of needs is based on the concept that there is a hier archy of biogenic and psychogenic needs that humans must progress through. Maslow hypothesizes that the higher needs in this hierarchy only come into focus once all the needs that are lower down in the 133
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TABLE 4-1. LEARNING TIIEORIES
TIIEORY Algo-heuristic
Androgeny (adult learning)
Adult learning
PRINCIPLE ELEMENTS Identifying the mental processes (conscious and subconscious) that underlie expert learning, thinking and performance in any area. All cognitive activities can be analyzed into operations of an algorithmic, semi-algOrithmic, heuristic, or semi-heuristic nature. Teaching students how to dL~cover processes is more valuable than providing them already formulated. Adults need to know why they need to learn something. Adults need to learn experientially. Adults approach learning as problem-solving. Adults learn best when the topic is of immediate value.
Integrates other theoretical frameworks for adult learning such as andragogy (Knowles), experiential learning (Rogers), and lifespan psychology. Consists of two classes of variables: personal characteristics (aging, life phases, and developmental stages) and situational characteristics (part-time versus full-time learning, and voluntary versus compulsory learning).
STRATEGIES
PROMINENT TIIEORISTS
CLINICAL APPLICATION
Once discovered, the operations and their systems can serve as the basis for instructional strategies and methods.
1. Landa
Performing a task or solving a problem always requires a certain system of elementary knowledge of units and operations.
There is a need to explain why specific things are being taught (e.g., certain commands, functions, operations, etc.). Instruction should be task-oriented instead of memorization; learning activities should be in the context of common tasks to be performed. Instruction should take into account the wide range of different backgrounds of learners; learning materials and activities should allow for different levels/types of previous experience with computers. Since adults are self-directed, instruction should allow learners to discover things for themselves, providing guidance and help when mistakes are made. The three dimensions of personal characteristics (affect, cognition, and behavior) must be taken into consideration. Aging results in the deterioration of certain sensory-motor abilities (e.g., eyesight, hearing, reaction time) while intelligence abilities (e.g., decision-making skills, reasoning, and vocabulary) tend to improve.
M. Knowles
Can be applied to any form of adult learning. Has been used extensively in the design of organizational training programs.
K.P. Cross
Adult learning programs should capitalize on the experience of participants. Adult learning programs should adapt to the aging limitations of the participants. Adults should be challenged to move to increasingly advanced stages of personal development. Adults should have as much choice as possible in the availability and organiza tion of learning programs.
Learning is a function of a change Behaviorist (stimulus-response in overt behavior. theory)--operant Changes in behavior are the result of an conditioning individual's response to events (stimuli) and their consequences that occur in the environment. The response of one behavior becomes the stimulus for the next response. Learning occurs when an individual engages in specific behaviors in order to receive certain consequences (learned association). Behavior can be controlled or shaped by operant conditioning. Desired or correct behaviors are identified so that frequent and scheduled reinforcements (positive reinforcement) can be given to reinforce the desired behaviors. Negative behaviors are ignored (negative reinforcement) so that these behaviors become weakened to the pOint where they disappear (extinction). First model of learning to be studied Classical conditioning in psychology. Demonstrate the environment's control over behavior. Type of associative learning. Relates the capacity of animals/humans to learn new stimuli and connect them to natural reflexes, allowing non-natural cues to elicit a natural reflex. The conditioned stimulus, or conditional stimulus, is an initially neutral stimulus that elicits a response-known as a conditioned response that is learned by the organism. Conditioned stimuli are associated psychologically with conditions such as anticipation, satisfaction (both immediate and prolonged), and fear. The relationship between the conditioned stimulus and conditioned response is known as the conditioned (or conditional) reflex. The process by which an individual learns to associate an unconditional stimulus with a conditional stimulus but receives no benefit from doing so.
Positive reinforcement is used through the use of rewards that are meaningful to the individual. Timing of Reinforcement ~ Continuous reinforcement: a behavior is reinforced every time it occurs. ~ Partial reinforcement: a behavior is reinforced intermittently. ~ Fixed interval: the period of time between the occurrences of each instance of reinforcement is fixed or set. ~ Variable interval: the period of time between the occurrences of each instance of reinforcement varies around a constant average.
B.P. Skinner, G. Watson
Limited clinical use: behavior modification techniques may be used when working with adults with impaired or limited cognitive abilities or young children. Repetition is a necessary prerequisite for learning.
Therapies associated with classical conditioning are aversion therapy, flooding, systematic desensitization, and implOSion therapy. Much of what we like or dislike is a result of classical conditioning.
I. Pavlov, ].B. Watson
These techniques have been criticized for being unethical since they have the potential to cause trauma. Perhaps the strongest application of classical conditioning involves emotion. Common experience and careful research both confirm that human emotion conditions vary rapidly and easily, particularly when the emotion is intensely felt or negative in direction; then it will condition quickly.
(Continued)
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TABLE 4-1. LEARNING THEORIES (Continued)
C'
THEORY Cognitive dissonance
Cognitive flexibility
PRINCIPLE ELEMENTS There is a tendency for individuals to seek consistency among their cognitions (i.e., beliefs, opinions). When there is an inconsistency between attitudes or behaviors (dissonance), something must change to eliminate the dissonance. In the case of a discrepancy between attitudes and behavior, it is most likely that the attitude will change to accommodate the behavior. Focuses on the nature of learning in complex and ill-structured domains. Emphasis is placed upon the presentation of information from multiple perspectives and use of many case studies that present diverse examples. Effective learning is context-dependent. Stresses the importance of constructed knowledge; learners must be given an opportunity to develop their own representations of information in order to properly learn.
Cognitive load
Learning happens best under conditions that are aligned with human cognitive architecture. The contents of long-term memory are sophisticated structures (schema) that permit us to perceive, think, and solve problems, rather than a group of rote learned facts. Schemas are acquired over a lifetime of learning, and may have other schemas contained within themselves. The difference between an expert and a novice is that a novice hasn't acquired the schemas of an expert.
Constructivist theory
Learning is an active process in which learners construct new ideas or concepts based upon their current/past knowledge.
STRATEGIES
PROMINENT THEORISTS
There are three ways to eliminate L. Festinger dissonance: 1. Reduce the importance of the dissonant beliefs. 2. Add more consonant beliefs that outweigh the dissonant beliefs. 3. Change the dissonant beliefs so that they are no longer inconsistent. Learning activities must provide R. Spiro, multiple representations of content. P. Feltovitch, Instructional materials should avoid R. Coulson oversimplifying the content domain and support context-dependent knowledge. Instruction should be case-based and emphasize knowledge construction, not transmission of information. Knowledge sources should be highly interconnected rather than compartmentalized. Change problem-solving methods J. Sweller to use goal-free problems or worked examples. Eliminate the working memory load associated with having to mentally integrate several sources of information by physically integrating those sources of information. Eliminate the working memory load associated with unnecessarily processing repetitive information by reducing redundancy. Increase working memory capacity by using auditory as well as visual information under conditions where both sources of information are essential (i.e., nonredundant) to understanding. Instruction must be concerned with J. Bruner the experiences and contexts that make the student willing and able to learn (readiness).
CLINICAL APPLICATION Dissonance theory is especially relevant to decision-making and problem-solving.
Limited: cognitive flexibility theory is especially formulated to support the use of interactive technology.
Cognitive load theory has many implications in the design of learning materials such as handouts and home exercise programs.
Much of this theory is linked to child development.
Cognitive structure (Le., schema, mental models) provides meaning and organization to experiences and allows the individual to "go beyond the information given."
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Experiential learning
Two types of learning: 1. Cognitive (meaningless): academic knowledge such as learning vocabulary or multiplication tables. 2. Experiential (significant): applied knowledge such as personal change and growth.
Genetic epistemology
Cognitive structures (i.e., development stages) are patterns of physical or mental action that underlie specific acts of intelligence and correspond to stages of child development. There are four primary cognitive structures: 1. Sensorimotor stage (0-2 years): intelligence takes the form of motor actions. 2. Preoperation period (3--7 years): intelligence is intutive in nature. 3. Concrete operational stage (8-11 years): cognition is logical but depends upon concrete referents. 4. Formal operations (12-15 years): thinking involves abstractions.
Modes of learning
Three modes of learning: 1. Accretion: the addition of new knowledge to existing memory. The most common form of learning. 2. Structuring: involves the formation of new conceptual structures or schema. 3. Tuning: the adjustment of knowledge to a specific task, usually through practice. The slowest form of learning. Accounts for expert performance.
Instruction must be structured so that it can be easily grasped by the student (spiral organization). Instruction should be designed to facilitate extrapolation and or fill in the gaps (going beyond the information given). Significant learning takes place when the subject matter is relevant to the personal interests of the student. Learning that is threatening to the self (e.g., new attitudes or perspectives) is more easily assimilated when external threats are at a minimum. Learning proceeds faster when the threat to the self is low. Self-initiated learning is the most lasting and pervasive. Children will provide different explanations of reality at different stages of cognitive development. Cognitive development is facilitated by providing activities or situations that engage learners and require adaptation (i.e., assimilation and accomodation). Learning materials and activities should involve the appropriate level of motor or mental operations for a child of given age; avoid asking students to perform tasks that are beyond their current cognitive capabilities. Use teaching methods that actively involve students and present challenges. Instruction must be designed to accommodate different modes of learning.
C. Rogers
Applies primarily to adult learners and adult learning.
J. Piaget
The theory has been applied extensively to teaching practice and curriculum design in elementary education.
D. Rumelhart, Multiple applications to D. Norman physical therapy general model for human learning.
Practice activities affect the refmement of skills but not necessarily the initial acquisition of knowledge.
(Continued)
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TABLE 4-1. LEARNING TI-lEORIES (Continued)
TI-lEORY Humanist
Social learning
PRINCIPLE ELEMENTS Emphasis placed on personal freedom and dignity of the individual and the learner's needs and feelings during the learning process. The learner experiences unconditional positive regard, acceptance, and understanding. Promotes active learning rather than passive. Social learning theory emphasizes the importance of observing and modeling the behaviors, attitudes, and emotional reactions of others. Social learning theory explains human behavior in terms of continuous reciprocal interaction between cognitive, behaVioral, and environmental influences.
STRATEGIES Teacher must function as a facilitator and resource finder.
PROMINENT TI-lEORISTS A.H. Maslow
Used in clinical situations that emphasize self discovery, self appropriated learning, and experimental learning.
A. Bandura
Applied extensively to the understanding of aggression and psychological disorders, particularly in the context of behavior modification.
Learning must address relevant problems and issues. The highest level of observational learning is achieved by first organiZing and rehearsing the modeled behavior symbolically and then enacting it overtly. Coding modeled behavior into words, labels, or images results in better retention than simply observing. Individuals are more likely to adopt a modeled behavior if it results in outcomes they value, or if the model is similar to the observer and has admired status and the behavior has functional value.
CLINICAL APPLICATION
CHAPTER 4. EDUCATION
pyramid are mainly or entirely satisfied. Maslow's hierarchy is often depicted as a pyramid consisting of five levels (Fig. 4-1). The lower lev els (from bonom to top: physiologic and safety needs) are referred to as defiCiency needs, while the top three levels (from bonom to top: lovelbelonging, status, and self-actualization needs) are referred to as a being needs. According to Maslow, in order for an individual to progress up the hierarchy to the being needs, his or her deficiency needs must be met. Growth forces create upward movement in the hierarchy, whereas regressive forces create downward movement in the hierarchy.
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5. Actualization 4. Status (esteem)
LEARN ING TH EORI ES
3. Love/belonging 2. Safety 1. Physiological (biological needs)
The following provides a synopsis on the various theories of learning.
Figure 4-1. Maslow's hierarchy of needs.
DOMAINS Of LEARNING
Educational Activities. Bloom! identified three domains of educational activities: ~
Cognitive: mental skills (knowledge). Involves knowledge and the development of intellectual skills. Includes the recall or recognition of specific facts, proce dural panerns, and concepts that serve in the development of intellectual abilities and skills. There are six major categories (degrees of difficulties) starting from the simplest behavior to the most complex, with the first one having to be mastered before the next one can take place (Table 4-2).
TABLE 4-2. COGNITIVE DOMAIN CATEGORY Knowledge: Recall data or information.
Comprehension: Understand the meaning, translation, interpolation, and interpretation of instructions and problems. Application: Use a concept in a new situation or unprompted use of an abstraction. Apply what was learned in the classroom into novel situations in the workplace. Analysis: Separate material or concepts into component parts so that the organizational structure may be understood. Distinguish between facts and inferences. SynthesL~: Build a structure or pattern from diverse elements. Put parts together to form a whole, with emphasL~ on creating a new meaning or structure. Evaluation: Make judgments about the value of ideas or materials.
EXAMPLES AND KEYWORDS Able to recite a poem; quote prices from memory. Keywords: defmes, identifies, labels, lists, matches, recalls, recognizes, reproduces, selects. Able to rewrite a policy and procedures manual; can explain the steps for performing a complex task. Keywords: comprehends, distinguishes, estimates, interprets, paraphrases, predicts, summarizes. Can use a manual to set up a DVD player can apply the laws of statistics to evaluate a research study. Keywords: applies, computes, constructs, demonstrates, manipulates, modifies, operates, prepares, produces, relates, shows, solves. Can fix a piece of exercise equipment by using logical deduction; can gather information and select the required tasks for staff training. Keywords: analyzes, breaks down, compares, contrasts, differentiates, distinguL~hes, identifies, illustrates, infers, outlines, separates. Can design or revise a process to perform a specific task; is able to integrate training from several sources to solve a problem. Keywords: categorizes, combines, compiles, composes, creates, devises, designs, generates, modifies, rearranges, reconstructs, reorganizes, summarizes. Can select the most effective solution; hire the most qualified candidate; explain and justify a new budget. Keywords: appraises, compares, concludes, contrasts, critiques, discriminates, interprets, justifies, summarizes.
Data from www.nwlink.com/-donclarklhrdlbloom.html.
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TABLE 4-3. AFFECTIVE DOMAIN: THE FIVE MAJOR CATEGORIES (LISTED FROM THE SIMPLEST BEHAVIOR TO THE MOST COMPLEX) CATEGORY Receiving phenomena: Awareness, willingness to hear, selected attention.
Responding to phenomena: Active participation on the part of the learner. Learning outcomes may emphasize compliance in responding, willingness to respond, or satisfaction in responding (motivation). Valuing: The worth or value a person attaches to a particular object, phenomenon, or behavior.
Organization: Organizes values into priorities by contrasting different values, resolving conflicts between them, and creating a unique value system.
InternaliZing values (characterization): Has a value system that controls their behavior. The behavior is pervasive, consistent, predictable, and most importantly, characteristic of the learner. Instructional objectives are concerned with the patient's general patterns of adjustment (personal, social, emotional).
EXAMPLE AND KEYWORDS Able to listen to others with respect; listens for and remember the names of newly introduced people. Keywords: chooses, describes, follows, identifies, locates, names, points to, selects. Is an active participant in discussions; able to present an inservice; asks many questions about new ideas and concepts in order to fully understand them. Keywords: answers, assists, complies, conforms, discusses, labels, performs, practices, reads, recites, reports, tells, writes. Is sensitive towards individuals and the various cultural differences; informs management on matters that one feels strongly about. Keywords: completes, demonstrates, differentiates, initiates, invites, joins, justifies, proposes, reports, selects, shares. Able to recognize the need for balance between freedom and responsible behaVior; accepts professional ethical standard~; prioritizes time effectively to meet the needs of the organization, family, and self. Keywords: adheres, alters, arranges, combines, compares, completes, defends, generalizes, identifies, integrates, modifies, organizes, relates, synthesizes. Demonstrates self-reliance and can work independently, but also cooperates in group activities as a team player; uses an objective approach in problem-solving; values people for what they are, not how they look. Keywords: discriminates, displays, influences, listens, modifies, performs, proposes, qualifies, questions, revises, solves, verifies.
Data from www.nwlink.com/-donclarklhrd/bloom.html.
~
~
Affective: growth in feelings or emotional areas (attitude) (Table 4-3), Includes the manner in which matters are dealt with from an emotional aspect. Includes feelings, values, appreciation, enthusiasms, motiva tions, and attitudes. Psychomotor: manual or physical skills (skills). Includes physical movement, coordination, and use of the motor-skill areas. Development of these skills requires practice and is measured in terms of speed, precision, distance, procedures, or tech niques in execution. The seven major categories listed the Simplest behavior to the most complex (Table 4-4).
Decision-Making. Both at a personal level and in the context of organizations, decision-making skill strongly affects the quality of life and success. A major focus of research on decision-making is the fre quent departure from purely rational choices. Most theories accept the idea that decision-making consists of a number of steps or stages such as recognition, formulation, the generation of alternatives, an information search, and then selection and action. Furthermore, it is well recognized that routine cognitive processes such as memory,
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TABLE 4-4. PSYCHOMOTOR DOMAIN CATEGORY Perception: The ability to use sensory cues to guide motor activity.
Set: Readiness to act; includes mental, physical, and emotional sets. Guided response: The early stages in learning a complex skill that includes imitation and trial and error. Mechanism: The intermediate stage in learning a complex skill.
Complex overt response: The skillful performance of motor acts that involve complex movement patterns in a quick, accurate, and highly coordinated manner and with a minimum expenditure of energy. Adaptation: Skills are well developed and the individual can modify movement patterns to fit special requirements. Origination: Can create new movement patterns to fit a particular situation or specific problem.
EXAMPLES AND KEYWORDS Able to detect nonverbal communication cues; can estimate where a moving ball will land and can move to the correct location to catch the ball. Keywords: chooses, detects, differentiates, distinguishes, identifies, isolates, relates, selects. Knows and acts upon a sequence of steps in a construction process; is able to recognize own abilities and limitations. Keywords: initiates, displays, explains, proceeds, reacts, states, volunteers. Can perform an exercise as demonstrated; follows instructions well. Keywords: copies, traces, follows, reproduces. Can use a personal computer effectively; able to perform simple DIY projects at home; can drive a car. Keywords: assembles, calibrates, constructs, dismantles, fixes, manipulates, measures, mends, organizes. Can parallel park a car into a tight spot; displays skill and competence while playing sports. Keywords: the same as for Mechanism, except that the performance is quicker, better, more accurate, etc. Responds effectively to unexpected experiences; able to modify instructions to meet the needs of the learners. Keywords: adapts, alters, changes, rearranges, reorganizes, revises, varies. Able to independently develop a new and comprehensive training program, or exercise protocol. Keywords: arranges, builds, combines, composes, constructs, creates, deSigns, initiates.
Data from www.nwlink.com/-donclarklhrdlbloom.html.
reasoning, and concept formation play a primary role in decision making. The study of attitudes, creativity, and problem-solving is closely associated with decision-making. In addition, decision-making behavior is affected (usually adversely) by anxiety and stress.
Problem-Solving. Problem-solving skills appear to be related to many other aspects of cognition such as schema (the ability to remem ber similar problems), pattern recognition (recognizing familiar prob lem elements), and creativity (developing new solutions). The issue of transfer is highly relevant to problem-solving. Sensory Motor Learning. Motor skills can be classified as con tinuous (e.g., tracking), discrete, or procedural movements (e.g., typing). Behavioral psychology emphasizes practice variables in sensory-motor skills such as massed (concentrated--eoncentrating the learning or practice in a short period of time) versus spaced (distributed-spreading out the learning or practice over a longer period of time) practice; part versus whole task learning; and feedback/reinforcement schedules. Long-term retention of motor skills depends upon regular practice; however, continuous responses show less forgetting in the absence of practice than discrete or procedural skills. Repetition after task profi ciency is achieved (overtraining) and refresher training reduce the
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effects of forgetting. Unlike verbal learning, sensory-motor learning appears to be the same under massed and spaced practice. Learning and retention of sensory-motor skills is improved by both the quantity and quality of feedback (knowledge of results) during training. Two ways in which learning/teaching of motor skills can be facil itated include: 1. Slowing down the rate at which the information is presented. 2. Reducing the amount of information that needs to processed. There is evidence that mental rehearsal, especially involving imagery, facilitates performance. This may be because it allows addi tional memory processing related to physical tasks (e.g., the forma tion of schema) or because it maintains arousal or motivation for an activity.
Study Pearl LEARNING STYLES There are several different theories regarding learning styles, including those proposed by lung, Witkin, Kolb and Barbe, and Swassing. Litzinger and Osif2 briefly describe each theory. However, as the authors point out, it would be impossible to incorporate every learning theory into every session, and therefore each clinician might choose to focus on one. Litzinger and Osif focus mainly on the 4MAT theory of David Kolb as adapted by Bernice McCarthy: ~
~
~
~
Accommodators. This type of learner looks for the significance of the learning experience. These learners enjoy being active participants in their learning, and will ask many questions such as "What ill" and "Why not?" Divergers. This type of learner is motivated to discover the relevancy of a given situation, and prefers to have infor mation presented in a detailed, systematic, and reasoned manner. Assimilator. This type of learner is motivated to answer the question, "what is there to know?" They like accurate, organ ized delivery of information and they tend to respect the knowledge of the expert. These learners are perhaps less "instructor intensive" than some other learning styles. They will carefully follow prescribed exercises, provided a resource per son is clearly available and able to answer questions. Convergers are motivated to discover the relevancy or "how" of a situation. The instructions given to this type of learner should be interactive, not passive.
Another series of learning styles that are used frequently was devised by Taylor,3 who proposed that there are three common learn ing styles: ~
~
Visual. As the name suggests, the visual learner assimilates infor mation by observation, using visual cues and information such as pictures, anatomic models, and physical demonstrations. Auditory. Auditory learners prefer to learn by having things explained to them verbally.
CHAPTER 4. EDUCATION ~
Tactile. Tactile learners, who learn through touch and interac tion, are the most difficult of the three groups to teach. Close supervision is required with this group until they have demon strated to the clinician that they can perform the exercises cor rectly and independently. PNF techniques, with the emphasis on physical and tactile cues, often work well with this group.
Bicknell-Holmes and Hoffman4 describe a variety of teaching methods that would appeal to most learning styles. These techniques involve active or discovery learning-the patient is able to actively par ticipate in the learning process, which is in direct contrast with a teach ing method like lecturing, where the patient is a passive observer. Discovery learning has certain attributes: ~ ~ ~
~
Emphasizes learning over content.
Uses failure as an opportunity to learn.
More is learned by doing than by watching.
Involves patients in higher levels of cognitive processing.
Some of the methods of discovery learning include the following. ~
~
~
~
~
~
~
~
Case-based learning: a fairly common active learning strategy in which the patients are able to participate in the decision making or problem-solving process. Incidental learning: learning is linked to game-like scenarios. Learning by exploring: a collection of questions and answers on a particular topic are organized into a system and patients can explore the various topics at their own pace. Learning by reflection: a type of active learning that involves higher-level cognitive skills. Patients are expected to model certain skills or concepts that they have acquired through their instructor or through another system of learning. Simulation-based learning: the clinician creates an artificial environment in which patients can practice skills or apply con cepts that they have learned, without the pressure of a real world situation. Real-life examples: using real-life problems and examples in a variety of scenarios (buying a house!car, using a bus schedule, etc.). Relevant instruction: instruction should be practical and the examples and exercises should be important and meaningful to the patients, because patients often need to know why they need to learn a particular skill or concept, or how it will be use ful to them in their everyday lives. Humor: to help keep the patients engaged and interested and to make their sessions more enjoyable.
Analytical Learner. The analytical/objective learner processes information in a step-by-step order, perceives information in an objec tive manner, and is able to use facts and easily understand the rela tionships between them. This type of learner perceives information in an abstract, conceptual manner; information does not need to be related to personal experience. As this type of learner may have diffi culty comprehending the big picture, a step-by-step learning process with some form of structure is recommended.
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Intuitive/Global Learner. The intuitive/global leaner processes information all at once, and not in an ordered sequence. Global learn ers are spontaneous and intuitive, and tend to learn in layers, absorbing material almost randomly without seeing connections, and then sud denly "getting it." The learning of this type reflects personal life expe riences and is thus subjective. As this type of learner tries to relate the subject matter to things he or she already knows, information needs to be presented in an interesting manner using attractive materials. Reasoning: Inductive Versus Deductive Reasoning. Inductive and deductive reasoning are two methods of logic used to arrive at a conclusion based on information assumed to be true. Both are used in research to establish hypotheses. 1. Deductive reasoning: involves a hierarchy of statements or truths and the arrival at a specific conclusion based on generalizations. 2. Inductive reasoning: inductive reasoning is essentially the opposite of deductive reasoning. It involves trying to create general principles by starting with many specific instances.
Initiative: Active Versus Passive Learning 1. Active/aggressive learner: exhibits initiative, actively seeks information; may reach conclusions qUickly before all infor mation is gathered. 2. Passive learner: often exhibits little initiative; responds best to direct learning.
IMPROVING COMPLIANCE WITH LEARNING AND PARTICIPATION A number of factors have been outlined to improve compliance, including the following. 5 7 ~ ~
~ ~ ~
~ ~ ~
Involving the patient in the intervention planning and goal setting. Realistic goal setting for both short- and long-term goals. Promoting high expectations regarding final outcome. Promoting perceived benefits. Projecting a positive attitude. Providing clear instructions and demonstrations with appro priate feedback. Keeping the exercises pain-free or with a low level of pain. Encouraging patient problem-solving.
COMMUNITY AND STAFF EDUCATION The strengths and weaknesses of various teaching methods when pre senting community education programs, or when educating staff, are outlined in Table 4-5.
USING VISUAL AIDS A number of guidelines when using visual aids are outlined in Table 4-6.
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TABLE 4-5. TEACHING ME1HODS STRENG1HS
TEACHING ME1HOD Lecture
~
~
~
Presents factual material in direct, logical manner. Contains experience that inspires. Useful for large groups.
~ ~ ~ ~
Lecture with discussion
Panel of experts
Brainstorming
Videotapes/slides
Discussion
Small group discussion
~
Involves audience, at least after the lecture. ~ Audience can question, clarify, and challenge. ~ Allows experts to present different opinions. ~ Can provoke better discussion than a one-person discussion. ~ Frequent change of speaker keeps attention from lagging. ~ Listening exercise that allows creative thinking for new ideas. ~ Encourages full participation because all ideas equally recorded. ~ Draws on group's knowledge and experience. ~ Spirit of congeniality is created. ~ One idea can spark off other ideas. ~ Entertaining way of teaching content (colorful) and raising issues. ~ Keep group's attention. ~ Looks professional. ~ Stimulates discussion. ~ Demonstrates three dimensional movement. ~ Pools ideas and experiences from group. ~ Effective after a presentation, mm, or experience that needs to be analyzed. ~ Allows everyone to participate in an active process. ~ Allows participation of everyone. ~ People often more comfortable in small groups. ~ Can reach group consensus.
PREPARATION
WEAKNESSES
~ ~ ~ ~ ~
~ ~ ~
~
~
~ ~ ~
~ ~ ~ ~
~
~ ~
Experts are not always good teachers. Audience is passive. Learning is difficult to gauge. Communication is one way. Time may limit discussion period. Quality is limited to quality of questions and discussion. Experts may not be good speakers. Personalities may overshadow content. Subject may not be in logical order.
~ ~
~ ~
~
~
Can be unfocused. Needs to be limited to 5 to 7 minutes. People may have difficulty getting away from known reality. If not facilitated well, criticism and evaluation may occur.
~
Can raise too many issues to have a focused discussion. Discussion may not have full participation. Only as effective as following discussion. Can be expensive.
~
Not practical with more that 20 people. Few people can dominate. Others may not participate. Is time consuming. Can get off the track.
~
Needs careful thought as to purpose of group. Groups may get side tracked.
~
~
~
~
Needs clear inrroduction and summary. Needs time and content limit to be effective. Should include examples, anecdotes. Requires that questions be prepared prior to discussion.
Facilitator coordinates focus of panel, introduces, and summarizes. Briefs panel.
Facilitator selects issue. Must have some ideas if group needs to be stimulated.
Need to set up equipment. Effective only if facilitator prepares questions to discuss after the show.
Requires careful planning by facilitator to guide discussion. Requires question outline.
Need to prepare specific tasks or questions for group to answer.
(Continued)
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TABLE 4-5. TEACHING METIlODS (Continued)
Role-playing
Case studies
Guest speaker
WEAKNESSES
STRENGTIlS
TEACHING METIlOD ~
Introduces problem situation dramatically. ~ Provides opportunity for people to assume roles of others and thus appreciate another point of view. ~ Allows for exploration of solutions. ~ Provides opportunity to practice skills. ~ Develops analytic and problem-solving skills. ~ Allows for exploration of solutions for complex issues. ~ Allows patient to apply new knowledge and skills. ~ Personalizes topic. ~ Breaks down audience's stereotypes.
~
~ ~
~
~
~
PREPARATION
People may be too self conscious. Not appropriate for large groups. People may feel threatened.
~
People may not see relevance to own situation. Insufficient information can lead to inappropriate results.
~
May not be a good speaker.
~
~
~
~
Trainer has to defme problem situation and roles clearly. Trainer must give very clear instructions.
Case must be clearly defined in some cases. Case study must be prepared.
Contact speakers and coordinate. Introduce speaker appropriately.
Data from http://honolulu.hawaiLedu/intranet!committees/facdevcomiguidebk!teachtip!comteach.htm.
TABLE 4-6. GUIDELINES FOR TIlE USE OF VISUAL AIDS OVERHEADS ~
Use the most professional lettering available. ~ Use transparencies of one color only and secure transparencies to cardboard frames (if available). ~ Number each transparency. ~ Prior to the session, check overheads for readability of type size by audience at far end of room. Printing should be no smaller than 1/4 inches high. Information should be placed on the top two-thirds of the transparency. ~ Be familiar with the operation of the projector and make sure projector works. Have extra bulbs available. ~ While presenting, be certain neither you nor the projector blocks anyone's view. ~ Use a pencil rather than a finger to note a detail on the transparency. ~ If you have a list of points, black out all but the first point, and then move the cover sheet and one point at the time.
FLIPCHARTS ~ Choose
a chart size that is appropriate for the design, your height, and the size of the audience. ~ Draw the art to fit the vertical shape of the chart. ~ Make the lettering dark enough and large enough to be read by everyone in the audience. ~ During preparation, leave several blank pages between each one to allow for corrections and additions. For the fmal presentation, remove all but one blank page at the beginning so that you can turn to that blank page when there is no relevant visual. ~ Securely attach charts to the easel and adjust the easel height for the presentation. ~ When writing on the flipchart, don't speak to the chart.
SLIDES ~ ~
Slides should be used instead of flipcharts if the group is large. Design the visuals for continuous Viewing and as notes.
~ Maintain
continuity: have all slides horizontal or vertical, not mixed.
~
Allow sufficient production time. Place no more than 15 words per slide. ~ Use black or blue background with bright colors. ~ Check the position and order of the slide in the carousel or tray. ~ Use a conventional pointer. ~ Keep on as many lights as possible. ~
CHAPTER 4. EDUCATION
CULTURAL INFLUENCES It is important that clinicians are sensitive to cultural issues in their inter
actions with patients. Cultural influences shape the framework within which people view the world, define and organize reality, and function in their everyday life. In many cases, individuals group themselves on the basis of cul tural similarities, and as a result form cultural groups. Cultural groups share behavioral patterns, symbols, values, beliefs, and other charac teristics that distinguish them from other groups. At the group level, cultural differences are generally variations of differing emphasis or value placed on particular practices.
REFERENCES 1. Bloom BS. Taxonomy ofEducational Objectives, Handbook I The Cognitive Domain. New York: David McKay; 1956. 2. Litzinger ME, Osif B. Accommodating diverse learning styles: designing instruction for electronic information sources. In: Shirato L, ed. What is Good Instruction Now? Library Instruction for the 90s. Ann Arbor: Pierian Press; 1993. 3. Taylor ]A. A practical tool for improved communications. Supervision. 1998;59: 1&-19. 4. Bicknell-Holmes T, Hoffman PS. Elicit, Engage, Experience Explore: Discovery Learning in Library Instruction. Ref Serv Rev. 2000; 28:313-322. 5. Blanpied P. Why won't patients do their home exercise programs? ] Orthop Sports Phys Ther. 1997;25:101-102. 6. Chen CY, Neufeld PS, Feely CA, et al. Factors influencing compli ance with home exercise programs among patients with upper extremity impairment. Am] Occup Ther. 1999;53:171-180. 7. Friedrich M, Cermak T, Madebacher P. The effect of brochure use versus therapist teaching on patients performing therapeutic exer cise and on changes in impairment status. Phys Ther. 1996;76: 1082-1088.
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Comprehension Questions "I
1. Maslow's hierarchy of needs is based on what concept? 2. What is the lowest need according to Maslow? 3. What is the highest need according to Maslow? 4. According to the 4MAT theory, how do accommodators learn? 5. According to the 4MAT theory, how do convergers learn? 6. What are the three learning styles devised by Taylor?
7. Outline three factors that can be used to improve patient compliance 8. You have just returned from an inservice offering new treatment techniques in wound care and would like to share the information with interested members of the hospital staff. What is the best way to share this information? A. Prepare a handout and give it to the members of the hospital staff. B. Schedule a mandatory inservice during lunch for those hospital staff that partici pate in wound care. C. Post bulletins in view of all hospital staff and send memos to the department heads inviting everyone to attend an inservice during lunch. D. None of the above.
Answers 1. That there is a hierarchy of biogenic and psychogenic needs that humans must progress through. 2. Physiologic need. 3. Self-actualization. 4. This type of learner looks for the significance of the learning experience. 5. Convergers are motivated to discover the relevancy or "how" of a situation. 6. Visual, auditory, and tacti Ie.
7. Involving the patient in the intervention planning and goal setting, setting realistic short- and long-term goals, and promoting high expectations regarding final outcome. 8. The answer is C.
Fundamentals and Core Concepts
TISSUES OF THE BODY Based on morphology and function, the tissues of the body are classified into four basic kinds: epithelial, nervous, connective, and muscle tissue.! EPITHELIAL TISSUE
Epithelial tissue is found throughout the body in two forms: membra nous and glandular. ~
~
Membranous epithelium forms such structures as the outer layer of the skin, the inner lining of the body cavities and lumina, and the covering of visceral organs. Glandular epithelium is a specialized tissue that forms the secretory portion of glands.
NERVOUS TISSUE
Nervous tissue helps coordinate movements via a complex motor con trol system of prestructured motor programs and a distributed network of reflex pathways mediated throughout the CNS.2 CONNECTIVE TISSUE
Connective tissue (CT) is found throughout the body and serves to pro vide structural and metabolic support for other tissues and organs of the body. Connective tissue includes bone, cartilage, tendons, liga ments, and blood tissue. The CT types are differentiated according to the extracellular matrix that binds the cells!: ~ ~
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Embryonic CT. Connective tissue proper. • Loose CT. • Dense regular CT. 149
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Study Pearl ~ ~
~
~
• Dense irregular CT. • Elastic CT.
Reticular CT.
Adipose CT.
Cartilage and bone tissue.
• Hyaline cartilage. • Fibrocartilage. • Elastic cartilage.
Blood (vascular) tissue.
Connective Tissue Proper. Connective tissue proper (crP) has a loose, flexible matrix, called ground substance. The most common cell within CTP is the fibroblast. Fibroblasts produce collagen, elastin, and reticulin fibers. Collagen and elastin are vital constituents of the musculoskeletal system. Collagen. The collagens are a family of extracellular matrix proteins that play a dominant role in maintaining the structural integrity of var ious tissues and in providing tensile strength to tissues. The major forms of collagen are outlined in Table 5-1. 4 Elastin. Elastic fibers are composed of a protein called elastin. As its name suggests, elastin provides the tissues in which it is situated with elastic properties. Elastin fibers can stretch, but they normally return to their original shape when the tension is released. The elastic fibers of elastin determine the patterns of distension and recoil in most organs including the skin, lungs, blood vessels, and CT. Arrangement of Collagen and Elastin. Collagenous and elastic fibers are sparse and irregularly arranged in loose CT, but are tightly packed in dense CT. 5 ~
Fascia is an example of loose CT.
~ Tendons and ligaments are examples of dense regular CT. 6
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Fascia. Fascia is viewed as the CT that provides support and protec tion to the joint, and acts as an interconnection between tendons aponeurosis, ligaments, capsules, nerves, and the intrinsic components of muscle. 7 •B This type of CT may be categorized as fibrous or nonfi brous, with the fibrous components consisting mainly of collagen and elastin fibers, and the nonfibrous portion consisting of amorphous ground substance, which is a viscous gel composed of long chains of carbohydrate molecules (GAG) bound to a protein and water. 9
Tendons and Ligaments.
Histologically, tendons and ligaments are similar in composition-they are densely packed CT structures that consists largely of directionally oriented, high tensile strength colla gen. lO Due to their function as supporting cables in an environment of high tensile forces, ligaments and tendons must be relatively inextensi ble to minimize transmission loss of energy. The collagen structural organization of tendons and ligaments is similarY Both are mostly type I collagenY The fibers are arranged in a quarter-stagger arrangement, which gives collagen its characteristic band ing pattern and provides high strength and stability. A loose connective tissue matrix surrounds the bundles of collagen fibrils. Bundles of
CHAPTER 5. FUNDAMENTALS AND CORE CONCEPTS
collagen and elastin combine to form a matrix of CT fascicles. This matrix is organized within the primary collagen bundles as well as between the bundles that surround them. 13
Tendons. Tendons are cordlike structures that function to attach mus cle to bone and to transmit the forces generated by muscles to bone in order to achieve movement or stability of the body in space. 13 The thickness of each tendon varies and is proportional to the size of the muscle from which it originates. Within the fascicles of tendons, the collagen components are uni directionally oriented. The fascicles are held together by a loose CT called endotenon. Endotenon contains blood vessels, lymphatics, and nerves, and permits longitudinal movements of individual fascicles when tensile forces are applied to the structure. The CT surrounding groups of fascicles and/or the entire structure is called the epitenon. ~
~
Gliding tendons, such as the flexor tendons of the hand, are enclosed by a tendon sheath with discrete parietal (inside sur face of the sheath) and visceral (epitenon or outside layer of the tendon) synovium layers. These tendons receive vascular access only through vincula-small loose, flexible strips of CT that connect with the mesotenon and paratenon, the loose con nective tissues around the sheath. 13 Vascular tendons are surrounded by a peritendinous CT paratenon, which is connected to the epitenon. If there is syn ovial fluid between these two layers, the paratenon is called tenosynovium; if not, it is termed tenovagium. 13
As the tendon joins the muscle, it fans out into a much wider and thinner structure. The site where the muscle and tendon meet is called the myotendinous junction (MTJ). Despite its viscoelastic mechanical characteristics, the MTJ is very vulnerable to tensile failure. 14,15 Tendon injuries. Tendon injuries account for up to half of all sports related injuries. Both extrinsic and intrinsic forces can cause injuries to tendons. ~
~
Extrinsic factors may include training errors, training surfaces, environmental conditions, footwear, and improper or faulty equipment. Intrinsic causes are due to an athlete's body alignment, muscle imbalances, or structural deformities.
Tendonitis is an inflammatory condition characterized by pain at tendinous insertions into bone. More specifically, it is the sympto matic degeneration of the tendon with vascular disruption and inflam matory repair. Tendonopathy is the current umbrella term applied to sports-related tendon injuries that cause pain, swelling, and impaired performance. Common sites of tendonopathy include the rotator cuff of the shoulder e.g., supraspinatus, bicipital tendons), insertion of the wrist extensors (e.g., lateral epicondylitis, tennis elbow) and flexors (e.g., medial epicondylitis) at the elbow, patellar and popliteal tendons and iliotibial band at the knee, insertion of the posterior tibial tendon in the leg (e.g., shin splints), and the Achilles tendon at the heel.
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TABLE 5-1. MAJOR TYPES OF COLLAGEN TYPE
I II III IV
LOCATION
Bone, skin, ligament, and tendon Cartilage, nucleus pulposus Blood vessels, gastrointestinal tract Basement membranes
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SECTION I. THE PROFESSION
TABLE 5-2. MAJOR LIGAMENTS OF TIlE UPPER QUADRANT JOINT Shoulder complex Glenohumeral
Elbow
FUNCTIOI\
LIGAMENT Coracoclavicular Costoclavicular Coracohumeral Glenohumeral ("Z") Coracoacromial Annular Ulnar (medial) collateral Radial (lateral) collateral
Wrist
Fingers
Extrinsic palmar Intrinsic Interosseous Volar and collateral interphalangeal
Fixes the clavicle to the coracoid process Fixes the clavicle to the costal cartilage of the fir.;t Ii> Reinforces the upper portion of the joint capsule Reinforces the anterior and inferior aspect of the joinI. c:apsuIe Protects the superior aspect of the coracoacromial joinI. Maintains the relationship between the head of the r.ldius and the humerus and ulna Provides stability against valgus (medial) stress, pamcularly in the range of 20-130 degrees of flexion and extension Provides stability against varus (lateral) stress and functions to maintain the ulnohumeral and radiohumeral joints in a reduced position when the elbow is loaded in supination Provides the majority of the wrist stability Serves as rotational restraint, binding the proximal carpal row into a unit of rotational stability Binds the carpal bones together Prevent displacement of the interphalangeal joints
Typically, repeated loading causes partial rupture of the fibrils, which leads to tendon fatigue and microscopic destruction. When this microscopic destruction exceeds the tendon's reparative capacity, cumulative microtrauma occurs. As the metabolic rate of tendons is low, the increased demand for collagen and matrix production is eas ily exceeded and pathologic changes occur (cell atrophy, calcium deposits [i.e., calcific tendinitis]). Inadequate repair will set off a vicious cycle of tenocyte death with further reduction of reparative capacity and subsequent predis position to injury. The end result of this overload mechanism or failed healing response is the formation of a tendinosis zone within the tendon.
Ligaments. Skeletal ligaments are fibrous bands of dense cr that con nect bones across joints (Tables 5-2 and 5-3). Ligaments contribute to the stability of joint function by preventing excessive motion,20 acting as guides to direct motion, and by providing proprioceptive information for joint function. 21 Inman 22 feels that the ligaments are more important as checkreins than as providers of stability during movement. The cellular organization of ligaments makes them ideal for sus taining tensile load. 23 Small amounts of elastin are present in ligaments, with the exception of the ligamentum flavum and the nuchal ligament of the spine. The collagen has a less unidirectional organization in lig aments than it does in tendons, but its structural framework still pro vides stiffness (resistance to deformation). 11 Pathology of the ligament. See Table 5-4.
Bone. Bone, the most rigid of the connective tissues, is a highly vas cular form of cr, composed of collagen, calcium phosphate, water, amorphous proteins, and cells. Despite its rigidity, bone is a dynamic tissue, which undergoes constant metabolism and remodeling. A dif ferent cell, the osteoblast, produces the collagen of bone in the same
CHAPTER 5. FUNDAMENTALS AND CORE CONCEPTS
153
TABLE 5-3. MAJOR LIGAMENTS OF THE SPINE AND LOWER QUADRANT LIGAMENT
JOINT Spine
Sacroiliac
Hip
Knee
Ankle
Foot
FUNCTION
Functions as a minor assistant in limiting anterior translation, and vertical separation of the vertebral body Resists vertical separation of the vertebral body Resists posterior shearing of the vertebral body Acts to limit flexion over a number of segments Provides some protection against intervertebral disk protrusions Ligamentum flavum Resists separation of the lamina during flexion Resists separation of the spinous processes during flexion Interspinous Iliolumbar (lower lumbar) Resists flexion, extension, axial rotation, and side bending of L5 on Sl Creates greater sciatic foramen Sacrospinous Resists forward tilting of the sacrum on the hip bone during weight bearing of the vertebral column Creates lesser sciatic foramen Sacrotuberous Resists forward tilting of the sacrum on the hip bone during weight bearing of the vertebral column Resists anterior and inferior movement of the sacrum Interosseous Dorsal sacroiliac (long) Resists backward tilting of the sacrum on the hip bone dUring weight bearing of the vertebral column Transports nutrient vessels to the femoral head Ligamentum teres Limits hip extension Iliofemoral Limits anterior displacement of the femoral head Ischiofemoral Pubofemoral Limits hip extension Medial collateral Stabilizes medial aspect of tibiofemoral joint against valgus stress Stabilizes lateral aspect of tibiofemoral joint against varus stress Lateral collateral Resists anterior translation of the tibia and posterior translation of the femur Anterior cruciate Resists posterior translation of the tibia and anterior translation of the femur Posterior cruciate Medial collaterals Provides stability between the medial malleollus, navicular, talus, and calcaneus against (deltoid) eversion Static stabilizers of the lateral ankle especially against inversion Lateral collaterals Provides indirect plantar support to the calcaneocuboid joint, by limiting the amount of Long plantar flattening of the lateral longitudinal arch of the foot Bifurcate Supports the medial and lateral aspects of the foot when weight bearing in a plantar flexed position Provides plantar support to the calcaneocuboid joint and possibly helps to limit flattening Calcaneocuboid of the lateral longitudinal arch Anterior longitudinal ligament Posterior longitudinal ligament
TABLE 5-4. LIGAMENT INJURIES GRADE First degree (mild)
Second degree (moderate)
Third degree (complete)
SIGNS Minimal loss of structural integrity No abnormal motion Little or no swelling Localized tenderness Minimal bruising Significant structural weakening Some abnormal motion Solid end-feel to stress More bruising and swelling Often associated hemarthrosis and effusion Loss of structural integrity Marked abnormal motion Significant bruising Hemarthrosis
IMPLICATIONS Minimal functional loss Early return to training-some protection may be necessary
Tendency to recurrence Need protection from risk of further injury May need modified immobilization May stretch out further with time Needs prolonged protection Surgery may be considered Often permanent functional instability
Reproduced, with pennission, from Reid DC. Sports Injury Assessment and Rehabilitation. New York: Churchill Iivingstone; 1992. Copyright © Elsevier.
l
154
SECTION I. THE PROFESSION
TABLE 5-5. GENERAL STRUCTURE OF BONE SITE Epiphysis
Physis
Metaphysis
Diaphysis
COMMENT Mainly develops under pressure Apophysis forms under traction Forms bone ends Supports articular surface Epiphyse~growth plate Respong(ye to ~rowth and sex hormones Vulnerable prior to growth spurt Mechanically weak Remodeling expanded bone end Cancellous bone heals rapidly Vulnerable to osteomyelitis Affords ligament attachment Forms shaft of bone Large surface for muscle origin Significant compact cortical bone Strong in compression
CONDITIONS
RESULT
Epiphyseal dysplasias Joint surface trauma Overuse injury Damaged blood supply Physeal dysplasia Trauma
Distorted joints Degenerative changes Fragmented development Avascular necrosis Short stature Deformed or angulated growth or growth arrest
Slipped epiphysis Osteomyelitis Tumors Metaphyseal dysplasia
Sequestrum formation Altered bone shape Distorted growth
Fractures Diaphyseal dysplasias Healing slower than at metaphysis
Able to remodel angulation Cannot remodel rotation Involucrum with infection Dysplasia give altered density and shape
Reproduced, with permission, from Reid DC. Sports Injury Assessment and Rehabilitation. New York: Churchi11 Livingstone; 1992. Copyright © Elsevier.
manner as that of ligament and tendon. 5 At the gross level, each bone has a distinct morphology comprising both cortical bone and cancel lous bone. ~ ~
Cortical bone is found in the outer shell. Cancellous bone is found within the epiphyseal and metaphy seal regions of long bones as well as throughout the interior of short bones (Table 5-5).14
The function of bone is to provide support, enhance leverage, protect vital structures, provide attachments for both tendons and liga ments, and to store minerals, particularly calcium. Bones may also serve as useful landmarks during the palpation phase of the examina tion. The strength of a bone is related directly to its density.
Study Pearl C~n'lplications • . following .. a.•.• fracture
.. (;arl<Jrslu~~ il1f~ction!fqt .·.~ijlbol.jsm,
VoolRroann's .isObE:!rnicP0L!iIii« sur faces. These relative compression or distractions affect the lewd of aRI grnity of the opposing surfaces. The position of maximmn of the opposing joint surfaces is termed the close-packed pusiIii:a of me joint. The position of least congruity is termed the open-pa::J!ll!Jll p0si tion. Thus, movements toward the close-packed posiIioo of a joint involve an element of compression, whereas moveIDeIJIS 0Ul of Ibis position involve an element of distraction.
COIIf:l""
Close-Packed Position. The close-packed position of a , . . fi joint position that results in:
me
~
Maximal tautness of the major ligaments.
Maximal surface congruity.
~ The least transarticular pressure.
~ The minimal joint volume.
~ The maximal stability of the joint.
~
Once the close-packed position is achieved, no further motion in that direction is possible. This is the often-cited reason why IDOSl frac tures and dislocations occur when an external force is applied (0 a joint that is in its close-packed position. The close-packed positions for the various joints are depicted in Table 5-18.
Open-Packed Position. In essence, any position of the joinl adler than the close-packed position could be considered an open-packed
TABLE 5-18. CLOSE-PACKED POSITION OF THE JOINTS JOINT Zygapophysial (spine) Temporomandibular Glenohumeral Acromioclavicular Sternoclavicular Ulnohumeral Radiohumeral Proximal radioulnar Distal radioulnar Radiocarpal (wrist) Metacarpophalangeal Carpometacarpal Interphalangeal Hip Tibiofemoral Talocrural (ankle) Subtalar Midtarsal Tarsometatarsal Metatarsophalangeal Interphalangeal
POSITION Extension Teeth clenched Abduction and external rotation Arm abducted to 90 degrees Maximum shoulder elevation Extension Elbow flexed 90 degrees; forearm supinated 5 degrees 5 degrees of supination 5 degrees of supination Extension with radial deviation Full flexion Full opposition Full extension Full extension, internal rotation, and abduction Full extension and external rotation of tibia Maximum dorsiflexion Supination Supination Supination Full extension Full extension
CHAPTER 5. FUNDAMENTALS AND CORE CONCEPTS
TABLE 5-19. OPEN-PACKED (RESTING) POSITION OF THE JOINTS JOINT
t
POSITION
Zygapophysial (spine) Temporomandibular Glenohumeral Acromioclavicular Sternoclavicular Ulnohumeral Radiohumeral Proximal radioulnar Distal radioulnar Radiocarpal (wrist) Carpometacarpal Metacarpophalangeal Interphalangeal Hip
Tibiofemoral Talocrural (ankle) Subtalar Midtarsal Tarsometatarsal Metatarsophalangeal Interphalangeal
Midway between flexion and extension Mouth slightly open (freeway space) 55 degrees of abduction, 30 degrees of horizontal adduction Arm resting by side Arm resting by side 70 degrees of flexion, 10 degrees of supination Full extension, full supination 70 degrees of flexion, 35 degrees of supination 10 degrees of supination Neutral with slight ulnar deviation Midway between abduction-adduction and flexion-extension Slight flexion Slight flexion 30 degrees of flexion, 30 degrees of abduction, slight lateral rotation 25 degrees of flexion 10 degrees of plantar flexion, midway between maximum inversion and eversion Midway between extremes of range of movement Midway between extremes of range of movement Midway between extremes of range of movement Neutral Slight flexion
position. The open-packed pOsItion, also referred to as the loose packed position of a joint, is the joint position that results in: ~ ~
~ ~ ~
The slackening of the major ligaments of the joint.
Minimal surface congruity.
Minimal joint surface contact.
Maximal joint volume.
Minimal stability of the joint.
The open-packed position permits maximal distraction of the joint surfaces. Because the open-packed position causes the brunt of any external force to be borne by the joint capsule or surrounding liga ments, most capsular or ligamentous sprains occur when a joint is in its open-packed position. The open-packed positions for the various joints are depicted in Table 5-19.
Capsular and Noncapsular Patterns of Restriction. Broadly speaking, there are two patterns of range of motion used in the interpretation of joint motion: ~
~
A capsular pattern of restriction is a limitation of pain and movement in a joint specific ratio, which is usually present with arthritis, or following prolonged immobilization (Table 5-20). A noncapsular pattern of restriction is a limitation in a joint in any pattern other than a capsular one, and may indicate the presence of either a derangement, a restriction of one part of the joint capsule, or an extra-articular lesion, that obstructs joint motion.
Study Pearl Theopert"pa~~~d
monly;u~dufingj
techniques.
.
177
178
SECTION I. THE PROFESSION
TABLE 5-20. CAPSULAR PATTERNS OF RESTRICTION LIMITATION OF MOTION (PASSIVE ANGULAR MOTION)
JOINT Glenohumeral Acromioclavicular Sternoclavicular Humeroulnar Humeroradial Superior radioulnar Inferior radioulnar Wrist (carpus) Radiocarpal Carpometacarpal Midcarpal First carpometacarpal Carpometacarpal 2-5 Metacarpophalangeal 2-5
External rotation> abduction> internal rotation (3:2: I) No true capsular pattern. Possible loss of horizontal adduction, pain (and sometimes sIigm Iais of end range) with each motion See above: acromioclavicular joint Flexion> extension (± 4:1) No true capsular pattern. Possible equal limitation of pronation and supination No true capsular pattern. Possible equal limitation of pronation and supination with pain at end ranges No true capsular pattern. Possible equal limitation of pronation and supination ~ith pain at end ranges Flexion = extension See above (carpus)
~
Retroposition Fan> fold Flexion> extension (± 2:1)
Interphalangeal Proximal (PIP) Distal (DIP) Hip Tibiofemoral Superior tibiofibular Talocrural Talocalcaneal (subtalar)
Internal rotation > flexion > abduction = extension> other motions Flexion> extension (± 5: I) No capsular pattern: pain at end range of translatory movements Plantar flexion> dorsiflexion Varus > valgus
Midtarsal Talonavicular calcaneocuboid 1st Metatarsophalangeal Metatarsophalangeal 2-5
Inversion (plantar fleXion, adduction, supination) > dorsiflexion Extension> flexion (± 2: I) Flexion ~ extension
Interphalangeal 2-5 Proximal Distal
Flexion Flexion
Flexion> extension (± 2: I)
~ ~
extension extension
Data from Cyriax J. Textbook of Orthopaedic Medicine: Diagnosis of Soft Tissue Lesions. 8th ed. London: Bailliere Tindall; 1982.
End-Feels. End-feels can be defined as the quality of resistance at end range. The end-feel can indicate to the clinician the cause of the motion restriction (Tables 5-21 and 5-22).
Study Pearl
Arc of Pain. The term "painful arc" is used to describe an occur rence of temporary pain during active or passive motion that disap pears before the end of the movement. The presence of a painful arc indicates that some structure is being compressed. Measuring Range of Motion Overview. The term "goniometry" is derived from two Greek words: gonia, meaning angle, and metron, meaning measure. Thus, a goniometer is an instrument used to measure angles. Within the field of physical therapy, goniometry is used to measure the total amount of available motion at a specific joint. Goniometry can be used to meas ure both active and passive range of motion.
J
CHAPTER 5. FUNDAMENTALS AND CORE CONCEPTS
179
TABLE 5-21 NORMAL END-FEELS
TYPE
CAUSE
CHARACTERISTICS AND EXAMPLES
Bony
Produced by bone-to-bone approximation
Muscular
Insufficiency: produced by the muscle tendon unit May occur with adaptive shortening 2. Slow guarding: resistance that is felt, slowly releases with sustained force
Soft-tissue approximation
Produced by the contact of two muscle bulks on either side of a flexing joint where the joint range exceeds other restraints
Capsular
Produced by capsule or
Abrupt and unyielding with the impression that further forcing will break something Examples Normal: elbow extension Abnormal: cervical rotation (may indicate osteophyte) Stretch with elastic recoil and exhibits constant-length phenomenon. Similar to Capsular (see below). Further forcing feels as if it will snap something Examples Normal; wrist flexion with finger flexion, the straight leg raise, and ankle dorsiflexion with the knee extended Abnormal; decreased dorsiflexion of the ankle with the knee flexed A very forgiving end-feel that gives the impression that further normal motion is possible if enough force could be applied Examples Normal: knee flexion, elbow flexion in extremely muscular subjects Abnormal; elbow flexion with the obese subject. Various degrees of stretch without elasticity. Stretch ability is dependent on thickness of the tissue ~ Strong capsular or extracapsular ligaments produce a hard capsular end-feel while a thin capsule produces a softer one ~ The impression given to the clinician is, if further force is applied something will tear Examples Normal: wrist flexion (soft), elbow flexion in supination (medium), and knee extension (hard), Abnormal: inappropriate stretch ability for a specific joint. If too hard, may indicate a hypomobility due to arthrosis; if too soft, a hypermobility
1.
ligament~
Goniometers are produced in a variety of sizes and shapes and are usually constructed of either plastic or metal. The two most common types of instruments used to measure joint angles are the bubble incli nometer and the traditional goniometer. Bubble goniometer. The bubble goniometer, which has a 360-degree rotating dial and scale with fluid indicator, can be used for flexion and extension; abduction and adduction; and rotation in the neck, shoul der, elbow, wrist, hip, knee, ankle, and spine. Traditional goniometer. The traditional goniometer, which can be used for flexion and extension; abduction and adduction; and rotation in the shoulder, elhow, wrist, hip, knee, and ankle, consists of three parts; A body. The body of the goniometer is designed like a protractor and may form a full or half circle. A measuring scale is located around the body. The scale can extend either from 0 to 180 degrees and 180 to 0 degrees for the half-circle models, or from 0 to 360 degrees and from 360 to 0 degrees on the full-circle models. The intervals on the scales can vary from 1 to 10 degrees.
180
SECTION I. THE PROFESSION
TABLE 5-22. ABNORMAL END-FEELS 1YPE
Springy
Boggy
Fast guarding (spasm)
Empty
Facilitation
CAUSES
CHARACTERISTICS AND EXAMPLES
Produced by the articular surface rebounding from an intra-articular meniscus or disc. The impression is that if forced further, something will collapse Produced by viscous fluid (blood) within a joint
A rebound sensation as if pushing off from a Sorbo rubber pad Examples Normal: axial compression of the cervical spine Abnormal: knee flexion or extension with a displaced meniscus A "squishy" sensation as the joint is moved toward its end range. Further forcing feels as if it will burst the joint
Produced by reflex and reactive muscle contraction in response to irritation of the nociceptor predominantly in articular structures and muscle. Forcing it further feels as if nothing will give
Produced solely by pain. Frequently caused by serious and severe pathologic changes that do not affect the joint or muscle and so do not produce spasm. Demonstration of this end-feel is, with the exception of acute subdeltoid bursitis, de facto evidence of serious pathology. Further forcing simply increases the pain to unacceptable levels Not truly an end-feel, as facilitated hypertonicity does not restrict motion. It can, however, be perceived near the end range
•
Examples Normal: none Abnormal: hemarthrosis at the knee An abrupt and "twangy" end to movement that is unyielding while the structure is being threatened, but disappears when the threat is removed (kicks back) With joint inflammation, it occurs early in the range, especially toward the close pack position to prevent further stress With an irritable joint hypermobility it occurs at the end of what should be normal range as it prevents excessive motion from further stimulating the nociceptor Spasm in grade II muscle tears becomes apparent as the muscle is passively lengthened and is accompanied by a painful weakness of that muscle Note: muscle guarding is not a true end-feel as it involves a co-contraction Examples Normal: none Abnormal: significant traumatic arthritis, recent traumatic hypermobility, grade II muscle tears The limitation of motion has no tissue resistance component and the resistance is from the patient being unable to tolerate further motion due to severe pain. It is not the same feeling as voluntary guarding but rather it feels as if the patient is both resisting and trying to allow the movement simultaneously Examples Normal: none Abnormal: acute subdeltoid bursitis, sign of the buttock A light resistance as from a constant light muscle contraction throughout the latter half of the range that does not prevent the end of range being reached. The resistance is unaffected by the rate of movement Examples Normal: none Abnormal: spinal facilitation at any level
A stationary arm. The stationary arm is structurally a part of the body and therefore cannot move independently of the body. A moving arm. The moving arm is attached to the fulcrum in the center of the body by a rivet or screw-like device that allows the moving arm to move freely on the body of the device. In some instruments, the screw-like device can be tightened to fix the mov ing arm in a certain position or loosened to permit free movement.
\ J j
t
CHAPTER 5. FUNDAMENTALS AND CORE CONCEPTS
I
181
The correct selection of which goniometer device to use depends on the joint angle to be measured. The length of arms varies among instru ments and can range from 3 to 18 inches. Extendable goniometers allow varying ranges from 91/ 2 to 26 inches. The longer-anned goniometers, or the bubble inclinometer, are recommended when the landmarks are fur ther apart, such as when measuring hip, knee, elbow, and shoulder movements. In the smaller joints such as the wrist and hand and foot and ankle, a traditional goniometer with a shorter arm is used.
Procedure. The patient is positioned in the recommended testing position. While stabilizing the proximal joint component, the clinician gently moves the distal joint component through the available range of motion until the end-feel is determined. An estimate is made of the available range of motion and the distal joint component is returned to the starting position. The clinician palpates the relevant bony landmarks and aligns the goniometer (Tables 5-23 and 5-24). A record is made of the starting measurement. The goniometer is then removed and the patient moves the joint through the available range of motion. Once the joint has been moved through the available range of motion, the goniometer is replaced and realigned, and a measurement is read and recorded.
•
•
Grading Accessory Movements. The range of motion at a joint is defined as the available range, not the full range, and is usually in one direction only (Fig. 5-5). Each joint has an anatomic limit (AL), which is determined by the configuration of the joint surfaces and the surrounding soft tissues. The point of limitation (Pi) is that point in the range which is short of the anatomic limit and which is reduced by either pain or tissue resistance. Maitland advocated five grades of accessory movements at a joint, each of which falls within the available range of motion that exist'> at the joint-a point somewhere between the beginning point and the anatomic limit (Fig. 5-5). These grades can be used to assess arthrokine matic motion of the joint (see the next section in the chapter). Hypomobility, Hypermobility, and Instability. If a joint moves less than what is considered normal, or when compared to the same joint on the opposite extremity, it may be deemed hypomobile. Hypomobility may be caused by a number of factors including con tracture of cr. A joint that moves more than considered normal when compared to the same joint on the opposite extremity may be deemed hypermobile. Hypermobility may occur as a generalized phenomenon or be localized to just one direction of movement-the result of dam aged CT. The term stability, specifically related to the joint, has been the subject of much research. 1l9- 134 In contrast to a hypermobile joint, an unstable joint involves a disruption of the osseous and ligamentous structures of that joint, and results in a loss of function. Joint stability may be viewed as a factor of joint integrity, elastic energy, passive stiff ness, and muscle activation: ~
Joint integrity. Joint integrity is enhanced in those ball- and socket joints with deeper sockets or steeper sides as opposed to those with planar sockets and shallower sides. Joint integrity
Study Pearl Caution musti~eused Wh~f1~~sing clinical judgments Qn.th.e.resultsof accessoryl'l'lotion testing because feIN studies have·.• exarl"dn~dthe validity and reliabHityofaccessory motion testlng. of the spine or extremities. ~.?~ little lsknQwnabou~~~yalidityof these tests for most inferences. l1B
Study Pearl ~ The . presence. ofhYPPn1pbHitY"'in
tire absence of contraind15ations is an indication for jointTobiJiz.1. tionsasthe intervention of choice. ~ The presence of hypermobil1tyis a contralndicati()nt()joiritmobi~ Iizations.
182
SECTION I. THE PROFESSION
TABLE 5-23. GONIOMETRIC TECHNIQUES FOR THE UPPER EXTREMITY JOINT Shoulder
MOTION
Forearm
Wrist
MOVABLE AR\i
Acromion process
Midaxillary line of the thorax
Extension
Acromion process
Midaxillary line of the thorax
Abduction
Anterior aspect of the acromion process Anterior aspect of the acromion process Olecranon process
Parallel to the midline of the anterior aspect of the sternum Medial midline of the humerus Parallel to the midline of the anterior aspec1 of the sternum Ulna using the olecranon process Parallel or perpendicular to and ulnar styloid for reference the floor Ulna using the olecranon process Parallel or perpendicular to and ulnar styloid for reference the floor Lateral midline of the radius Lateral midline of the humerus using the center of the using the radial head and radial acromion process for reference styloid process for reference Lateral midline of the humerus Lateral midline of the radius using using the center of the the radial head and radial acromion process for reference styloid process for reference Parallel to the anterior midline Dorsal aspect of the forearm, just proximal to the styloid of the humerus process of the radius and ulna Parallel to the anterior midline Ventral aspect of the forearm, just proximal to the styloid of the humerus process of the radius and ulna Lateral midline of the ulna Lateral midline of the fifth using the olecranon and metacarpal ulnar styloid process for reference Lateral midline of the fifth Lateral midline of the ulna using the olecranon and metacarpal ulnar styloid process for reference Dorsal midline of the forearm Dorsal midline of the third using the lateral epicondyle metacarpal of the humerus for reference
Internal rotation External rotation Flexion
Olecranon process Lateral epicondyle of the humerus
Extension
Lateral epicondyle of the humerus
Pronation
Lateral to the ulnar styloid process
Supination
Medial to the ulnar styloid process
Flexion
Lateral aspect of the wrists over the triquetrum
Extension
Lateral aspect of the wrists over the triquetrum
Radial deviation
Over the middle of the dorsal aspect of the wrist over the capitate Over the middle of the dorsal aspect of the wrist over the capitate Over the palmar aspect of the first carpo metacarpal joint
Ulnar deviation
Thumb
STATIONARY ARM
Flexion
Adduction
Elbow
AXIS
Carpometacarpal flexion
Carpometacarpal extension
Carpometacarpal abduction
Over the palmar aspect of the first carpometacarpal joint Over the lateral aspect of the radial styloid process
Lateral midline of the humerus using the lateral epicondyle of the humerus for reference Lateral midline of the humerus using the lateral epicondyle of the humerus for reference Medial midline of the humerus
Dorsal midline of the forearm using the lateral epicondyle of the humerus for reference
Dorsal midline of the third metacarpal
Ventral midline of the radius using the ventral surface of the radial head and radial styloid process for reference Ventral midline of the radius using the ventral surface of the radial head and radial styloid process for reference Lateral midline of the second metacarpal using the center of the second metacarpal or phalangeal joint for reference
Ventral midline of the first metacarpal
Ventral midline of the first metacarpal Lateral midline of the first metacarpal using the center of the first metacarpal or phalangeal joint for reference
CHAPTER 5. FUNDAMENTALS AND CORE CONCEPTS
183
TABLE 5-23. GONIOMETRIC TECHNIQUES FOR THE UPPER EXTREMITY (Continued) JOINT
Fingers
.
MOTION Carpometacarpal adduction
Over the lateral aspect of the radial styloid process
Metacarpophalangeal flexion
Over the dorsal aspect of the metacarpo phalangeal joint Over the dorsal aspect of the metacarpophalangeal joint Over the dorsal aspect of the metacarpo phalangeal joint Over the dorsal aspect of the metacarpo phalangeal joint Over the dorsal aspect of the proximal interphalangeal joint Over the dorsal aspect of the proximal interphalangeal joint Over the dorsal aspect of the proximal interphalangeal joint Over the dorsal aspect of the proximal interphalangeal joint
Metacarpophalangeal extension Metacarpophalangeal abduction Metacarpophalangeal adduction Proximal interphalangeal flexion Proximal interphalangeal extension Distal interphalangeal flexion Distal interphalangeal extension
~
~
~
AXIS
STATIONARY ARM
MOVABLE ARM
Lateral midline of the second metacarpal using the center of the second metacarpal or phalangeal joint for reference Over the dorsal midline of the metacarpal
Lateral midline of the first metacarpal using the center of the first metacarpal or phalangeal joint for reference Over the dorsal midline of the proximal phalanx
Over the dorsal midline of the metacarpal
Over the dorsal midline of the proximal phalanx
Over the dorsal midline of the metacarpal
Over the dorsal midline of the proximal phalanx
Over the dorsal midline of the metacarpal
Over the dorsal midline of the proximal phalanx
Over the dorsal midline of the proximal phalanx
Over the dorsal midline of the middle phalanx
Over the dorsal midline of the proximal phalanx
Over the dorsal midline of the middle phalanx
Over the dorsal midline of the middle phalanx
Over the dorsal midline of the distal phalanx
Over the dorsal midline of the middle phalanx
Over the dorsal midline of the distal phalanx
is also dependent on the attributes of the supporting structures around the joint, and the extent of joint disease. Elastic energy. Connective tissues are elastic structures, and as such are capable of storing elastic energy when stretched. This stored elastic energy may then be used to help return the joint to its original position when the stresses are removed. Passive stiffness. Individual joints have passive stiffness that increases toward the joint end range. An injury to these passive structures causing inherent loss in the passive stiffness results in joint laxity .135 Muscle activation. Muscle activation increases stiffness, both within the muscle and within the joint(s) it crosses. 136 However, the synergists and antagonist muscles that cross the joint must be activated with the correct and appropriate activation in terms of magnitude or timing. A faulty motor control system can lead to inappropriate magnitudes of muscle force and stiffness, allowing for a joint to buckle or undergo shear translation. 136
Pathologic breakdown of the above factors may result in instabil ity. Two types of instability are recognized: articular and ligamen tous.-Articular instability can lead to abnormal patterns of coupled and translational movements. 137-Ligamentous instability may lead to multiple planes of aberrant joint motion. l38
184
SECTION I. THE PROFESSION
TABLE 5-24. GONIOMETRIC TECHNIQUES FOR THE LOWER EXTREMITY JOINT Hip
MOTION Flexion
Extension
Abduction
Knee
Ankle
Subtalar
AXIS
STATIONARY ARM
MOVABLE ARM
Over the lateral aspect of the hip joint using the greater trochanter of the femur reference Over the lateral aspect of the hip joint using the greater trochanter of the femur reference Over the anterior superior iliac spine (ASIS) of the extremity being measured
Lateral midline of the pelvis
Lateral midline of the femur
using the lateral epicondyle
for reference
Lateral midline of the femur using the lateral epicondyle for reference Anterior midline of the femur using the midline of the patella for reference
Adduction
Over the anterior superior iliac spine (ASIS) of the extremity being measured
Internal rotation
Anterior aspect of the patella
External rotation
Anterior aspect of the patella
Lateral midline of the pelvis
Aligned with imaginary horizontal line extending from one ASIS to the other ASIS Aligned with imaginary horizontal line extending from one ASIS to the other ASIS Perpendicular to the floor or parallel to the supporting surface
Perpendicular to the floor or parallel to the supporting surface
Flexion
Lateral epicondyle of the femur
Lateral midline of the femur using the greater trochanter for reference
Extension
Lateral epicondyle of the femur
Lateral midline of the femur using the greater trochanter for reference
Dorsiflexion
Lateral aspect of the lateral malleolus
Plantar flexion
Lateral aspect of the lateral malleolus
Lateral midline of the fibula using the head of the fibula for reference Lateral midline of the fibula using the head of the fibula for reference Anterior midline of the lower leg using the tibial tuberosity for reference Anterior midline of the lower leg using the tibial tuberosity for reference Posterior midline of the lower leg Posterior midline of the lower leg
Inversion
Anterior aspect of the ankle midway between the malleoli
Eversion
Anterior aspect of the ankle midway between the malleoli
Inversion
Posterior aspect of the ankle midway between the malleoli Posterior aspect of the ankle midway between the malleoli
Eversion
Anterior midline of the femur using the midline of the patella for reference Anterior midline of the lower leg using the crest of the tibia and a point midway between the two malleoli for reference Anterior midline of the lower leg using the crest of the tibia and a point midway between the two malleoli for reference Lateral midline of the fibula using the lateral malleolus and fibular head for reference Lateral midline of the fibula using the lateral malleolus and fibular head for reference Parallel to the lateral aspect of the fifth metatarsal Parallel to the lateral aspect of the fifth metatarsal
,
J
I•
I t
t
• Anterior midline of the second metatarsal
Anterior midline of the second metatarsal
Posterior midline of the calcaneus Posterior midline of the calcaneus
•
f
CHAPTER 5. FUNDAMENTALS AND CORE CONCEPTS
..
Grade I
I,
I
185
Grade III
Grade II
-I
Grade IV at limit of range
I Grade V
Pl
BP
AL
(Point of limitation)
(Beginning point in range of motion)
(Anatomic limit)
Figure 5-5. Maitland's five grades of motion. (PL, point of limitation; AL, anatomic limit.) (Reproduced, with permission, from Dutton M. Manual Therapy of the Spine. New York: McGraw-Hili; 2002:44.)
•
KINESIOLOGY
I
,
'1
GENERAL PRINCIPLES OF BIOMECHANICS The science of biomechanics involves the application of mechanical principles in the study of the structure and function of movement. For the physical therapist designing and supervising rehabilitation pro grams, a working knowledge of biomechanics is essential: a funda mental skill of the physical therapist is to identify, analyze, and solve problems related to human movement. When describing joint movements it is necessary to have a start ing position as the reference position. This starting position is referred to as the anatomic reference position. The anatomic reference posi tion for the human body is described as the erect standing position with the feet just slightly separated and the arms hanging by the side, the elbows straight, and with the palms of the hand facing forward (Fig. 5-6).
DIRECTIONAL TERMS Directional terms are used to describe the relationship of body parts or the location of an external object with respect to the body.139 The fol lowing are commonly used directional terms: Superior or cranial--doser to the head.
Inferior or caudal----eloser to the feet.
Anterior or ventral-toward the front of the body.
Posterior or dorsal-toward the back of the body.
Medial-toward the midline of the body.
Lateral-away from the midline of the body.
Proximal----eloser to the trunk.
Distal-away from the trunk.
Superficial-toward the surface of the body.
Deep--away from the surface of the body in the direction of the
inside of the body.
I
L I
A
B
Figure 5-6. Standing positions. A. Funda mental standing position. B. Anatomic stand ing position. (Reproduced, with permission, from Luttgens K, Hamilton N. Kinesiology: Scientific Basis of Human Motion. 10th ed. New York: McGraw-Hili; 2002:38.)
186
SECTION I. THE PROFESSION
MOVEMENTS OF THE BODY SEGMENTS Movements of the body segments occur in three dimensions along imaginary planes and around various axes of the body.
Planes of the Body. There are three traditional planes of the body corresponding to the three dimensions of space: sagittal, frontal, and transverse (Fig. 5-7).139 ~
Sagittal. The sagittal plane, also known as the anterior-posterior
or median plane, divides the body vertically into left and right
halves of equal size
Frontal. The frontal plane, also known as the lateral or coronal
plane, divides the body equally into front and back halves
Transverse. The transverse plane, also known as the horizontal
plane, divides the body equally into top and bottom halves.
~ ~
\
I
Axes of the Body.
Three reference axes are used to describe human motion: frontal, sagittal, and longitudinal. The axis around which the movement takes place is always perpendicular to the plane in which it occurs. ~
Frontal. The frontal axis, also known as the transverse axis, is perpendicular to the sagittal plane
Sagittal. The sagittal axis is perpendicular to the frontal plane
Longitudinal. The longitudinal axis, also known as the vertical
axis, is perpendicular to the transverse plane.
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\~ I
I'
:\
r
"-o£ten described as deep,tQMstant~l1db()r ing, and is apt to be more noticeable and more intense at night}9
Intensity. One of the simplest methods to quantify the intensity of pain is to use a lO-point visual analogue scale. The visual analog scale (VAS) is a numerically continuous scale that requires the pain level be identified by making a mark on a 100-mm line. 17 The patient is asked to rate his or her present pain compared with the worst pain ever experienced, with 0 representing no pain, 1 representing minimally perceived pain, and 10 representing pain that requires immediate attention. 18 Pain Perception. It is important to remember that pain perception is highly subjective. Pain is a broad and significant symptom that can be described using many descriptors. The symptoms of chronic pain typically behave in a mechanical fashion, in that they are provoked by activity or repeated movements, and reduced with rest, or a movement in the opposite direction.
L
Study Pearl Patients' with chroQkpi:lln may be more prone to ,depression' and dis rupted ihterpersonal relationships.20-23
Quality of Symptoms. The quality of the symptoms depends on the type of receptor being stimulated. ~ ~ ~ ~
Stimulation of the cutaneous A-delta nociceptors leads to prick ing pain. 24 Stimulation of the cutaneous C nociceptors results in burning or dull pain. 25 Activation of the nociceptors in muscle by electrical stimulation produces aching pain. 26 Electrical stimulation of visceral nerves at low intensities results in vague sensations of fullness and nausea, but higher intensi ties cause a sensation of pain. 27
Peripheral neuropathies can manifest as abnormal, frequently unpleasant sensations, which are variously described by the patient as numbness, pins and needles, and tingling. 28 When these sensations occur spontaneously without an external sensory stimulus, they are called paresthesias (Table 6-3).28 Patients with paresthesias typically demonstrate a reduction in the perception of cutaneous and proprio ceptive sensations. Motivational-affective circuits can also mimic pain states, most notably in patients with anxiety, neurotic depression, or hysteria. 22 The MADISON mnemonic outlines the behavioral indicators that suggest motivational-affective pain 29 ,30:
_
~
tudY Pearl
I
I
Because motorand sensory axonsruh in thesameMerves,disord~rsof the P,eri P,'"heral nerves (neuropathies) usu~ ally affect both motor and sensory functions.
264
SECTION II. TESTS AND MEASURES
TABLE 6-3. CAUSES OF PARESTHESIA PROBABLE CAUSE
PARESTHESIA LOCATION Lip (perioral) Bilateral lower or bilateral upper extremities All extremities simultaneously One half of body Segmental (in dermatomal pattern) Glove-and-stocking distribution Half of face and opposite half of body
Vertebral artery occlusion Central protrusion of disk impinging on spine Spinal cord compression Cerebral hemisphere lesion Disk or nerve root Diabetes mellitus neuropathy, lead or mercury poisoning Brainstem impairment
Multiple complaints, including complaints about unrelated body
parts.
Authenticity claims in an attempt to convince the clinician the
symptoms exist.
Denial of the negative effect the pain is having on function.
Interpersonal variability, manifested by different complaints to dif
ferent clinicians or support staff.
Singularity of symptoms, where the patient requests special con
sideration due to their type and level of pain.
Only you, where the clinician is placed at a special level of expertise. Nothing works.
Study Pearl
Frequency and Duration. The frequency and duration of the patient's symptoms can help the clinician to classify the injury accord ing to its stage of healing: acute (inflammatory), subacute (migratory and proliferative), and chronic (remodeling) (see Table 5-31). Aggravating and Easing Factors. Of particular importance are the patient's chief complaint and the relationship of that complaint to specific aggravating activities or postures. Musculoskeletal condi tions are typically aggravated with movement and alleviated with rest (Table 6-4). If no activities or postures are reported to aggravate the symptoms, the clinician needs to probe for more information. Nonmechanical events that provoke the symptoms could indicate a nonmusculoskeletal source for the pain32 : ~ ~
Night pain. Pain at night, unrelated to movement, that disturbs or prevents sleep may indicate a malignancy. Eating. Pain that increases with eating may suggest gastroin testinal involvement.
TABLE 6-4. DIFFERENTIATION BETWEEN MUSCULOSKELETAL AND SYSTEMIC PAIN MUSCULOSKELETAL PAIN
SYSTEMIC PAIN
Usually decreases with cessation of activity Generally lessens at night Aggravated with mechanical stress Usually continuous or intermittent Reproduced, with permission, from Meadows York: McGraw-Hili; 1999.
Reduced by pressure Disturbs sleep Not aggravated by mechanical stress Usually constant or in waves
J. Orthopedic Differential Diagnosis in Physical Therapy. New
CHAPTER 6. THE HISTORY AND SYSTEMS REVIEW ~ ~ ~
Stress. An increase in overall muscle tension prevents muscles from resting. Cyclical pain. Cyclical pain can often be related to systemic events, as with menstrual pain. If aggravating movements or positions have been reported, they should be tested at the end of the tests and measures, to avoid any overflow of symptoms, which could confuse the clinician.
location. The clinician should determine the location of the symp toms, as this can indicate which areas need to be included in the physi cal examination. Information about how the location of the symptoms has changed since the onset can indicate whether a condition is wors ening or improving. In general, as a condition worsens the symptom dis tribution becomes more Widespread and distal (peripheralizes). As the condition improves, the symptoms tend to become more localized (cen tralized). A body chart may be used to record the location of symptoms. It must be remembered that the location of symptoms for many musculoskeletal conditions is quite separate from the source, espe cially in those peripheral joints that are more proximal, such as the shoulder and the hip. The term referred pain is used to describe those symptoms that have their origin at a site other than where the patient feels the pain. If the extremity appears to be the source of the symp toms, the clinician should attempt to reproduce the symptoms by load ing the peripheral tissues. If this proves unsuccessful, a full investiga tion of the spinal structures must ensue. Behavior of Symptoms. The behavior of the symptoms aids the clinician in determining the stage of healing and the impact it has on the patient's function. Whether the pain is worsening, improving, or unchanging provides information on the effectiveness of an interven tion. In addition, a gradual increase in the intensity of the symptoms over time may indicate to the clinician that the condition is worsening or is nonmusculoskeletal in nature. 16.32 Maitland33 introduced the concept of the degree of irritability. An irritable structure has the following characteristics: ~
~
~
A progressive increase in the severity of the pain with move ment or a specific posture. An ability to reproduce constant pain with a specific motion or posture indicates an irritable structure. Symptoms increased with minimal activity. An irritable struc ture is one that requires very little to increase the symptoms. Increased latent response of symptoms. Symptoms do not usually resolve within a few minutes following a movement or posture.
According to McKenzie and MaY,31 the intervention for the ortho pedic patient whose symptoms have a low degree of irritability, and are gradually resolving, should focus on only education initially. However, if the improvement ceases, a mechanical intervention may then be necessary,3l
Nature of the Symptoms. The clinician must determine whether pain is the only symptom, or whether there are other symptoms that accompany the pain, such as dizziness, bowel and bladder changes, tin gling (paresthesia), radicular pain/numbness, weakness, and increased sweating.
Study Pearl
Study Pearl
265
266
SECTION II. TESTS AND MEASURES ~ ~ ~
~
Study Pearl ~
Dizziness (discussed later). Bowel or bladder dysfunction usually indicates a compromise (compression) of the cauda equine. Paresthesia. The seriousness of the paresthesia depends upon its distribution. While complaints of paresthesia can be the result of a relatively benign impingement of a peripheral nerve, the reasons for its presence can vary in severity and seriousness (Table 6-3). Radicular pain is produced by nerve root irritation. This type of pain is typically sharp, or shooting. Numbness that is a der matomal pattern indicates spinal nerve root compression. Radiating pain refers to an increase in pain intensity and distri bution. Radiating pain typically travels distal from the site of the injury. Weakness. Any weakness should be investigated by the clinician to determine whether it is the result of a neurological lesion (e.g., cerebral hemisphere lesion, spinal nerve root compression, or a peripheral nerve lesion), disuse, inhibition due to pain or swelling, an injury to the contractile or inert tissues (muscle, ten don, bursa, etc.), or a more serious pathology such as a fracture.
Past History of Current Condition. It is important for the clinician to determine whether the patient has had successive onsets of similar symptoms in the past, as recurrent injury tends to have a detri mental affect on the potential for recovery. If it is a recurrent injury, the clinician should note how often, and how easily, the injury has recurred, and the success or failure of previous interventions. PAST MEDICAL AND SURGICAL HISTORY The patient's past medical history (PMH) can be obtained through a questionnaire (Table 6-5). The PMH can provide information with regard to allergies, childhood illnesses, and previous trauma. In addi tion, information on any health conditions such as cardiac problems, high blood pressure, or diabetes, should be elicited, as these may impact exercise tolerance (cardiac problems, high blood pressure) and speed of healing (diabetes). If the surgical history (Table 6-5) is related to the current problem, the clinician should obtain as much detail about the surgery as possi ble from the surgical report, including any complications, precautions, or postsurgical protocols.
FAMILY HISTORY AND GENERAL HEALTH STATUS Certain diseases, such as rheumatoid arthritis, diabetes, cardiovascular disease, and cancer have familial tendencies. The general health status refers to a review of the patient's health perception, physical and psychological function, as well as any specific questions related to a particular body region or complaint. 6
MEDICATIONS Although the dispensing of medications is out of the scope of practice for a physical therapist, questioning patients about their prescribed medications can reveal medical conditions that the patient might not
CHAPTER 6. THE HISTORY AND SYSTEMS REVIEW
267
TABLE 6-5. SAMPLE MEDICAL HISTORY QUESTIONNAIRE General Information Date: Last Name First Name The information requested may be needed if you have a medical emergency. Person to be notified in emergency Phone Are you currently working? (Y) or (N) If not, why? Type of work
_
Relationship
_
General Medical History Please check ('1/) if you have been treated for: ( ) Heart problems () Lung disease/problems ( ) Arthritis ( ) Fainting or dizziness ( ) Swollen and painful joints ( ) Shortness of breath ( ) Calf pain with exercise ( ) Irregular heartbeat ( ) Severe headaches ( ) Stomach pains or ulcers ( ) Pain with cough or sneeze ( ) Recent accident ( ) Back or neck injuries ( ) Head trauma/concussion ( ) Diabetes ( ) Muscular weakness ( ) Stroke(s) () Cancer ( ) Joint dislocation(s) ( ) Balance problems ( ) Muscular pain with activity ( ) Broken bone ( ) Difficulty sleeping ( ) Swollen ankles or legs ( ) Frequent falls ( ) Jaw problems ( ) Unexplained weight loss ( ) Circulatory problems () Tremors ( ) Epilepsy/seizures/convulsions ( ) High blood pressure (hypertension) ( ) Chest pain or pressure at rest ( ) Allergies (latex, medication, food) ( ) Kidney disease ( ) Constant pain unrelieved by rest ( ) Liver disease ( ) Pregnancy ( ) Weakness or fatigue ( ) Hernias ( ) Night pain (while sleeping) ( ) Blurred vision ( ) Nervous or emotional problems ( ) Bowellbladder problems ( ) Any infectious disease (TE, AIDS, hepatitis) ( ) Difficulty swallowing ( ) Tingling, numbness, or loss of feeling. If yes, where? ( ) A wound that does not heal ( ) Constant pain or pressure during activity ( ) Unusual skin coloration Do you use tobacco? (Y) or (N) If yes, how much? Are you presently taking any medications or drugs? (Y) or (N) If yes, what are you taking them for? 1. Pain
On the line provided, mark where your "pain status" is today.
I
No pain
I
Most severe pain
2. Function. On a scale of 0 to 10, with 0 being able to perform all of your normal daily activities, and 10 being unable to perform
any of your normal daily activities, give yourself a score for your current ability to perform your activities of daily living.
Please list any major surgery or hospitalization:
Hospital: _ Approx. Date: _ Reasons: Hospital: _ Approx. Date: _ Reasons: Have you recently had an x-ray, MRI, or CT scan for your condition? (Y) or (N) Facility: Approx. date: _ Findings: Please mention any additional problems or symptoms you feel are important: Have you been evaluated and/or treated by another physician, physical therapist, chiropractor, osteopath, or health care practitioner for this condition? (Y) or (N) If yes, please circle which one.
268
SECTION II. TESTS AND MEASURES
consider related to his or her present problem.! Medications can also have an impact on clinical findings and the success of an intervention (see Chapter 19).34
SYSTEMS REVIEW The purpose of the systems review is to: ~
~
~ ~ ~ ~ ~
Help determine the anatomic and physiologic status of all systems (i.e., musculoskeletal, neurologic, cardiovascular, pulmonary, integumentary, gastrointestinal, urinary, and reproductive; see the discussion later in this chapter).35 Provide information about communication skills, affect, cogni tion, language abilities, education needs, and learning style of the patient.35 Narrow the focus of subsequent tests and measures.
Define areas that may cause complications or indicate a need for
precautions during the examination and intervention processes. Screen for physical, sexual, and psychological abuse. Make a determination of the need for further physical therapy services based on an evaluation of the information obtained. Identify problems that require consultation with, or referral to, another health care provider.
With the majority of states now permitting direct access to physical therapists, many physical therapists now have the primary responsibility for being the gatekeepers of health care and for making medical refer rals. In light of the APTA's movement toward realizing Vision 2020, an operational definition of autonomous practice and the related term autonomous physical therapist practitioner is defined by the APTA's Board as follows: ~
~
Autonomous physical therapist practice is practice character ized by independent, self-determined professional judgment and action. An autonomous physical therapist practitioner within the scope of practice defined by the Guide to Physical Therapist Practice, provides physical therapy services to patients who have direct and unrestricted access to their services, and may refer as appropriate to other health-care providers and other profes sionals and for diagnostic tests. 36
Through the history and physical examination, physical therapists diagnose and classify different types of conditions for use in their clinical reasoning and intervention. 5 The Guide clearly articulates the physical therapist's responsibility to recognize when a consultation with, or referral to, another health care provider is necessary.6 The systems review, in addition to the scanning examination (see Table 6-6 and the discussion later in this chapter), is the critical part of the examination that identifies possible health problems that require consultation With, or referral to, another health care provider. 6 The sys tems review is based on the clinician's knowledge of body system physiology so that malfunctions of the various systems can be detected through comprehensive questioning.
CHAPTER 6. THE HISTORY AND SYSTEMS REVIEW
269
TABLE 6-6. COMPONENTS OF lHE SCANNING EXAMINATION AND lHE STRUcruRES TESTED Active ROM Passive ROM Resisted Stress Dural Neurologic Dermatome Myotome Reflexes
Willingness to move, ROM, integrity of contractile and inert tissues, pattern of restriction (capsular, or noncapsular), quality of motion, and symptom reproduction Integrity of inert and contractile tissues, ROM, end-feel, sensitivity Integrity of contractile tissues (strength, sensitivity) Integrity of inert tissues (ligamentous/disc stability) Dural mobility Nerve conduction Afferent pathway (sensation) Efferent pathway (strength, fatigability) Afferent-efferent pathways, and central nervous systems
All patients should be questioned about their general health. This is usually obtained using a patient self-report questionnaire (Table 6-5). The self-report questionnaire should be designed to address such issues as 37 : ~
~
Fatigue: complaints of feeling tired or run down are extremely common, and therefore often only become significant if the patient reports that tiredness interferes with the ability to carry out typical daily activities and when the fatigue has lasted for 2 to 4 weeks or longer. Many serious illnesses can cause fatigue (Table 6-7). Malaise: a sense of uneasiness or general discomfort that is often associated with conditions that generate fever.
TABLE 6-7. CONDITIONS PRESENTING AS CHRONIC FATIGUE Psychological
Endocrine/metabolic
Infectious
Neoplasms Cardiopulmonary Connective tissue disease Sleep disturbances
Depression Anxiety Somatization disorder Hypothyroidism Diabetes mellitus Pituitary insufficiency Addison's disease Chronic renal failure Hyperparathyroidism Endocarditis Tuberculosis Mononucleosis Hepatitis HIV infection Occult malignancy Congestive heart failure Chronic obstructive pulmonary disease Rheumatic disorders Sleep apnea Esophageal reflux
Allergic rhinitis Reproduced, with permISSIon, from Boissonnault WG. Review of Systems. In: Boissonnault WG, ed. Primary Care for the Physical1berapist: Examination and Triage. St. Louis: Elsevier W.B. Saunders; 2005:87-104. Copyright © Elsevier.
270
SECTION II. TESTS AND MEASURES ~
~
~
~
~ ~
Feverlchills/sweats: these are signs and symptoms that are most often associated with systemic illnesses such as cancer, infections, and connective tissue disorders such as rheumatoid arthritis. To qualify as a red flag, the fever should have some longevity (2 weeks or longer). Unexpected weight change: a sensitive but nonspecific finding that can be a normal physiologic response, but may also be associated with depression, cancer, or gastrointestinal disease. Nausea/vomiting: persistent vomiting is an uncommon com plaint reported to a physical therapist, as the physician will have already been contacted. However a low-grade nausea, which can be caused by systemic illness or an adverse drug reaction, may be reported. Dizziness/lightheadedness: dizziness (vertigo) is a nonspecific neurologic symptom that requires a careful diagnostic workup. A report of vertigo, although potentially problematic, is not a contraindication to the continuation of the examination. Differential diagnosis includes primary central nervous system diseases, vestibular and ocular involvement, and more rarely, metabolic disorders. 38 Careful questioning can help in the dif ferentiation of central and peripheral causes of vertigo. Dizziness provoked by head movements or head positions could indicate an inner ear dysfunction. Dizziness provoked by certain cervical motions, particularly extension or rotation, also may indicate vertebral artery compromise. Paresthesia/numbness/weakness (Table 6-3). Change in mentation/cognition: can be a manifestation of mul tiple disorders including delirium, dementia, head injury, stroke, infection, fever, and adverse drug reactions. The clini cian notes whether the patient's communication level is age appropriate, whether the patient is oriented to person, place, and time, and whether emotional and behavioral responses appear to be appropriate to circumstances.
The systems review includes an assessment of the anatomic and physiologic status of all systems (Le., musculoskeletal, neurologic, car diovascular, pulmonary, integumentary, gastrointestinal, urinary, and reproductive), including the following. 35 ~
For the cardiovascular/pulmonary system, the assessment of heart rate, respiratory rate, blood pressure, and edema. The four so-called vital signs, which are standard in most medical settings, include temperature, heart rate and blood pressure, and respiratory rate. Pain is considered by many to be the fifth vital sign (see Chapter 9 ).39--48 The clinician should monitor at least heart rate and blood pressure in any person with a history of cardiovascular disease or pulmonary disease, or those at risk for heart disease. 49 The equipment needed to assess these vital signs is a thermometer, a blood pressure (BP) cuff with a stethoscope (or an automatic BP machine), and a watch or clock. • Temperature. Body temperature is one indication of the metabolic state of an individual; measurements provide infor mation concerning basal metabolic state, possible presence or
CHAPTER 6. THE HISTORY AND SYSTEMS REVIEW
absence of infection, and metabolic response to exercise. 50 "Normal" body temperature of the adult is 98.6°F (37°C). (Great Britain uses 98.4°F l36.9°Cl as "normal"). However, temperatures in the range of 965°F (35.8°C) to 99.4°F (37.4°C) are not at all uncommon. Fever or pyrexia is a tem perature exceeding lOO°F (37.7°C).51 Hyperpyrexia refers to extreme elevation of temperature above 41.1°C or lO6°F. 50 Hypothermia refers to an abnormally low temperature (below 35°C or 95°F). The temperature is generally taken by placing the bulb of a thermometer under the patient's tongue for 1 to 3 minutes depending on the device. In most individ uals there is a diurnal (occurring every day) variation in body temperature of 05° to 2°F. The lowest ebb is reached during sleep. Menstruating women have a well-known temperature pattern that reflects the effects of ovulation, with the temper ature dropping slightly before menstruation, and then drop ping further 24 to 36 hours prior to ovulation.51 Coincident with ovulation, the temperature rises and remains at a some what higher level until just before the next menses. It is also worth noting that in adults over 75 years of age and in those who are immunocompromised (e.g., transplant recipients, corticosteroid users, persons with chronic renal insufficiency, or anyone taking excessive antipyretic medications), fever response may be blunted or absent. 50 • Heart rate. In most people, the pulse is an accurate meas ure of heart rate. The heart rate or pulse is taken to a contain information about the resting state of the cardiovascular sys tem and the system's response to activity or exercise and recovery. 50 It is also used to assess patency of the specific arteries palpated, and the presence of any irregularities in the rhythm50 (see Chapter 11). • Respiratory rate. The normal chest expansion difference between the resting position and the fully inhaled position is 2 to 4 cm (females > males). The clinician should compare measurements of both the anterior-posterior diameter and the transverse diameter during rest and at full inhalation. Normal respiratory rate is between 8 and 14 per minute in adults, and slightly qUicker in children. The examination of breathing patterns is described in Chapter 10. • Blood pressure. Blood pressure is a measure of vascular resistance to blood flow (see Chapter 12).50 • Edema. Edema is an observable swelling from fluid accu mulation in certain body tissues. Edema most commonly occurs in the feet and legs, where it also is referred to as peripheral edema. Swelling or edema may be localized at the site of an injury or diffused over a larger area due to a sys temic disorder (e.g., congestive heart failure or renal dis ease). In general, the amount of swelling is related to the severity of the condition. The swelling occurs as a result of changes in the local circulation and an inability of the lym phatic system to maintain equilibrium, which causes an accumulation of excess fluid under the skin in the interstitial spaces or compartments within the tissues that are outside of the blood vessels.
271
L
272
SECTION II. TESTS AND MEASURES
~ ~
~
~
The more serious reasons for swelling include fracture, tumor, congestive heart failure, and deep vein thrombosis. See Chapters 11 and 12 for more details regarding the lym phatic system and the various types of edema. For the integumentary system, the assessment of skin integrity, skin color, and presence of scar formation (see Chapter 13). For the musculoskeletal system, the assessment of gross sym metry, gross range of motion, gross strength, weight, and height (see Chapter 8). For the neuromuscular system, a general assessment of gross coordinated movement (e.g., balance, locomotion, transfers, and transitions). In addition, the clinician observes for peripheral and cranial nerve integrity (see Chapter 9) and notes any indication of neurologic compromise such as tremors or facial tics. For communication ability, affect, cognition, language, and learning style, it is important to verify that the patient can com municate his or her needs. The clinician should determine whether the patient has a good understanding about his or her condition, the planned intervention, and the prognosis. The cli nician should also determine the learning style that best suits the patient.
Finally, it is well worth investigating the possibility that the pre senting signs and symptoms are because of an adverse drug reaction (Table 6-8).
THE SCANNING EXAMINATION FOR NEUROMUSCULOSKELETAL CONDITIONS Designed by Cyriax,52 the scanning (screening) examination for the orthopedic patient traditionally follows the history and is often incor porated as part of the systems review. Although two studies 53 ,54 ques tioned the validity of some aspects of the selective tissue tension exam ination, no defmitive conclusions were drawn from these studies. The scarcity of research to refute the work of Cyriax would suggest that its principles are sound, and that its use should be continued. The purpose of the scanning examination is to help rule out the possibility of symptom referral from other areas, and to ensure that all possible causes of the symptoms are examined. In addition, the scan ning examination helps narrow the search for the source(s) of symp toms to a specific body region and to identify any red flags that were alluded to during the history or physical examination. It was Grieve 55 who coined the term masqueraders to indicate those conditions that may not be musculoskeletal in origin and that may require skilled inter vention elsewhere (Table 6-9). The scanning examination is divided into two examinations: one for the lower quarter/quadrant (Table 6-10) and the other for the upper quarter/quadrant (Table 6-11). The tests that comprise the scanning examination are designed to detect neurologic weakness, the patient's ability to perceive sensations, and the inhibition of the deep tendon reflexes (DTR) and other reflexes by the central nervous system.
CHAPTER 6. THE HISTORY AND SYSTEMS REVIEW
273
TABLE 6-8. MEDICATION SIDE EFFECTS AND SUBJECTIVE SYMPTOMS SIDE EFFECfS AND SUBJECTIVE SYMPTOMS Gastrointestinal distress (dyspepsia, heartburn, nausea, vomiting, abdominal pain, constipation, diarrhea, bleeding)
Pulmonary (bronchospasm, shortness of breath, respiratory depression)
Central nervous system (dizZiness, drowsiness, insomnia, headaches, hallucinations, confuSion, anxiety, depression, muscle weakness)
Dermatologic (skin rash, itching, flushing of face)
MEDICATIONS (IN ORDER OF MOST COMMON OCCURRENCE) Salicylates Nonsteroidal anti-inflammatory drugs (NSAlDs) Opioids Corticosteroids Beta-blockers Calcium-channel blockers Skeletal muscle relaxants Diuretics Angiotensin-converting enzyme (ACE) inhibitors Digoxin Nitrates Cholesterol-lowering agents Antiarrhythmic agents Antidepressants (tricyclic antidepressants, monoamine oxidase inhibitors, lithium) Neuroleptics Antiepileptic agents Oral contraceptives Estrogens and progestins Theophylline Salicylates NSAlDs Opioids Beta-blockers ACE inhibitors NSAlDs Skeletal muscle relaxants Opioids Corticosteroids Beta-blockers Calcium-channel blockers Nitrates ACE inhibitors Digoxin Antianxiety agents Antidepressants (tricyclic antidepressants, monoamine oxidase inhibitors) Neuroleptics Antiepileptic agents Oral contraceptives Estrogens and progestins NSAlDs Corticosteroids Beta-blockers Opioids Calcium-channel blockers ACE inhibitors Nitrates Cholesterol-lowering agents Antiarrhythmic agents Antidepressants (monoamine oxidase inhibitors, lithium) Oral contraceptives Estrogens and progestins Antiepileptics ( Continued)
274
SECTION II. TESTS AND MEASURES
TABLE 6-8. MEDICATION SIDE EFFECTS AND SUBJECTIVE SYMPTOMS (Continued)
SIDE EFFECTS AND SUBJECTIVE SYMPTOMS Musculoskeletal (weakness, fatigue, cramps, arthritis, reduced exercise tolerance, osteoporosis)
Cardiac (bradycardia, ventricular irritability, AV block, congestive heart failure, PVCs, ventricular tachycardia)
Vascular (claudication, hypotension, peripheral edema, cold extremities)
Genitourinary (sexual dysfunction, urinary retention, urinary incontinence)
Head, eyes, ears, nose, and throat (tinnitus, loss of taste, headache, light-headedness, dizziness)
MEDICATIONS (IN ORDER OF MOST COM,\10N OCCURRENCE) Corticosteroids Beta-blockers Calcium-channel blockers ACE inhibitors Diuretics Digoxin Antianxiety agents Antiepileptic agents Antidepressants Neuroleptic agents Opioids Diuretics Beta-blockers Calcium-channel blockers Digoxin Antiarrhythmic agents Tricyclic antidepressants Neuroleptics Oral antiasthmatic agents NSAIDs Corticosteroids Diuretics Beta-blockers Calcium-channel blockers ACE inhibitors Nitrates Antidepressants (tricyclic antidepressants, monoamine oxidase inhibitors) Neuroleptics Oral contraceptives Estrogens and progestins Opioids Diuretics Beta-blockers Antiarrhythmic agents Antidepressants (tricyclic antidepressants, monoamine oxidase inhibitors) Neuroleptics Oral contraceptives Estrogens and progestins Salicylates NSAIDs Opioids Skeletal muscle relaxants Beta-blockers Nitrates Calcium-channel blockers ACE inhibitors Digoxin Antiarrhythmic agents Antianxiety agents Antidepressants (tricyclic antidepressants, monoamine oxidase inhibitors) Antiepileptic agents
Reproduced, with permission, from Boissonnault WG. Review of systems. In: Boissonnault WG, ed. Primary Care for the Physical Therapist: Examination and Triage. Sr. Louis: Elsevier W.B. Saunders; 2005:87-104; and Data from Cain SO, Janos sc. Clinical pharmacology for the physical therapist. In: Boissonnault W, ed. Examination in Physical Therapy Practice: Screening for Medical Disease. 2nd ed. New York: Churchill Livingstone; 1995:350-351. Copyright © Elsevier.
CHAPTER 6. THE HISTORY AND SYSTEMS REVIEW
275
TABLE 6-9. EXAMINATION FINDINGS AND TIfE POSSIBLE CONDITIONS CAUSING THEM FINDINGS
POSSIBLE CONDITION
Dizziness
Upper cervical impairment, vertebrobasilar ischemia, craniovertebral ligament tear; may also be relatively benign Cord compression, vertebrobasilar ischemia Cord compression, vertebrobasilar ischemia Cord compression, vertebrobasilar ischemia Cord compression, vertebrobasilar ischemia Instability, retropharyngeal hematoma, rheumatoid arthritis
Quadrilateral paresthesia Bilateral upper limb paresthesia Hyperreflexia Babinski or clonus sign Consistent swallow on transverse ligament stress tests Nontraumatic capsular pattern Arm pain lasting> 6--9 mo Persistent root pain < 30 yr Radicular pain with coughing Pain worsening after 1 mo > 1 level involved (cervical region) Paralysis Trunk and limb paresthesia Bilateral root signs and symptoms Nontraumatic strong spasm Nontraumatic strong pain in elderly patient Signs worse than symptoms Radial deviator weakness Thumb flexor weakness Hand intrinsic weakness and/or atrophy Horner's syndrome Empty end-feel Severe post-traumatic capsular pattern Severe post-traumatic spasm Loss of range of motion post-trauma Post-traumatic painful weakness
Rheumatoid arthritis, ankylosing spondylitis, neoplasm Neoplasm Neoplasm Neoplasm Neoplasm Neoplasm Neoplasm or neurologic disease Neoplasm Neoplasm Neoplasm Neoplasm Neoplasm Neoplasm Neoplasm Neoplasm, thoracic outlet syndrome, carpal tunnel syndrome Superior sulcus tumor, breast cancer, cervical ganglion damage, brainstem damage Neoplasm Fracture Fracture Fracture Fracture
Reproduced, with permission, from Meadows J. Orthopedic Differential Diagnosis in Physical Therapy. New York: McGraw-Hill; 1999.
TABLE 6-10. THE LOWER QUARTER SCANNING MOTOR EXAMINATION MUSCLE TESTED
MUSCLE ACTION
ROOT LEVEL
PERIPHERAL NERVE
Hip flexion
Iliopsoas
11-L2
Knee extension Hamstrings
Quadriceps Biceps femoris, semimembranosus, and semitendinosus Tibialis anterior Extensor hallicus longus Fibularis (peroneus) longus and brevis Gastrocnemius and soleus Gluteus maximus
L2-L4 L4-S3
Femoral to iliacus and lumbar plexus to psoas Femoral Sciatic
Primarily L4 Primarily L5 Primarily 51
Deep peroneal Deep fibular (peroneal) nerve Superficial fibular (peroneal) nerve
Primarily SI L5-S2
Tibial Inferior gluteal nerve
Dorsiflexion with inversion Great toe extension Ankle eversion Ankle plantarflexion Hip extension
276
SECTION II. TESTS AND MEASURES
TABLE 6-11. TIlE UPPER QUARTER SCANNING MOTOR EXAMINATION RESISTED ACTION
MUSCLE TESTED
ROOT LEVEL
Shoulder abduction Elbow flexion Elbow extension Wrist extension
Deltoid Biceps brachii Triceps brachii Extensor carpi radialis longus, brevis, and extensor carpi ulnaris Flexor carpi radialis and flexor carpi ulnaris Flexor digitorum superficialis, flexor digitorum profundus, and lumbricales
Primarily C5 Primarily c6 Primarily C7 Primarily c6
Axillary Musculocutaneous Radial Radial
Primarily C7
Median nerve for radialis and ulnar nerve for ulnaris Median nerve superficialis, both median and ulnar nerve for profundus and lumbricales Ulnar
Wrist flexion Finger flexion
Finger abduction
Dorsal interossei
Primarily C8
Primarily T1
PERIPHERAL NERVE
The tests used in the scanning examination (Table 6-6) produce a medical diagnosis, rather than a physical therapy one. 56 Those diag noses can include: ~
Fracture. Neurologic pathology, which can either be treated (mechanical netve root compression from a disc protrusion, or inflamma tion), or is out of the scope of a physical therapist (tumor, upper motor neuron impairment, and cauda equina impairment) (Table 6-2). ~ Tendinitis, bursitis, muscle tear. ~ Tendon avulsion. ~
If a diagnosis is rendered from the scan, an intetvention may be initiated using the guidelines outlined in Table 6-12. The scan and/or history may also have indicated to the clinician that the patient's con dition is in the acute stage of healing. While this is not a diagnosis in the true sense, it can be used for the purpose of the intetvention plan. Often the scanning examination does not generate enough signs and symptoms to formulate a working hypothesis or a diagnosis. In this case, further testing with the tests and measures is required in order to proceed.
TABLE 6-12. SCAN FINDINGS AND INTERVENTIONS CONDITIONS
FINDINGS
PROTOCOL
Severe pain, all movements reduced
Gentle manual traction in progressive extension Traction and/or traction manipulation in extension PRICEMEM (Protection, Rest, Ice, Compression, Elevation, Medication Electrotherapeutics, Manual therapy) Exercises in pain-free direction Exercises in pain-free direction
Intervertebral disk protrusion, prolapse, and extrusion Anterior-posterior instability of vertebral segment Arthritis
Flexion and extension reduction greater than rotation Hot capsular pattern
Subluxation of vertebral segment Arthrosis of vertebral segment
One direction restricted
All directions restricted
CHAPTER 6. THE HISTORY AND SYSTEMS REVIEW
REFERENCES 1. Boissonnault WG. Examination in Physical Therapy Practice: Screening for Medical Disease. New York: Churchill Livingstone; 1991. 2. Meadows J. Orthopedic Differential Diagnosis in Physical Therapy. New York: McGraw-Hill; 1999. 3. Boissonnault W, Goodman C. Physical therapists as diagnosticians: drawing the line on diagnosing pathology. ] Orthop Sports Phys Ther. 2006;36:351-353. 4. Boissonnault WG, Bass C. Medical screening examination: not optional for physical therapists. ] Orthop Sports Phys Ther. 1991; 14:241-242. 5. OuVall RE, Godges J. Introduction to physical therapy differential diagnosis: the clinical utility of subjective examination. In: Wilmarth MA, ed. Medical Screening for the Physical Therapist. Orthopaedic Section Independent Study Course 14.1.1 La Crosse, WI: Orthopaedic Section, APTA; 2003:1-44. 6. American Physical Therapy Association. Guide to physical thera pist practice. Phys Ther. 2001;81:S13-S95. 7. Steinberg MH. Management of sickle cell disease. N EnglJ Med. 1999;340:1021-30. 8. Haslock 1. Ankylosing spondylitis. Baillieres Gin Rheumatol. 1993; 7:99. 9. Potosky AL, Feuer EJ, Levin OL. Impact of screening on incidence and mortality of prostate cancer in the United States. Epidemiol Rev. 2001;23:181-186. 10. Wingo PA, Tong T, Bolden S. Cancer statistics, 1995. CA Cancer ] Clin. 1995;45:8. 11. Parkin OM, Muir CS. Cancer incidence in five continents. Comparability and quality of data. /ARC Sci Pub. 1992;66:45. 12. Ries LAG, Eisner MP, Kosary CL, et al. SEER Cancer Statistics Review, 1973-1997. Bethesda: National Cancer Institute; 2000. 13. Martinez JC, Otley Cc. The management of melanoma and non melanoma skin cancer: a review for the primary care physician. Mayo Clin Proc. 2001;76:1253-1265. 14. McKenzie R, May S. Mechanical diagnosis. In: McKenzie R, May S, eds. The Human Extremities: Mechanical Diagnosis and Therapy. Waikanae, New Zealand: Spinal Publications; 2000:79-88. 15. Judge RD, Zuidema GO, Fitzgerald FT. The medical history and physical. In: Judge RD, Zuidema GO, Fitzgerald FT, eds. Clinical Diagnosis. 4th ed. Boston: Little, Brown; 1982:9-19. 16. Maitland G. Vertebral Manipulation. Sydney: Butterworth; 1986. 17. Huskisson EC. Measurement of pain. Lancet. 1974;2:127. 18. Halle JS. Neuromusculoskeletal scan examination with selected related topics. In: Flynn TW, ed. The Thoracic Spine and Rib Cage: Musculoskeletal Evaluation and Treatment. Boston: Butterworth-Heinemann; 1996:121-146. 19. Judge RD, Zuidema GO, Fitzgerald FT. Musculoskeletal system. In: Judge RD, Zuidema GO, Fitzgerald FT, eds. Clinical Diagnosis. 4th ed. Boston: Little, Brown; 1982:365-403. 20. Bonica JJ. Neurophysiological and pathological aspects of acute and chronic pain. Arch Surg. 1977;112:750-761.
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SECTION II. TESTS AND MEASURES
21. Burkhardt CS. The use of the McGill Pain Questionnaire in assess ing arthritis pain. Pain. 1984;19:305. 22. Chaturvedi SK. Prevalence of chronic pain in psychiatric patients. Pain. 1987;29:231-237. 23. Dunn D. Chronic regional pain syndrome, type 1: part 1. AORN]. 2000;72:421. 24. Konietzny F, Perl ER, Trevino D, et al. Sensory experiences in man evoked by intraneural electrical stimulation of intact cutaneous afferent fibers. Exp Brain Res. 1981;42:219-222. 25. Ochoa J, Torebjork E. Sensations evoked by intraneural micros timulation of C nociceptor fibres in human skin nerves. ] Physiol. 1989;415:583-599. 26. Torebjork HE, Ochoa JL, Schady W. Referred pain from intraneural stimulation of muscle fascicles in the median nerve. Pain. 1984;18:145-156. 27. Ness TJ, Gebhart GF. Visceral pain: a review of experimental stud ies. Pain. 1990;41:167-234. 28. Rowland LP. Diseases of the motor unit. In: Kandel ER, Schwartz JH, Jessell TM, eds. Principles of Neural Science. 4th ed. New York: McGraw-Hill; 2000:695-712. 29. Goldstein R. Psychological evaluation of low back pain. Spine: State of the Art Rev. 1986;1:103. 30. Norris TR. History and physical examination of the shoulder. In: Nicholas JA, Hershman EB, Posner MA, eds. The Upper Extremity in Sports Medicine. 2nd ed. St Louis, MO: Mosby Year-Book; 1995:39-83. 31. McKenzie R, May S. History. In: McKenzie R, May S, eds. The Human Extremities: Mechanical Diagnosis and Therapy. Waikanae, New Zealand: Spinal Publications; 2000:89-103. 32. Goodman CC, Snyder TEK. Differential Diagnosis in Physical Therapy. Philadelphia: Saunders; 1990. 33. Maitland G. Peripheral Manipulation. 3rd ed. London: Butterworth; 1991. 34. Magarey ME. Examination of the cervical and thoracic spine. In: Grant R, ed. Physical Therapy ofthe Cervical and Thoracic Spine. 2nd ed. New York: Churchill Livingstone; 1994:109-144. 35. American Physical Therapy Association. Guide to Physical Therapist Practice. 2nd ed. Phys Ther. 2001;81:1-746. 36. American Physical Therapy Association. Guide to Physical Therapist Practice. 2nd ed. Phys Ther. 2001;81:9-746. 37. Boissonnault WG. Review of systems. In: Boissonnault WG, ed. Primary Care for the Physical Therapist: Examination and Triage. St. Louis, MO: Elsevier Saunders; 2005:87-104. 38. Mohn A, di Ricco L, Magnelli A, et al. Celiac disease-associated vertigo and nystagmus. ] Pediatr Gastroenterol Nutr. 2002;34: 317-318. 39. Davis MP, Walsh D. Cancer pain: how to measure the fifth vital sign. Cleve Clin] Med. 2004;71:625-632. 40. Salcido RS. Is pain a vital sign? Adv Skin Wound Care. 2003;16:214. 41. Sousa FA. Pain: the fifth vital sign. Rev Lat Am Enfermagem. 2002; 10:446-447. 42. Lynch M. Pain: the fifth vital sign. Comprehensive assessment lead., to proper treatment. Adv Nurse Pract. 2001;9:28-36. 43. Lynch M. Pain as the fifth vital sign.] Intraven Nurs. 2001;24:85-94.
CHAPTER 6. THE HISTORY AND SYSTEMS REVIEW
44. Merboth MK, Barnason S. Managing pain: the fifth vital sign. Nurs Clin North Am. 2000;35:375-383. 45. Torma 1. Pain-the fifth vital sign. Pulse. 1999;36:16. 46. Newman, BY Pain as the fifth vital sign. ] Am Optom Assoc. 1999;70:619-620. 47. Joel LA. The fifth vital sign: pain. Am] Nurs. 1999;99:9. 48. McCaffery M, Pasero CL. Pain ratings: the fifth vital sign. Am] Nurs. 1997:97:15-16. 49. Frese EM, Richter RR, Burlis TV. Self-reported measurement of heart rate and blood pressure in patients by physical therapy clin ical instructors. Phys Ther. 2002;82: 1192-2000. 50. Bailey MK. Physical examination procedures to screen for serious disorders of the low back and lower quarter. In: Wilmarth MA, ed. Medical Screening/or the Physical Therapist. Orthopaedic Section Independent Study Course 14.1.1. La Crosse, WI: Orthopaedic Section, APTA; 2003:1-35. 51. Judge RD, Zuidema GD, Fitzgerald FT. Vital signs. In: Judge RD, Zuidema GD, Fitzgerald FT, eds. Clinical Diagnosis. 4th ed. Boston: Little, Brown; 1982:49-58. 52. Cyriax]. Diagnosis of soft tissue lesions. In: Cyriax]. Textbook 0/ Orthopaedic Medicine. 8th ed. London: Bailliere Tindall; 1982. 53. Hayes KW. An examination of Cyriax's passive motion tests with patients having osteoarthritis of the knee. Phys Ther. 1994:74:697. 54. Franklin ME. Assessment of exercise induced minor lesions: the accuracy of Cyriax's diagnosis by selective tissue tension para digm. ] Orthop Sports Phys Ther. 1996;24: 122. 55. Grieve GP. The masqueraders. In: Boyling JD, Palastanga N, eds. Grieve's Modern Manual Therapy. 2nd ed. Edinburgh: Churchill Livingstone; 1994:841-856. 56. Meadows JTS. Manual Therapy: Biomechanical Assessment and Treatment, Advanced Technique. Calgary: Swodeam Consulting; 1995.
279
l
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SECTION II. TESTS AND MEASURES
Comprehension Questions
1. Give three reasons for taking a patient history. 2. Information about the patient's age, height, weight, marital status, and primary lan guage spoken is covered by which component of the history according to The Guide? 3. Which component of the history, according to The Guide, is concerned about the patient's developmental background and hand or foot dominance? 4. True or false: Pain that is not alleviated by rest, and that is not associated with acute trauma, may indicate the presence of aserious disorder such as atumor or aneurysm. A. True. B. False.
5. What do the letters in the MADISON mnemonic represent, and what type of patient does the mnemonic help detect? 6. True or false: Symptoms that are distal and superficial are more difficult for the patient to specifically localize than those that are proximal and deep. A. True. B. False. 7. What are the three characteristics of an irritable structure? 8. Radicular pain is produced by what? 9. Which portion of the examination helps determine the anatomic and physiologic sta tus of all systems (i.e., musculoskeletal, neurologic, cardiovascular, pulmonary, integumentary, gastrointestinal, urinary, and genital reproductive)? 10. Give five examples of red flags during an examination. 11. What are the four vital signs? 12. What is the purpose of the upper and lower quarter scanning examinations?
Answers 1. To elicit reports of potentially dangerous symptoms, or red flags that require an immediate medical referral; to determine the chief complaint, its mechanism of injury, its severity, and its impact on the patient's function; and to gather information about the patient's past general medical and surgical history. 2. General demographics. 3. Growth and development. 4. The answer is A. This statement is true. 5. Multiple complaints, including complaints about unrelated body parts; Authenticity claims in an attempt to convince the clinician the symptoms exist; Denial of the
CHAPTER 6. THE HISTORY AND SYSTEMS REVIEW
negative effect the pain is having on function; Interpersonal variability, manifested by different complaints to different clinicians or support staff; Singularity of symptoms, where the patient requests special consideration due to his or her type and level of pain; Only you, where the clinician is placed at a special level of expertise; and Nothing works. The mnemonic is used to help detect patients with motivational affective pain. 6. The answer is B. This statement is false.
7. A progressive increase in the severity of the pain with movement or a specific pos ture, syrnptoms increased with minimal activity, and increased latent response of syrnptoms. 8. Nerve root irritation 9. Systems review. 10. Examples include fever (for more than 2 weeks), unexpected weight loss, night sweats, changes in cognition, dizziness, and vomitting. 11. Temperature, heart rate, blood pressure, and respiratory rate. 12. To help rule out the possibility of symptom referral from other areas, and to ensure that all possible causes of the symptoms are examined.
281
Gait, Posture, Ergonomics, and Occupational Health
GAIT Normal human gait is a method of bipedal locomotion involving the complex synchronization of the neuromuscular and cardiovascular sys tems.! The major requirements for successful walking include 2 : ~ ~
~ ~ ~
Support of body mass by the lower extremities. Production of locomotor rhythm. For the most part, the loco
motor rhythm relies on reflexes-the stretch reflex and the
extensor thrust. 3 The stretch reflex is involved in the
extremes of joint motion, while the extensor thrust may facil
itate the extensor muscles of the lower extremity during
weight bearing. 4
Dynamic balance control of the moving body.
Propulsion of the body in the intended direction.
Adaptability of locomotor responses to changing task and envi
ronmental demands.
The major elements of physical therapy intervention that comprise locomotor training are outlined in Table 7-1.
Study Pearl
THE GAIT CYCLE
The gait cycle is defined as the interval of time between any of the repetitive events of walking. Such an event could include the point when the foot initially contacts the ground, to when the same foot con tacts the ground again. s The gait cycle consists of two periods: stance and swing (Fig. 7-1): ~
The stance period. This period constitutes approximately
60% of the gait cycle,6,7 and describes the entire time the foot
is in contact with the ground and the limb is bearing weight.
The stance period begins with the initial contact of the foot on
the ground, and concludes when the ipsilateral foot leaves the
ground.
283
284
SECTION II. TESTS AND MEASURES
TABLE 7-1. mE MAJOR COMPONENTS OF LOCOMOTOR TRAINING INSTRUCTION AND TRAINING IN
FUNCTIONAL COMPONENT Preparation
Parallel bar progression
Overground progression (with and then without assistive device) with appropriate gait pattern
Body weight support
Bridging/pelvis elevation Hands on knees and quadruped Kneeling Half kneeling Sitting and sitting balance Modified plantigrade (position involving large base of support and high center of mass) Moving from sitting to standing and reverse with and without assistive device Supported standing and weight shifting with and without assistive device Standing with progressively diminishing base of support Stepping, sidestepping, cross-stepping Use of appropriate gait pattern, forward progression, and turning Indoor Forward progression and turning
Walking backward
Sidestepping, cross-stepping, and braiding
Stair climbing
Falling techniques (for individuals who are active ambulators)
Outdoor Opening doors and passing through thresholds Curb climbing; negotiating ramps, stairs, and sloped surfaces Entering/exiting transportation vehicles Walking on even and uneven surfaces Walking with imposed timing requirements Use of open community environments (use of elevators, revolving doors etc.) Walking on treadmill using body weight support progressing to no body weight support Slow speed progressing to faster speeds Dynamic balance control of the moving body Reciprocal stepping patterns: assisted movements to unassisted Short duration to longer durations
Data from Schmitz 1J. Locomotive training. In: O'Sullivan SB, Schmitz 1J, eels. PhYSical Rehabilitation. 5th ed. Philadelphia: FA Davis; 2007:523-560.
~
The swing period. The swing period constitutes approXimately 40% of the gait cycle,6,7 and describes the period when the foot is not in contact with the ground. The swing period begins as the foot is lifted from the ground and ends with initial contact with the ipsilateral foot. 5
Stance Period. Within the stance period, two tasks and four inter vals are recognized. 6,8,9 The two tasks include weight acceptance and single limb support. The four intervals include loading response, mid stance, terminal stance and pre-Swing (Fig. 7-1).9 Initial contact and toe-off are instantaneous events. The initial contact, which occurs when one foot makes contact with the ground, takes place at the beginning of the stance period and represents the first 0% to 2% of the gait cycle. As the initial contact of one foot is occurring, the contralat eral foot is preparing to come off the floor. Weight Acceptance. The weight acceptance task occurs during the first 10% of the stance period.
CHAPTER 7. GAIT, POSTURE, ERGONOMICS, AND OCCUPATIONAL HEALTH
285
Double
support
(10%)
Double support
(10%)
J - - - - . . . . . L - - - Stance (60%) ----L-------J-----Stance (40%) ------...,~
10% Loading response
30%
Mid-stance
50%
Terminal stance
70%
Pre-swing
Initial swing
85%
Mid-swing
Terminal swing
Toe-off Initial contact
Initial contact
1... 4-------------Stride(100%)---------------I-/
Figure 7-1. Approximate values for the two phases of gait. (Reproduced, with permission, from Dutton M. Orthopaedic Examination, Evaluation, and Intervention. New York: McGraw Hill; 2004:374.)
The Loading Response. The loading response interval begins as one limb bears weight while the other leg begins to go through its swing period. This interval may be referred to as the initial double stance period, and consists of the first 0% to 10% of the gait cycle.9 Single Leg Support. The middle 40% of the stance period is divided equally into mid-stance and terminal stance. Stability during single limb support arises primarily from the action of the calf muscles, which restrain excessive forward collapse of the tibia. 1O In addition, move ment of the subtalar joint into inversion functions to lock the midtarsal joints, creating a rigid forefoot lever over which the body weight can progress. 10
Mid-Stance. The mid-stance interval, representing the first half of the single limb support task, begins as one foot is lifted, and continues until the body weight is aligned over the forefoot. 9 The mid-stance interval comprises the 10% to 30% phase of the gait cycle. 9 Terminal Stance. The terminal stance interval is the second half of the single limb support task. It begins when the heel of the weight bearing foot lifts off the ground and continues until the contralateral foot strikes the ground. Terminal stance comprises the 30% to 50% phase of the gait cycle.9 In the late single limb support, movement of the subtalar joint into inversion functions to lock the midtarsal joints and create a rigid forefoot over which body weight can progress. 10 Limb Advancement Pre-Swing. The pre-swing interval represents the 50% to 60% phase of the gait cycle. The pre-swing interval refers to the last 10% of the stance period. This interval begins with initial contact of the contralateral limb and ends with ipsilateral toe-off. As both feet are on the floor at the same time during this interval, double support occurs for the second
Study Pearl
~l
A number of ta{:tors contribute to shock absorption during weight acceptance. These include Hl: ... Eccentric control of knee flexion to 15 degrees allow$ the dissipation of forces generated by the abrupt transfer of body weight onto the limb. . . ... Movement of the foot into 4 to 6
degrees of ever$ion functions to
unlock the midtarsal joints (talon
avicular and calcaneocuboid), cre
ating a more flexible foot that· is
able to adapt to uneven surfaces.•
~
286
SECTION II. TESTS AND MEASURES
time in the gait cycle. This last portion of the stance period is therefore referred to as the terminal double stance. Each interval of double stance lasts about 0.11 seconds. Timing for the phases of stance is 100/0 for each double stance interval and 400/0 for single limb support, so that the period of single limb support of one limb equals the period of swing for the other. 9
Swing Period. Gravity and momentum are the primary sources of motion for the swing period. 4 Within the swing period, one task and four intervals are recognized. 6,8,9 The task involves limb advancement. The four intervals include pre-swing, initial SWing, mid-SWing, and terminal sWing. 9 Limb Advancement. The swing period involves the forward motion of the non-weight-bearing foot. The four intervals of the swing period are described in the next sections. 9
Pre-Swing. In addition to representing the final portion of the stance period and single limb support task, the pre-swing interval is consid ered as part of the swing period. Initial Swing. This interval begins with the lift of the foot from the floor, and ends when the swinging foot is opposite the stance foot. It represents the 600/0 to 730/0 phase of the gait cycle. 9 Knee flexion to 60 degrees (owing to passive and active factors) assists in clearing the limb. 1o
Study Pearl Hip flexion to 25 degrees, in.combina tion with~rlkle dor?iflexion ton~utral, is necessatJ'tp achieve foot c1earance,10
Mid-Swing. This interval begins as the swinging limb is opposite the stance limb, and ends when the swinging limb is forward and the tibia is vertical. It represents the 730/0 to 870/0 phase of the gait cycle. 9 Terminal Swing. This interval begins with a vertical tibia of the swing leg with respect to the floor, and ends the moment the foot strikes the floor. It represents the last 870/0 to 1000/0 of the gait cycle.
Study Pearl
Gait Cycle Duration. The precise duration of the gait cycle intervals depends on a number of factors, including age, impairment, and the patient's walking velocity.
As gait speed increases, it develops
into jogging and then running, with changes occurring with each of the intervals. For example, as speed increases, the stance period decreases and the terminal double stance phase disappears altogether. This produces a double unsupported phase. 12 ~
~
~
~
Normal free gait velocity on a smooth and level surface aver ages about 82 m/min for adults, with men being about 50/0 faster than womenY Walking velocity declines with age at a rate of 30/0 to 110/0 in healthy adults > 60 years oldY
The primary determinants of gait velocity are the repetition rate (cadence), physical conditioning, and length of the person's stride. ll ~
Cadence. Cadence is defined as the number of separate steps taken in a certain time. Normal cadence is between 90 and 120 steps per minute, with an average of 113 steps per minute. 13,14 The cadence of women is usually 6 to 9 steps per minute slower than that of men. 14 Cadence is also affected by age, with
CHAPTER 7. GAIT, POSTURE, ERGONOMICS, AND OCCUPATIONAL HEALTH
~
cadence decreasing from the age of 4 to the age of 7, and then again in advancing years. 15 Step length/stride length. Step length is measured as the distance between the same point of one foot on successive footprints (ipsilateral to the contralat eral foot fall). Stride length, on the other hand, is the distance between suc cessive points of foot-to-floor contact of the same foot. A stride is one full lower extremity cycle. • Two step lengths added together make the stride length. • The average stride length for normal individuals is 1.41 meters,u • Typically, the stride length does not vary more than a couple of inches between tall and short individuals. • Men typically have longer stride lengths than women. • Stride length decreases with age, pain, disease, and fatigue. 16 It also decreases as the speed of gait increasesY A decrease in stride length may also result from a forward-head posture, a stiff hip, or a decrease in the availability of motion at the lum bar spine. The decrease in stride length that occurs with aging is thought to be the result of the increased likelihood of falling during the swing period of ambulation due to diminished con trol of the hip musculature. 18 This lack of control prevents the aged person from being able to intermittently lose and recover the same amount of balance that the younger adult can lose and recover. 18
287
TABLE 7-2. GAIT PARAMETERS
Cadence (steps/min) = velocity (m/sec) x 120/stride length (m) Stride length (m) = velocity (m/sec) x 120/cadence (steps/min) Velocity (m/sec) = cadence (steps/min) x stride length (m)/120 Reproduced, with permission, from Levine D, Whittle M. Gait Analysis: The Lower Extremities. La Crosse, WI: Orthopaedic Section, APTA, Inc.; 1992.
I
Sludy_P_ea_rl
_
A mathematical relationship exists
between cadence, stride length, and velocity, such that if two of them are directly measured, the third maybe derived by calculation (Table 7-2).5
CHARACTERISTICS OF NORMAL GAIT Although the presence of symmetry in gait appears to be important, asymmetry in of itself does not guarantee impairment. It must be remembered that the definition of what constitutes "normal" gait is elu sive. Perry, and Gage and associates, list five priorities of normal gait I3 ,15:
Study Pearl ~ ~ ~ ~ ~
Stability of the weight-bearing foot throughout the stance period. Clearance of the non-weight-bearing foot during the swing period. Appropriate prepositioning (during terminal swing) of the foot for the next gait cycle.
Adequate step length.
Energy conservation.
In order for gait to be efficient and to conserve energy, the center of gravity (COG) must undergo minimal displacement. The three-dimensional excursion of the center of gravitylbody mass is minimized through the intricate interactions of the segments of the lower extremity, especially at the knee and pelvis. 15 During the gait cycle, the COG is displaced both vertically and laterally: ~
Vertical displacement of the whole trunk occurs twice during each cycle-the lowest in double support, and the highest around mid-stance and mid-swing. 5 This vertical displacement
l
The COG of the. body is located approximately midline in the frontal < . plane and slightly anterior to the sec ond sacral vertebra· in the sagittal plane. The COG in men is at a point that corresponds to 56.18% of their height. In women the COG is. at a point that corresponds to 55044% of theirheight. 19
l
288
SECTION II. TESTS AND MEASURES
~
of the COG is minimized through pelvic rotation, flexion, and extension movements at the hip and knee, and rotation of the tibia and subtalar joint. 20 Lateral displacement of the COG occurs during the left and right stance periods. 5 Under normal conditions, the lateral dis placement of the COG occurs in a sinusoidal manner.
JOINT MOTIONS DURING GAIT
Trunk and Upper Extremities.
During the gait cycle, the swing of the arms is out of phase with the legs. As the upper body moves for ward, the trunk twists about a vertical axis. The thoracic spine and the pelvis rotate in opposite directions to each other to enhance stability and balance. In contrast, the lumbar spine tends to rotate with the pelvis. The shoulders and trunk rotate out of phase with each other during the gait cycle. 20 Unless they are restrained, the arms tend to swing in opposition to the legs, the left arm swinging forward as the right leg swings forward, and vice versa. 4 Maximum flexion of both the elbow and shoulder joints occurs at initial contact interval of the opposite foot and maximum extension occurs at initial contact of the foot on the same side. 21 Although the majority of the arm swing results from momentum, the pendular actions of the arms are also produced by gravity and muscle action. 4 ,22 ~ ~ ~
Study Pearl the
the
-epancy, ess, the latter Trendelenburg enburg sign is lvis lists toward side during
L-________________
The posterior deltoid and teres major appear to be involved during the backward swing, The posterior deltoid serves as a braking mechanism at the end of the forward swing. The middle deltoid is active in both the forward and backward swing, perhaps to prevent the arms from brushing against the sides of the body during the swing.
Pelvis. The pelvis serves the double function of weight transfer and of acetabulum placement during gait. For normal gait to occur, the pelvis must both rotate and tilt. This combination of rotation and tilting serves to prevent excessive motion of the trunk. The rotation of the pelvis (approximately 4 degrees to each side) normally occurs about a vertical axis in the transverse plane toward the weight-bearing limb. 15 In addition to decreasing the lateral deviation of the COG, the pelvic rotation also results in a relative lengthening of the femur, and thus step length, during the termination of the swing period. 9 During the swing period, there is a slight pelvic tilt to the unsup ported leg (approximately 5 degrees). The downward tilting of the pelvis occurs in the frontal plane on the contralateral side of the stance limb. The pelvic tilt results in a relative adduction of the weight-bearing limb and a relative abduction of the non-weight-bearing limb. 9,20 Hip. ~
Hip motion occurs in all three planes during the gait cycle. Hip rotation occurs in the transverse plane. The hip rotates approx imately 40 to 45 degrees in the sagittal plane during a normal stride. 23 The hip begins in internal rotation during the loading response. Maximum internal rotation is reached near mid-stance.
CHAPTER 7. GAIT, POSTURE, ERGONOMICS, AND OCCUPATIONAL HEALTH
~
~
The hip externally rotates during the swing period, with maxi
mal external rotation occurring in terminal swing. 24
The hip flexes and extends once during the gait cycle, with the
limit of flexion occurring at the middle of the swing period, and
the limit of extension being achieved before the end of the
stance period (Table 7-3). At the point of initial contact, the hip
is in approximately 35 degrees of flexion, where it begins to
extend. Maximum hip flexion of 30 to 35 degrees occurs in late
swing period at about 85% of the gait cycle; maximum exten
sion of approximately 10 degrees is reached near toe-off at
approximately 50% of the cycle 23--2S (Table 7-3).
In the coronal plane, hip adduction occurs throughout early
stance and reaches a maximum at 40% of the cycle. 2s Hip
adduction totaling 5 to 7 degrees occurs in the early swing
period, which is followed by slight hip abduction at the end of
the swing phase, especially if a long stride is taken. 4•23 ,2s
The movements of the thigh and lower leg occur in conjunction with the rotation of the pelvis. The pelvis, thigh, and lower leg nor mally rotate toward the weight-bearing limb at the beginning of the swing period. 20
Knee. The knee flexes twice and extends twice during each gait cycle: once during weight bearing and once during non-weight bear ing (Table 7-3). It is fully extended before initial contact, flexes early in the stance period, extends again around mid-stance, then starts flexing again, reaching a peak early in the swing period. The flexion occurs so that the lower limb can be advanced during the swing period with min imum vertical displacement of the COG. During weight-bearing activities such as gait, the tibiofemoral joint is subject to constant large muscular loads, bending, and rotational moments. These forces become particularly significant during sports activities, which place additional stresses on the joint. The knee flexes to about 20 degrees during the loading response interval, and this serves to act as a shock-absorbing mechanism. The knee then begins to extend and, as the heel rises during the terminal stance interval, it is almost fully extended, but flexes again as the swing period begins. It then continues to flex as the leg moves into the swing period, before extending again prior to initial contact. s In normal walk ing, about 60 degrees of knee motion is required for adequate clearance of the foot in the swing period. The peak flexion is required during ini tial swing, right after toe-off, because at that point in the gait cycle, the toe is still pointed toward the ground. IS Tibiofemoral joint reaction forces increase to 5 to 6 times the body weight for running and stair climbing, and 8 times body weight with downhill walking. 26-28 A loss of knee extension, which can occur with a flexion defor mity, results in the hip being unable to extend fully, which can alter the gait mechanics. Foot and Ankle. Ankle joint motion during the gait cycle occurs primarily in the sagittal plane (Table 7-3). During normal gait, the initial contact with the ground is made by the heel. In individuals with poor
Study Pearl
289
"..
N ID Q
TABLE 7-3. JOINT MOTIONS AND MUSCLE ACTIVITY AT lHE HIP AND KNEE, AND JOINT POSITIONS AND MOTIONS OF lHE TIBIA, FOOT, AND ANKLE DURING GAIT PHASE Heel strike
Foot flat
Mid-stance
Heel-off
Toe-off
HIP Gluteus maximus and hamstrings work eccentrically to resist flexion moment at the hip. Erector spinae working eccentrically to control trunk flexion. The hip begins to extend from a position of 20 to 40 degrees of flexion. Reaction force anterior to the hip joint creating a flexion moment. Hip positioned in slight adduction and external rotation. Gluteus maximus and hamstrings contract concentrically to move hip toward extension. Hip moving into extension, adduction, and internal rotation. Hip moves through neutral position. Pelvis rotates posteriorly. Reaction force now posterior to hip joint creating an extension moment. Iliopsoas contracting eccentrically to resist hip extension. Gluteus medius creating reverse action to stabilize opposite pelvis. Hip positioned in 10 to 15 degrees of hip extension, abduction and external rotation. Iliopsoas activity continuing. Extension moment decreases after double-limb support begins. Hip moving toward 10 degrees of extension, abduction, and external rotation. Continued decrease of extension moment. Iliopsoas activity continuing. Adductor magnus working eccentrically to control pelvis.
KNEE
TIBIA
ANKLE
FOOT
Positioned in full extension before heel contact, but flexing as heel makes contact. Reaction force behind knee causing flexion moment. Quadriceps femoris contracting eccentrically to control knee flexion.
Slight external rotation
Moving into plantarflexion
Supination
In 20 degrees of knee flexion, moving toward extension. Flexion moment. After foot is flat, quadriceps femoris activity becoming concentric to bring femur over tibia. In 15 degrees of flexion, moving toward extension. Maximum flexion moment. Quadriceps femoris activity decreasing.
Internal rotation
Plantarflexion to dorsiflexion over a fixed foot
Pronation, adapting to support surface
Neutral rotation
3 degrees of dorsiflexion
Neutral
In 4 degrees of flexion, moving toward extension. Maximum flexion moment. Quadriceps femoris activity decreasing.
External rotation
Supination as foot becomes rigid for push-off
Moving from near full extension to 40 degrees of flexion. Reaction forces moving posterior to knee as knee flexes. Flexion moment. Quadriceps femoris contracting eccentrically.
External rotation
15 degrees of dorsiflexion toward plantarflexion Maximum dorsiflexion moment 20 degrees of plantarflexion Dorsiflexion moment
Supination
CHAPTER 7. GAIT, POSTURE, ERGONOMICS, AND OCCUPATIONAL HEALTH
control of dorsiflexion (e.g., hemiplegics), the initial contact is made with the low part of the heel and forefoot simultaneously. Ibis is usu ally accompanied by a toe drag during the swing period. The ankle is usually within a few degrees of the neutral position at the time of initial contact, with the heel slightly inverted and the sub talar joint slightly supinated. 30 The initial impact is taken through the lateral tubercle of the calcaneus, a structure unique to humans and designed to tolerate the shock of heel strike via the calcaneal fat pad. As the heel contacts the ground, its forward momentum comes to an abrupt halt. During the loading response interval, plantar flexion occurs at the talocrural joint, with pronation occurring at the subtalar joint.30 The pronation of the subtalar joint unlocks the foot and allows maximal range of motion of the midtarsal joint, which brings the artic ulating surfaces of the cuboid and navicular to a position relatively par allel to the weight-bearing surface and allows the forefoot to become supple. 31 ,32 This increase in midtarsal joint mobility enhances the abil ity of the foot to adapt to uneven terrain. At the end of the mid-stance interval, the talocrural joint is maxi mally dorsiflexed, and the subtalar joint begins to supinate. During the latter part of the stance period, the foot must become a rigid lever. From the mid-stance to the terminal stance interval, the foot is in supination (plantar flexion of the ankle, external rotation of the tibia, dorsiflexion and abduction of the talus, and inversion of the calca neus)Y Supination at the subtalar joint locks the foot into a rigid lever30 ,33 by promoting supination at the midtarsal joint, which results in the articulating surfaces of the cuboid and calcaneus adopting a position that is perpendicular to one another, thus stabi liZing their articulation. 32 The fixed cuboid acts as a fulcrum for the fibularis (peroneus) longus muscle, facilitating plantar flexion of the first metatarsal in push-offY Once the ankle is fully close-packed, the heel is lifted by a com bination of passive force and contraction from the taut gastrocnemius, and the soleus, The lifting of the heel accentuates the force applied to the mid- and forefoot, and reinforces the close packing of this area, while simultaneously unclose packing the ankle joint. As ankle plantar flexion reaches its peak at the end of the terminal stance interval, the first metatarsophalangeal joint is extended. The dorsiflexion of the first MTP places tension on the plantar fascia and helps to elevate the medial longitudinal arch through the windlass mechanism of the plantar fascia. This windless mechanism creates a dynamic stable arch and hence a more rigid lever for push-oEfY While the forefoot is on the ground and the heel is off, the heel is inverted and the foot is supinated. 30 The heel rise coincides with the opposite leg swinging by the stance legY Approximately 40% of the body weight is borne by the toes in the final stages of foot contact. 35 ,36 Muscle activity during push-off is designed to initiate propulsionY From initial contact to early mid-stance, the tibia moves anteriorly, internally rotating within the ankle mortise, and prodUcing talar adduc tion and plantar flexion, and calcaneal eversion (weight-bearing pronation of the subtalar joint)Y The forward tibial advancement requires approximately 10 degrees of ankle joint dorsiflexion to pre vent excessive pronation at the subtalar and oblique midtarsal joints,7,32,37
291
Study Pearl An .arlaptiyeJYsho#t~nedg~str()cne, mius.rnosclemayprodufeffiByement impairment{)}' restriQting.n.()rmal.dor3 siflexion .of the.ankJe fr(.jmoccurring duriJjlg·the . m'd3stancT.toh~?I·raise
portio~orthe gaitcyde'1lli~m()ti(}nis
l
compensated·rot·· b~increased.prona tionof·the· subt~la' .'...• ycre~ intertlalrota~ionoft . . > . y an~~sult. ant '''-in the Io1w jin\.F""'PIex. :'-.J
I
292
SECTION II. TESTS AND MEASURES
During the swing period, the ankle must dorsiflex in order for the forefoot to clear the ground. The ankle adopts a neutral position in terms of dorsiflexion and plantar flexion prior to the next initial contact.
MUSCLE ACTIONS The ankle and hip muscles are responsible for the majority of positive work performed during walking (54% of the hip and 36% of the ankle).38 The knee contributes the majority of the negative work (56%). 38 The muscle actions that occur dUring the stance period of gait are depicted in Tables 7-3 and 7-4.
Spine and Pelvis.
During the swing period, the semispinalis, rotatores, multifidus, and external oblique muscles are active on the side toward which the pelvis rotates. 4 The erector spinae and internal oblique abdominal muscles are active on the opposite side. The psoas
TABLE 7-4. MUSCLE FUNCTIONS OF 1HE LOWER LEG DURING 1HE STANCE PHASE OF GAIT MUSCLE
Heel Strike to Weight Acceptance Anterior tibialis Extensor hallucis longus Extensor digitorum Posterior tibialis Soleus Gastrocnemius
Mid-stance Posterior tibialis Soleus Flexor hallucis longus Flexor digitorum longus Posterior tibialis Soleus Gastrocnemius
ACTION
Eccentric--control pronation of subtalar joint Eccentric---clecelerate plantar flexion and posterior shear of tibia on talus Eccentric---clecelerate pronation of subtalar joint and internal rotation of the tibia
Eccentric---clecelerate fOIWard movement of tibia
Concentric-supinate subtalar and midtarsal joints
Push-off and Propulsion Peroneus longus Abductor hallucis
Concentric-plantar flexion of first ray
Peroneus brevis
Antagonist to supinators of subtalar and midtarsal joints
Flexor digitorum longus Extensor hallucis longus and brevis
Concentric-stabilize toes against ground Concentric-stabilize first metatarsophalangeal joint
Abductor hallucis Abductor digit quinti Flexor hallucis brevis Flexor digitorum brevis Extensor digitorum brevis Interossei, lumbricals
Concentric-stabilize midtarsal and forefoot, raise medial arch of foot in push-off
Data from Norkin CC: Examination of gait. In: O'Sullivan SB, Schmitz T], eels. Physical Rehabilitation. 5th ed. Philadelphia: FA Davis; 2007:317-363.
l
CHAPTER 7. GAIT, POSTURE, ERGONOMICS, AND OCCUPATIONAL HEALTH
293
major and quadratus lumborum help to support the pelvis on the side of the swinging limb, while the contralateral hip abductors also provide support.
Hip. During the early to mid portion of the swing phase, the iliop soas is the prime mover with assistance from the rectus femoris, sarto rius, gracilis, adductor longus, and possibly the tensor fascia latae, pectineus, and the short head of the biceps femoris during the initial swing interval. Perry notes the adductor longus muscle to be "the first and most persistent hip flexor."9 In terminal swing, there is no appre ciable action of the hip flexors when ambulating on level ground. Instead, the hamstrings and gluteus maximus are strongly active to decelerate hip flexion and knee extension. 23.25 Both these superficial muscles and their deeper counterparts, such as the hip adductors, the gemelli, and the short rotators, certainly contribute. 39 In rapid walking, there is increased activity of the sartorius and the rectus femoris dUring the swing period. 4 During initial contact, the gluteal muscles and the hamstrings contract isometrically with moderate intensity. The loading response interval is accompanied by hamstrings and gluteus maximus activity, which aid hip extension.23.25.41 The adductor magnus muscle supports hip extension and also rotates the pelvis externally toward the for ward leg. In mid-stance, coronal plane muscle activity is greatest as the abductors stabilize the pelvis. 42 --46 The muscle activity initially is eccentric as the pelvis shifts laterally over the stance leg. The gluteus medius and minimus remain active in terminal stance for lateral pelvic stabilization. The iliacus and anterior fibers of the tensor fas ciae latae are also active in the terminal stance and pre-swing inter vals. 23 ,25 Notable, but inconsistent, muscle activity of the rectus femoris is described by several authors. 23 ,25.41 The only muscles of the hip that contract significantly during the last part of the stance period are the adductor magnus, longus, and possibly brevis. 4 Knee. During the swing period, there is very little activity from the knee flexors. The knee extensors contract slightly at the end of the swing period prior to initial contact. During level walking the quadriceps achieve peak activity dUring the loading response interval (25% maxi mum voluntary contraction) and are relatively inactive by mid-stance as the leg reaches the vertical position and "locks," making quadriceps con traction unnecessary.47-50 Hamstring involvement is also important to normal knee function. The hamstrings provide dynamic stability to the knee by resisting both medial-lateral and anterior translational forces on the tibia. 27 The coactivation of the antagonist muscles about the knee during the loading response aids the ligaments in maintaining joint sta bility, by equalizing the articular surface pressure distribution and con trolling tibial translation. 51 ,52 The hamstrings also demonstrate activity at the end of the stance period. Hamstring activity during graded walking and increased speed demonstrates increased activity and for a longer duration. 4 Foot and Ankle. During the beginning of the swing period, the tibialis anterior, extensor digitorum longus (EDL), extensor hallucis
Study Pearl The passive hip extension moment at initial contact has been calculated to be approximately 60% to 100% of the total moment occurring during the stance period, suggesting that passive elastic energy is stored and released during gait. 40
J
Study Pearl Electromyographic activity of the hamstrings during level walking has shown that the hamstrings decelerate the leg prior to heel contact and then act synergistically with the quadri ceps during the stance period to sta bilize the knee. 49,53
L
294
SECTION II. TESTS AND MEASURES
Study Pearl In the presence of calf muscle weak ness there is an inability to control forward advancement of the tibia, resulting in excessive dorsiflexion during single limb support and a lack of heel rise during late stance. 10
Study Pearl During the stance period, three ankle rocker periods are recognized. 1. The first rocker occurs between the initial contact and when the foot is fJat on the floor. This rocker involves the ankle dorsiflexors working eccentrically to gradually permit the foot to come into full contact with the ground. 2. During the second rocker, the foot remains flat on the ground while the tibia advances. This motion is due to the plantar flexors working eccentrically to control the· ankle dorsiflexion that occurs. 3. The third rocker is the push-off required for advancement of the limb. This is the period of power generation. Thus, the first two rockers are decel eration rockers, where the perspective muscles are working eccentrically by undergoing a lengthening contraction with energy absorption. The third rocker is an acceleration rocker and aids in propulsion.
longus (EHL), and possibly the fibularis (peroneus) tertius contract concentrically with slight to moderate intensity tapering off during the middle of the swing period. 4,54,55 As the swing period begins, the fibu laris (peroneus) longus also contracts concentrically to evert the entire foot and bring the sole of the foot parallel with the substrate. At the point where the leg is perpendicular to the ground during the swing period, the tibialis anterior, EDL and EHL group of muscles contract concentrically to dorsiflex and invert the foot in preparation for the ini tial contact,4,54,55 There is very little activity, if any, from the plantar flexors during the swing period. Following initial contact, the anterior tibialis works eccentrically to lower the foot to the ground during the loading response intervaP4,55 Calcaneal eversion is controlled by the eccentric activity of the poste rior tibialis, and the anterior movement of the tibia and talus is limited by the eccentric action of the gastrocnemius and soleus muscle groups as the foot moves toward mid-stance. 56 Pronation occurs in the stance period to allow for shock absorption, ground terrain changes, and equilibrium. 32 ,57 The triceps surae become active again from mid stance to the late stance period, contracting eccentrically to control ankle dorsiflexion as the COG continues to move forward. In late stance period, the Achilles tendon is stretched as the triceps surae contracts and the ankle dorsiflexes. 58 At this point the heel rises off the ground and the action of the plantar flexors changes from one of eccentric contraction to one of concentric contraction. The energy stored in the stretched tendon helps to initiate plantar flexion and the initiation of propulsion.58 The fibularis (peroneus) longus provides important stability to the forefoot during propulsion.
INflUENCES ON GAIT
Pain. Refer to "Abnormal Gait Syndromes" later in this chapter. Posture. The patient's posture is examined for the presence of asymmetry, or any deviations in the relaxed standing stance (see the discussion of posture later in this chapter). Good alignment of the weight-bearing segments of the body: ~ ~
Study Pearl The consequences of a triple arthrodesis on gaitfunction include 10 ; ~ Loss of subtalar joint motion, resulting in reduced shock absorp tion during weight acceptance. ~ An inability to supinate in terminal stance, diminishing the forefoot rocker effect. .. Compromised ability to progress beyond the supporting foot. .. Diminished stride fength,
~
Reduces the likelihood of strain and injury by reducing joint friction and tension in the soft tissues. Improves the stability of the weight-bearing limb and the bal ance of the trunk. The stability of the body is directly related to the size of the base of support. In order to be stable, the inter section of the line of gravity with the base of support should be close to the geometric center of the base. 59 Reduces excess energy expenditure.
Flexibility and the Amount of Available Joint Motion. A decrease in flexibility and/or joint motion may result in an increase in "internal resistance" and an increase in the energy expenditure required.
Endurance-Economy of Mobility. Economy of mobility is a measurement of submaximal oxygen uptake (submax VO) for a
CHAPTER 7. GAIT, POSTURE, ERGONOMICS, AND OCCUPATIONAL HEALTH
given speed. 60 ,6l A decline in functional performance may be evi denced by an increase in submax V0 2 for walking. 62 This change in economy of mobility may be indicative of an abnormal gait pattern. 62 Some researchers have reported no gender differences for economy of mobility,6.}-- 20 cm) Deformity such as hip abductor muscle contracture Genu valgus Fear of losing balance Leg length discrepancy
Decreased walking base
«
10 cm) Hip adductor muscle contracture Genu varum
Excessive eversion of calcaneus during initial contact through mid-stance Excessive tibia vara (refers to the frontal plane position of the distal 1/3 of the leg as it relates to the supporting surface) Forefoot varus Weakness of tibialis posterior Excessive lower extremity internal rotation (due to muscle imbalances, femoral anteversion)
Excessive pronation during mid-stance through terminal stance Insufficient ankle dorsiflexion (less than 10 degrees) Increased tibial varum Compensated forefoot or rearfoot varus deformity Uncompensated forefoot valgus deformity Pes planus Long limb Uncompensated medial rotation of tibia or femur Weak tibialis anterior
Excessive supination during initial contact through mid-stance Limited calcaneal eversion Rigid forefoot valgus Pes cavus Uncompensated lateral rotation of the tibia or femur Short limb Plantar flexed first ray Upper motor neuron muscle imbalance
Excessive dorsiflexion Compensation for knee flexion contracture Inadequate plantar flexor strength Adaptive shortening of dorsiflexors Increased muscle tone of dorsiflexors Pes calcaneus deformity
Excessive plantar flexion Increased plantar flexor activity Plantar flexor contracture (Continued)
308
SECTION II. TESTS AND MEASURES
TABLE 7-7. SOME GAIT DEVIATIONS AND THEIR CAUSES (Continued)
GAIT DEVIATIONS
REASONS
Excessive varus Contracture Overactivity of the muscles on the medial aspect of the foot
Excessive valgus Weak invertors Foot hypermobility
Decreased or absence of propulsion (plantar flexor gait) Inability of plantar flexors to perform function resulting in a shorter step length on the involved side. Data from Giallonardo LM. Clinical evaluation of foot and ankle dysfunction. Phys Ther. 1988;68:1850--1856; Epler M. Gait. In: Richardson JK, 19larsh ZA, eds. Clinical Orthopaedic Physical Therapy. Philadelphia: Saunders; 1994:602--625; Hunt GC, Brocato RS. Gait and foot pathomechanics. In: Hunt GC, ed. Physical Therapy o/the Foot and Ankle. Edinburgh: Churchill Livingstone; 1988; Krebs DE, Robbins CE, Lavine L, et al. Hip biomechanics dUring gait. J Orthop Sports Phys Ther. 1998;28:51-59; Larish DD, Martin PE, Mungiole M. Characteristic panerns of gait in the healthy old. Ann NY Acad Sci. 1987;515:18--32; Levine D, Whinle M. Gait Analysis: The Lower Extremities. La Crosse, WI, Orthopaedic Section, APTA, Inc. 1992; Perry J. Gait Analysis: Normal and Pathological hmction. Thorofare, NJ: Slack; 1992; and Song KM, Ha1liday SE, Linle DG. The effect of limb-length dis crepancy on gait. J BoneJoint Surg. 1977;79A:1690--1698.
The patient's foot is also examined for callus formation, blisters, corns, and bunions. Callus formation on the sole of the foot is an indicator of dysfunction and provides the clinician with an index to the degree of shear stresses applied to the foot, and clearly outlines abnormal weight-bearing areas llO Adequate amounts of calluses may provide protection, but in excess amounts they may cause pain. Callus formation under the second and third metatarsal heads could indicate excessive pronation in a flexible foot, or Morton's neuroma if just under the former. A callus under the fifth, and sometimes the fourth, metatarsal head may indicate an abnormally rigid foot. The patient is then asked to walk in his or her usual manner and at his or her usual speed. The clinician begins the gait assessment with an overall look at the patient while he or she walks, noting the cadence, stride length, step length, and velocity. The arm swing during gait should also be observed. If an individual has a problem with the foot and/or ankle on one side, the opposite arm swing is often decreased. 34 The patient is observed from head to toe and then back again, from the side, from the front, and then from the back. In addition to observing the patient walking at his or her normal pace, the clinician should observe the patient walking at varying speeds, as appropriate. This can be achieved on a treadmill by adjust ing speed, or by asking the patient to change his or her walking speed. Once an overall assessment has been made of the patient's gait, the clinician can focus attention on the various segments of the kinetic chain of gait, including the trunk, pelViS, lumbar spine, hip, knee, and ankle and foot (Table 7-3). Attempts are made to determine the pri mary cause of any gait deviations or compensations (Table 7-7).
Anterior View. When observing the patient from the front, the cli nician can note the following;
CHAPTER 7. GAIT, POSTURE, ERGONOMICS, AND OCCUPATIONAL HEALTH ~
~ ~ ~ ~
~
~ ~
~
~
~ ~
~
~
~ ~
The subject's head should not move too much during gait in a lateral or vertical direction, and should remain fairly stationary during the gait cycle. The amount of lateral tilt of the pelvis.
The amount of lateral displacement of the trunk and pelvis.
Whether there is excessive swaying of the trunk or pelvis.
The amount of vertical displacement. Vertical displacement can
be assessed by observing the patient's head. A "bouncing gait" is characteristic of adaptively shortened gastrocnemii, or increased tone of the gastrocnemius and soleus. The reciprocal arm swing. Movements of the upper trunk and limbs usually occur in the opposite directions to the pelvis and the lower limbs. Whether the shoulders are depressed, retracted, or elevated.
Whether the elbows are flexed or extended.
The amount of hip adduction/abduction that occurs. Causes of
excessive adduction include an excessive coxa vara angle, hip abductor weakness, hip adductor contracture or spasticity, or contralateral hip abduction contracture. Excessive hip abduc tion may be caused by an abduction contracture, a short leg, obeSity, impaired balance, or hip flexor weakness. 1lI The amount of valgus or varus at the knee. During gait, there may be an obvious varus-extension thrust. According to Noyes and aSSOciates, this gait pattern is characteristic of chronic injuries to the posterolateral structures of the knee. ll2 The width of the base of support. The degree of toe out. The term toe-out refers to the angle formed by the intersection of the foot's line of progression and the line extending from the center of the heel through the second metatarsal. The normal toe-out angle is approximately 7 degrees, which decreases as the speed of gait increases. lLl Whether any circumduction occurs. Hip circumduction can indicate a leg length discrepancy, decreased ability of the knee to flex, or hip abductor shortening or overuse. Whether any hip hiking occurs. Hip hiking can indicate a leg length discrepancy, hamstring weakness, or quadratus lumbo rum shortening. Evidence of thigh atrophy. The degree of rotation of the whole lower extremity. Because positioning the lower extremity in external rotation decreases the stress on the subtalar joint complex, an individual with a foot/ankle problem will often adopt this position during gaitY Excessive internal or external rotation of the femur can indicate adaptive shortening of the medial (anteversion) or lateral ham strings (retroversion).
Lateral View ~ ~
The amount of thoracic and shoulder rotation. Each shoulder and arm should swing reciprocally with equal motion. Orientation of trunk. The trunk should remain erect and level during the gait cycle as it moves in the opposite direction to the pelvis. Compensation can occur in the lumbar spine for a loss of motion at the hip. A backward lean of the trunk may result from weak hip extensors or inadequate hip flexion. A forward lean of the trunk may result from pathology of the hip, knee, or
309
310
SECTION II. TESTS AND MEASURES
~
~
~
~
~ ~
~
~
~
ankle, abdominal muscle weakness, decreased spinal mobility, or hip flexion contracture. Forward leaning dUring the loading response and early mid-stance intelVals may indicate hip exten sor weakness. 89 Orientation of the pelVic tilt. An anterior pelvic tilt of 10 degrees is considered normal. Excessive anterior tilting can be due to weak hip extensors, a hip flexion contracture, or hip flexor spasticity. Excessive posterior pelvic tilting during gait usually occurs in the presence of hip flexor weakness. Degree of hip extension. Causes of inadequate hip extension and excessive hip flexion contracture, iliotibial band contrac ture, hip flexor spasticity, or pain. 111 Causes of inadequate hip flexion may include hip flexor weakness or a hip joint arthrodesis. lll Knee flexion and extension. The knee should be extended dur ing the initial contact intelVal, followed by slight flexion during the loading response intelVal. During the swing period there must be sufficient knee flexion. Causes of excessive knee flex ion and inadequate knee extension include inappropriate ham string activity, knee flexion contracture, soleus weakness, or excessive ankle plantar flexion. Causes of inadequate flexion and excessive extension at the knee include quadriceps weak ness, pain, quadriceps spasticity, excessive ankle plantar flex ion, hip flexor weakness, or knee extension contracturesY4 Individuals with genu reculVatum may have a functional strength deficit in the quadriceps muscle or gastrocnemius that allows knee hyperextension. lIS Ankle dorsiflexion and plantar flexion. During the mid-stance, the ankle dorsiflexes, and the body pivots over the stationary foot. At the end of the stance period, the ankle should be seen to plantarflex to raise the heel. At the beginning of the swing period the ankle is plantarflexed, moving into dorsiflexion as the swing period progresses, reaching a neutral position at the time of heel contact at the termination of the swing. Excessive plantar flexion in mid-swing, initial contact, and loading response may be due to pretibial (especially the anterior tib ialis) weakness. Excessive plantar flexion may also be due to a plantar flexion contracture, soleus and gastrocnemius spastic ity, or weak quadricepsy6 Excessive dorsiflexion may be due to soleus weakness, ankle fusion, or persistent knee flexion during the mid-stance period. 89 The stride length of each limb. Cadence. The cadence should be normal for the patient's age (Table 7-7). Heel rise. An early heel rise indicates an adaptively short ened Achilles tendon. 34 Delayed heel rise may indicate a weak gastrocnemius-soleus complex. Heel contact. A low heel contact during initial contact may be due to a plantar flexion contracture, tibialis anterior weakness, or premature action by the calf muscles. 116 Pre-swing. An exaggerated pre-swing is manifested by the patient walking on his or her toes. The causes for this include pes equines deformity, adaptive shortening or increased tone of the triceps surae, weakness of the dorsiflexors, and knee flex ion occurring at mid-stance. A decreased pre-swing is often
CHAPTER 7. GAIT, POSTURE, ERGONOMICS, AND OCCUPATIONAL H£ALTH
311
characterized by a lack of plantar flexion at terminal stance and pre-swing. The causes for this can be ankle or foot pain or weakness of the plantar flexor muscles.
Posterior View ~
~
~ ~
~ ~
The amount of subtalar inversion (varus)/eversion (valgus). Excessive inversion and eversion usually relate to abnormal muscular control. Generally speaking, varus tends to be the dominant dysfunction in spastic patients, while valgus tends to be more common with flaccid paralysis. 116 Base of support.
Pelvic list.
Degree of hip rotation. As in standing, excessive femoral inter
nal rotation past the mid stance of gait will accentuate genu recurvatum. Causes of excessive external hip rotation may include gluteus maximus overactivity and excessive ankle plan tar flexion. III Cause of excessive internal hip rotation include medial hamstring overactivity, hip adductor overactivity, ante rior abductor overactivity, or quadriceps weakness. 1 11 The amount of hip adduction/abduction. The amount of knee rotation.
QUANTITATIVE GAIT ANALYSIS Quantitative gait analysis (Table 7-8) is used to obtain information on spatial and temporal gait variables, as well as motion patterns. 1l7 Imaging-based systems are the most sophisticated and expensive methods of obtaining quantitative data.
Gait Analysis Profiles and/or Scales ~
Functional ambulation profile (FAP). DeSigned to examine gait skills on a continuum from standing balance in the parallel bars to independent ambulation. 118 A more recent version of the FAP, which incorporates five environmental challenges that the individual may negotiate with or without use of orthotics or assistive devices, is called the Emory Functional Ambulation Profile (EFAP).
TABLE 7-8. GAlT VARIABLES FOR QUANTITATIVE GAlT ANALYSIS VARIABLE Speed Cadence Velocity Acceleration Stride time Step time Stride length Swing time Step width Foot angle
DESCRIPTION A scalar quantity that has magnitude but not direction The number of steps taken by a patient per unit of time A measure of a body's motion in a given direction The rate of change of velocity with respect to time The amount of time that elapses during one stride. Both stride times should be measured The amount of time that elapses between consecutive right and left foot contacts (heel strikes). Both right and left step times should be measured The linear distance between two successive points of contact of the same foot The amount of time during the gait cycle that one foot is off the ground The width of the walking base (base of support) L~ the linear distance between one foot and the opposite foot The angle of foot placement with respect to the line of progression (degree of toe-out or toe-in)
Data from Norkin Cc. Examination of gait. In: O'Sullivan SB, Schmitz T], eels. Physical Rehabilitation. 5th ed. Philadelphia: FA Davis; 2007:317-363.
312
SECTION II. TESTS AND MEASURES ~
Functional independence measure (FIM)y9-122 A multidimen sional scale that assesses locomotion as one dimension of over all functional status. The FIM has two domains of function: motor (self-care, sphincter control, ability to transfer, and loco motion) and cognitive (communication and social cognition). The scoring criteria for the ambulation component of the loco motion subscale are summarized in Table 7-9. ~ Iowa Level of Assistance Scale. Examines four functional tasks (one of which involves gait): getting out of bed, standing from bed, ambulating 15 feet (4.57 m), and walking up and down three steps. ~ Gait Abnormality Rating Scale (GARS).123 Designed to iden tify patients living in nursing homes who were at risk for falling. The Modified GARS (GARS-M) is a modified seven-item version. ~ Fast Evaluation of Mobility Balance and Fear (FEMBAF). An instrument designed to identify risk factors, functional per formance, and factors that hinder mobility. ~ Functional ambulation classification (FAC) .124.1 25 Six functional categories are defined: 1. Nonfunctional ambulation. 2. The assistance of another for support and balance is required. 3. Light touch assistance is required. 4. The patient needs verbal cueing for occasional safety assistance. 5. Patient is independent in ambulation on level surfaces. 6. Patient is independent in ambulation on all surfaces, includ ing stairs and inclines. ~ Timed up and go. 126--130 Patients are asked to rise from a seated position in a standard high chair, walk 3 meters on a level sur face, turn, walk back to the chair, and return to a seated posi tion, moving as quickly as they are safely able. Performance is based on total time to complete the task. 117
TABLE
7-9. SCORING CRITERIA FOR THE LOCOMOTION COMPONENT OF THE FIM™
SCORE
7
6 5
4
3 2 1
CRITERIA
Able to walk at least 150 feet (50 m) completely independently, without any type of assistive device or wheelchair, safely and within a reasonable (functional) period of time Able to walk at least 150 feet (50 m) independently but requires an assistive device (orthosis, prosthesis, wheelchair, special shoes, cane, crutches, walker), or takes more than reasonable time, or has safety concerns Requires stand by supervbion, cueing, or coaxing to walk or propel wheelchair at least 150 feet (50 m) Requires minimum contact assistance (patient contributes 75% effort) to walk or propel wheelchair at least 150 feet (50 m) Requires moderate assistance (patient contributes 50% to 74% effort) to walk or propel wheelchair a minimum of 150 feet (50 m) Requires maximal assistance of one person (patient contributes 2'i% to 49% effort) to walk or propel wheelchair 'i0 feet (17 m) Requires total assistance (patient contributes less than 25% effort), or requires assistance of more than one helper, or is unable to walk or propel wheelchair at least 50 feet (17 m)
Dam from Dickson HG, Kohler F. FumIiunal independence measure (FIM). Scand] RehabilMed. 1999:31:63-64: Grey N, Kennedy P. The Functional Independence Measure: a comparative study of clinician and self ralings. Paraplegia. 1993:31:457--461; Hamilton BB, Laughlin ]A, Fiedler RC, ela1. Intenater reliability of the 7-level functional independence measure (FIM). Scand] Rehabil Med. 1994;26:115-119: and Keith RA, Granger CV, Hamilton BB, el OIL The functional independence measure: a new 1001 for rehabilitation. Adv Clin Rehabil. 1987;1:6-18.
CHAPTER 7. GAIT, POSTURE, ERGONOMICS, AND OCCUPATIONAL HEALTH
POSTURE Posture describes the relative positions of different joints at any given moment,131 Like "good movement," "good posture" is a subjective term based on what the clinician believes to be correct based on ideal models. Over the course of time, various definitions have been put forward to describe the attributes of good posture. 25 ,13 2- 136 Postural control is fundamental to movement, allowing an indi vidual to 137 : .. .. .. ..
313
Study Pearl
system to perform ,actions ,requiring
the least amount of ~nergy to achieve the desired effect."132
""
,
Maintain a position.
Move into and out of positions.
Recover from instability.
Anticipate and prepare for instability.
Postural control is described under three conditions 137 : .. Steady-state adjustments: require movement strategies that con trol a stable, quiet position in which the center of body mass is kept within the base of support. .. Anticipatory adjustments: require movement strategies that recover stability in response to a planned, voluntary movement. .. Reactive adjustments: require strategies that recover stability in response to an unexpected, external disturbance. The postural examination may be assessed statically, when the body is at rest, or dynamically with the body in motion. The clinician observes the patient from the front, back, and sides, ideally with a patient standing near a plumbline for vertical reference for each view and with the clinician positioned to be able to see the patient's entire body: .. Standing: when observing from the anterior or posterior view, the plumbline should be aligned with a point midway between the feet and should divide the patient equally into the left: and right halves. When observing the patient from the side, the plumbline should be aligned slightly anterior to the lateral malleolus. .. Dynamic: refer to "Clinical examination of Gait" earlier in this chapter. The postural assessment gives an overall view of the patient's muscle function in both chronic and acute pain states. The examina tion enables the clinician to differentiate between possible provocative causes, such as structural variations, altered joint mechanics, muscle imbalances, and/or the residual effects of pathology. Skeletal malalignment may be defined as either abnormal joint alignment or deformity within a bone. Abnormal, or nonneutral, align ment is defined as "positioning that deviates from the midrange posi tion of function.,,138 To be classified as abnormal, nonneutral alignment must produce physical functional limitations. Nonneutral alignment may produce neuromusculoskeletal pathology at adjacent or distal
Study Pearl
. ext1ernal auditory meatus, acromio clavicular joints, greater trochanters, and lateral malleoli. .. In the anteroposterior view, approx imate skeletal symmetry allows division of the body into symmetri cal halves with bisection of the fol lowing points: glabella, frenulum, episternal notch, xiphoid process, symphysis pubis, and a point mid way between the medial malleoli of the ankle joints.
314
SECTION II. TESTS AND MEASURES
Study Pearl
I
Amuscle.·imJjalance~cursWhen.the
r~~ti?? .'eng~~:.~f~~~gonist • . an~~h.Y
antag()nis~.~hang~s):,with· one ·a(lopt..
in~as~orer restinglen?th than nor m~ll~ndthe other a~9Ptin~a.tonger resting length than norrnal.T~~.inert tissues,. suc:h as the ligaments and joint c:apsules, reatt in asirnilar fash ion, therehy alteringjoinrpl.ay, which in turn alters arthrokinernatic:func:tion aridforc:e transmission as. thernusdes around that joint..\llit~~·,their length in an attempt to mini:mi.ze the stresses at that Joint. 139 ,144,145
---------------------,
Study Pearl WhiTe most dinidatls tan apprec:iate
that repeated movement patterns per
formed In a Jherapeutic manner can
beR~nen¢j(l,l,jtmust als.? berernern:'
beredthat repeatedl)'lotions per
formed.erroneously can ··produce
changes in l)'I1,lsdetension, muscle
strength, length,.andsliffness. 15o
Study Pearl A sustained change in muscle length is postulated toinfJuence the informa tion sent hy the proprioceptors,which can c.ause alterations in recruitment patterns and the domihanee of one synergist over andther. 150,152
Study Pearl Postural imbalances involve the entire body, as should any corrections. It is important to remember. that prior to any intervention an appropriate exam . ination must take place. ~
joints through compensatory motions or postures. Nonneutral alignment, whether maintained statically, or performed repetitively, appears to be a key precipitating factor in soft-tissue and neurologic pain. 139 This may be due to an alteration in joint load distribution or the force transmis sion of the muscles. Nonneutral alignment can occur in the frontal (scoliosis, a leg length discrepancy) and sagittal planes (forward head, anteriorly rotated pelvis, a decrease in the lumbar lordosis, knee recurvatum, shoulder protraction), and can progress to a somatic dysfunction. 14 o 142 Sustained postures can also produce muscle imbalances and pain, especially if the joint is held at the end of its range. 143 It is theorized that if a muscle lengthens as part of a compensation, muscle spindle activity increases within that muscle, producing recip rocal inhibition of that muscle's functional antagonist, and resulting in an alteration in the normal force-couple and arthrokinematic relation ship, thereby effecting the efficient and ideal operation of the move ment system. 146-150 The pain from sustained positions is thought to result from ischemia of the isometrically contracting muscles, localized fatigue, or an excessive mechanical strain on the structures. Intramuscular pres sure can compress the blood vessels and prevent the removal of metabolites, and the supply of oxygen, either of which can cause tem porary painy,l It is quite normal for muscles to frequently change their lengths during movements. However, this change in resting length becomes pathologic when it is sustained through incorrect habituation, or as a response to pain. Muscles maintained in a shortened or lengthened position will eventually adapt to their new positions. Although these muscles are initially incapable of producing a maximal contraction in the newly acquired positions,153 changes at the sarcomere level allow the muscle to eventually produce maximal tension at this new length. 150 While this may appear to be a satisfactory adaptation, the changes in length produce changes in tension development, as well as changes in the angle of pull,1'i4 For example, a passively insufficient muscle is acti vated earlier in a movement than a normal muscle, and has a tendency to be more hypertonic, thereby producing a reflex inhibition of the antagonists. 146,147,155,156 For the vast majority of people, static postures are a rarity, while dynamic postures are more functional. JulP56 and Janda157 developed a system that characterized muscles based on common patterns of kinetic chain dysfunction into two functional divisions: a movement group, and a stabilization group (Table 7-10). More recently, Sahrmannl'iO has stressed the importance of obser vation along both directions of the kinetic chain, and the importance of examining joints proXimal to the site of the disorder, or symptomology, to determine the mechanical cause of the symptoms rather than iden tifying the painful tissues. Once the mechanical source is identified, the focus of the intervention is the simultaneous retraining of the muscles, by contracting the lengthened muscle when it is in a shortened posi tion, and stretching the shortened muscle. 150 Common lower limb skeletal malalignments and possible cor related and compensatory motions or postures are compiled in Table 7-11. Common postural deformities of the thoracic region include l'i8:
CHAPTER 7. GAIT, POSTURE, ERGONOMICS, AND OCCUPATIONAL HEALTH
315
TABLE 7-10. FUNCTIONAL DIVISION OF MUSCLE GROUPS TONIC (MOVERS) GROUP
POSTURAL (STABILIZERS) GROUP
Examples Gastrocnemius/soleus Tibialis posterior Short hip adductors Hamstrings Rectus femoris Tensor fascia lata Erector spinae Quadratus lumborum Pectoralis major Upper portion of trapezius Levator scapulae Sternocleidomastoid Scalenes Upper limb flexors
Examples Peronei Tibialis anterior Vastus medialis and lateralis Gluteus maximus, medius, minimus Serratus anterior Rhomboids Lower portion trapezius Short/deep cervical flexors Upper limb extensors Rectus abdominis
Characteristics Primarily type IIa muscle fibers Prone to adaptive shortening Prone to develop hypertonicity Dominate in new movement situations Generally cross two or more joints
Characteristics Primarily type I muscle fibers Prone to develop weakness and muscle inhibition Dominate in postural or sustained activities Primarily cross one joint
Reproduced. with permission, from .lull GA, Janda V. Muscle and motor control in low back pain. In: Twomey LT, Taylor JR, cill,. Physicallberapy a/the Low Back: Clinics in Physical Therapy. New York: Churchill Livingstone; 1987:258. Copyright © Elsevier. ~
~
~ ~
Dowager's hump. 'nus deformity is characterized by a severely
kyphotic upper dorsal region, which result'> from multiple anterior
wedge compression fractures in several vertebrae of dle middle to
upper moracic spine, usually caused by postmenopausal osteo
porosis or long-term corticosteroid merapy (specificity, 0.99).159
Hump back. This deformity is a localized, sharp, posterior
angulation, called gibbus, produced by an anterior wedging of
one of two thoracic vertebra as a result of infection (tuberculo
sis), fracture, or congenital bony anomaly of the spine 160
Round back. This deformity is characterized by decreased
pelvic inclination and excessive kyphosis.
Flat hack. This deformity is characterized by decreased pelVic
inclination, increased kyphosis, and a mobile thoracic spine.
Other deformities associated with this region include: ~
~
~
Barrel chest. In this deformity, a forward and upward project
ing sternum increases the anteroposterior diameter. The barrel
chest results in respiratory difficulty, stretching of the inter
costal and anterior chest muscles, and adaptive shortening of
the scapular adductor muscles.
Pigeon chest. In this deformity, a forward and downward project
ing sternum increases me anteroposterior diameter. The pigeon
chest results in a lengthening of dle upper abdominal muscles and
an adaptive shortening of me upper intercostal muscles.
Funnel chest. In this deformity, a posterior-projecting sternum
occurs secondary to an outgrowili of dle ribs. 161 The funnel chest
results in adaptive shortening of me upper abdominals, shoulder
adductors, pectoralis minor, and intercostal muscles, and in length
ening of me moracic extensors and middle and upper trapezius.
316
SECTION II. TESTS AND MEASURES
TABLE 7-11. SKELETAL MALALIGNMENT OF THE LOWER QUARTER AND CORRELATED AND COMPENSATORY MOTIONS OR POSTURES
MALALIGNMENT
POSSIBLE CORRELATED MOTIONS OR POSTURES
POSSIBLE COMPENSATORY MOTIONS OR POSTURES
Ankle and Foot
Ankle equinus
Rearfoot varus Excessive subtalar supination (calcaneal valgus)
Tibial; tibial and femoral; or tibial, femoral, and pelvic external rotation
Rearfoot valgus Excessive subtalar pronation (calcaneal valgus)
Tibial; tibial and femoral; or tibial, femoral, and pelvic internal rotation Hallux valgus Subtalar supination and related rotation along lower quarter
Forefoot varus
Hypermobile first ray Subtalar or midtarsal excessive pronation Hip or knee flexion Genu recurvatum Excessive internal rotation along the lower quarter chain Hallux valgus Plantar flexed first ray Functional forefoot valgus Excessive or prolonged midtarsal pronation Excessive external rotation along the lower quarter chain Functional forefoot varus Plantar flexed first ray Hallux valgus Excessive midtarsal or subtalar pronation or prolonged pronation Excessive tibial; tibial and femoral; or tibial, femoral, and pelvic internal rotation, or all with contralateral lumbar spine rotation Excessive midtarsal or subtalar supination Excessive tibial; tibial and femoral; or tibial, femoral, and pelvic external rotation, or all with ipsilateral lumbar spine rotation
Forefoot valgus
Hallux valgus Subtalar pronation and related rotation along lower quarter
Metatarsus adductlis
Hallux valgus Internal tibial torsion Flat foot
Hallux valgus
Forefoot valgus Subtalar pronation and related rotation along the lower quarter33
Excessive tibial; tihial and femoral; or tibial, femoral, and pelvic external rotation, or all with ipsilateral lumbar spine rotation
Pes planus Excessive subtalar pronation External tibial torsion Lateral patellar subluxation Excessive hip adduction Ipsilateral hip excessive internal rotation Lumbar spine contralateral rotation Excessive lateral angulation of tihia in frontal plane; (tibial varum); (tihia vaw) Internal tibial torsion Ipsilateral hip external rotation Excessive hip abduction Ankle plantar flexion Excessive anterior pelvic tilt
Forefoot varus Excessive suhtalar supination to allow lateral heel to contact ground In-toeing to decrease lateral pelvic sway during gait Ipsilateral pelvic external rotation
In~toeing
Knee and Tibia Genu valgus
Genu varus
Genu recUlvatum
Forefoot valgus Excessive subtalar pronation to allow medial heel to contact ground Ipsilateral pelvic internal rotation
Posterior pelvic tilt Flexed trunk posture Excessive thoracic kyphosis
CHAPTER 7. GAIT, POSTURE, ERGONOMICS, AND OCCUPATIONAL HEALTH
317
TABLE 7-11. SKELETAL MALALIGNMENT OF THE LOWER QUARTER AcI\lD CORRELATED AND COMPENSATORY MOTIONS OR POSTURES (Continued)
MALALIGNMENT External tibial torsion
Internal tibial torsion
Excessive tibial retroversion (posterior slant of tibial plateaus) Inadequate tibial retrotorsion (posterior deflection of proximal tibia due to hamstrings pull) Inadequate tibial retroflexion (bowing of the tibia) Bowleg deformity of tibia (tibia vard, tibial varum)
Hip and Femur Excessive femoral anteversion (anteversion)
POSSIBLE CORRELATED MOTIONS OR POSTURES Out-toeing Excessive suhtalar supination with related rotation along lower quarter In-toeing Metatarsus adductus Excessive subtalar supination with related rotation along lower quarter Genu recurvatum
Functional forefoot varus Excessive suhtalar pronation with related rotation along lower quarter Functional forefoot valgus Excessive subtalar pronation with related rotation along lower quarter
Flexed knee posture
Altered alignment of Achilles tendon causing altered associated joint motion Internal tibial torsion
In-toeing Excessive suhtalar pronation Lateral patellar subluxation
Femoral retrotorsion (retroversion)
Out-toeing Excessive suhtalar supination
Excessive femoral neck to shaft angle (coxa valga)
Long ipsilateral lower limb and correlated motions or postures of a long limh Posterior pelvic rotation Supinated subtalar joint and related external rotation along the lower quarter Pronated subtalar joint and related internal rotation along lower quarter Short ipsilateral lower limb and correlated motions or postures along lower quarter; anterior pelvic rotation
Decreased femoral neck to shaft angle (coxa vara)
POSSIBLE COMPENSATORY MOTIONS OR POSTImES
Forefoot valgus Excessive subtalar pronation Excessive external tibial torsion Excessive knee external rotation Excessive tibial; tibial and femoral; or tibial, femoral, and pelvic external rotation; or all with ipsilateral lumbar spine rotation Excessive knee internal rotation Excessive tibial; tibial and femoral; or tibial, femoral, and pelvic internal rotation; or all with contralateral lumhar spine rotation Excessive ipsilateral subtalar pronation Excessive contralateral subtalar supination Contralateral plantar flexion Ipsilateral genu recurvatum Ipsilateral hip or knee flexion Ipsilateral forward pelvis with contralateral lumbar spine rotation Excessive ipsilateral suhtalar supination Excessive contralateral subtalar pronation Ipsilateral plantar flexion Contmlateral genu recurvatum Contralateral hip or knee flexion Ipsilateral backward pelvic rotation with ipsilateral lumhar spine rotation
Reproduced, with permission, from Riegger-Krugh C, Keysor JJ. Skeletal malalignments of the lower quarter: correlated and compensatory motions and postures. J Orthop Sports Phys Ther. 1996;23:164-170. With permission of the Orthopaedic and Sports Physical Therapy Section of the American Physical Therapy Association.
318
SECTION II. TESTS AND MEASURES
LATERAL CURVATURE Of THE SPINE
Two terms, scoliosis and rotoscoliosis, are used to describe the lateral curvature of the spine. Scoliosis is the older term and refers to an abnormal side bending of the spine, but gives no reference to the coupled rotation that also occurs. Rotoscoliosis is a more detailed definition, used to describe the curve of the spine by detailing how each vertebra is rotated and side flexed in relation to the vertebra below. For example, with a left lumbar convexity, the L5 vertebra would be found to be side flexed to the right and rotated to the left in relation to the sacrum. The same would be true with regard to the relation between L4 and L5. This rotation, toward the convexity, con tinues in small increments until the apex at L3. L2, which is above the apex, is right rotated and right side-flexed in relation to L3. The small increments of right rotation continue up until the thoracic spine, where the side bending and rotation return to the neutral position. Lateral curvature of the spine can be described as being structural or functionaI 162 ,163: ~
Study Pearl The curve patterns are named accord ing to the level of the apex of the curve. For exam, p. Ie'1 a right thora~ic' c' Il't~e, ,h,as a convexIty toward ,the fight; and '(he apex .of the cut'VIO'isin the thoracic spine. ' •'
~
I
Functional: this type of scoliosis is classified as postural, which disappears on foward bending; and compensatory, which is most conunonly due to a short leg. Structural: may be genetic, congenital, or idiopathic, producing a structural change to the bone and a loss of spinal fleXibility. With a structural scoliosis, the vertebral bodies rotate toward the convexity of the curve (the spinous processes deviate toward the concave side), producing a distortion, called a rib hump.164 The rib hump occurs on the convex side of the curve. Persistent scoliosis during forward bending (Adam's sign) is indicative of a structural curve.
The curvature results in an adaptive shortening of the intrinsic trunk muscles on the concave side, and lengthening of the intrinsic muscles on the convex side. A number of radiographic classification systems exist to describe the types of scoliotic curves, including: ~
Ponseti-Friedman classification.16S-l67 There are five types: I. A Single major lumbar curve at Tll-L3 with an apex at 11-2. II. A single major dorsolumbar curve at T6-7 to 11-2 with an apex at Tll-12. III. Combined thoracic and lumbar with a dorsal curve on the right side at T5-6 or TlO-ll and an apex at T7-8 and a lum bar curve on the left side at TIO-ll to L3-4 with an apex at 11-2. IV. A single major thoracic curve at T5-6 to Tll-12 with an apex at T8-9. V. Cervicothoracic at C7-Tl or T4-5 with an apex at T3. ~ King-Moe classification. 16B There are four types: I. Lumbar dominant and S-shaped. II. Thoracic dominant and S-shaped. III. Thoracic where the thoracic and lumbar curves do not cross the midline. IV. Long thoracic or double thoracic with Tl tilted into the upper curve.
CHAPTER 7. GAIT, POSTURE, ERGONOMICS, AND OCCUPATIONAL HEALTH ~
Lenke classification. 169,170 There are three components: • Type of curves: I. Primary thoracic. II. Double thoracic scoliosis. III. Double major scoliosis. IV. Triple major scoliosis. V. Dorsolumbar-lumbar scoliosis. • Lumbar modifier: based on the relationship of the central sacral vertical line to the apex of the lumbar curve. Classified into A, B, and C categories. • Sagittal thoracic modifier: the sagittal curve measurement from T5-12. Designations are: - for less than 10 degrees, N for 10 to 40 degrees, and + for greater than 40 degrees.
A number of techniques, measures, and indices are used to assess scoliosis. These include the Cobb-Webb technique, the Ferguson tech nique, the Greenspan method, the Nash-Moe technique of measuring vertebral rotation, the Cobb method of assessing vertebral rotation, the Risser index, the observation for ossification of the vertebral ring apophysis, the difference in the rib-vertebral angle, the Perdriolle method, and the Lytilt method. There is no literature that examines why patients and/or their sur geons choose surgical versus nonsurgical treatment. Parameters to consider include preoperative risks, radiographic measures, clinical symptoms, functional limitations and appearance, and social issues. The conservative approach for scoliosis runs the gamut from bracing to monitoring.
POSTURE AT WORK
Posture for Standing, Sitting in Office Chairs, or Driving Standing Posture.
It is important to maintaining the natural curve of the spine when standing. The patient should be advised to: ~ ~ ~
~ ~
Keep the head directly over the shoulders and the shoulders over the pelvis. Tighten the abdominal muscles and tuck in the buttocks. Place the feet slightly apart with one foot in front of the other and knees slightly flexed. Use a railing or box to prop one foot up while standing. Wear shoes with good support and cushioning. A rubber mat can ease the pressure and enhance favorable ergonomic conditions. Change feet positions every 20 minutes.
Sitting Posture. Many of the problems associated with sitting may be avoided by a combination of the following techniques. ~
Provide support for the lumbar spine. Maintaining a similar lumbar lordosis in sitting as one maintains in standing is gener ally thought to be better than either a reduced lordosis or a kyphotic lumbar spine posture.m,173
319
Study Pearl
The significant incidence of scoliosis in' toe, ,adolescent popl,ll~tion' has prompted the creation,of ,. school s~reenihg programs in aliSO states. From the fifth grade onward/ children ",s,hould be, seree.ned, ,approximately e\'lery 6 to 9 months.
Study Pearl ical stimulation of muscles for the rrection f scoliosis has not been found to e in preventing sco liosis progression, 71
320
SECTION II. TESTS AND MEASURES ~
Study Pearl
=
Nach~~~~~JouJ1dth~tJ~l~rv~~~r of pronation and supination Equallimitarion of flexion and extension None Equal limirarion of flexion and extension Thumb: abduction then extension
Distal radioulnar
10 degrees of supination
5 degrees of supination
Radiocarpal (wrist)
Neutral with slight ulnar deviation
Extension
Intercarpal Midcarpal
Exten:>ion Extension with ulnar deviation Thumb: full opposition
Metacarpophalangeal
Neutral or slight flexion Neutral or slight flexion with ulnar deviation Thumb: midway between abduction and adduction and midway between flexion and extension Fingers: midway between flexion and exten:>ion Slight flexion
Interphalangeal
Slight flexion
Carpometacarpal
Fingers: full flexion
Thumb: full oppOSition Fingers: full flexion Full extension
Fingers: equal limitation in
all directions rlexion then extension Flexion, extension
Study Pearl Movement of the Hand on the Forearm. The proximal and distal radioulnar joints are intimately related biomechanically, with the function and stability of both joints dependent on the configuration of, and distance between, the two bones. Due to the morphology of the wrist, movement at this joint complex involves a coordinated inter action between a number of articulations including the radiocarpal joint, the proximal row of carpals, and the distal row of the carpals.
TABLE 8-14. ACTNE RANGE OF MOTION NORMS FOR THE FOREARM, WRIST, AND HAND MOTION Forearm pronation Forearm supination Radial deviation Ulnar deviation Wrist flexion Wri:>t extension Finger flexion Finger extension Finger abduction Finger adduction Thumb flexion Thumb extension Thumb adduction Thumb abduction
DEGREES 85-90 85-90 15 30-45 80-90 70-90 MCP: 85-90; PIP: 100-115; DIP: 80-90 MCP: 30-45; PIP: 0; DIP: 20 20-30
o CMC: 45-50; MCP: 50-55; IP: 85-90 MCP: 0; IP: 0-5 30 60-70
CMC, carpometacarpal; DIP, distal interphalangeal; IP, interphalangeal; MCP, metacar pophalangeal; PIP, proximal interphalangeal.
Kienb6ck's disease is in . avascular necrosis of the lunate, UsLiallyas a result of trauma. It has alsobeel'lasso dated with relative shoi'teri irig ofthe ulnar compared.· IN rin. ineradi!;!sPol'lil'L The fouf stages of thedis(;!l:tse are sde rosis, fragmentation/collapse/and arthritis.
370
SECTION II. TESTS AND MEASURES TABLE 8-15. FUNCTIO NAL RANGE OF MOTION OF lHE HAND AND WRIST
JOINT MOTION
Wrist flexion Wrist extension Radial deviation Ulnar deviation MCP flexion PIP flexion DIP flexion Thumb MCP flexion
FUNCTIONAL RANGE OF MOTION (DEGREES)
5--40 30--40
10-20 15-20
60 60 40
20
DIP, distal interphalangeal; MCP, metacarpophalangeal; PIP, proximal interphalangeal. Data from Blair 5J, McCormick E, Bear-Lehman J, et aI. Evaluation of impairment of the upper extremity. Clin Orthop. 1987;221:42-58; Brumfield RH, Champoux JA. A biome chanical study of normal functional wrist motion. Clin Orthop ReI Res. 1984;187:23-25; Lamereaux L, Hoffer MM. The effect of wrist deviation on grip and pinch strength. Clin Orthop. 1995;314:152-155; Kapandji IA. The Physiology ofthejoints, Upper Limb. New York: Churchill Livingstone; 1991; Tubiana R, Thomine J-M, Mackin E. Examination of the Hand and Wrist. London: Mosby; 1996; Palmer AK, Werner FW, Murphy D, et al. Functional wrist motion: a biomechanical study. j Hand Surg. 1985; lOA:39-46; and Ryu J, Cooney WP, Askew LJ, et al. Functional ranges of motion of the wrist joint. j Hand Surg. 1991 ;l6A:409--420.
Flexion and Extension Movements of the Wrist. Wrist movements occur around a combination of three functional axes: longi tudinal, transverse, and anterior-posterior. In a neutral wrist position, the scaphoid contacts the radius, and the lunate contacts the radius and disc. The movements of flexion and extension of the wrist are shared among the radiocarpal articulation and the intercarpal articulation, in varying proportions. ~
~
During wrist flexion, most of the motion occurs in the mid carpal joint (60% or 40 degrees versus 40% or 30 degrees at the radiocarpal joint), and is associated with slight ulnar deviation and supination of the forearmY During wrist extension, most of the motion occurs at the radio carpal joint (66.5% or 40 degrees versus 33.5% or 20 degrees at the midcarpal joint), and is associated with slight radial devia tion and pronation of the forearm. 17
Frontal Lateral Movements of the Wrist. There is a phys iologic ulnar deviation at rest, easily demonstrated clinically and radi ographically. The amount of deviation is approximately 40 degrees of ulnar deviation and 15 degrees of radial deviation.
Radial Deviation. Radial deviation occurs primarily between the proximal and distal rows of the carpal bones. TIle motion of radial deviation is limited by impact of the scaphoid onto the radial stylOid, and ulnar collateral ligament. The abductor pollicus longus and extensor pol licis brevis are best suited to produce radial deviation of the wrist.
CHAPTER 8. MUSCULOSKELETAL PHYSICAL THERAPY
Ulnar Deviation. Ulnar deviation occurs primarily at the radio carpal jointY Ulnar deviation is limited by the radial collateral liga mentY The muscle with the best biomechanical advantage to pro duce ulnar deviation of the wrist in pronation is the extensor carpi ulnaris. The position of the wrist in flexion or extension influences the tension of the long or "extrinsic" muscles of the digits. Neither the flexors nor the extensors of the fingers are long enough to allow max imal range of motion at the wrist and the fingers simultaneously.
Thumb Movements.
Thumb flexion and extension occur around an anterior-posterior axis in the frontal plane (Fig. 8-6) that is perpendicular to the sagittal plane of finger flexion and extension. In this plane, the metacarpal surface is concave and the trapezium sur face is convex. Flexion occurs with a conjunct rotation of internal rota tion of the metacarpal. Extension occurs with a conjunct rotation of external rotation of the metacarpal. A total range of 50 to 70 degrees is available. Thumb abduction and adduction occur around a medial-lateral axis in the sagittal plane (Fig. 8-6), which is perpendicular to the frontal
a. Abduction
d. Flexion
b. Hyperadduction
e. Hyperflexion
c. Extension
f. Opposition
Figure 8-6. Movements of the thumb at the carpometacarpal joint. (Reproduced, with permission, from Luttgens K, Hamilton N. Kinesiology. Scientific Basis of Human Motion. 10th ed. New York: McGraw-Hili; 2002:141.)
171
372
SECTION II. TESTS AND MEASURES
Study Pearl Given that the hip region is also a common. source of symptom. referral from other regIons, the examination of the hlp rarely occurs in Isolation, andalmosralways involves an assess mentofthe lumbar spine, pelvis, and k:nee joint complex.
Study Pearl
HIP
Eno-range hip flexion is associated with a posteriQF rotation of the ilium bone. Theenl;l range of hipextep slol'lJs asSociated with an anterior rotation of theili lIfn. Hip abductionl . ·a. •. dd. . •. uc.. •. t•. '.·o. •.•. n areassociatedwith a tilt of the. pelvis. I
Study Pearl Iheangle betweenthefelTloral shaft alldthe neck is called the collum! inclination angle. This angle Is approxImately 125 to 130 degrees,22 buttanvarywith body types. Ina tall person,. thecbllum angle is larger
(~alga).The
. Q.•••. .•...p.!JS. p it. shorter individual..
plane of finger abduction and adduction. During thumb abduction and adduction, the convex metacarpal surface moves on the concave tra peZium. Abduction occurs with a conjunct rotation of internal rotation. Adduction occurs with a conjunct rotation of external rotation. A total range of 40 to 60 degrees is available. Opposition of the thumb involves a wide arc motion comprised of sequential palmar abduction and flexion from the anatomic position, accompanied by internal rotation of the thumb. Retroposition of the thumb returns the thumb to the anatomic position, a motion that incor porates elements of adduction with extension and external rotation of the metacarpal.
inn.,
with a
Anatomy. The acetabulum is made up of three bones: the ilium, ischium, and pubis (Fig. 8-7). The acetabular labrum deepens the acetabulum and increases articular congruence. A number of muscles act across the hip (Table 8-16). The femur is held in the acetabulum by five separate ligaments: .. The iliofemoral ligament attaches to the anterior inferior iliac spine of the pelvis and the intertrochanteric line of the femur. .. The pubofemoral ligament originates at the superior ramus of the pubis, also attaching to the intertrochanteric line of the femur. .. The ischiofemoral ligament connects the ischium to the greater trochanter of the femur. .. The transverse acetabular ligament consists of the labrum cov ering the acetabular notch. .. The femoral head ligament joins the femoral head with the transverse ligament and acetabular notch.
Vascular Supply. The proximal shaft of the femur and the femoral neck receive a plentiful blood supply from the medial circumflex femoral artery and its branches. The femoral head, on the other hand, has an extremely tenuous blood supply from a small branch of the obturator artery that passes with the femoral ligament. Biomechanics. The hip joint is classified as an unmodified ovoid (ball and socket) joint. This arrangement permits motion in three planes: sagittal (flexion and extension around a transverse axis), frontal (abduction and adduction around an anterior-posterior axis), and transverse (internal and external rotation around a vertical axis). All three of these axes pass through the center of the femoral head. Due to its location, design, and function, the hip joint transmits truly impressive loaels, both tensile and compressive. Loads of up to eight times body weight have been demonstrated in the hip joint during jog ging, with potentially greater loads present during vigorous athletic competition. IS Motions about the hip joint can occur independently; however, the extremes of motion require motion at the pelvis. 19
CHAPTER 8. MUSCULOSKELETAL PHYSICAL THERAPY
Symphysis
Figure 8-7. Anterior view of the sacroiliac joint showing bones and joints. (Reproduced, with permission, from Luttgens K, Hamilton N. Kinesiology: Scientific Basis of Human Motion. 10th ed. New York: McGraw-Hili; 2002:160.)
In the anatomic position, the orientation of the femoral head causes the contact force between the femur and acetabulum to be high in the anterior-superior region of the joint 20 Because the anterior aspect of the femoral head is somewhat exposed in this position, the joint has more flexibility in flexion than in extension. 2i The collum angle has an important influence on the hips. An increase in the collum angle causes the femoral head to be directed more superiorly in the acetabulum, and is known as coxa valga. Coxa valga has the following effects at the hip joint: ~
~
~
It changes the orientation of the joint reaction force from the
normal vertical direction to one that is almost parallel to the femoral shaft. 23,24 This lateral displacement of the joint reaction force reduces the weight-bearing surface, resulting in an increase in stress applied across joint surfaces not specialized to sustain such loads. It shortens the moment arm of the hip abductors, placing them in a position of mechanical disadvantage. 24 This causes the abductors to contract more vigorously to stabilize the pelVis, producing an increase in the joint reaction force. 2i It increases the overall length of the lower extremity, affecting other components in the kinetic chain. Coxa valga has the effect of decreasing the normal physiologic angle at the knee. This places an increased mechanical stress on the medial aspect of the knee joint and more tensile stress on the lateral aspect of the joint.
373
~
TABLE 8-16. MUSCLES ACONG ACROSS THE HIP JOINT
""
MUSCLE Adductor brevis Adductor longus
ORIGIN External aspect of the body and inferior ramus of the pubis Pubic crest and symphysis
Adductor magnus
Inferior ramus of pubis, ramus of ischium, and the inferolateral aspect of the ischial tuberosity
Eiceps femoris (long head)
Arises from the sacrotuberous ligament and posterior aspect of the ischial tuberosity
Gemelli (superior and inferior) Gluteus maximus
Gluteus medius
Gluteus minimus
Gracilis
Iliacus Obturator externus
Obturator internus Pectineus
Superior-dorsal surface of the spine of the ischium, inferior-upper part of the tuberosity of the ischium Posterior gluteal line of the ilium, iliac crest, aponeurosis of the erector spinae, dorsal surface of the lower part of the sacrum, side of the coccyx, sacrotuberous ligament, and intermuscular fascia Outer surface of the ilium between the iliac crest and the posterior gluteal line, anterior gluteal line and fascia Outer surface of the ilium between the anterior and inferior gluteal lines, and the margin of the greater sciatic notch The body and inferior ramus of the pubis
Super two-thirds of the iliac fossa, upper surface of the lateral part of the sacrum Rami of the pubis, ramus of the ischium, medial two-thirds of the outer surface of the obturator membrane Internal surface of the anterolateral wall of the pelvis and obturator membrane Pecten pubis (pectineal line of the pubis)
INSERTION By an aponeurosis to the line from the greater trochanter of the linea aspera of the femur By an aponeurosis to the middle third of the linea aspera of the femur By an aponeurosis to the linea aspera and adductor tubercle of the femur By way of a tendon, on the lateral aspect
of the head of the fibula, the lateral condyle of the tibial tuberosity, the lateral collateral ligament, and the deep fascia of the leg Superior and inferior-medial surface of the greater trochanter Iliotibial tract of the fascia lata, gluteal tuberosity of the femur
INNERVATION Obturator nerve, L3 Obturator nerve, L3 Obturator nerve and tibial portion of the sciatic nerve, L2-L4 Tibial portion of the sciatic nerve, Sl
Sacral plexus, L5-S1 Inferior gluteal nerve, 51-52
Lateral surface of the greater trochanter
Superior gluteal nerve, L5
A ridge laterally situated on the anterior
Superior gluteal nerve, L5
surface of the greater trochanter The anterior-medial aspect of the shaft of the proximal tibia, just proximal to the tendon of the semitendinosus Fibers converge with tendon of the psoas major to lesser trochanter Trochanteric fossa of the femur
Obturator nerve, L2
Femoral nerve, L2 Obturator nerve, L4
Medial surface of the greater trochanter
Sacral plexus, Sl
Along a line leading from the lesser trochanter to the linea aspera
Femoral or obturator or accessory obturator nerves, L2
Piriformis
Psoas major
Quadratus femoris
Sartorius
By two heads, from the anterior inferior iliac spine, and a reflected head from the groove above the acetabulum Anterior superior iliac spine and notch below it
Semimembranosus
Ischial tuberosity
Semitendinosus
Ischial tuberosity
Tensor fasciae latae
Outer lip of the iliac crest and the lateral surface of the anterior superior iliac spine
Rectus femoris
~
'I
I.n
Front of the sacrum, gluteal surface of the ilium, capsule of the sacroiliac joint, and sacrotuberous ligament Transverse processes of all the lumbar vertebrae, bodies, and intervertebral discs of the lumbar vertebrae Ischial body next to the ischial tuberosity
Upper border of the greater trochanter of femur
Sacral plexus, Sl
Lesser trochanter of the femur
Lumbar plexus, L2-L3
Quadrate tubercle on femur
Nerve to quadratus femoris Femoral nerve, L3-L4
Base of the patella
Upper part of the medial surface of the tibia in front of the gracilis The posterior-medial aspect of the medial condyle of the tibia Upper part of the medial surface of the tibia behind the attachment of the sartorius and below that of the gracilis Iliotibial tract
Femoral nerve, L2-L3 Tibial nerve, LS-S1 Tibial nerve, LS-S1
Superior gluteal nerve, L4-L5
376
SECTION II. TESTS AND MEASURES
==l
If the collum angle is reduced, it is known as coxa vara. The mechanical effects of coxa vara are, for the most part, the opposite of those found in coxa valga, although they appear to be less deleterious Version is the normal angutardiffer
than those of coxa valga. 25 ence between the transverse axes of
Femoral alignment in the transverse plane also influences the each endof a long bone. The terms
mechanics of the hip joint. femoral anteversion (FA) and retrover
Anteversion is defined as the anterior position of the axis through sion refer to this relationship between
the femoral condyles. 26 ,27 Retroversion is defined as a femoral neck axis the neck of the femur and the femoral
that is parallel or posterior to the condylar axis. 21 The normal range for shaft,enging in the femoralcondyles,
femoral alignment in the transverse plane in adults is 12 to 15 degrees that dictates tbe position of the
of anteversion. 27 ,28 femoral head. Wh~n the knee ispoll'lt
Excessive anteversion directs the femoral head toward the anterior ing straightahe.1d.
aspect of the acetabulum when the femoral condyles are aligned in their normal orientation. Some studies have supported the hypothesis that a persistent increase in femoral anteversion predisposes to osteoarthritis of the hip, although other studies have refuted this. Study Pearl Hip flexion averages 110 to 120 degrees, extension 10 to 15 degrees, abduction 30 to 50 degrees, and adduction 25 to 30 degrees. Hip exter Subjet:;tsVv'ith excessive I nal rotation averages 40 to 60 degrees and internal rotation averages 30 u5uall~ have morehipl.?t:rnal rota
to 40 degrees (Table 8-17). tion rangeDf motion than external
The degree of pelvic tilt, which is measured as the angle between rotation; .• andgravitat~lcr the typical
the horizontal plane and a line connecting the ASIS with the posterior "frog~sitting"po5ture asa position of
superior iliac spine, varies from 5 to 12 degrees in normal individuals. 29 com.·.·•fort. T.h..ere is also .asso.. c. i.a.ted in
Both a low ASIS in women, and a structurally flat back in men, can toeing while weight-bearing.21
cause stnrctural variations in pelvic alignment, which can be misinter preted as acquired postural impairments. The most stable position of the hip is the normal standing posi tion: hip extension, slight abduction, and slight internal rotation. 30-32 Study Pearl .... I
Study Pearl
I
ant~verSio:-
Th~~xnTlmonly
cited open-pack (rest
ing)posltioHs oithe hip are between
10 and JOdegrees of flexion, 10 and
30 degrees of abduction, and 0 and
5 degrees of external rotation.
According to Cyriax, lJ,34 the capsular
pattern of thehipIs a.marked limita
tion of flexion, abduction, and inter"
na I rotation. Kaltenborn 3o considers
the>capsular pattern at the hip to be
extenSi2
The subtalar joint controls supination and pronation in close con junction with the transverse tarsal joints of the midfoot. In normal indi viduals, there is an inversion to eversion ratio of 2:3 to 1:3, which amounts to approximately 20 degrees of inversion and 10 degrees of eversion. Stability for the subtalar joint is provided by the calcaneofibular ligament, the cervical ligament, the interosseous ligament, the lateral talocalcaneal ligament, the fibulotalocalcaneal ligament (ligament of Rouviere), and the extensor retinaculum.
Midtarsal (Transverse Tarsal) Joint Complex. The func tion of the midtarsal joint complex is to provide the foot with an addi tional mechanism for raising and lowering the arch, and to absorb some of the horizontal-plane tibial motion that is transmitted to the foot during stance. 59 .65 The talocalcaneal joint has two degrees of freedom: plantar flexion/dorsiflexion and inversion/eversion, with motion occurring around a longitudinal and oblique axis, both of which are independent of each other. 63 Cuneonavicular Joint. The cuneonavicular joint has one to two degrees of freedom: plantar/dorsiflexion and inversion/eversion.
Intercuneiform and Cuneocuboid Joints. Due to their very plane curvature, these joints have only one degree of freedom: inversion/eversion. Metatarsophalangeal Joints. The MTP joints have two degrees of freedom: flexion/extension and abduction/adduction. Range of motion of these joint is variable (Table 8-22).
First Metatarsophalangeal Joint. The function of the great toe is to provide stability to the medial aspect of the foot, and to provide for normal propulsion during gait. Normal alignment of the first MTP jomt varies between 5 degrees varus and 15 degrees valgus. The great toe is characterized by having a remarkable discrepancy between active and passive motion. ApproXimately 30 degrees of active plantar flexion is present, and at least 50 degrees of active exten sion, which can be frequently increased passively to between 70 and 90 degrees.
CHAPTER 8, MUSCULOSKELETAL PHYSICAL THERAPY
Interphalangeal (IP) Joints. Each of the IP joints has one degree of freedom: flexion/extension.
CRANIOVfRTfBRAL JOINTS The craniovertebral (CV) junction is a collective term that refers to the region of the cervical spine where the skull and vertebral column artic ulate. It comprises the bony structures of the foramen magnum, occiput, atlas, axis, and their supporting ligaments. The posterior portion of the foramen magnum houses the brainstem-spinal cord junction.
Occipito-Atlantal (OA) Joint. The oCcipito-atlantal (GA) joint is formed between the occipital condyles and the superior articular facets of the atlas (Cl). The paired occipital condyles are ovoid structures with their long axis situated in a posterolateral to anteromedial orientation.
Atlanto-Axial Joint. This is a relatively complex articulation, which consists of: ~
~
Two lateral zygapophyseal joints between the articular surfaces of the inferior articular processes of the atlas and the superior processes of the axis. Two medial joints: one between the anterior surface of the dens of the axis and the anterior surface of the atlas, and the other between the posterior surface of the dens and the anterior hyalinated surface of the transverse ligament.
Craniovertebral Ligaments ~
~
~
~
Capsule and accessory capsular ligaments. By necessity, these ligaments are quite lax, to permit maximal motion, so they pro vide only moderate support to the joints during contralateral head rotation. Apical. The apical ligament of the dens extends from the apex of the dens to the anterior rim of the foramen magnum. The apical ligament appears to be only a moderate stabilizer against posterior translation of the dens relative to both the atlas and the occipital bone. Vertical and transverse bands of the cruciform. The transverse portion stretches between tubercles on the medial aspects of the lateral masses of the atlas. The major responsibility of the transverse portion is to counteract anterior translation of the atlas relative to the axis, thereby maintaining the position of the dens relative to the anterior arch of the atlas. The trans verse ligament also limits the amount of flexion between the atlas and axis. 64 These limiting functions are of extreme impor tance, because excessive movement of either type could result in the dens compressing the spinal cord, epipharynx, vertebral artery, or superior cervical ganglion. Alar and accessory alar. The alar ligaments connect the superior part of the dens to fossae on the medial aspect of the occipital condyles, although they can also attach to the lateral masses of the atlas. The function of the ligament is to resist flexion, con tralateral side bending, and rotation. 6S Due to the connections of the ligament, side bending of the head produces a contralat eral rotation of the C2 vertebra. 66
387
388
SECTION II. TESTS AND MEASURES ~
~
~
Anterior occipito-atlantal membrane. The anterior occipito atlantal membrane is thought to be the superior continuation of the anterior longitudinal ligament. It extends from the anterior arch of vertebra CI to the anterior aspect of the foramen magnum. Posterior oCcipito-atlantal membrane. The posterior occipito atlanta I membrane is a continuation of the ligamentum flavum. This ligament interconnects the posterior arch of the atlas and the posterior aspect of the foramen magnum. Tectorial membrane. The tectorial membrane is the most pos terior of the three ligaments and interconnects the occipital bone and the axis. This ligament is the superior continuation of the posterior longitudinal ligament, and connects the body of vertebra C2 to the anterior rim of the foramen magnum. This bridging ligament is an important limiter of upper cervical flexion.
Craniovertebral Muscles Anterior Suboccipital Muscles ~
~
Rectus Capitis Anterior Rectus Capitis Lateralis
Posterior Suboccipital Muscles. These muscles function in the control of segmental sliding between CI and C2,67 and may have an important role in proprioception, having more muscle spindles than any other muscle for their size. 67 All of the posterior suboccipital mus cles are innervated by the posterior ramus of CI, and are also strongly linked with the trigeminal nerve. 68 ,69 The suboccipitals receive their blood supply from the vertebral artery.
Nerve Supply. The dorsal ramus of spinal nerve CI is larger than the ventral ramus and supplies most of the muscles that form that tri angle. It usually has no cutaneous distribution. The dorsal ramus of spinal nerve C2, also known as the greater occipital nerve, supplies most of the posterior aspect of the scalp, extending anteriorly to a line across the scalp that extends from one external auditory meatus to the other. Blood Supply. The cervical cord is supplied by two arterial sys tems, central and peripheral, which overlap but are discrete. The first is dependent entirely on the single anterior spinal artery (ASA). The second, without clear-cut boundaries, receives supplies from the ASA and both posterior spinal arteries.7° Biomechanics. The upper cervical spine is responsible for approximately 500/0 of the motion that occurs in the entire cervical spine. Motion at the AA joint occurs relatively independently, while below C2, normal motion is a combination of motion occurring at other levels. Occipito-atlantal Joint. The primary motion that occurs at this joint is flexion and extension, although side bending and rotation also occur. It is generally agreed that rotation and side bending at this joint occur to opposite sides when they are combined. Occipital rotation and, to some degree, anterior-posterior transla tion of the occiput on CI , is thought to be limited by the alar ligaments.
AI ~
with legs dangling over the end of the bed, with the knee flexed to 90 degrees and foot relaxed. The clinician stabilizes the lower leg with one hand and, using the oth~r hand, grasps the foot and rotates it laterally. Pain on the medial and lateral aspect of the
CHAPTER 8. MUSCULOSKELETAL PHYSICAL THERAPY
ankle, and/or displacement of the talus from the medial malleolus, depending on severity, may indicate a tear of the deltoid ligament. Thompson Test for Achilles Tendon Rupture. In this test, the patient is positioned prone or kneeling with the feet over the edge of the bed. With the patient relaxed, the clinician gently squeezes the calf muscle and observes for the production of plantar flexion. An absence of plan tar flexion indicates a complete rupture of the Achilles tendon. Patla Test for Tibialis Posterior Length. The patient is positioned prone, with the knee flexed to 90 degrees. Un The clinician stabilizes the cal caneus in eversion and the ankle in dorsiflexion with one haml. With the other hand, the clinician contacts the plantar surface of the bases of the second, third, and fourth metatarsals with the thumb, while the index and middle fingers contact the plantar surface of the navicular. The clinician then pushes the navicular and metatarsal heads dorsally and compares the end-feel and patient response with the uninvolved side. A positive test is indicated with reproduction of the patient's symptoms. Feiss Line. The Feiss line test is used to assess the height of the medial arch, using the navicular position. With the patient non-weight-bearing, the clinician marks the apex of the medial malleolus and the plantar aspect of the first MTP joint, and a line is drawn between the two points. The navicular is palpated on the medial aspect of the foot, and an assessment is made as to the position of the navicular relative to the imaginary line. The patient is then asked to stand with the feet about 3 to 6 inches apart. In weight-bearing, the navicular normally lies on, or very close to the line. If the navicular falls one-third of the distance to the floor, it represents a first-degree flat foot; if it falls two thirds of the distance, it represents a second-degree flat foot; and if it rests on the floor, it represents a third-degree flat foot. "Too Many Toes" Sign. The patient is asked to stand in a normal relaxed position while the clinician views the patient from behind. If the heel is in valgus, the forefoot abducted, or the tibia externally rotated more than normal, the clinician will observe more toes on the involved side than on the normal side.
Articular Stability Tests Navicular Drop Test. The navicular drop test is a method of assessing the degree to which the talus plantar-flexes in space on a calcaneus that has been stabilized by the ground, during subtalar joint pronation. The clinician palpates the position of the navicular tubercle as the patient's foot is non-weight-bearing but resting on the floor surface with the subtalar joint maintained in neutral. The clinician then attempts to quantify inferior displacement of the navicular tubercle as the patient assumes 50% weight-bearing on the tested foot. A navicular drop greater than 10 mm from the neutral position to the relaxed stand ing position suggests excessive medial longitudinal arch collapse of abnormal pronation. Talar Rock. The talar rock is an articular stability test for the subtalar joint. The test is performed with the patient positioned in side lying, the
435
436
SECTION II. TESTS AND MEASURES
hip and knee flexed. The clinician sits on the table with the back to the patient, and places both hands around the ankle just distal to the malle oli. The clinician applies a slight distraction force to the ankle, before applying a rocking movement to the foot in a upward or downward direction. A "clunk" should be felt at the end of each of the movements.
Passive Foot Rotation. This test assesses the integrity of the midtarsal and tarsometatarsal joints. A rotational movement is applied to the mid tarsal and tarsometatarsal joints. At the midtarsal joint, the proximal row of the tarsal bones (navicular, calcaneus, and talus) is stabilized, and the distal row (cuneiforms and cuboid) is rotated in both direc tions. At the tarsometatarsal joints, the distal row of the tarsals is stabi lized and the metatarsals are rotated in both directions. Neurovascular Status Homan's Sign. The patient is positioned supine with the knee extended. The clinician stabilizes the thigh with one hand, and pas Sively dorsiflexes the patient's ankle with the other. Pain in the calf with this maneuver may indicate a positive Homan's sign for deep vein thrombophlebitis, especially if there are associated signs including pal lor and swelling in the leg and a loss of the dorsal pedis pulse.
Buerger's Test. The patient is positioned supine with the knee extended. The clinician elevates the patient's leg to about 45 degrees and maintains it there for at least 3 minutes. Blanching of the foot is positive for poor arterial circulation, especially if, when the patient sits with the legs over the end of the bed, it takes 1 to 2 minutes for the limb color to be restored. Morton's Test. The patient is positioned supine. The clinician grasps the foot around the metatarsal heads and squeezes the heads together. The reproduction of pain with this maneuver indicates the presence of a neuroma or a stress fracture. Ouchenne's Test. The patient is positioned in supine with their legs straight. The clinician pushes through the sole on the first metatarsal head, and pushes the foot into dorsiflexion. The patient is asked to plantar flex the foot. If the medial border dorsiflexes and offers no resistance while the lateral border plantar-flexes, a lesion of the superficial per oneal nerve, or a lesion of the L4, L5, and Sl nerve root, is indicated. Tinel's Sign. There are two locations around the ankle where Tinel's sign can be elicited. The anterior tibial branch of the deep peroneal nerve can be tapped on the anterior aspect of the ankle. The posterior tibial nerve may be tapped behind the medial malleolus. Tingling or paresthesia with this test is considered a positive finding.
Dorsal Pedis Pulse. The dorsal pedis pulse can be palpated just lateral to the tendon of the extensor hallucis longus over the dorsum of the foot.
Special Tests of the Spine and SIJ Special Tests of the Upper Cervical Spine Vertebral Artery Tests. A positive vertebral artery test is one in which signs or symptoms change, especially if the changes evoked include
CHAPTER 8. MUSCULOSKELETAL PHYSICAL THERAPY
upper motor neuron signs and symptoms. More subtle examination findings can include a significant delay in verbal responses to ques tions of orientation, with some inconsistency of answers; changes in pupil size; and nystagmus.!3 7 Clinical testing of the vertebral artery should stop once positive signs or symptoms are noted. Throughout the tests, the clinician should observe the patient's eyes for possible nystagmus or changes in pupil size, and should have the patient COLlnt backward to assess the quality of speech. The patient is asked to report any changes in symptoms, however insignificant he or she may feel the changes to be.
Initial Test. The initial test consists of having the patient rotate the head to each side while in sitting position. The longus colli and sca lene muscles rotate the cervical spine and can squeeze the vertebral artery on the side contralateral to the rotation. 1.,8 The presence of mus cular compression of the artery can be further tested by combining cervical flexion with rotation to place the inferior oblique capitis on stretch. 138 Barre's Test. Barre's test can be used to test for vertebral artery insuffi ciency, especially if the patient is unable to lie supine. The patient is seated with the arms outstretched, forearms supinated. The patient is asked to close the eyes and move the head and neck into maximum extension and rotation. A positive test is one in which one of the outstretched arms sinks toward the Hoor and pronates, indicating the side of the compromise. Hautard's (Hautant's, Hautart; or Hautarth's) Test. As with Barre's test, proprioceptive loss rather than dizziness is sought in Hautard's test. 139,140 The test has two parts. The patient is seated, Both arms are actively flexed to 90 degrees at the shoulders. The eyes are then closed for a few seconds while the clinician observes for any loss of position of one or both arms. If the arms move, the proprioception loss has a nonvascular cause. If the first part of the test is negative, the patient is asked to extend and rotate the neck. Because the second part of the test is performed to elicit a vascular cause for the dizzi ness, the eyes can be open or closed. Having the eyes open allows the clinician to observe for nystagmus and changes in pupil size. Each position is held for 10 to 30 seconds. If wavering of the arms occurs with the second part of the test, a vascular cause for the symp toms is suspected. Cervical Quadrant Test. The patient is positioned supine.!4! The supine position is reported to result in an increase in passive motion at the cervical spine compared with sitting, and therefore may better test the ability of the vertebral artery to sustain a stretch. The clinician pas sively moves the patient's head into extension and side bending. Maintaining this position, the clinician rotates the patient's head to the same side as the side bending and holds it there for 30 seconds. A pos itive test is one in which referring symptoms are produced if the oppo site artery is involved. OeKleyn-Nieuwenhuyse Test. The patient is positioned supine.!42 The clinician passively moves the patient's head into extension and
437
438
SECTION II. TESTS AND MEASURES
Study Pearl Following a positive vertebral artery test or positive responses in the his tory, the patient must be handled very carefully! and .. further' intervention, icularlY!Jl;;tnipulation.of the cer spine, should not bedeIivered. The patienuhould not,.lInder any cir cumstance, be..a.lloweCl tQ. leave the dinicunti!his or her physiCian has been contacted, and.. until the neces sary .arrangements . have been. made for the safe transport ot the patient to an appropriate facility.
----------
rotation. A positive test is one in which referring symptoms are pro duced if the opposite artery is involved. Despite its Widespread appear ance in a number of texts, this test is not recommended because of the severe traction stresses it places on the vertebral artery.140
Dix-Hallpike Test. This test can be used to help determine if the cause of the patient's dizziness is because of a vestibular impairment due to an accumulation of utricle debris (otoconia), which can move within the posterior semicircular canals and stimulate the vestibular sense organ (cupula). This test is only usually performed if the vertebral artery test and instability tests do not provoke symptoms. The test involves haVing the patient suddenly lie down from a sit ting position with the head rotated in the direction that the clinician feels is the provocative position. 140 The end point of the test is when the patient's head overhangs the end of the table so that the cervical spine is extended. A positive test is the reproduction of the patient's symptoms. Modified Sharp-Purser Test. This test was originally designed to test the sagittal stability of the AA segment in rheumatoid arthritic patients, as a number of pathologic conditions can affect the stability of the osseoligamentous ring of the median joints of this segment in this patient population. These changes result in degeneration and thinning of the articular cartilage between the odontoid process and the anterior arch of the atlas, or the dens can become softened. The aim of the test is to determine whether the instability was sig nificant enough to provoke central nervous system's signs and/or symptoms. lbe patient is positioned in sitting. The patient is asked to segmentally flex the head and relate any signs or symptoms that this might evoke to the clinician. In addition, a positive test may be indi cated by the patient hearing or feeling a clunk. Local symptoms such as soreness are ignored for the purposes of evaluating the test. If no serious signs or symptoms are provoked, the clinician stabilizes C2 with one hand, and applies a posteriorly oriented force to the head. In the presence of a positive test, a provisional assumption is made that the symptoms are caused by excessive translation of the atlas compromising one or more of the sensitive structures listed above. The test is considered positive and the physical examination is terminated. No intervention should be attempted other than the issuing of a cervical collar to prevent craniovertebral flexion and an immediate referral to the patient's physician.
Special Tests of the Cervical Spine and TMJ Temporomandibular Joint Screen. As the temporomandibular joint can refer pain to this region, the clinician is well advised to rule out this joint as the cause for the patient's symptoms. The patient is asked to open and close the mouth, and to laterally deviate the jaw as the clinician observes the quality and quantity of motion and notes any reproduction of symptoms. Lhermitte's Symptom or "Phenomenon./I This is not so much a test as a symptom described as an electric shock-like sensation that radiates down the spinal column into the upper or lower limbs when flexing
CHAPTER 8. MUSCULOSKELETAL PHYSICAL THERAPY
the neck. It can also be precipitated by extending the head, coughing, sneezing, bending forward, or moving the limbs. I ';3 Lhermitte's symp tom and abnormalities in the posterior part of the cervical spinal cord on MRI are strongly associated. I44
Brachial Plexus Tests Stretch Test. This test is similar to the straight leg raise for the lower extremity as it stretches the brachial plexus. The patient is in sitting position. The patient is asked to side bend the head to the uninvolved side and to extend the shoulder and elbow on the involved side. Pain and paresthesia along the involved arm are indicative of a brachial plexus irritation. Compression Test. The patient is positioned sitting. The patient is asked to side bend the head to the uninvolved side. The clinician applies firm pressure to the brachial plexus by squeezing the plexus between the thumb and fingers. Reproduction of shoulder or upper arm pain is positive for mechanical cervical lesions. H5 Tinel's Sign. The patient is positioned sitting. The patient is asked to side bend the head to the uninvolved side. The clinician taps along the trunks of the brachial plexus using the fingertips. Local pain indicates a cervical plexus lesion. A tingling sensation in the distribution of one of the trunks may indicate a compression or neuroma of one or more trunks of the brachial plexus. 146
Thoracic Outlet Tests. Despite their widespread use, no studies documenting the reliability of the common thoracic outlet maneuvers of Adson's, Allen's, or the costoclavicular maneuver have been per formed. 106 The specificity of these tests, determined in asymptomatic patients, has been reported to be between 18% and 87%,147-150 while the sensitivity has been documented at 94%.106,149 When performing thoracic outlet syndrome tests, evaluation for either the diminution or disappearance of pulse or reproduction of neurologic symptoms indicates a positive test. However, the aim of the tests should be to reproduce the patient's symptoms rather than to obliterate the radial pulse, as more than 50% of normal, asymptomatic people will exhibit obliteration of the radial pulse during classic provocative testing. I5 ! A baseline pulse should be established first, before performing the respective test maneuvers. Adson's Vascular Test. The patient extends the neck, turns the head toward the side being examined, and takes a deep breath. This test, if positive, tends to implicate the scalenes because this test increases the tension of the anterior and middle scalenes, and compromises the interscalene triangle. 152 Allen's Pectoralis Minor Test. Allen's test increases the tone of the pec toralis minor muscle. The shoulder of the seated patient is pOSitioned in 90 degrees of glenohumeral abduction, 90 degrees of glenohumeral external rotation, and 90 degrees of elbow flexion on the tested side. While the radial pulse is monitored, the patient is asked to turn the head away from the tested side. This test, if positive, tends to implicate pectoralis tightness as the cause for the symptoms.
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SECTION II. TESTS AND MEASURES
Costoclavicular Maneuver. During this test, the shoulders are drawn back and downward in an exaggerated military position to reduce the volume of the costoclavicular space. Hallstead's Maneuver. The patient is positioned sitting on the edge of a table. The clinician grasps the arm on the symptomatic side, passively depresses its shoulder girdle, and then pulls the arm down toward the floor, while palpating the radial pulse. The patient is asked to extend the head and to turn away from the tested side. Roos's Test. The patient is positioned sitting. 153 The arm is positioned in 90 degrees of shoulder abduction and 90 degrees of elbow flexion. The patient is asked to perform slow finger clenching for 3 minutes. The radial pulse may be reduced or obliterated during this maneuver, and an infraclavicular bruit may be heard. If the patient is unable to maintain the arms in the start position for 3 minutes or reports pain, heaviness, or numbness and tingling, the test is considered positive for TOS on the involved side. This test is also referred to as the bands-up test or the elevated arm stress test (EAST).
Overhead Test. The overhead exercise test is useful to detect thoracic outlet arterial compression. The patient elevates both arms overhead, and then rapidly flexes and extends the fingers. A positive test is achieved if the patient experiences heaviness, fatigue, numbness, tin gling, blanching, or discoloration of a limb within 20 seconds. 152 Hyperabduction Maneuver (Wright's Test). This test is considered by many to be the best provocative test for thoracic outlet compression caused by compression in the costoclavicular space. 147 The test L'i per formed by asking the patient to turn the head away from the side being examined, and take a deep breath while the clinician passively abducts and externally rotates the patient's arm. Passive Shoulder Shrug. This Simple but effective test is used with patient') who present with TOS symptoms to help rule out thoracic outlet syndrome. The patient is seated with arms folded and the clini cian stands behind. The clinician grasps the patient's elbows and pas sively elevates the shoulders up and forward. This position is main tained for 30 seconds. Any changes in the patient's symptoms are noted. The maneuver has the affect of slackening the soft tissues and the plexus.
Upper Limb Tension Tests Special Tests of the Lumbar Spine and SI} Neurodynamic Mobility Testing Straight Leg Raise Test. The straight leg raise (SLR) test should be a rou tine test during the examination of the lumbar spine among patients with sciatica or pseudoclaudication. However, the test is often negative in patients with spinal stenosis. 154 A leg elevation of less than 60 degrees is abnormal, suggesting compression or irritation of the nerve roots. A positive test reproduces the symptoms of sciatica, with pain that radi ates below the knee, not merely back or hamstring pain. 154 Ipsilateral straight-leg raising has sensitivity but not specificity for a herniated NU, whereas crossed straight-leg raising is insensitive but highly specific.
CHAPTER B. MUSCULOSKELETAL PHYSICAL THERAPY
The clinician must remember that the SLR test stresses a number of structures, including: ~ ~ ~ ~
The The The The
lumbosacral nerve roots.
hamstrings.
hip joint.
sacroiliac joint.
The following guidelines can be used to interpret the results from the test lSS : ~
~ ~ ~
Symptom.') reproduced in the 0- to 30-degree range may indicate hip pathology or a severely inflamed nerve root. Symptoms reproduced in the 30- to 50-degree range may indicate sciatic nerve root involvement. Symptoms reproduced in the 50- to 70-degree range may indicate hamstring involvement. Symptoms reproduced in the 70- to 90-degree range may indi cate involvement of the sacroiliac joint.
Pheasant's Test. The patient is positioned prone. While monitoring for motion at the patient's pelvis, the clinician passively flexes the patient's knees. Pheasant's test introduces an anterior pelvic tilt/increase in lor dosis through the pull of the rectus femoris. Once motion occurs at the pelvis, the clinician determines whether the low back symptoms have been reproduced. lS6 A pulling sensation on the anterior aspect of the thighs is a normal finding. If full knee flexion is achieved before the tilting occurs, the patient is positioned prone on the elbows and the test is repeated. Patients who test positive for this maneuver tend to have the following subjective complaints: ~ ~ ~
~
Pain with supine lying with the legs straight, unless the rectus and hip flexors are especially fleXible. Pain with prone lying. Pain with sitting erect. Pain with prolonged standing.
The cause of the pain is thought to be due to the passive stretch ing or compression of pain-sensitive structures. These structures include the zygapophyseal joints, the segmental ligaments, and the anterior aspect of the IVD. Anterior SI Joint Stress Test. The anterior stress test, also called the gap
ping test, is performed with the patient supine. The clinician stands to one side of the patient and, crossing the arms, places the palms of the hands on the patient's anterior superior iliac spines. Crossing the arms ensures that the applied force is in a lateral direction, thereby gapping the anterior aspect of the sacroiliac joint. The stress is maintained for 7 to 10 seconds, or until an end-feel is felt. The procedure stresses the ven tralligament and compresses the posterior aspect of the joint. A positive test is one in which the patient's groin and/or sacroiliac joint pain is reproduced anteriorly, posteriorly, unilaterally, or bilaterally.157 The anterior gapping test, and its posterior counterpart are believed to be sensitive for severe arthritis or ventral ligament tears,33 although they have been shown to be poorly reproducible. ls8
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SECTION II. TESTS AND MEASURES
Posterior Sacroiliac Joint Stress Test. The posterior stress test, also called the compression test, is performed with the patient in side lying. The clinician, standing behind the patient, applies a downward force on the side of the patient's uppermost innominate using both hands. The procedure creates a medial force that tends to gap the posterior aspect of the joint while compressing its anterior aspect. The repro duction of pain over one or both of the sacroiliac joints is considered positive. FADE (Flexion, Adduction, Extension) Positional Test. The setup for the FADE test is similar to that of the FABER test, except that the start position involves moving the patient's hip into flexion and adduc tion. 159 From that position, the clinician moves the patient's hip into extension and slight abduction. A positive test is indicated by pain or loss of motion as compared with the uninvolved side. Posterior-Anterior Pressures. Posterior-anterior pressures, advocated by Maitland,141 are applied over the spinous, mammillary, and trans verse processes of this region. The clinician should apply the posterior anterior force in a slow and gentle fashion using the index and middle finger of one hand, while monitoring the paravertebrals with the other hand. While these maneuvers are capable of eliciting pain, restricted movement and/or muscle spasm, they are fairly nonspecific in deter mining the exact level involved or the exact cause of the symptoms, and have been found to have poor inter-rater reliability in the absence of corroborating clinical data. 160 However, as a screening tool, the posterior-anterior pressures have their uses, and help detect the presence of excessive motion and/or spasm.
INTERVENTION PRINCIPLES FOR MUSCULOSKELETAL INJURIES A number of principles should guide the intervention through the var ious stages of musculoskeletal tissue healing. These include: ~ Control pain, inflammation, and swelling (edema). .. Promote and progress healing. .. Instructions to the patient on a therapeutic exercise program tl1at: • Corrects any imbalances between strength and flexibility . • Addresses postural and movement dysfunctions. • Integrates the open and closed kinetic chains. • Incorporates neuromuscular re-education. • Maintains or improves overall strength and cardiovascular fitness. • Improves the functional outcome of the patient.
CONTROL PAIN AND INFLAMMATION The clinician has a number of tools at his or her disposal to help to con trol pain, inflammation, and swelling (edema). These include the appli cation of electrotherapeutic and physical modalities (refer to Chapter 18),
CHAPTER 8. MUSCULOSKELETAL PHYSICAL THERAPY
gentle range-of-motion exercises, and graded manual techniques. During the acute stage of healing, the principles of PRICEMEM (Protection, Rest, Ice, Compression, Elevation, Manual therapy, Early motion, and Medications) are recommended. The modalities used dur ing the acute phase involve the application of cryotherapy, electrical stimulation, pulsed ultrasound, and iontophoresis. Modalities used during the later stages of healing include thermotherapy, phonophore sis, electrical stimulation, ultrasound (US), iontophoresis, and diathermy. The applications of cold and heat are taught to the patient at the earliest opportunity. Gentle manual techniques (grade I or II joint mobilizations) may also be used to help with pain (refer to Chapter 18). As the patient pro gresses, gentle passive muscle stretching may be introduced. Self stretching and self-mobilization techniques are taught to the patient at the earliest appropriate opportunity. The goals of the acute phase should include: ~
~ ~ ~ ~
~ ~ ~ ~ ~ ~ ~
Maximizing patient comfort by decreasing pain and inflammation. Protection of the injury site. Restoration of pain-free range of motion throughout the entire kinetic chain. Retardation of muscle atrophy. Minimizing the detrimental effects of immobilization and activity restriction. 161-16i, Attainment of early neuromuscular control. Improving soft-tissue extensibility. Increasing functional tolerance. Maintaining general fitness. Appropriate management of scar tissue. Encouraging the patient toward independence with the home exercise program. Progression of the patient to the functional stage.
PROMOTE AND PROGRESS HEALING The promotion and progression of tissue repair involves a delicate bal ance between protection and the application of controlled functional stresses to the damaged structure. Tissue repair can be viewed as an adaptive life process in response to both intrinsic and extrinsic stim Uli. 167 These stimuli can be in the form of manual techniques and/or therapeutic exercises. Although physical therapy cannot accelerate the healing process, it can ensure that the healing process is not delayed or disrupted, and that it occurs in an optimal environment,168 In addition to excess stress, detrimental environments include prolonged immobi lization, which must be avoided (see Table 17-9). The rehabilitation procedures chosen to progress the patient will depend on the type of tissue involved, the extent of the damage, and the stage of healing (see Chapter 5). The intervention must be related to the signs and symp toms present rather than the actual diagnosis. The functional phase addresses any tissue overload problems and functional biomechanical deficits. The goals of the functional phase should address: ~ ~
Attainment of full range of pain-free motion.
Restoration of normal joint kinematics.
443
444
SECTION II. TESTS AND MEASURES ~ ~ ~
~ ~
Improvement of muscle strength to within normal limits.
Improvement of neuromuscular control.
Restoration of normal muscle force couples.
Correction of any deficits in the whole kinetic chain that are
involved in an activity to which the patient is planning to return. Performance of activity-specific progressions before full return to function.
The selection of intervention procedures, and the intervention pro gression, must be guided by continuous reexamination of the patient's response to a given procedure, making the reexamination of patient dysfunction before, during, and after each intervention, essentiaJ.32 There are three possible scenarios following a reexamination: ~ ~
~
The patient's function has improved. In this scenario, the inten sity of the intervention may be incrementally increased. The patient's function has diminished. In this scenario, the intensity and the focus of the intervention must be changed. Further review of the home exercise program may be needed. The patient may require further education on activity modifica tion and the use of heat and ice at home. The working hypoth esis must be reviewed. Further investigation is needed. There is no change in the patient's function. Depending on the elapse of time since the last visit, there may be a reason for the lack of change. This flnding may indicate the need for a change in the intensity of the intervention. If the patient is in the acute or subacute stage of healing, a decrease in the intensity may be warranted, to allow the tissues more of an opportunity to heal. In the chronic stage, an increase in intensity may be warranted.
COMMON ORTHOPEDIC CONDITIONS Examples of diagnoses involving the musculoskeletal system include fracture, rheumatoid arthritis, osteoarthritis, joint dislocation, tendinitis, bursitis, and ligament sprain/rupture. Many pathologic conditions that initially affect other body systems such as the neurologic, cardiovascular, or pulmonary systems can result in secondary or indirect impairment of the musculoskeletal system. Examples include traumatic brain injury, peripheral vascular disease, cerebral vascular accident, cerebral palsy, spinal and peripheral nerve injury, burns, and myocardial infarction. ACHILLES TENDINITIS Achilles tendinitis is the most common overuse syndrome of the lower leg. 169 A number of factors appear to contribute to the development of Achilles tendinitis: ~
Biomechanical factors. The rapid and repeated transitions from pronation to supination cause the Achilles tendon to undergo a "whipping" or "bow-string" action. 169 Moreover, if the foot remains in a pronated position after knee extension has begun, the lateral tibial rotation at the knee and the medial tibial rota tion at the foot results in a "wringing" or twisting action of the tendon. 170
CHAPTER 8. MUSCULOSKELETAL PHYSICAL THERAPY ~
~
~
~
~
~
445
Training variables. The lack of stretching programs, a faster training pace, and hill training have all been found to correlate with increased incidence. 169 Fatigue. Overtraining has been found to correlate to calf mus cle fatigue and microtears of the tendon 170,171 Isokinetic variables. Muscular insufficiency has been cited as a significant factor in the inability to eccentrically restldin dorsiflex ion during the beginning of the support phase of running. 169.m-171 Anthropometric variables. The compensatory overpronation resulting from the inflexibility of the cavus foot is a precursor to Achilles tendinitis. Shoe type. Spike shoes lock the feet on the surface during the single support phase in running and increase the athlete's foot grip but also transfer lateral and torque shear forces directly to the foot and ankle and through to the Achilles tendon. Sacroiliac joint dysfunction. Changes in sacroiliac joint mechanics as compared with the contralateral side. m
Achilles tendinitis typically occurs as one of two types l76 ; ~ ~
Insertional: involving the tendon-bone interface. Noninsertional: occurring just proximal to the tendon insertion on the calcaneus in or around the tendon substance. Can be referred to as peritendinitis, peritendinitis with tendinosis, and tendinosis. 176,177
Clinical symptoIIL'i consist of a gradual onset of pain and swelling in the Achilles tendon 2 to 3 em proximal to the insertion of the tendon, which is exacerbated by activity. Some patients will present with pain and stiffness along the Achilles tendon when rising in the morning, or pain at the start of activity that improves as the activity progresses. In fact, in the early stages of Achilles tendinitis, morning stiffness may be the only symptom, whereas pain is felt even at rest in the advanced stages 17H Upon observation, the patient will often be found to have pronated feet and the presence of swelling is common. Observation during gait may reveal an antalgic gait, with the involved leg held in external rotation both during the stance and swing phase. ~
Localization of the tenderness with palpation is extremely important. • Tenderness that is located 2 to 6 em proximal to the insertion is indicative of noninsertional tendinitis. • Pain at the bone-tendon junction is more indicative of inser tional tendinitis. • If there is an area in the tendon itself that is discrete and painful with side-to-side pressure of the fingers, this often indicates an area of mucoid degeneration or a small partial ru pture of the tendon. • If the tenderness is in the area of the retrocalcaneal bursa, which is noted by side-to-side pressure in that area, this is the primary area of involvement.
A lack of 20 to 30 degrees of dorsiflexion in knee extension signi fies gastrocnemius tightness, and inability to dorsiflex 30 to 35 degrees in knee flexion implicates the soleus as well.
Study Pearl The differential diagnosis for.posterlor heel pain includes retrocalca.neal bursitis, 179 m~tabolic diseases, arthri tis and cho ndropaticdJseasesof the ankle joint, tibiavara, os trigonum, calcaneal contusion,plantar fasciitis, calcaneal stress fracture impingement syndrome, and stress fractures ofthe fibula or tibia.
446
SECTION II. TESTS AND MEASURES
Study Pearl For the treatment of a tendon injury, the following five-step plan is recom mended: 1. The principles of '" PRICEMEM (Prot~cti~n, Rest, ,Ice",Compression, Elevation, Manual therapy, Early motion, and Medications) to aid healing. 2. Agradual pr~gressiQn of t,herapeu tic exercise, (ocusingon eccentric exercises and the removal of intrin sic deficits: inCreasing flexibility, and muscle, imbalances. I. Removal oLany extrinsic factors (damaging stimuli). This often irivblvesabseflcefrom abuse rather than absolute rest. 4. Identification of any faulty m~hanics/techn ique, 5 .,A."ppliytition.' ofc;ross-secti()n mas sagetot~~"tend()fl(l~~ptefated .
There is often pain with resisted testing of the gastrocnemius/ soleus complex. The intervention for Achilles tendinitis varies, with the recommended amount of rest depending on the severity of the symptoms180: ~ ~
~
Type 1. Characterized by pain that is only experienced after activity. These patients should reduce their exercise by 25%. Type II. Characterized by pain that occurs both during and after activity but does not affect performance. These patients should reduce their training by 50%. Type III. Characterized by pain during and after activity that does affect performance. These patients should temporarily discontinue running.
Achilles stretching and strengthening; manual techniques; the cor rection of any lower-chain asymmetries, particularly low back and pelvic and hip t1exor asymmetries; electrotherapeutic modalities as appropriate; conect shoe wear; and orthotics (made from a mold of the foot held in subtalar neutral and non-weight-bearing) can be of signif icant benefit.
ACROMIOCLAVICULAR JOINT INJURIES InjUries to the AC joint can be categorized as either acute traumatic or chronic injuries 2 The chronic disorder may be atraumatic or post traumatic, with the fonner being attributed to generalized osteoarthri tis, inflammatory arthritis, or mechanical problems of the meniscus of this joint,18] The majority of traumatic injuries occur from a fall onto the shoulder with the arm adducted at the side. The ground reaction force produces displacement of the scapula in relation to the distal clavicle. 2 Injuries to the AC joint were originally classified by Tossy and col leagues 182 and Allman 183 as incomplete (grades I and II) and com plete (grade III). This classification has been expanded to include six types of injuries based on the direction and amount of displacement (Table 8_36)3,4,184,185: ~
~
~
~
Types I, II, III, and V all involve inferior displacement of the acromion with respect to the clavicle. They differ in the severity of injury to the ligaments and the amount of resultant displacement. 186 Types I and II usually result from a fall or a blow to the point on the lateral aspect of the shoulder, or a fall on an outstretched hand (FOOSH), producing a sprain. Types III and IV usually involve a dislocation (commonly called AC separations) and a distal clavicle fracture, both of which commonly disrupt the coracoclavicular ligaments. 2 In addition, damage to the deltoid and trapezius fascia, and rarely the skin, can occur. 2 Type IV injuries are characterized by posterior displacement of the clavicle. Type VI injuries have a clavicle inferiorly dis placed into either a subacromial or subcoracoid position. These types (IV, V, VI) also have complete rupture of all the ligament complexes and are much rarer injuries than types I through III. 2
CHAPTER 8. MUSCULOSKELETAL PHYSICAL THERAPY
447
TABIE 8-36. CLASSIFICATION OF AC INJURIES AND CLINICAL FINDINGS Type I
Type II
Type III
Type IV
Type V
Type VI
Isolated sprain of acromioclavicular ligaments Coracoclavicular ligaments intact Deltoid and trapezoid muscles intact Tenderness and mild pain at AC joint High (160-180 degrees) painful arc Resisted adduction is often painful Intervention is with TFM, ice, and pain-free AROM AC ligament is disrupted Sprain of coracoclavicular ligament AC joint is wider; may be a slight vertical separation when compared to the normal shoulder Coracoclavicular interspace may be slightly increased Deltoid and trapezoid muscles intact Moderate to severe local pain Tenderness in coracoclavicular space PROM all painful at end range with horizontal adduction being the most painful Resisted abduction and abduction are often painful Intervention initiated with ice and pain-free AROM!PROM; TFM introduced on day 4 AC ligament is disrupted AC joint dislocated and the shoulder complex displaced inferiorly Coracoclavicular interspace 25-100% greater than normal shoulder Coracoclavicular ligament is disrupted Deltoid and trapezoid muscles are usually detached from the distal end of the clavicle A fracture of the clavicle is usually present in patients under 13 years of age Arm held by patient in adducted position Obvious gap visible between acromion and clavicle AROM all painful; PROM painless if done carefully Piano key phenomenon (clavicle springs back after being pushed caudally) present AC ligament is disrupted AC joint dislocated and the clavicle anatomically displaced posteriorly into or through the trapezius muscle Coracoclavicular ligaments completely disrupted Coracoclavicular interspace may be displaced but may appear normal Deltoid and trapezoid muscles are detached from the distal end of the clavicle Clavicle displaced posteriorly; surgery indicated for types N-VI AC ligaments disrupted Coracoclavicular ligaments completely disnlpted AC joint dislocated and gross disparity between the clavicle and the scapula (300-500% greater than normal) Deltoid and trapezoid muscles are detached from the distal end of the clavicle Tenderness over entire lateral half of the clavicle AC ligaments disnlpted Coracoclavicular ligaments completely disrupted AC joint dislocated and the clavicle anatomically clisplaced inferiorly to the clavicle or the coracoid process Coracoclavicular interspace reversed with the clavicle being inferior to the acromion or the coracoid process Deltoid and trapezoid muscles are detached from the distal end of the clavicle Cranial aspect of shoulder is flatter than oppOSite side; Often accompanied with clavicle or upper rib fracture and/or brachial plexus injury
AROM, active range of motion; PROM, passive range of motion; TFM, transverse friction massage.
Data from Allman FL Jr. Fractures and ligamentous injuries of the clavicle and its articulation. j Bonejoint Surg. 1967;49A:774--784; Rockwood CA Jr.
Injuries to the acromioclavicular joint. In: Rockwood CA Jr., Green DP, eds. Fractures in Adults. 2nd ed. Philadelphia: Lippincott; 1984:860-910; and
Rockwood CA Jr., Young DC. Disorders of the acromioclavicular joint. In: Rockwood CA Jr., Matsen FA III, ed,. The Shoulder. Philadelphia: W.B.
Saunders; 1990:413-468.
448
SECTION II. TESTS AND MEASURES
TABLE 8-37. PHYSICAL THERAPY INTERVENTION FOR AC JOINT INJURIES INTERVENTION
INJURY TYPE Type I
Type II
Type III
Does not require immobilization. Ice is recommended for pain. If return to sport involves contact or impact forces, a donut pad placed over the shoulder helps to protect the joint. Patients are typically prescribed a sling as desired. ROM exercises are initiated as tolerated, often beginning with PROM to minimize muscle activation of the trapezius and deltoid. However, because the deltoid and trapezius fibers reinforce the AC joint capsule, specific strengthening exercises for these muscles are part of the long-term rehabilitation program. Return to function usually occurs within 2 to 3 weeks after injury. The most appropriate intervention is somewhat controversial and can be either surgical or conservative. The most commonly used device for reduction is the Kenny-Howard harness.
Physical therapy intervention varies according to injury severity (Table 8-37).
ADHESIVE CAPSULlTIS Adhesive capsulitis, often termed frozen shoulder, is associated with female gender, age older than 40 years, post-trauma, diabetes, pro longed immobilization, thyroid disease, post-stroke or myocardial infarction, ceItain psychiatric conditions, and the presence of certain autoimmune diseases. IH7 Nash and Hazelman 1HH have described the concept of primary and secondary frozen shoulder: ~ ~
Primary: idiopathic in origin and insidious onset. Secondary: either traumatic in origin, or related to a disease process, neurologic condition, or cardiac condition.
Adhesive capsulitis is diagnosed primarily by physical examination patients demonstrate limited active and passive range of motion with a capsular pattern of restriction. The six ROM measurements that should be taken include flexion, external rotation at the side, external rotation in abduction, internal rotation in abduction, horizontal abduction, and functional internal rotation up the back. The three classic stages of adhesive capsulitis inc1ude I89 : ~
~ ~
The early painful stage (freeZing): lasts 2 to 9 months. Patients have diffuse pain, difficulty with sleeping on the affected side, and restricted movement secondary to pain. The stiffening stage (freeZing): lasts 4 to 12 months. Characterized by progressive loss of ROM and decreased function. Recovery stage (thawing): lasts 5 to 24 months. Characterized by gradual increases in ROM and decreased pain.
The primary goal of physical therapy is the restoration of the range of motion and focuses on the application of controlled tensile stresses to produce elongation of the restricting tissues. Exercise has been found to be more effective than modalities, nonsteroidal anti inflammatory drugs, or steroid injections.I90.191 Nichoison I92 found that mobilization significantly improved range of motion into abduction
CHAPTER 8. MUSCULOSKELETAL PHYSICAL THERAPY
449
but offered no significant advantage of exercise alone in other motions. ~ ~
~
The patient with capsular restriction and low irritability may require aggressive soft-tissue and joint mobilization. The patient with high irritability may require pain-easing man ual therapy techniques. The patient with limited ROM due to nonstructural changes is aimed at addressing the cause of the pain.
Surgical intervention (manipulation) is reserved for those patients who do not respond to conservative intervention.
ANKLE SPRAINS Ankle sprains are the most common injuries in sports and recreational activities, and if left untreated can lead to chronic instability and impairment. Most acute ankle injuries occur in people 21 to 30 years old, although injuries in the younger and older age groups tend to be more serious.
Lateral Ankle (Inversion) Sprain. Sprains of the lateral liga mentous complex represent 85% of ankle ligament sprains. 193 ,194 In the younger population, serious ankle sprains are unusual in the skeletally immature because the ligaments are usually stronger than the bone, 195-197 necessitating ruling out a physeal fracture.198.199 Lateral ligament sprains are more common than medial ligament sprains for two major reasons 200 ; ~
~
The lateral malleolus projects more distally than the medial malleolus, producing less bony obstruction to inversion than eversion. The deltoid ligament is much stronger than the lateral ligaments.
Lateral ankle sprains can be graded according to severity: ~
~
~
Grade I sprains are characterized by minimum to no swelling and localized tenderness over the ATFL. These sprains require on average 11.7 days before the full resumption of athletic activities. 201 Grade II sprains are characterized by localized swelling and more diffuse lateral tenderness. These sprains require approxi mately 2 to 6 weeks for return to full athletic function. 202 ,20:\ Grade III sprains are characterized by significant swelling, pain, and ecchymosis and should be referred to a specialist. 204 Grade III injuries may require more than 6 weeks to return to full function. For acute grade III ankle sprains, the average duration of disability has been reported anywhere from 45 to 26 weeks, and only 25% to 60% of patients are symptom-free 1 to 4 years after injury.205
Conservative intervention has been found to be uniformly effec tive in treating grade I and II ankle sprains and generally patients are completely asymptomatic and functionally stable at follow-up.206 Intervention in the acute stage centers around aggressive attempts to:
Study Pearl In the neutral position or dorsiflexion, the ankle is stable because the widest part of the talus' is in the mortise. However, in plantar' f ankle stability is decreased...a~ .n·23o The appearance of the nodules is followed by the formation of tendon-like cords, which are due to the pathologic change in normal fascia. 231 - m The thickening and shortening of the fascia cause contracture, which behaves similarly to the contracture and maturation of wound healing. 230 The contractures form at the MCP joint, the PIP joint, and occasionally the DIP joint. 23.j The diagnosis of Dupuytren's disease in its early stages may be dif ficult, and is based on the palpable nodule, characteristic skin changes, changes in the fascia, and progressive joint contracture. The skin changes are caused by a retraction of the skin, resulting in dimples or pits. Dupuytren's disease can be classified into three biologic stages 2J2 : ~
~ ~
First stage: the proliferative stage, characterized by an intense proliferation of myofibroblasts (the cells believed to generate the contractile forces responsible for tissue contraction) and the formation of nodules. Second stage: the involutional stage, represented by the align ment of the myofibroblasts along lines of tension. Third stage: the residual stage, where the tissue becomes mostly acellular and devoid of myofibroblasts, and only thick bands of collagen remain.
The disease is usually bilateral, with one hand being more severely involved. However, there appears to be no association with hand dominance. The patient may have one, two, or three rays involved in the more severely affected hand. The most commonly involved digit is the little finger, which is involved in approximately 70% of patients. Conservative interventions have not yet proven to be clinically useful or of any long-term value in the treatment of established contractu res. Surgery is the intervention of choice when the MCP joint contracts to 30 degrees and the deformity becomes a functional problem. 235 Scar management and splinting are an important part of the postoperative management. Active, active assisted, and passive exercises are usually initiated at the first treatment session. EPICONDYLITIS
Lateral Epicondylitis (Tennis Elbow). Lateral epicondylitis represents a pathologic condition of the tendons of the muscles that control wrist extension and radial deviation, resulting in pain on the lateral side of the elbow. This pain is aggravated with movements of the wrist, by palpation of the lateral side of the elbow, or by contrac tion of the exensor muscles of the wrist. Tennis elbow is usually the result of overuse, but can be traumatic in origin. Individuals who perform repetitive wrist extension against resistance are particularly at risk, including participants in tennis, base ball, javelin, golf, squash, racquetball, swimming, and weight lifting. The pain of tennis elbow is often activity related. Diffuse achiness and morning stiffness are also common complaints. Occasionally the pain is experienced at night and the patient may report frequent drop ping of objects, especially if they are carried with the palm facing down.
Study Pearl While the terms "epicondylitis" and "tendinitis" are commonly used to describe tenniselbowlthey are mis nomers as histopathologic studies have demonstrated that tennis elbow is not an inflammatory condition; ratherl it is a degenerative condition, ~ a tendinosis. 236,237
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SECTION II. TESTS AND MEASURES
Tenderness is usually found over the ECRB and ECRL, especially at the lateral epicondyle. The site of maximum tenderness is most com monly over the anterior aspect of the lateral epicondyle. Tennis elbow is a self-limiting complaint; without intervention, the symptoms will usually resolve within 8 to 12 months. 238 More than 40 treatments have been suggested, indicating that the ideal remedy has yet to be found, although there is agreement that management of the patient who presents for the first time with tennis elbow should be con servative. Poor technique, particularly with racket sports, is the cause of many elbow problems. Emphasis should be placed on recruiting the whole of the shoulder and trunk when hitting the ball, so as to dissi pate the forces as widely as possible. In addition to correcting poor technique, patient education should address racket size, grip size, and string tension. An exercise regimen consisting of progressive resistance exercise to the wrist extensors, with the elbow flexed to 90 degrees and also with the elbow straight, is recommended. 239 This should be performed as a ten-repetition maximum, morning and night. Gradually the weight must be increased so that the ten-repetition maximum is always main tained. Pain will be increased for the first week or two or three, but by the fifth or sixth weeks, the elbow pain will be better. An ice pack or heating pad can be a mitigating modality during the painful period. 239 Counterforce bracing 240 (such as the Count-R-Force brace from Medical Sports, Arlington, Virginia) has been shown to: ~
Have a beneficial effect on the force couple imbalances, and altered movements associated with tennis elbow.241-243 ~ Decrease elbow angular acceleration. 244 ~ Decrease electromyographic activity.244 However, contrary to popular belief, tennis elbow braces have been shown to have little effect in vibrational dampening. 245 Surgery is indicated if the symptoms do not resolve despite prop erly performed nonoperative treatments lasting 6 months.
MEDIAL EPICONDYLITIS (GOLFER'S ELBOW) Medial epicondylitis is only one-third as common as tennis elbow and primarily involves a tendinopathy of the common flexor origin, specif ically the flexor carpi radialis and the humeral head of the pronator teres. 246 To a lesser extent the palmaris longus, flexor carpi ulnaris, and flexor digitorum superficialis, may also be irlvolved. 247 The mechanism for golfer's elbow is not usually related to direct trauma, but rather to overuse. This commonly occurs for three reasons: ~ ~
~
The flexor-pronator tissues fatigue in response to repeated stress. There is a sudden change irl the level of stress that predisposes the elbow to medial ligamentous injury.248 The ulnar collateral ligament fails to stabilize the valgus forces sufficiently. 249
Chronic symptoms result from a loss of extensibility of the tissues, leavirlg the tendon unable to attenuate tensile loads. The typical clinical presentation is pain and tenderness over the flexor-pronator origin, slightly distal and anterior to the medial
CHAPTER 8, MUSCULOSKELETAL PHYSICAL THERAPY
epicondyle, in an aggressive advanced-level athlete. The symptoms are typically exacerbated with either resisted wrist flexion and pronation, or passive wrist extension and supination. Differential diagnosis for medial elbow symptoms inciudes 250 : ~
Medial ulnar collateral ligament injury or insufficiency. 251-253 ~ Ulnar nerve entrapment. ~ Medial elbow intra-articular pathology.25 4 The conservative intervention for this condition initially involves rest, activity modification, and local modalities. Once the acute phase has passed, the focus is to restore the range of motion, and correct imbalances of flexibility and strength. The strengthening program is progressed to include concentric and eccentric exercises of the flexor pronator muscles. Splinting, or the use of a counterforce brace, may be a useful adjunct.
FINGER IN/URIES
Boutonniere Deformity. The boutonniere or "buttonhole" deformity occurs when the common extensor tendon that inserts on the base of the middle phalanx is damaged. The realignment of the extensor mechanism, coupled with the loss of certain muscle influ ence, produces a deformity of extension of the MCP and DIP joints, and flexion of the PIP jOint-the classic boutonniere deformity. If trau matic in origin, this condition can be difficult to diagnose, due to the degree of swelling, but if more than a 30-degree extension lag is pres ent at the PIP joint, a boutonniere lesion should be suspected. The presence of a mobile correctable deformity requires little more than immobiliZing the PIP in full extension for 6 to 8 weeks, and the DIP and MCP joints held free. Gentle AROM exercises can begin for flexion and extension of the PIP joint at 4 to 8 weeks, with the splint being reapplied between exercises. General strengthening usually begins at 10 to 12 weeks. For a return to competition, an additional 2 months is reqUired. Swan-Neck (Recurvatum) Deformity. The swan-neck deformity is characterized by a flexion deformity at the DIP joint, and hyperextension of the PIP joint. This rearrangement leads to an increased extensor force across the PIP joint with a resulting hyperex tension of the PIP joint. The resultant loss of function includes an inability to bring the tips of the fingers into grasp. Clinical findings include a hyperextended PIP joint with a flexed DIP joint of the same digit. The intervention for swan-neck deformity depends on the etio logic status of the PIP joint and its related anatomic structures. The intervention for a swan-neck deformity with no loss of PIP joint flexion is usually conservative, with a silver ring splint used for the correction of the PIP hyperextension. Mallet Finger.
Mallet finger deformity is a traumatic disruption of the terminal tendon resulting in a loss of active extension of the DIP joint. This is one of the most common hand injuries sustained by the athletic population, and is especially conunon in the baseball catcher and football receiver.
455
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SECTION II. TESTS AND MEASURES
The physical examination reveals a flexion deformity of the distal interphalangeal (DIP) joint, which can be extended passively but not actively. This lack of active extension at the DIP joint is due to the zero tension being provided by the extensor digitorum communis (EDC), in addition to the resulting increased tone in the flexor digitorum profun dus (FDP). Conservative intervention involves 6 weeks of immobilization. Mallet deformities with an associated large fracture fragment are typically treated with 6 weeks of immobilization following open reduction and internal fIxation, usually with K-wires. 2S5 Closed reduction is used for other types, followed by 6 weeks of continuous dorsal splinting of the DIP in 0° of extension to 15° of hyperextension. 255 The PIP joint should be free to move. Gentle progressive resistive exercises (PREs) using putty or a hand exerciser are initiated at week 8. Usually the splint is dis continued at 9 weeks if the DIP extension remains at 0 to 5 degrees and there is no extensor lag. Unrestricted use usually occurs after 12 weeks.
R.upture of the Terminal Phalangeal Flexor (Jersey Fmger). The rupture of the FDP tendon from its insertion on the dis tal phalanx (jersey finger) is often misdiagnosed as a sprained or "jammed" finger, as there is no characteristic deformity associated with it,25s The injury is typically caused by forceful passive extension while the flexor digitorum profundus muscle is contracting. A common example is in football when the flexed finger is caught in a jersey while the athlete is attempting to make a tackle; hence the term jersey finger. To test the integrity of the tendon, the clinician isolates the FDP by holding the MCP and PIP joints of the affected finger in full extension, and asks the patient to attempt to flex the DIP. If it flexes, it is intact. If not, it is ruptured. The intervention can involve doing nothing if function is not seri ously affected, or surgical reattachment of the tendon, which requires a 12-week course of rehabilitation.
FRACTURES The following fractures are described in Chapter 14: .. .. .. .. .. ..
Pathologic fractures. Stress fractures . Proximal humeral fractures. Distal radius fractures. Proximal femur/hip fractures. Fractures of the spine.
GROIN PAIN The hip adductor muscleS-including the graCilis, pectineus, and adductor longus, brevis, and magnus-are the most frequent cause of groin region pain, with the adductor longus being the most commonly injured. 256 ,257 Adductor strains have been known to cause long-standing problems. There are a number of causative factors for an adductor strain including a muscular imbalance of the combined action of the muscles stabilizing the hip joint, resulting from fatigue or an abduction over load, especially as the adductor muscles act as important stabilizers of
CHAPTER 8, MUSCULOSKELETAL PHYSICAL THERAPY
the hip joint. Adductor strains are associated with jumping, running, kicking, and twisting activities, particularly when external rotation of the affected leg is an added component of the activity. The signs and symptoms are easily recognizable: 258 .. Twinging or stabbing pain in the groin area with qUick starts and stops, .. Edema or echemosis several days post injury. .. Pain with manual resistance to hip adduction when tested in different degrees of hip flexion: 0 degrees (gracilis), 45 degrees (adductor longus and brevis), 90 degrees (if combined with adduction; pectineus). .. Possibly a palpable defect in severe ruptures. .. Muscle guarding. The differential diagnosis for groin pain includes abdominal mus cle strains, inguinal hernia, osteitis pubis, and referred pain from the hip joint or lumbar spine. The intervention of adductor strains involves the principles of PRICEMEM in the acute stage. This is followed by heat applications, hip adductor isometrics, and gentle stretching dUring the subacute phase, progressing to a graded resistive program and then a gradual return to full activity. As part of the rehabilitation program, any imbal ance between the adductors and the abdominals needs to be addressed. In addition, the clinician should examine the patient's tech nique in his or her required activity, as poor technique can overload and fatigue the adductors.
HALLUX VALGUS Hallux valgus is the term used to describe a deformity of the first MTP joint in which the proximal phalanx is deviated laterally with respect to the first metatarsal. Hallux valgus has been observed to occur almost exclusively in populations that wear shoes, although some predispos ing anatomic factors make some feet more vulnerable than others to the effects of extrinsic factors. 25 9--264 Women have been observed to have hallux valgus in a ratio of 9:1 compared to men. 265 With increasing lateral deviation of the hallux, the MTP joint becomes incongruent, the sesamoids subluxate laterally, the hallux pronates, the medial aspect of the first metatarsal head becomes more prominent, and weight-bearing shifts from the first metatarsal head to the second metatarsal and possibly the third. The intervention includes recommendations for wider shoes and orthotics. Achilles stretching should be used in cases of Achilles con tracture. A simple toe spacer can be used between the first and second toes. In cases of pes planus associated with hallux valgus, a medial lon gitudinal arch support with Morton's extension under the first MTP joint may also alleviate symptoms. If pain persists, however, structural realignment of the first metatarsal varus is usually necessary, as the bunion deformity becomes more severe and decompensated.
LUMBAR HERNIATED NUCLEUS PULPOSUS The water-retaining ability of the nucleus pulposus progressively declines with age resulting in a decrease in the mechanical stiffness of
457
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SECTION II. TESTS AND MEASURES
the disk, allowing the annulus to bulge with a corresponding loss of disk and foramina height. The etiology of pain for a particular individual cannot be deter mined because of the multiplicity of potential sources. However, the degenerating disk is known to have neurovascular elements associated with the periphery, including pain fibers. Disk deterioration and loss of disk height may shift the balance of weight-bearing to the facet joint. Nuclear material, which is displaced into the spinal canal, is associated with a significant inflammatory response-macrophages respond to this displaced foreign material and seek to clear the spinal canal. Compression of a motor nerve results in weakness, and compression of a sensory nerve results in numbness. Radicular pain results from inflammation of the nerve, explaining the lack of correlation between the actual size of a disk herniation or even the consequent degree of neural compression with the correlating clinical symptoms. Furthermore, degeneration may result in radial tears and leakage from the nuclear material, which is toxic to the nerves. The resultant inflammatory response causes neural irritation with radiating pain without numbness, weakness, or loss of reflex, as neural compression is absent. The pertinent historical information begins with an analysis of the chief complaint. ~
~
~ ~
~ ~ ~
~
Does the patient's complaint concern dominant leg pain, dom inant back pain, or a mixture of significant problems with both? A pain drawing can be very helpful in assessing the pattern of pain regarding a dermatomal distribution or in assessing the organicity of the complaints. Is the onset acute, subacute, or chronic? Under what circumstances does onset occur? What positions or actions cause problems? Which activities is the patient unable or less able to perform, and which activities exacerbate or moderate the pain? What is the patient's prior history, particularly of similar symp toms or response to treatment? The physical demands of the patient's occupation and daily activities.
It is important to specifically exclude red flags, such as nonme chanical pain-pain at night unrelated to activity or movement, which may be indicative of a tumor or infection. The physical examination is essentially a neurologic assessment of weakness; dermatomal numbness; reflex change; or most importantly in the lumbar spine, sciatic or femoral nerve root tension. The provocation of radiating pain down the leg is the most sensi tive test for a lumbar disk herniation. For a higher lumbar lesion, reverse straight-leg raising or hip extension stretching the femoral nerve is analogous to a straight-leg raising sign. Other causes of signif1cant back pain in the absence of neurologic findings should be considered. Sciatic nerve irritation may result from sacroiliac dysfunction or degenerative joint disease due to the proximity of the sciatic notch to the sacroiliac joint. The intervention focus should address the reduction of inflamma tion. Therefore, a period of rest is appropriate, and warm moist heat or modalities and gentle exercises based on patient's tolerance. Exercises
CHAPTER 8. MUSCULOSKELETAL PHYSICAL THERAPY
mobilize muscles and joints to facilitate the removal of edema and pro mote recovery. A transcutaneous electrical nerve stimulation (TENS) unit may be helpful in some patients with chronic conditions. Patients should be encouraged to maintain flexibility by initiating life-long exercise regi mens, including aerobic conditioning, particularly swimming, which allows gravity relief.
ILIOTIBIAL BAND FRICTION SYNDROME (ITBFS) As its name suggests, ITBFS is a repetitive stress injury, common in runners and cyclists, that results from friction of the iliotibial band as it slides over the prominent lateral femoral epicondyle at approximately 30 degrees of knee flexion. The friction has been found to occur at the posterior edge of the band, which is felt to be tighter against the lateral femoral condyle than the anterior fibers. The friction causes a gradual development of a reddish brown bursal thickening at the lateral femoral epicondyle. Subjectively the patient reports pain with the repetitive motions of the knee. There is rarely a history of trauma. Although walking on level surfaces does not generally reproduce symptoms, especially if a stiff legged gait is used, climbing or descending stairs often aggravates the pain. Patients do not complain of pain during sprinting, squatting, or during such stop-and-go activities as tennis, raquetball, or squash. The progression of symptoms is often associated with changes in training surfaces, increased mileage, or training on crowned roads. The lateral knee pain is described as diffuse and hard to localize. Objectively, there is localized tenderness to palpation at the lateral femoral condyle and/or Gerdy's tubercle on the anterior-lateral portion of the proximal tibia. The resisted tests are likely to be negative for pain. The special tests for the ITB (Ober's test, prone-lying test, and retinacular test) should be positive for pain, crepitus, or both. In addi tion to the finding of a tight iliotibial band, a cavus foot (calcaneal varus) structure, leg length difference (with the syndrome developing on the shorter side), fatigue, internal tibial torsion (increased lateral retinaculum tension), an anatomically prominent lateral femoral epi condyle, and genu varum, have all been associated with ITB friction problems, although they have yet to be substantiated. The intervention for ITBFS consists of activity modification to reduce the irritating stress (decreasing mileage, changing the bike seat position, and changing the training surfaces), using new running shoes, heat or ice applications, strengthening of the hip abductors, and stretching of the iliotibial band. Surgical intervention, consisting of a resection of the posterior half of the ITB at the level that passes over the lateral femoral condyle, is reserved for the more recalcitrant cases.
LITTLE LEAGUER'S ELBOW Little Leaguer's elbow is a common term for an avulsion lesion to the medial apophysis. The repetitive motions involved in the various phases of throwing place enormous strains on the elbow, particularly during the late cocking and acceleration phases, which can result in inflammation, scar formation, loose bodies, ligament sprains or ruptures, and the more serious conditions of osteochondritis or an avulsion fracture. Little
459
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SECTION II. TESTS AND MEASURES
Leaguer's elbow may start insidiously or suddenly. Usually, a sudden onset of pain is secondary to fracture at the site of the lesion. Clinical findings include a history of pain on the medial side of the elbow, with and without throwing. Physical findings relate to the spe cific lesion, but are commonly a persistent elbow discomfort or stiff ness due to aggravation by the injury. A locking or "catching" sensation indicates a loose body. Management is conservative, involving rest and elimination of the offending activity for 3 to 6 weeks. If osteochondritis dissecans is pres ent, the joint needs protection for several months. The patient cannot return to pitching until full and normal motion has returned. To pre vent elbow disorders, young athletes should adhere to the rules of the Little League, which limit the number of pitches per game, per week, and per season, and the number of days of rest between pitching. The pitch count is the most important of these statistics. Surgical intervention is reserved for those patients with symptoms of a loose body, osteochondritis, or who fail to respond to conserva tive therapy.
MENISCAl INJURIES Meniscal injuries are a common sports-related problem and the most frequent injury to the knee joint. Such injuries are especially prevalent among competitive athletes, particularly those who play soccer, foot ball, and basketball. Meniscal tears can be classified into two types: traumatic and degenerative. ~
~
Traumatic tears are most commonly found in young, athleti cally active individuals, not necessarily associated with contact injuries, and are frequently associated with ACL tears and less commonly with PCL tears. Vertical longitudinal tears are the most common; transverse or radial tears are also common. Degenerative tears tend to occur in patients older than 40 years. No history of a traumatic event is present. These tears have minimal or no healing capacity, and horizontal cleavage tears, flap tears, and complex tears are most common.
The most common report is one of jOint-line pain. The patient may also report joint clicking or locking, and the knee giving way. Injuries to the healthy meniscus are usually produced by a combination of compressive forces coupled with rotation of the flexed knee as it starts to move into extension. The differential diagnosis for meniscal tears is extensive and includes bone contusion, plica syndromes, popliteus tendinitis, osteo chondritis desiccans, chondral damage from trauma, loose bodies, patellofemoral pain and instability, fat pad impingement syndrome, inflammatory arthritis, fracture, meniscotibial ligament sprain, discoid meniscus (DM), and synovial lesions. Tests to evaluate the menisci are outlined in "Special Tests of the Knee Complex" earlier in this chapter. Treatment options depend on knowledge of the exact type, loca tion, and extent of the meniscal tear. Severe damage, and loss or removal of the menisci, frequently lead to joint instability and later accelerated degenerative joint disease (DJD), resulting in further dis ability and joint replacement.
CHAPTER 8. MUSCULOSKELETAL PHYSICAL THERAPY
461
OSTEOARTHRITIS
See Chapter 5.
PATELLA TENDINITIS
Patellar tendinitis (jumper's knee) and quadriceps tendinitis are over use conditions that are frequently associated with eccentric overload ing during deceleration activities (repeated jumping and landing, downhill running, etc.). The high stresses placed upon these areas during closed kinetic chain functioning place them at high risk for overuse injuries. The diagnosis of tendinitis is based on a detailed history and careful palpation of the tendons in both flexion and extension. Pain upon palpation near the patellar insertion is present in both patel lar and quadriceps tendinitis. These are usually self-limiting condi tions that respond to rest, stretching, eccentric strengthening, brac ing, and other conservative techniques. When treating overuse injuries, it is essential that the clinician limits both the chronic inflammation and degeneration by working on both sides of the problem-tissue strength should be maximized through proper training, and adequate healing time must be allowed before return ing to full participation. A number of protocols have been advocated for the conservative intervention of patella tendinitis: ~
~
Grade I lesions, which are characterized by no undue functional impairment and pain only after the activity, are addressed with adequate warm-up before training and ice massage after. Grade II or III strains: activity modification, localized heating of the area, a detailed flexibility assessment, and an evaluation of athletic techniques. In addition, a concentric-eccentric program for the anterior tibialis muscle group is prescribed, which progresses into a purely eccentric program as the pain decreases. 266
Surgical intervention is only usually required if significant tendi nosis develops, and is successful in the majority of patients.
PATELLOFEMORAL DYSFUNCTION
Anterior knee pain or patellofemoral pain syndrome is a commonly rec ognized symptom complex characterized by pain in the vicinity of the patella, which is worsened by sitting, climbing stairs, inclined walking, and squatting. It is a common reason for referral to physical therapy. Although anterior knee pain can occur in anyone, particularly athletes, women who are not athletic appear to be more prone to this problem than men who are not athletic. The impairments resulting from patellofemoral dysfunction have been related to problems that cannot be improved by physical therapy, and those that can. The former include anatomic variance (femoral trochlear dysplasia, patellar morphology and the amount of congruence of the patellofemoral, the natural positioning of the patella, [altalbajaJ joint) and gender (females are more predisposed).
Some.feeltbat the.· terrnP?-te1l9t·t~f1~ di?itis, is a • misnomer 'ause(tbe Patell~r/!;ten<J()newhicfl, ' nectstwo bones, isbyd~tif1itionaJ ent.
Study Pearl ply a mismatch between structure and the ture to dissipate the forces, resulting in inflammatory changes.
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SECTION II. TESTS AND MEASURES
Patients presenting with various patellofemoral conditions invari ably report similar symptoms, which has previously led to the indis criminate use of such terms as "anterior knee pain" and "chondroma lacia patellae." Knee pain is the most common presentation of patellofemoral pain syndrome. The pain characteristically is located behind the kneecap (i.e., retropatellar) and most often manifests dur ing activities that require knee flexion and forceful contraction of the quadriceps (e.g., during squats, ascending/descending stairs). The pain may worsen in intensity, duration, and rapidity of onset if the aggravating activity is performed repeatedly. Sitting with the knee flexed for a protracted period of time may exacerbate the pain, such as while watching a movie ("movie-goer's knee."). Patients with this condition often may prefer to sit at an aisle seat, where they may more frequently keep the knee extended. Symptoms often occur during the activity, such as playing volley ball for 30 minutes, or may occur later after the activity has been com pleted. Sometimes symptoms manifest as late as the next day. The usual physical findings are localized around the knee: ~
~
~
~ ~
~ ~
Tenderness often is present along the facets of the patella. The facets are most accessible to palpation while the knee is fully extended and the quadriceps muscle is relaxed. An apprehension sign may be elicited by manually fixing the position of the patella against the femur and having the patient contract the ipsilateral quadriceps. Crepitus may be present, but if present in isolation, crepitus does not allow for definitive diagnosis. An alteration in the Q-angle. Gait analysis may demonstrate excessive foot pronation, exces sive knee valgus, or an antalgic gait pattern.
Repetitive squatting may reproduce knee pain.
Genu recurvatum and hamstring weakness.
Ice packs frequently are used to decrease pain and inflammation associated with this condition. Other modalities that may be useful and commonly are incorporated into physical therapy include electrical stimulation and biofeedback. The basic exercise principles for man agement are: ~
~
~ ~ ~
~
Restoration of muscle balance within the quadriceps group. Quadriceps strengthening traditionally is performed while the knee is flexed 0 to 30 degrees. Controversy remains as to the extent that the individual muscle groups comprising the quadri ceps can selectively be strengthened. Stretching of the quadriceps should be of long duration (20 to 30 seconds) and with low force. Improving fleXibility. Exercises to stretch the iliotibial band, hip, hamstring, and gastrocnemius. Manual stretching of the lat eral retinaculum may be used as a conservative approach, par tially mimicking the effect of lateral retinacular release. Improving range of motion.
Restricting the offending physical activity.
Home exercise programs that include both stretching and
strengthening exercises. Patellar taping techniques (McConnell method) can be used to reduce the friction on the patella. If successful, the clinician can teach the patient self-taping techniques to use at home.
CHAPTER 8. MUSCULOSKELETAL PHYSICAL THERAPY ~
~
Proper footwear also is important. The clinician can evaluate the patient's biomechanics and recommend proper shoes and/or orthotics. Soft knee braces may also be of benefit. Bracing involves con trol of the tracking position of the patella and restriction of full knee flexion.
PLANTAR FASCIITIS
Plantar fasciitis is an inflammatory process of the plantar fascia and is reported to be the most common cause of inferior heel pain. The role of the heel spur in plantar fasciitis is controversial. Common findings include a history of pain and tenderness on the plantar medial aspect of the heel, especially dUring initial weight-bearing in the morning. Interference with daily activities is common. Plantar fasciitis is usually unilateral, although both feet can be affected. The heel pain often decreases during the day but worsens with increased activity (such as jogging, climbing stairs, or going up on the toes) or after a period of sitting. Upon physical examination, there will be localized pain on palpa tion along the medial edge of the fascia or at its origin on the anterior edge of the calcaneus, although firm finger pressure is often necessary to localize the point of maximum tenderness. The main area of tender ness is typically just over and distal to the medial calcaneal tubercle, and usually there is one small exquisitely painful area. Tenderness in the center of the posterior part of the heel may be due to bruising or atrophy of the heel pad or to subcalcaneal bursitis. Slight swelling in the area is common. To test for plantar fasciitis, the fascia needs to be put on stretch with a bowstring-type test. The patient's heel is manually fixed in ever sion. The clinician takes hold of the first metatarsal and places it in dor siflexion, before extending the big toe as far as possible. Pain should be elicited at the medial tubercle. A number of interventions have been suggested over the years for plantar fasciitis. These include: ~
Night splinting. ~ Orthotics. ~ Taping. ~ Heel cups. ~ Stretching (gastrocnemius) and strengthening of the leg muscles and foot intrinsics. ~ Deep frictional massage. ~ Corticosteroid injection. ~ Dexamethasone iontophoresis. ~ Shoe modifications. ~ NSAIDs. ~ Casting. ~ Extracorporeal shock-wave lithotripsy.267 ~ Open and endoscopic plantar fasciotomy and surgical neurolysis (in extremely recalcitrant cases). RHEUMATOID DISEASES
Gout. Gout is the most common form of inflammatory arthritis in men older than 40 years of age, and appears to be on the increase. 268
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SECTION II. TESTS AND MEASURES
Gout is caused by the accumulation of uric acid crystals in synovial joints. The rising prevalence of gout is thought to stem from dietary changes, environmental factors, increasing longevity, subclinical renal impairment, and the increased use of drugs causing hyperuricemia, particularly diuretics. 269
Ankylosing Spondylitis.
Study Pearl
I
f:-
CaHn and colleagues273 describe screening>questions fot AS: 1. Is there morning stiffness? 2. Is there improvement in discomfort
I
with exercise?
3. Was the onsetof backpaitlDefore
age 40 years?
4. Didthe problem.beginslowly? I . .•.·S.• ·.. . . •. .H.•·. as the. p.•. a. in persisted for at.. lea.st
. 3··months?
.
I
Ankylosing spondylitis (AS, also known as Bekhterev's or Marie-Strlimpell disease) is a chronic rheuma toid disorder. Thoracic involvement in AS occurs almost universally. The patient is usually between 15 and 40 years of age. 270 Although males are affected more frequently than females, mild courses of AS are more common in the latter. 271 The disease includes involvement of the anterior longitudinal lig ament and ossification of the disk, thoracic zygapophysial joints, cos tovertebral joints, and manubriosternal joint. This multijoint involve ment makes the checking of chest expansion measurements a reqUired test in this region. In time, AS progresses to involve the whole spine and results in spinal deformities, including flattening of the lumbar lordosis, kypho sis of the thoracic spine, and hyperextension of the cervical spine. These changes in turn result in flexion contractures of the hips and knees, with significant morbidity and disability.271 The most characteristic feature of the back pain associated with AS is pain at night. 272 Patients often awaken in the early morning (between 2 and 5 AM) with back pain and stiffness, and usually either take a shower or exercise before returning to sleep.271 Backache during the day is typically intermittent irrespective of exertion or rest. 271 Using at least four positive answers to define a "positive" result, the sensitivity of these questions was 0.95 and the specificity 0.85. 273 A human leukocyte antigen (HLA) haplotype association (HLA-B27) has been found with ankylosing spondylitis and remains one of the strongest known associations of disease with HLA-B27, but other dis eases are also associated with the antigen. 271 Peripheral arthritis is uncommon in AS, but when it occurs, it is usu ally late in the course of the arthritis. 274 Peripheral arthritis developing early in the course of the disease is a predictor of disease progression. 275 The arthritis usually occurs in the lower extremities in an asymmetric dis tribution, with involvement of the "axial" joints, including shoulders and hips, more common than involvement of more distal joints. 271 ·276 Inspection usually reveals a flat lumbar spine and gross limitation of side bending in both directions. Mobility loss tends to be bilateral and symmetric. There is loss of spinal elongation on flexion (Schober's test), although this can occur in patients with chronic low back pain or spinal tumors and is thus not specifiC for inflammatory spondy 10pathies. 277 The patient may relate a history of costochondritis and, upon examination, rib springing may give a hard end-feeL Basal rib expansion often is decreased. The glides of the costotransverse joints and distraction of the sternoclavicular joints are decreased, and the lumbar spine exhibits a capsular pattern. As the disease progresses, the pain and stiffness can spread up the entire spine, pulling it into forward flexion, so that the patient adopts the typical stooped-over position. The patient gazes downward, the entire back is rounded, the hips and knees are semiflexed, and the arms cannot be raised beyond a limited amount at the shoulders. 278 Exercise is particularly important for these patients to maintain the mobility of the spine and involved joints for as long as possible, and to
CHAPTER 8. MUSCULOSKELETAL PHYSICAL THERAPY
465
prevent the spine from stiffening in an unacceptable kyphotic position. A strict regimen of daily exercises, which include positioning and spinal extension exercises, breathing exercises, and exercises for the peripheral joints, must be followed. 279 Several times a day, patients should lie prone for 5 minutes, and they should be encouraged to sleep on a hard mattress and avoid the side-lying position. Swimming is the best routine sport.
Systemic Lupus Erythematosus. Systemic lupus erythemato sus (SLE), sometimes referred to as lupus, is a chronic inflammatory autoimmune disorder that can affect any organ or system of the body. According to the American Rheumatism Association, a person is con sidered to have SLE if 4 of the following 11 criteria are present: ~ ~ ~ ~ ~ ~ ~
Abnormal titer of antinuclear antibodies. Butterfly rash. Discoid rash. Hemolytic anemia, leukopenia, or thrombocytopenia. Non-erosive arthritis of two or more peripheral joints charac terized by tenderness, swelling, or effusion. Photosensitivity. Pleuritis or pericarditis.
Clinical manifestations for the physical therapist to note include: ~ ~ ~ ~
Musculoskeletal involvement: arthralgias and arthritis consti tute the most common presenting manifestations of SLE. Cardiopulmonary signs: pleuritis, pericarditis, and dyspnea. Central nervous system involvement: headaches, depression, seizures, and peripheral neuropathy (Raynaud's phenomenon). Kidney dysfunction or failure.
Study Pearl The.. serQn~~tiv~.art~roPatniesii.in:GIl.lde anf45°C, 45°C, hrenia and anxiety.ll2 ------
Study Pearl - - - - - - - - - - - - -
Hyporeflexia, if not generalized to the whole body, indicates a lower motor neuron (LMN) or sensory paresis, which may be segmental (root), multi segmental (cauda equina), or nonS€g mental (peripheral nerve).
I S::d:s'-:-:-:-:-j-S--de-f-i-n-e-d-as-v-e--Io-c-it-y_
dependent (resistance increases with velocity) hypertonia and, hyperactive tendon reflexes (increased deep ten don reflexes, DTRs) resulting from hyperexcitability of the stretch reflex. Spasticity is a common sequela of an anatomic or physiologic anomaly of the eNS, specifically an injury to the corticospinal system (suprasegmentall upper motor neuron lesions).ll3-115 If left untreated, spasticity can lead to the development of secondary impairment such as contracture, pO,slural asymme tries, and deformity (see later).4
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SECTION II. TESTS AND MEASURES
a flexed or semiflexed position. The Jendrassik maneuver can be used during testing to enhance a muscle reflex that is difficult to elicit. 116 ~ ~
For the upper extremity reflexes, the patient is asked to cross the ankles and then to isometrically attempt to abduct the legs. For the lower extremity reflexes, the patient is asked to inter lock the fingers and then to isometrically attempt to pull the elbows apart.
The superficial (cutaneous) and pathologic reflexes (Table 9-26) can also be tested. Various substitutes for Babinski's sign have been described, and some are occasionally useful. They are described in the next sections.
Oppenheim. The clinician applies noxious stimuli to the crest of the patient's tibia by running a fingernail along the crest. A positive test, demonstrated by Babinski's signs, is indicative of an UMN impairment. Clonus.
The clinician passively applies a sudden dorsiflexion of the patient's ankle and the stretch is maintained during the test. The clini cian notes a gradual increase in tone and then the transient occurrence of ankle clonus. In some patients, there is a more sustained clonus, and in others there is only a very short-lived finding. During the testing, the patient should not flex the neck as this can often increase the number of beats. A positive test, demonstrated by four or five reflex twitches of the plantar flexors (two or three twitches are considered norma]), is indicative of an upper motor neuron impairment.
Hoffmann's Sign. Hoffmann's sign is the upper limb equivalent of Babinski's sign. However, unlike Babinski's sign, some normal indi viduals can exhibit Hoffmann's sign.7 9 The clinician holds the patient's middle finger and briskly pinches the distal phalalLx, thereby applying a noxious stimulus to the nail bed of the middle finger. 79 Denno and Meadows ll7 devised a dynamic version of Hoffman's sign, which involves the patient performing repeated flexion and extension of the TABLE 9-26. PATHOLOGIC REFLEXES ELICITATION
REFLEX Babinski's
Stroking of lateral aspect of side of foot
Chaddock's
Stroking of lateral side of foot beneath lateral malleolus Stroking of anteromedial tibial surface Squeezing of calf muscles firmly Passive flexion of one lower limb "Flicking" of terminal phalanx of index, middle, or ring finger
Oppenheim's Gordon's Brudzinski's Hoffmann's
Lhermitte's
Neck flexion
POSITIVE RESPONSE Extension of big toe and fanning of four small toes Normal reaction in newborns Same response as above Same response as above Same response as above Similar movement occurs in opposite limb Reflex flexion of distal phalan.x of thumb and of distal phalanx of index or middle finger (whichever one was not "flicked") An electric shock-like sensation that radiates down the spinal column into the upper or lower limbs
Data from Magee DJ. OTtbopedic Pbysical Assessment. 4th ed. Philadelphia: W.E. Saunders; 2002.
PATHOLOGY Pyramidal tract lesion Organic hemiplegia Pyramidal tract lesion Pyramidal tract lesion Pyramidal tract lesion Meningitis Increased irritability of sensory nerves in tetany Pyramidal tract lesion Abnormalities (demyelination) in the posterior part of the cervical spinal cord
CHAPTER 9. NEUROMUSCULAR PHYSICAL THERAPY
head before being tested. A positive response for this test is the pres ence of Hoffman's sign.
Supraspinal Reflex Testing ~
~
~
Visual fixation of a stationary target can be tested using the tip of a pencil. The patient is seated and is asked to look straight ahead and focus on the tip of the pencil, which is held by the clinician at arm's length from the patient. The test is repeated with the patient's eyes turned to the extremes of horizontal and vertical gaze, and the pencil tip positioned accordingly. The VOR can be tested by asking the patient to fIx vision on a dis tant object. The clinician holds the patient's head firmly with the palms of the hands against the patient's cheeks, and produces a rapid but small head turn. If the reflex movement of the eyes is too big or too small, the inappropriate eye movement will be fol lowed by a corrective (saccadic) movement. Presence of this cor rective action may indicate a lesion of the vestibular nerveY8 Smooth pursuit can be tested by having the patient fix the gaze on an object placed in front of them. The object is then moved to the right while the patient follows it with the eyes. The clini cian looks for the presence of corrective saccades, which indi cate that the pursuit is not holding the eye on the moving tar get. The object is then moved back to the start position before being moved to the left while the patient follows it with the eyes. The object can then be moved in a variety of directions, combining horizontal, vertical, and diagonal movements to test if the patient can follow the object without saccadic move ments. Difficulty with smooth pursuit may indicate a lesion of the cerebellum, reticular formation, or cerebral cortex, or a cra nial nerve lesion (oculomotor, trochlear, or abducens)' 118
EXAMINATION OF MOTOR FUNCTION ~
~
~ ~ ~
~
Posture: observe the patient while sitting, standing, or walking. Note where the patient is erect, bent forward, or leaning to either side, and whether changes in position alter posture. While patients are standing, they can be asked to place their feet together and close the eyes, while the clinician observes their inability to maintain normal posture (Romberg's sign). Apraxia: the inability to perform voluntary learned movement in the absence of loss of sensation, strength, coordination, atten tion, or comprehension. The presence of apraxia indicates the breakdown in the conceptual and/or motor production systems. Ideomotor apraxia: patient cannot perform the task upon com mand but can do the task when left on own. Ideational apraxia: patient cannot perform the task at all, either on command or on own. Muscle atrophy: determine muscle bulk, and firmness. If atro phy is present: • Determine whether it is due to denervation, disuse, or pri mary atrophy. • Check for the presence of persistent fasciculations Resistance to passive movement of the limbs: muscle tone is the term used for the resistance felt when the patient's joint is pas sively moved with the muscles of the limb relaxed. Even when
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SECTION II. TESTS AND MEASURES
Study Pearl Medica Ietiologies for increased spas ticity include a new or enlarged eNS lesion, genitourinary tract dysfunction (infection, obstruction etc.), gastroin testinal disorders (bowel impaction, hemorrhoids,etc.), venous thrombo sis, fracture, muscle strain, and pres sure ulcers.113-115
~
~
relaxed, all muscle groups and joints possess a certain amount of intrinsic resistance to passive movement. Neurologic disease produces both increases (hypertonia) and decreases (hypotonia) in muscle tone. Flaccidity (absent tone), hypotonia (reduced tone): characteris tic of segmental/lower motor neuron lesions (spinal nerve root and peripheral nerve injury), but may also be seen briefly with upper motor neuron lesions (spinal shock, cerebral shock). Presence of spasticity • Clasped knife phenomenon. This phenomenon is reflected by a sudden letting go by the patient when resistance is applied. • Clonus-an exaggeration of the stretch reflex. A maintained stretch stimulus produces a cyclical, spasmodic contraction. • Spasticity can be graded using the modified Ashworth Scale1l9-123
0: no increase in muscle tone. 1: slight increase in muscle tone, minimal resistance at end of range of motion. 1 +: slight increase in muscle tone, minimal resistance through less than half of range of motion. 2: more marked increase in muscle tone, through most of range of motion, affected part easily moved. 3: considerable increase in muscle tone, passive movement difficult. 4: affected part rigid in flexion or extension. ~ Hyperactive cutaneous/superficial reflexes (Babinski's sign). ~ Hyperreflexia. ~ Muscle weakness. ~ Rigidity: characteristic of lesions of the basal ganglia. In con trast to spasticity, increased resistance is encountered through out the range of the joint regardless of the velocity of passive movement. ~ Cogwheel phenomenon: a ratchet-like response to passive movement characterized by an alternate giving and increased resistance to movement. ~ Leadpipe: characterized by constant rigidity. Leadpipe rigidity is common in patients with Parkinson's disease. ~ Opisthotonos124.l25: prolonged severe spasm of muscles caus ing the head, back, and heels to arch backward; arms and hands are held rigidly flexed. Seen in severe meningitis, tetanus, and epilepsy. ~ Posturing. ~ Decorticate: upper extremities are held in flexion and the lower extremities in extension (Fig. 9-22). ~ Decerebrate: upper and lower extremities are held in extension (Fig. 9-22). ~ Muscle strength: manual muscle testing can be used to assess muscle strength with neurologic patients with the following provisos: • Passive restraint: soft-tissue changes (contractures) can restrict ability to move throughout the full range of motion. • Active restraint: spastic muscles can restrict ability to move. • Abnormal reflex activity can restrict ability to move. • Muscle recruitment problems.
) 1
CHAPTER 9. NEUROMUSCULAR PHYSICAL THERAPY Posturing in Comatose States
Decortication The arm, wrist, fingers are flexed with thumb trapped in palm. The arms are adducted and in position resting on chest. Legs are extended pronated. Seen in lesions of the thalamus.
Decerebration
The arms are extended, pronated. Legs extended. Seen in lesions of the midbrain.
Figure 9-22. The appearance of decorticate and decerebrate posturing. (Reproduced, with permission, from Gilman, S: Clinical Examination of the Nervous Tissue. New York: McGraw-Hili; 2000:60.)
EXAMINATION OF COORDINATION Coordination is the ability to execute smooth, accurate, controlled motor responses. Efficient motor control includes normal muscle tone and postural response mechanisms, selective movement, and coordi nation. Abnormalities of coordination are common in motor system disorders. Coordinated movements are characterized by appropriate speed, distance, direction, timing, and muscular tension. Two terms often associated with coordination are dexterity and agility: ~ ~
Dexterity: refers to the skillful use of the fingers during fine motor tasks. Agility: refers to the ability to rapidly and smoothly initiate, stop, or modify movement while maintaining postural control. 126
As the cerebellum, basal ganglia, and dorsal column medial lem niscal pathway provide input to, and act together with, the cortex in the production of coordinated movement, lesions in any of these areas impact higher level processing and execution of coordinated motor responses (Fig. 9_23).126 The examination of coordination involves the assessment of: ~
~
Finger opposition: the patient is asked to tap the index finger on the thumb. Standardized tests and measures for finger dex terity include, but are not limited to, the Jebsen-Taylor Hand Function Test,127 the Minnesota Rate of Manipulation Test,128--130 the Purdue pegboard, and the O'Connor tweezer test. Pronation/supination: the patient is asked to alternate between pronation and supination of the forearm in a rapid fashion.
569
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SECTION II. TESTS AND MEASURES ~ ~ ~
~
~
Mass grasp: the patient is asked to open and close a fist. Circle drawing: the patient is asked to draw a circle in the air with either the upper extremity or lower extremity. Finger-nose-finger movements: the clinician holds an object about 1 m from the patient's face and asks the patient to use an index finger to touch repeatedly and alternately. Heel-knee-shin test: the patient is positioned supine and asked to place the heel of one foot on the knee of the opposite leg and run the heel down the shin across the dorsum of the foot to the great toe. Rebound test: the patient is positioned with the elbow flexed. The clinician applies sufficient manual resistance to produce an isometric contraction of the biceps before suddenly releasing the tension.
For each of the above tests, the clinician should note: ~ ~
~ ~
~
Speed/rate versus control.
Precision of movement.
Degree of steadiness.
Consistency.
Correctness and accuracy of response.
~ Area of pathology
~\ I)))~'/IIF/'T;""
Manifestation
//
2"
\
Basalganglia
Akinesia Athetosis Bradykinesia Chorea Dystonia Hemiballismus Rigidity Resting tremor
Cerebellum
Asthenia Dysarthria Dysdiadochokinesia Dysmetria Gait ataxia Hypotonia Nystagmus Rebound phenomenon Tremor
Dorsal colu~n- { Varied medial lemnlscal
Figure 9-23. Manifestations of cerebellar, basal ganglia, and dorsal column-medial lem niscal pathology.
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CHAPTER 9. NEUROMUSCULAR PHYSICAL THERAPY
ASSESSMENT OF GAIT One of the most important aspect'i of the neurologic examination as walking is a highly demanding activity that requires the coordinated activity of the entire nervous system. Gait disorders have stereotyped patterns reflecting injury to different components of the motor system (see Chapter 7). ~
'!]
tI I
~
~
~
~
~
~
Involuntary movements: the patient should be observed sitting quietly to detect the presence of • Dysfunction of the extrapyramidal or basal ganglia systems • A parkinsonian (resting) tremor: consists of a distal 4- to 5 Hz rhythmic alternating flexion-extension of the fingers with adduction-abduction of the thumb and of the lips and eyelids when lightly closed. The trauma occurs with the limbs at rest and disappears briefly with active movement. • Tics: spasmodic contractions of individual muscles, commonly noticed in the face, head, neck, ancl/or shoulder muscles. • Chorea: consists of moderately rapid movements, flowing constantly between face, limbs, and trunk, involving facial grimacing, sweeping movements of the chin across the chest, piano-playing movements of the fingers, and eleva tion action of the shoulders and hips. • Athetosis: consist of a slow series of movements involving the limbs, face, and trunk, usually appearing in combina tion with dystonic postures. Cerebellar disorders. • Intention tremors occurring when voluntary movement is attempted.
Cortical disorders.
• Seizures. • Tonic/clonic convulsive movements. Heredofamilial or senile trauma: consist of a fine distal trem bling movement of the fingers when extended. A shaking trauma of the head is also common in this disorder. Rubral disorders: consist of a combined proximal trauma char acteristic of cerebellar disease and a distal tremor similar to heredofamilial tremor, usually with flexion-extension and adduction-abduction components to the movements of the fingers. Myoclonus: jerking, involuntary movements of the limb or trunk. Hemiballismus: consists of a flinging movement of the whole arm at the shoulder and the leg at the hip.
NEURODYNAMIC MOBILITY The examination of the neurodynamic mobility of the peripheral nerv ous system is performed using the theoretical concepts and techniques of adverse neural tension.
EXAMINATION OF SENSORY FUNCTION Indications for examination of sensory function are based on the his tory and systems review (Table 9-27). Sensory dysfunction may be associated with any pathology or injury affecting either the PNS or CNS, or with a combined involvement of both systems:
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SECTION II. TESTS AND MEASURES
TABLE 9-27. TERMINOLOGY OF COMMON SENSORY FUNCTIONS AND IMPAIRMENTS Allodynia Analgesia Causalgia Double simultaneous stimulation Dysesthesia Graphesthesia Hypalgesia Hyperalgesia Paresthesia Stereognosis Astereognosis Thigmesthesia Two-point discrimination
Pain produced by a non-painful stimulus Loss of the sensation of pain A syndrome of painful, burning sensations associated with vasomotor, trophic (connective tissue atrophy, changes to hair and nails), and sudomotor (sweat glands) changes The ability to attend to and identify a tactile stimulus that is applied to both sides of the body at the same time The sensation that damage is being done to tissue when none is occurring-tactile hallucination The ability of the patient to identify characters that are written on the skin using a dull pointed object. Diminished sensibility to pain Heightened sensibility to pain An abnormal sensation of the skin (numbness, tingling, pricking, burning, or creeping) that has no objective cause The ability to identify objects that are placed in the hand when the eyes are closed. The inability to identify objects The ability to recognize the application of a light touch The ability to recognize two points of stimulation applied
~
Study Pearl ~
It is worth remembering that few sys tematic reports addressi ng the reI ia bil ity of traditional sensory tests appear in the literature.
Pathology, disease, or injury to the peripheral nerves such as trauma, metabolic disturbances (diabetes, hypothyroidism, alcoholism), infections, impingement or compression, toxins, and nutritional deficits (vitamin B J ) . Cerebral vascular accident, transient ischemic attack, tumors, or multiple sclerosis.
A full examination of the sensory system involves testing pain, temperature, light touch, vibration, position, and discriminative sensa tions. For patients with no apparent neurologic symptoms or signs, an abbreviated examination may be substituted.
Description of Tests. Sensory function tests are described in the following sections. 131
Pain ~
Study Pearl As a degree of overlap exists with the segmental innervation of the ski n, 132 it is important to test the full area of the dermatome because the area of greater sensitivity changes. The area of sensitivity, or autogenous area, is a small region of the dermatome with no overlap, and is the only area within a dermatome that is supplied exclu Sively by a single segmental level. Because there is so much overlap in the dermatQme, spinal nerve root compression usually results in hypoes thesia rather· than anesthesia.· within the majority of th~ qerlT)iltdme! but anesthesia or near anesthesia ill the autogenous area of thedermiltome.
~
Origin: lateral spinothalamic tract. Test: pinprick. This test is performed using a sharp safety pin, occasionally substituting the blunt end for the point as a stimu lus. When investigating an area of cutaneous sensory loss, it is recommended that the clinician begin the pinprick test in the area of anesthesia and work outward until the border of normal sensation is located.
The clinician stimulates in the aforementioned patterns, and asks the patient "Is this sharp or dull?" or, when making comparisons using the sharp stimulus, "Does this feel the same as this?" (Note: It is impor tant that the clinician use as light a touch as the patient can perceive and not, under any circumstances, press hard enough to draw blood.)
Temperature ~
~
Origin: lateral spinothalamic tract. Test: using two test tubes, filled with hot and cold water, the cli nician touches the skin and asks the patient to identify "hot" or "cold." The impulses for temperature sensation travel together with pain sensation in the lateral spinothalamic tract. The testing of skin temperature can also help the clinician to differentiate between a venous insufficiency and arterial insufficiency. With
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CHAPTER 9. NEUROMUSCULAR PHYSICAL THERAPY
venous insufficiency, an increase in skin temperature is noted in the area of occlusion, and it will also appear bluish in color. Pitting edema, especially around the ankles, sacrum, and hands, may also be present. However, if pitting edema is pres ent and the skin temperature is normal, the lymphatic system may be at fault. With arterial insufficiency, a decrease in skin temperature is noted in the area of occlusion and the area appears whiter. The area is also extremely painful.
Pressure ~
~
Origin: spinothalamic tract. Test: firm pressure is applied to the patient's muscle belly.
Vibration ~ ~
Origin: dorsal column/mediallemniscal tract. Test: using a relatively low-pitched tuning fork, preferably of 128 Hz, the clinician taps it on the heel of his or her hand and places it firmly over a bony process of the patient such as the malleoli, patellae, epicondyles, vertebral spinous processes, or iliac crest. The patient is asked what he or she feels. To be cer tain, the patient is asked to inform the clinician when the vibra tion stops, and then the clinician touches the fork to stop the vibration. At this point, the patient should indicate that the vibration has stopped. If vibration sense is absent, then the cli nician should move proximally along the extremity and retest.
Position Sense (Proprioception) ~ ~
•
Origin: dorsal column/medial lemniscal tract. Test: the patient is tested for the ability to perceive passive move ments of the extremities, especially the distal portions. It is awareness of the position of joints at rest. The clinician grasps the patient's big toe, holding it by its sides between the thumb and index finger, and then pulls it away from the other toes to avoid friction and to prevent extraneous tactile stimulation from indi cating a change of position. "Down" and "up" are demonstrated to the patient as the clinician moves the patient's toe clearly upward and downward. Then, with the patient's eyes closed, the patient is asked for an "up" or "down" response, as the clinician moves the toe in a small arc. This is repeated several times on each side, avoiding simple alternation of the stimuli. If position sense is impaired, then the clinician should move proximally along the extremity and retest. Alternatively, the patient is asked to dupli cate the position with the oppOSite extremity.
Movement Sense (Kinesthesia) ~ ~
Origin: dorsal column/mediallemniscal tract. Test: the patient is asked to indicate verbally the direction of movement while the extremity is in motion. The clinician must grip the patient's extremity over neutral borders.
Stereognosis ~
~
Origin: dorsal column/mediallemniscal tract. Test: the patient is asked to recognize, through touch alone, a variety of small objects such as comb, coins, pencils, and safety pins that are placed in the hand.
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SECTION II. TESTS AND MEASURES
Graphesthesia ~ ~
Origin: dorsal column/mediallemniscal tract. Test: the patient is asked to recognize lellers, numbers, or designs traced on the skin. Using a blunt object, the clinician draws a large number in the patient's palm, asking the patient to identify the number, letter, or design.
Two-Point Discrimination ~ ~
Origin: dorsal column/medial lemniscII tract. Test: a measure is taken of the smallest distance between two stimuli that can still be perceived by the patient as two distinct stimuli.
1
Equilibrium Reactions. The patient's ability to maintain bal ance in response to alterations in the body's center of gravity and base of support is tested. ASSESSMENT OF POSTURAL CONTROL Postural control requires the dynamic integration of multiple sensory inputs, specifically the visual, somatosensory, and vestibular systems. Vision is appropriate for balance reactions when proprioceptive input conflicts and visual-vestibular input agree; proprioceptive input is appropriate when vestibular and proprioceptive input agree and con flict with vision; and vestibular input is appropriate when vision and proprioception conflict. 91
Visual system.
Examine the patient's visual acuity (see "CN II" under "Cranial Nerve Examination" earlier in this chapter) and depth perception and determine whether the patient has any visual field deficits.
Somatosensory System. Examine the patient's proprioception and cutaneous sensation (touch, pressure) of the lower extremities and trunk, especially of the feet and ankles. Alterations in joint range of motion or muscle strength due to pain may produce dysfunction in bal ance and affect the quantity and quality of movement. Vestibular System. Examine the patient's righting, equilibrium, and protective reactions. In addition, the clinician can assess for the presence of: ~
Movement strategies: the timing, sequencing, or scaling of ankle and hip strategies, the appropriateness of the chosen strategy, and the number of strategies in the patient's repertoire. • The ankle strategy is the first strategy to be elicited by a small range and low velocity perturbation when the feet are on the ground. • The hip strategy is elicited by a greater force, challenge, or perturbation through the pelvis and hips. The hips should move in the opposite direction to the head in order to main tain balance. • Suspensory strategy. Lowering the body's center of gravity. • Stepping strategy. Rapid steps are taken in an effort to realign the body's center of gravity over the base of support.
J
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CHAPTER 9. NEUROMUSCULAR PHYSICAL THERAPY ~
~
Quality of motion: Rood's concept of levels of control through out activities. • Mobility. • Stability. • Controlled mobility. • Skill.
Components of movement.
• Head control. • Trunk strength/rotation. • Extension/abduction of the limbs. • Midline orientation. • Weight shift.
The clinician should also assess the following components: ~
~
Joint range of motion of involved segments: restricted range of motion in the joints involved in maintaining good posture/ balance. Functional muscle strength/endurance: manual muscle testing may not provide a functional measure of strength or endurance.
ASSESSMENT OF AEROBIC CAPACITy/ENDURANCE Fatigue may be defined as a subjective state in which one feels tired or exhausted, and in which the capacity for normal work or activity is reduced. Each person's experience of fatigue depends on a variety of factors. These factors include culture, personality, the physical envi ronment Oight, noise, and vibration), availability of social support through networks of family members and friends, the nature of a par ticular fatiguing disease or disorder, and the type and duration of work or exercise. Physical reasons for fatigue include ~ ~
~
~
~ ~
~
~
Circulatory and respiratory impairment. Examples include lung disease, vascular disease, and anemia. Infection. Fatigue is an early primary symptom of chronic, non localized infections found in such diseases as acquired immune deficiency syndrome (AIDS), Lyme disease, and tuberculosis. Nutritional disorders or imbalances. Dehydration. Dehydration results from water and sodium imbalances in body tissues. Dehydration contributes to muscle weakness and mental confusion; it is a common and over looked source of fatigue. Deconditioning. This term refers to generalized organ system deterioration resulting from bed rest and lack of exercise. Pain. When pain is severe enough, it may disrupt sleep and lead to the development of such sleep disorders as insomnia or hypersomnia (excessive sleeping; discussed later), which in turn contributes to fatigue, deconditioning, and depression. Stress. Various chronic diseases are related to stress, including regional enteritis (intestinal inflammation), ulcerative colitis (a disease of the colon), gastric ulcers, rheumatoid arthritis, cardiac angina, and dysmenorrhea (painful menstruation). Sleep disorders. There are a variety of sleep disorders that cause fatigue, including insomnia, hypersomnia, sleep apnea, and restless legs syndrome.
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SECTION II. TESTS AND MEASURES
EXAMINATION OF AUTONOMIC NERVOUS SYSTEM fUNCTION ~
~
~ ~ ~
~
~
Pupils: Loss of function of the sympathetic innervation of the pupil leads to papillary constriction; Horner's syndrome, which consists of anihidrosis on the ipsilateral side of the face, ptosis, a small pupil, and enopthalmos. Loss of parasympathetic func tion results in a dilated pupil and possible blurred vision. Cardiovascular system: disorders of blood pressure, heart rate (see Chapter 11). • Sympathetic stimulation results in increased heart rate, force of contraction, blood pressure, and respiratory rate. • Parasympathetic stimulation results in decreased heart rate, force of contraction, blood pressure, and respiratory rate. Integumentary changes. Sympathetic stimulation results in increased sweating. Urinary function. Parasympathetic stimulation causes detrusor contraction and bladder emptying. Sexual dysfunction. Maybe the earliest manifestation of auto nomic insufficiency. • In males, the parasympathetic system functions principally in achieving erection and the sympathetic system in performing ejaculation. Gastrointestinal dysfunction: dysphagia, reflex, nausea, vomit ing, and upper abdominal pain. Sympathetic stimulation inhibits peristalsis and tone and causes contraction of the upper and lower esophageal, ileocecal, and anal sphincters.
DIAGNOSTIC PROCEDURES The clinician should review the results of any diagnostic tests that have been performed, if available.
Cerebral Angiography. Cerebral angiography is an x-ray pro cedure used to visualize the vascular system of the brain. 133-135 Radiopaque contrast material is injected into the carotid, subclavian, brachial, or femoral artery, and x-rays are taken at specific intervals. ~ ~ ~
Useful in determining areas of increased and decreased vascularity. Provides information about the dynamics of cerebral circulation. Disadvantages: invasive; may cause meningeal irritation, hem orrhage, vasospasm, anaphylactic reaction to dye.
Computed Tomography (CT Scan). Computed tomography uses x-rays emitted from a source and confined to a plane oriented perpendicular to the long axis of the body to provide a detailed cross section of tissue structure. 136-143 The narrowly collimated beam of x rays that rotates in a continuous 360-degree motion around the patient is transmitted through tissues of varying densities and is converted to an electrical signal. The computer-generated image uses multiple readings of the patient in cross-sectional slices to produce a three-dimensional picture.
CHAPTER 9. NEUROMUSCULAR PHYSICAL THERAPY ~ ~
~
Contrast enhancement can be used to provide more detail. CT is best at showing calcific structures, including the skull and calcific abnormalities in the brain; and blood, including sub arachnoid blood and epidural, subdural, and cerebral hematomas. It is also very good at showing the ventricles and cerebral spinal fluid spaces and for showing lesions of the spinal cord or the nerve roots. Its major advantages over MRI include speed, greater availabil ity, and less expense.
Electroencephalography (EEG). EEG is a process of meas uring and recording temporal changes in brainwave activity via elec trodes that are attached to various areas of the patient's head.144-146 The test can be used to diagnose seizure, alterations in mental status, and brainstem disorders, and to localize intracranial lesions of the brain. Electromyogram (EMG). The electromyogram is designed to record intrinsic electric activity in a skeletal muscle. 147- 151 Surface elec trodes are applied, or a needle electrode (needle EMG) is inserted, into the muscles. Electrical activity is detected within an oscilloscope and transmitted to a loudspeaker. Normal muscle is electrically silent away from the endplate region. With electrode movement, normal inser tional activity consists of a brief electrical discharge. An EMG study can be useful in diagnosing lower motor neuron or primary muscle disease (mononeuropathy, plexopathy, radiculopathy, polyneuropathy, and defective neuromuscular transmission at the neu romuscular junction). The burst of action potentials when the EMG needle is inserted is increased in denervated muscle. Alterations in the size, duration, and shape of the motor unit potentials occur with re-innervation of previ ously denervated muscles. The number of motor unit potentials is decreased in a lower motor neuron injury. Evoked Potential (EP). Evoked potentials are responses pro duced from different levels of the nervous system with a relatively fixed latency following a stimulus.15Z-157 Responses may be recorded from the nerves, the cortical tracts and nuclei, or cortical segments of a stimulated pathway. In clinical practice, the most commonly used potentials are visual, auditory, and somatosensory, with each produc ing a characteristic brainwave pattern. The evoked potential studies are useful in detecting lesions in multiple sclerosis (prolonged latency without loss in amplitude), eval uating visual or auditory function in patients who cannot cooperate with more formal testing of vision or hearing, and for providing useful prognostic information in comatose patients. Lumbar Puncture (LP). The most common purpose of lumbar puncture is to obtain cerebrospinal fluid (CSF). The CSF is obtained by using a hollow needle and stylet, which is inserted into the subarach noid space of the lumbar portion of the spinal canal at the level of the third and fourth lumbar vertebrae. The CSF sample is used to provide a specific diagnosis, such as some types of meningitis, leptomeningeal carcinoma, and subarachnoid hemorrhage. Two other purposes for a lumbar puncture include:
577
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SECTION II. TESTS AND MEASURES ~
~
Intrathecal injections (contrast agent for myelography).158-160 CSF pressure measurement,161-163 for example, when there is a suspected idiopathic intracranial hypertension or chronic hydrocephalus. The complications of this test may include severe headaches, infections, and epidural hematomas.
Contraindications to lumbar puncture include the presence of a large intracranial mass/lesion or obstructive hydrocephalus.
Magnetic Resonance Imaging (MRI). An MRI (see Chapter 5) uses a large magnet with a strong magnetic field and relies on the inter action of the spin and associated protons (and, to a lesser extent, neu trons) with its magnetic field (nuclear magnetic resonance).164-l71 MRI can be used for brain imaging for nearly any clinical indication, but because it costs more than CT, it is usually reserved for situations in which it has advantages over CT-it is clearly superior for evaluating patients with: ~
~ ~ ~ ~ ~ ~
~
Epilepsy. Cerebral vasculitis. Vascular malformations. Suspected multiple sclerosis and other white matter diseases. Small, deep infarcts. Lesions of any type in the brainstem and cerebellum. Tl-weighted images are useful for showing overall brain anatomy and for a valuation of CSF spaces; they are most useful for demonstrating hydrocephalus, atrophy, cysts, and malformations. T2-weighted images are sensitive to subtle changes in tissue characteristics. As with CT, enhancement of MRI, which is use ful for demonstrating vascular structures such as aneurysms and vascular malformations, can be utilized.
This procedure is noninvasive and painless for the patient, although some patients experience claustrophobia that interferes with completion.
Magnetic Resonance Angiography (MRA). MRA pro vides excellent visualization of large vessels and effectively shows thrombosis, embolism, stenosis, and dissection of large vessels in the head or neck. It is also good for showing aneurysms and arteriovenous and venous malformationsYZ-175 Myelography. Myelography is a radiographic process by which the spinal cord and spinal subarachnoid space are viewed and pho tographed. A contrast medium is introduced. This test is used to iden tify a variety of spinal lesionsy6-180 Nerve Conduction Velocity. Nerve conduction velocity (NCV) is a test that measures the speed with which an electrical impulse can be transmitted through excitable tissue. The speed of action potential conduction can he measured along any accessible nerve. Conduction velocities of the fastest-conducting fibers are deter mined hy stimulating the nerve at two sites, measuring and the latency from each stimulus to onset of response, and dividing the distance
CHAPTER 9. NEUROMUSCULAR PHYSICAL THERAPY
579
between the two sites by the difference in latency between the two responses. ~
~
~
Conduction velocity is expressed as meters per second. Decreased conduction velocities are seen in peripheral neu ropathies characterized by demyelination (e.g., Guillain-Barre syndrome). 181 Slowed conduction velocities are seen with focal compression of a peripheral nerve.182-187
Positron Emission Tomography (PET). PET is a neuroimag ing technique in which radioisotopes are injected and emissions are measured by a gamma ray detector system. 188- 190 This test provides information on the cerebral blood flow and brain metabolism, but it is not as detailed as CT or MRI. Ventriculography. Ventriculography is an x-ray examination of the head after an injection of air or another contrast medium into the cerebral ventricles; for example, an x-ray examination of the ventricle of the heart after an injection of a radiopaque contrast medium. 191 ,19 2 Electronystagmography. Electronystagmography (ENG) involves a battery of tests that assess central and peripheral vestibular function and organization. Central vestibular function is reflected in oculomotor tests for nystagmus, reflexes (optokinetic nystagmus), and integrated motion (saccade, pursuit). Peripheral VIII cranial nerve and labyrinthine function is evaluated in response to various stimuli (e.g., positional/positioning, caloric, rotational chair testing). Nystagmus can be observed, recorded, and quantified. Electro oculography (EOG) indirectly measures eye movement by detecting changes in the electrical charges produced by the corneal-retinal potential using skin electrodes. Eye movements can also be quantified directly using infrared oculography (IRO). IRO techniques allow direct observation of eye movements and eliminate many a1tifactual elements present on EOG.
NEUROLOGIC DYSFUNCTION At the most fundamental level, all neurologic dysfunctions can be clas sified as either an upper motor neuron lesion, a lower motor neuron lesion, or a combination of both.
UPPER MOTOR NEURON LESION
Study Pearl
The upper motor neuron (UMN) is located in the white columns of the spinal cord and the cerebral hemispheres. An upper motor neuron lesion is also known as a central palsy. One or more of the signs and symptoms described in the follow ing sections may be associated with a UMN lesion.
Nystagmus. In health, nystagmus occurs during self-rotation in order to hold images of the visual world steady on the retina and main tain clear vision.193-195 Pathologic nystagmus is characterized by an invol untary loss of control of the conjugate movement of the eyes (about one
I
An upper motor neuron lesion is characterized by spastic paralysis or paresis, little or no muscle atrophy, hyperreflexive stretch reflexes in a nonsegmental distribution, and the presence of pathologic signs and
~flexes.
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SECTION II. TESTS AND MEASURES
or more axes) involved with smooth pursuit or saccadic movement. Broadly, nystagmus may be divided into one of three categories: ~ ~
~
Physiologic (e.g., optokinetic, vestibular and end-point). Congenital or infantile nystagmus. Acquired (e.g., neurologic disease or drug toxicity).196,197
The more serious causes of nystagmus include lesions to the brain stem or cerebellum, although the mechanisms by which the cerebellum influences eye movements are still under investigation. Nystagmus can also be a characteristic sign of vertebrobasilar compromise.
Dysphasia. Dysphasia is defined as a problem with vocabulary, and results from a cerebral lesion in the speech areas of the frontal or temporal lobes. Wallenberg's Syndrome. Wallenberg's syndrome is the result of a lateral medullary infarction and is characterized by selective involvement of the spinothalamic sensory modalities with dissociated distribution (ipsilateral trigeminal and contralateral hemibody/limbs), contralateral or bilateral trigeminal sensory impairment, restricted sensory involvement, and a concomitant deficit of lemniscal sensations. 198 ,199 Ataxia.
Ataxia is often most marked in the extremities. In the lower extremities, it is characterized by the so-called "drunken-sailor" gait pattern, with the patient veering from one side to the other, and hav ing a tendency to fall toward the side of the lesion (see Chapter 7). Ataxia of the upper extremities is characterized by a loss of accuracy in the reaching for, or placing of, objects. Although ataxia can have a number of causes, it generally suggests CNS disturbance, specifically a cerebellar disorder, or a lesion of the posterior columns. zoo-zoz
Study Pearl
Spasticity. Spinal or neurogenic shock occurs immediately follow ing any trauma to the spinal cord sufficient to cause tetraplegia or para plegia (refer to "SpinaVNeurogenic Shock" later in this chapter).z03-Z05 This shock results in the loss of reflexes innervated by the portion of the cord below the site of the lesion; the muscles innervated by the traumatized portion of the cord, the portion below the lesion, as well as the bladder, become flaccid. Spinal shock, which wears off between 24 hours and approximately 3 months after injury, can be replaced by spasticity in some or all of these muscles. Spasticity occurs because the reflex arc to the muscle remains anatomically intact despite the loss of cerebral innervation and control via the long tracts. During spinal shock, the arc does not function, but as the spine recovers from the shock, the reflex arc begins to function without the inhibitory or regu latory impulses from the brain, creating local spasticity and clonus. Drop Attack. This is described as a loss of balance resulting in a fall, but with no loss of consciousness. The patient, usually elderly, will fall forward with the precipitating factor being extension of the head. Recovery is usually immediate. Causes include: ~ A vestibular system impairment. z06 ~
~
Neoplastic and other impairments of the cerebellum. Z07 Vertebrobasilar compromise. z08
CHAPTER 9. NEUROMUSCULAR PHYSICAL THERAPY ~
~ ~
~
581
Sudden spinal cord compression. Third-ventricle cysts. Epilepsy. Type 1 Chiari malformation. 209
Wernicke's Encephalopathy. This is an impairment, which is typically localized to the dorsal part of the midbrain,210 and which pro duces the classic triad of Wernicke's encephalopathy: abnormal mental state, ophthalmoplegia, and gait ataxia. 2l1 Vertical Diplopia. Patients with vertical diplopia complain of seeing two images ("double vision"), one atop or diagonally displaced from the other. 212 Dysphonia. Dysphonia presents as a hoarseness of the voice. Usually no pain is reported. Painless dysphonia is a common symptom of Wallenberg's syndrome. 198 Hemianopia. Hemianopia is defined as a loss in half of the visual field and is always bilateral. A visual field defect describes sensory loss restricted to the visual field and arises from damage to the primary visual pathways linking optic tract and striate cortex. Ptosis. Ptosis is defined as a pathologic depression of the superior eyelid such that it covers part of the pupil due to a palsy of the levator palpabrae and Muller's muscles. Miosis. Miosis is defined as the inability to dilate the pupil (dam age to sympathetic ganglia). It is one of the symptoms of Horner's syndrome. Horner's Syndrome. This is caused by an interference to cervi cothoracic sympathetic outflow due to a lesion of (1) the reticular for mation, (2) the descending sympathetic system, or (3) the oculomotor nerve caused by a sympathetic paralysis. 213 The other clinical signs of Horner's syndrome are ptosis, enopthalamus, facial reddening, and anhydrosis. If Horner's syndrome is identified, the patient should inune diately be returned or referred to a physician for further examination. Dysarthria. Dysarthria is defined as an undiagnosed change in articulation. Dominant or nondominant hemispheric ischemia as well as brainstem and cerebellar impairments may result in altered articulation. LOWER MOTOR NEURON LESION The lower motor neuron begins at the alpha motor neuron and includes the dorsal and ventral roots, the spinal nerve, the peripheral nerve, the neuromuscular junction, and the muscle fiber complex. 214 The lower motor neuron (LMN) consists of a cell body located in the anterior gray column, and its axon, which travels to a muscle by way of the cranial or peripheral nerve. Lesions to the LMN, also known as a peripheral palsy, can occur in the cell body or anywhere along the axon. These lesions can be due to direct trauma, toxins, infections, ischemia, and compression.
Study Pearl Thecharaderistic50f.ao·.t·MNJncll.lde muscle atrQphyand.hypotonus!> a diminished orabs¢nt stretcnreflexof the a~i:l5sel"\(edby q.spinalperveroot! ora. ·pt?ripheta1o¢o/ea.nq ahabsence of pathologi 10 degrees.
632
SECTION II. TESTS AND MEASURES
Surgical Management. The surgical management of spasticity can be divided into orthopedic and neurosurgical procedures. Careful preoperative evaluation is important in assessing patients with spastic contractures, and treatment of each individual area must be tailored to each patient's specific problems. In the upper and lower extremity, the general goals of surgical treatment are to improve function, improve hygiene, provide pain relief, and to facilitate total care of the patient. Functional Electrical Stimulation. While the short-term effect of functional electrical stimulation is to decrease spasticity, long term use has been associated with increasing spasticity in patients with incomplete spinal cord injury and quadriplegia. Thermotherapy and Cryotherapy. Superficial heat can reduce hypertonicity by facilitating uptake of released neurotransmit ters and return calcium to the sarcoplasmic reticulum. Cryotherapy is reported to reduce deep tendon reflexes and clonus. Sensory Stimulation. Mechanical vibration of large muscles has been shown to reduce spasticity. STRATEGIES TO MANAGE HYPOTONIA
Therapeutic Exercise. Therapeutic exercise may be applied in several forms: ~
~ ~
Active and passive range of motion techniques applied in con junction with proper positioning and splinting are recom mended. A daily program of stretching helps restore resting length of muscle, tendon, and joint capsule and can prevent contracture. Neurodevelopmental techniques invoking proprioceptive neu romuscular facilitation (PNF). Active or resisted exercises to strengthen limbs, which must include a balancing of agonist and antagonist muscle groups.
VESTIBULAR REHABILITATION THERAPY
Study Pearl An effective VRT program uses a team of healthcare providers to assess and treat patients with balance disorders. This team should include a physician trained in the evaluation and treat ment of balance disorders (typically a neuro~ototogist, otolaryngologist, or neurologist), a vestibular or physical therapist trained in balance testing and vestibular therapy, and an occu p(l.tional therapist.
Vestibular rehabilitation therapy (VRT) has been a highly effective modality for most individuals with disorders of the vestibular or central balance system, and is designed to promote habituation and compen sation for deficits related to a wide variety of balance disorders. 469 The goals of VRT are to improve balance, minimize falls, and decrease the subjective sensation of dizziness by improving vestibu lar function and promoting mechanisms of central adaptation and compensation. 469 VRT is based on the use of existing neural mechanisms for adap tation, plasticity, and compensation. The extent of vestibular compen sation and adaptation is closely related to the direction, duration, frequency, magnitude, and nature of the retraining stimulus. 469 VRT exercise protocols aim to improve vestibulo-ocular control, increase the gain of the vestibulo-ocular reflex (VOR), improve postural strategies, and increase levels of motor control for movement. The cervical-ocular
CHAPTER 9. NEUROMUSCULAR PHYSICAL THERAPY
633
reflex (COR) may be developed as a substitution strategy for visual sta bility for deficits in the VOR during head movements. VRT also takes advantage of the adaptive characteristics of the CNS to increase VOR accuracy, refine oculomotor skills, improve pos tural control, and encourage utilization of appropriate movement strategies. 469 Adaptation serves to extinguish symptoms of dizziness provoked by motion or visual stimulation. Several factors must be considered when designing a VRT pro gram for an individual patient, including ~ ~ ~ ~ ~ ~ ~
~
~
The status of visual and proprioceptive system,. Physical strength. Motor skills. Integrity of the cerebellum. General physical health. Decision-making and cognitive abilities. Age. Memory. Presence of psychological and anxiety disorders.
VRT is typically designed as a clinician-directed patient-motivated home-based exercise protocol, with individuals visiting the clinician on a limited basis. The patient engages in custom-designed exercises at home several times a day without clinician supervision. VRT exercises are graduated, beginning at the minimal skill level that the patient is capable of performing; complexity is increased as compensation and habituation occur. Patients have regular follow-up visits with the clini cian until compensation and habituation are complete and optimal bal ance is attained. The accurate diagnosis and assessment of a patient is critical for a successful individualized VRT program. VRT should be considered for patients with stable symptomatic vestibular deficits that have not com pletely resolved by means of natural compensation. 469 Individuals with unstable lesions (e.g., demyelinating disease, seizure disorder, migraine), progressive degenerative processes, or fluctuating or episodic symptoms of imbalance are not candidates for VRT. 469 Optimal candidates have stable central or peripheral vestibular deficits; symptoms provide specific activities or stimuli; and intact cognitive, cerebellar, visual, and proprioceptive systems. Patient motivation is a sig nificant factor in successful implementation of a VRT program. Although some reports are conflicting, vestibular exercises are generally effective regardless of patient's age and duration of symptoms.
Specific Exercises Xl Viewing. The patient holds a card with lettering at arm's length with the eyes focused on the letters. The patient moves the head from side to side, increasing speed with progressions. The entire cycle is repeated 20--30 times. The head can also be moved vertically and diag onally. The exercise is progressed in the following manner469 : ~ ~ ~
~
Sitting to standing with the feet shoulder width apart. Standing with the feet together. Standing partially pointed (i.e., one foot half way ahead of the other). Standing pointed (i.e., one foot completely in front of the other)
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SECTION II. TESTS AND MEASURES
The patient progresses from standing on a firm surface to standing on a compliant surface. The card is then posted on the wall with a plain background and progressed to being posted on a wall with a busy pat terned background.
X2 Viewing. The patient holds a card with lettering at arm's length with the eyes focused on the letters. The patient moves the head to the right and the card to the left, keeping the eyes focused on the letters. 469 Then the patient moves the head to the left and the card to the right, keeping the eyes focused on the letters. The exercise is performed slowly initially before increasing speed as the test progresses, while keeping the letters in focus. The entire cycle is repeated 20-30 times. The head can also be moved vertically. The exercise is progressed from sitting to standing as described above.
Ocular Motor Exercises Increasing Pursuit Gain. The patient holds a card with lettering at arm's length, and then moves the card from left to right across the visual field, tracking with eye movement and keeping the head still. The entire cycle is repeated 20-30 times. The head can also be moved vertically and diagonally increasing speed while keeping the letters in focus. The exercise is progressed from sitting to standing as described above (see VOR stimulation exercises above). Improving Saccade Latency, Velocity, and Accuracy. The patient holds a card with lettering in each hand approximately 15 inches apart at arm's length. Keeping the head still, the patient moves the eyes back and forth from card to card, 1 second per card. The entire cycle is repeated 20-30 times. The head can also be moved vertically and diag onally increasing speed while keeping the letters in focus. The exercise is progressed from sitting to standing as described above (see VOR stimulation exercises).
Balance Exercises ~
~
~
~ ~
The patient stands with feet together, maintaining balance by reaching out and touching the wall (in front of the patient). The patient takes the hands off the wall for progressively longer periods, beginning with 1 hand at a time, and alternat ing hands. The stance is then sharpened to narrow the base of support. The patient stands with feet shoulder width apart, looking at a target on the wall. The exercise is first performed with arms outstretched, then close to the body, then folded across the chest. The exercise is performed in sitting, then standing with the head bent forward 30°, and finally standing with the head bent backward 30°. The patient reaches up as though reaching for an object over the head. Progress to having patient standing on foam or pillow and then to standing on 1 leg. The patient hends over as though picking up an object from the floor. Progress from sitting to standing to a sharpened stance. Performing exercises with the room lights lowered and then with eyes closed.
CHAPTER 9. NEUROMUSCULAR PHYSICAL THERAPY
Gait Exercises ~
~
~
The patient begins by walking next to a wall, with the hand out for support. The patient gradually increases the number of steps without support. To make the exercise more challenging the patient can narrow the width of the gait, progressing even tually to heel-to-toe walking. The patient begins by walking while moving the head, left and right, with increasing speed. To make the exercise more chal lenging the patient can narrow the width of the gait. The patient then walks while moving the head in the vertical direc tion (i.e., nodding up and down). The patient practices turning when walking, first with large cir cles, then with gradually smaller turns, in both directions.
Combined Category Exercises ~
~
~
Exercises involving stepping over objects and around furni ture. The patient can also perform activities such as bending over, picking up objects, throwing and catching objects, bouncing them off walls, and walking on differing compliance surfaces. The patient is asked to walk at the grocery store, practicing with minimal and then no support from the cart. The patient then introduces slow, small head movements, gradually increasing the speed and degree. The patient is asked to walk at the mall, initially walking slowly and staying near the walls, and going with flow of the crowd. Gradually, the patient increases their speed, moves away from the walls, and goes against traffic.
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9. Bogduk N. Innervation and pain patterns of the cervical spine. In: Grant R, ed. Physical Therapy ofthe Cervical and Thoracic Spine. New York: Churchill Livingstone; 1988. 10. Fawcett DW. The nervous tissue. In: Fawcett DW, ed. Bloom and Fawcett: A Textbook of Histology. New York: Chapman & Hall; 1984:336-339. 11. Chusid JG. Correlative Neuroanatomy & Functional Neurology. 19th ed. Norwalk, CT: Appleton-Century-Crofts; 1985:144-148. 12. Daniels DL, Hyde JS, Kneeland JB, et al. The cervical nerves and foramina: Local-coil MRI imaging. AjNR. 1986;7:129-133. 13. Pech P, Daniels DL, Williams AL, et al. The cervical neural foramina: correlation of microtomy and CT anatomy. Radiology. 1985;155: 143-146. 14. Carter GT, Kilmer DD, Bonekat HW, et al. Evaluation of phrenic nerve and pulmonary function in hereditary motor and sensory neuropathy type 1. Muscle Nerve. 1999;15:459--466. 15. Bolton CF. Clinical neurophysiology of the respiratory system. Muscle Nerve. 1993;16:809-818. 16. Gozna ER, Harris WR. Traumatic winging of the scapula. j Bone joint Surg. 1979;61A:123Q-1233. 17. Kauppila U. The long thoracic nerve: possible mechanisms of injury based on autopsy study. j Shoulder Elbow Surg. 1993;2:244-248. 18. Kauppila LI, Vastamaki M. Iatrogenic serratus anterior paralysis: long-term outcome in 26 patients. Chest. 1996;109:31-34. 19. Post M. Orthopaedic management of neuromuscular disorders. In: Post M, Bigliani LU, Flatow EL, et al., eds. The Shoulder: Operative Technique. Baltimore: Williams & Wilkins; 1998:201-234. 20. Kuhn JE, Plancher KD, Hawkins R]. Scapular winging. jAm Acad Orthop Surg. 1995;3:319-325. 21. Reis FP, de Camargo AM, Vitti M, et al. Electromyographic study of the subclavius muscle. Acta Anatomica. 1979;105:284-290. 22. Hoffman GW, Elliott LF. The anatomy of the pectoral nerves and its significance to the general and plastic surgeon. Ann Surg. 1987;205:504. 23. Delagi EF, Perotto A. Arm. In: Delagi EF, Perotto A, eds. Anatomic Guide for the Electromyographer. 2nd ed. Springfield, IL: Thomas; 1981:66-71. 24. Sunderland S. The musculocutaneous nerve. In: Sunderland S, ed. Nerves and Nerve Injuries. 2nd ed. Edinburgh: Churchill Livingstone; 1978:796-801. 25. de Moura WG Jr. Surgical anatomy of the musculocutaneous nerve: a photographic essay. j Reconstr Microsurg. 1985;1:291-297. 26. Flatow EL, Bigliani LU, April EW. An anatomic study of the mus culocutaneous nerve and its relationship to the coracoid process. Clin Orthop. 1989;244:166-171. 27. Stern PJ, Kutz JE. An unusual variant of the anterior interosseous nerve syndrome: a case report and review of the literature. j Hand Surg. 1980;5:32-34. 28. Hope PG. Anterior interosseous nerve palsy following internal fix ation of the proximal radius. j Bone joint Surg. 1988;70B:28Q-282. 29. Amadio PC, Beckenbaugh RD. Entrapment of the ulnar nerve by the deep flexor-pronator aponeurosis. j Hand Surg Am. 1986; 11A:83-87. 30. Hirasawa Y, Sawamura H, Sakakida K. Entrapment neuropathy due to bilateral epitrochlearis muscles: a case report. j Hand Surg Am. 1979;4:181-184.
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31. Chen FS, Rokito AS, lobe FW. Medial elbow problems in the overhead-throwing athlete.] Am Acad 071hop Surg. 2001;9:99-113. 32. Mannheimer ]S, Lampe GN. Clinical Transcutaneous Electrical Nerve Stimulation. Philadelphia: FA Davis; 1984:440-445. 33. McGuckin N. The T4 syndrome. In: Grieve GP, ed. Modern Manual Therapy of the Ve71ebral Column. New York: Churchill Livingstone; 1986:370-376. 34. DeFranca GG, Levine IJ. The T 4 syndrome.] Manip PhysiolTher. 1995;18:34-37. 35. Grieve GP. Thoracic musculoskeletal problems. In: Boyling ]D, Palastanga N, eds. GrievesModernManualTherapyofthe Ve71ebral Column. 2nd ed. Edinburgh: Churchill Livingstone; 1994:401-428. 36. Warfel BS, Marini SG, Lachmann EA, et al. Delayed femoral nerve palsy following femoral vessel catheterization. Arch Phys Med Rehabil. 1993;74:1211-1215. 37. Hardy SL. Femoral nerve palsy associated with an associated pos terior wall transverse acetabular fracture.] 071hop Trauma. 1997; 11:40-42. 38. Papastefanou SL, Stevens K, Mulholland RC. Femoral nerve palsy: an unusual complication of anterior lumbar interbody fusion. Spine. 1994;19:2842-2844. 39. Fealy S, Paletta GA]r. Femoral nerve palsy secondary to traumatic iliacus muscle hematoma: course after nonoperative manage ment.] Trauma Inj Infect Crit Care. 1999;47:1150-1152. 40. Ecker AD, Woltman HW. Meralgia paresthetica: a report of one hundred and fifty cases.]AMA. 1938;110:1650-1652. 41. Keegan ]], Holyoke EA. Meralgia paresthetica: an anatomical and surgical study.] Neurosurg. 1962;19:341-345. 42. Reichert FL. Meralgia paresthetica; a form of causalgia relieved by interruption of the sympathetic fibers. Surg Clin No71h Am. 1933; 13:1443. 43. Sunderland S. Traumatized nerves, roots and ganglia: muscu loskeletal factors and neuropathological consequences. In: Knorr 1M, Huntwork EH, eds. The Neurobiologic Mechanisms in Manipulative Therapy. New York: Plenum Press; 1978:137-166. 44. Kenny P, O'Brien CP, Synnott K, et al. Damage to the superior gluteal nerve after two different approaches to the hip.] Bone Joint Surg. 1999;8IB:979-981. 45. Lu], Ebraheim NA, Huntoon M, et al. Anatomic considerations of superior cluneal nerve at posterior iliac crest region. Clin 071hop Rei Res. 1998;347:224-228. 46. Sogaard I. Sciatic nerve entrapment: case report. ] Neurosurg. 1983;58:275-276. 47. Robinson DR. Pyriformis syndrome in relation to sciatic pain. Am ] Surg. 1947;73:355-358. 48. Resnick D. Diagnosis ofBone and Joint Disorders. Philadelphia: WE Saunders; 1995. 49. Ohsawa K, Nishida T, Kurohmaru M, et al. Distribution pattern of pudendal nerve plexus for the phallus retractor muscles in the cock. Okajimas Folia Anat]pn. 1991;67:439-441. 50. Dommisse GF, Grobler 1. Arteries and veins of the lumbar nerve roots and cauda equina. Clin 071hop. 1976;115:22-29. 51. Halle ]S. Neuromusculoskeletal scan examination with selected related topics. In: Flynn TW, ed. The Thoracic Spine and Rib Cage: Musculoskeletal Evaluation and Treatment. Boston: Butterworth-Heinemann; 1996: 121-146.
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243. Hartl R. Back to basics, or the evolution of traumatic brain injury management since Scipione Riva-Rocci. Crit Care Med. 2007;35: 1196-1197. 244. Irdesel J, Aydiner SB, Akgoz S. Rehabilitation outcome after trau matic brain injury. Neurocirngia (Austr). 2007;18:5-15. 245. Teasell R, Bayona N, Lippert C, et al. Post-traumatic seizure disor der following acquired brain injury. Brain In). 2007;21:201-214. 246. Scherer M. Gait rehabilitation with body weight-supported tread mill training for a blast injury survivor with traumatic brain injury. Brain In}. 2007;21:93-100. 247. Pressman HT. Traumatic brain injury rehabilitation: case manage ment and insurance-related issues. Phys Med Rehabil Clin N Am. 2007;18:165-174, viii. 248. Young JA. Pain and traumatic brain injury. Phys Med Rehabil Clin N Am. 2007;18:145-163, vii-viii. 249. Yen HL, Wong JT. Rehabilitation for traumatic brain injury in chil dren and adolescents. Ann Acad Med Singapore. 2007;36:62-66. 250. Chua KS, Ng YS, Yap SG, et al. A brief review of traumatic brain injury rehabilitation. Ann Acad Med Singapore. 2007;36:31--42. 251. Ducrocq SC, Meyer PG, Orliaguet GA, et al. Epidemiology and early predictive factors of mortality and outcome in children with traumatic severe brain injury: experience of a French pediatric trauma center. Pediatr Crit Care Med. 2006;7:461--467. 252. Chesnut RM. The evolving management of traumatic brain injury: Don't shoot the messenger. Crit Care Med 2006;34:2262; author reply 2262-2263. 253. Fulk GD. Traumatic brain injury. In: O'Sullivan SB, Schmitz 1J, eds. Physical Rehabilitation. 5th ed. Philadelphia: FA Davis; 2007:895-935. 254. de Jong LD, Nieuwboer A, Aufdemkampe G. Contracture preven tive positioning of the hemiplegic arm in subacute stroke patients: a pilot randomized controlled trial. Clin Rehabil. 2006;20:656-667. 255. Chatterton HJ, Pomeroy VM, Gratton ]. Positioning for stroke patients: a survey of physiotherapists' aims and practices. Disabil Rehabil. 2001;23:413--421. 256. Osgood SL, Kuczkowski KM. Autonomic dysreflexia in a parturient with spinal cord injury. Acta Anaesthesiol Belg. 2006;57:161-162. 257. Wu KP, Lai PL, Lee LF, et al. Autonomic dysreflexia triggered by an unstable lumbar spine in a quadriplegic patient. Chang Gung Medj. 2005;28:50&-511. 258. Adiga S. Further lessons in autonomic dysreflexia. Arch Phys Med Rehabil. 2005;86:1891; author reply 1891. 259. Sullivan-Tevault M. Autonomic dysreflexia in spinal cord injury. Emerg Med Servo 2005;34:79-80, 85. 260. Jacob C, Thwaini A, Rao A, et al. Autonomic dysreflexia: the for gotten medical emergency. Hosp Med. 2005;66:294-296. 261. Bycroft J, Shergill IS, Chung EA, et al. Autonomic dysreflexia: a medical emergency. Postgrad Medj. 2005;81:232-235. 262. Taylor AG. Autonomic dysreflexia in spinal cord injury. Nurs Clin Notth Am. 1974;9:717-725. 263. Fulk GD, Schmitz TJ, Behrman AL. Traumatic spinal cord injury. In: O'Sullivan SB, Schmitz TJ, eds. Physical Rehabilitation. 5th ed. Philadelphia: FA Davis; 2007:937-996. 264. Czell D, Schreier R, Rupp R, et al. Influence of passive leg move ments on blood circulation on the tilt table in healthy adults. J Neuroengineering Rehabil. 2004;1:4.
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265. Jacobs PL, Mahoney ET, Robbins A, et al. Hypokinetic circulation in persons with paraplegia. Med Sci Sports Exerc. 2002;34: 1401-1407. 266. Houtman S, Colier WN, Oeseburg B, et al. Systemic circulation and cerebral oxygenation during head-up tilt in spinal cord injured individuals. Spinal Cord. 2000;38:15&-163. 267. Johnson RH, Spaulding ]M. Disorders of the autonomic nervous system. Some disorders of regional circulation. Contemp Neural Ser. 1974;11:114-128. 268. Spangler L1. Nonprogressive spinal cord disorders. In: Cameron MH, Monroe LG, eds. Physical Rehabilitation: Evidence-Based Examination, Evaluation, andInteroention. St. Louis: WB Saunders/ Elsevier; 2007;53&-579. 269. American Spinal Injury Association. International Standards for Neurological Classification of Spinal Cord Injury. Chicago: American Spinal Injury Association; 2002. 270. Folstein MF, Robins LN, Helzer ]E. The Mini-Mental State Examination. Arch Gen Psychiatry. 1983;40:812. 271. Folstein MF, Folstein SE, McHugh PRo "Mini-mental state." A prac tical method for grading the cognitive state of patients for the cli nician.] Psychiatr Res. 1975;12:189-198. 272. Field-Fote EC, Fluet GG, Schafer SD, et al. The Spinal Cord Injury Functional Ambulation Inventory (SCI-FAI).] Rehabil Med. 2001;33: 177-181. 273. Greitz D. Unraveling the riddle of syringomyelia. Neurasurg Rev. 2006;29:251-263; discussion 264. 274. Milhorat TH. Classification of syringomyelia. Neurosurg Focus. 2000;8:E1. 275. Pearce ]M. Syringes and syringomyelia. Eur Neurol. 2005;54:243. 276. Todor DR, Mu HT, Milhorat TH. Pain and syringomyelia: a review. Neurosurg Focus. 2000;8:El1. 277. Wollman DE. Syringomyelia: an uncommon cause of myelopathy in the geriatric population.] Am Geriatr Soc. 2004;52: 1033-1034. 278. Rusbridge C, Greitz D, Iskandar B]. Syringomyelia: current con cepts in pathogenesis, diagnosis, and treatment.] Vet Intern Med. 2006;20:469-479. 279. Ahn UM, Ahn NU, Buchowski ]M, et al. Cauda equina syndrome secondary to lumbar disc herniation: a meta-analysis of surgical outcomes. Spine. 2000;25:1515-1522. 280. Brown K1. Cauda equina syndrome. Implications for the orthopaedic nurse in a clinical setting. Orthop Nurs. 1998;17: 31-35; quiz 36-37. 281. Kennedy]G, Soffe KE, McGrath A, et al. Predictors of outcome in cauda equina syndrome. Eur Spine j. 1999;8:317-322. 282. Orendacova], Cizkova D, Kafka], et al. Cauda equina syndrome. Prag Neurobiol. 2001;64:613-637. 283. Small SA, Perron AD, Brady W]. Orthopedic pitfalls: cauda equina syndrome. Am] Emerg Med. 2005;23:159-163. 284. Karceski S. Multiple sclerosis: what have we learned? Neurology. 2007;68:E9-1O. 285. Antel], Arnold D. The search for the missing links in multiple sclerosis. Curr Neural Neurasci Rep. 2007;7:93-94. 286. Vanderlocht], Hellings N, Hendriks ]], et al. Current trends in multiple sclerosis research: an update on pathogenic concepts. Acta Neural Belg. 2006;106:180-190.
649
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1 t
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l
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SECTION II. TESTS AND MEASURES
287. Bruck W. New insights into the pathology of multiple sclerosis: towards a unified concept? ] Neurol. 2007;254Csuppl 1):13-19. 288. Holberg C, Finlayson M. Factors influencing the use of energy conservation strategies by persons with multiple sclerosis. Am] Occup Tber. 2007;61:96-107. 289. Sayao AL, Devonshire V, Tremlett H. Longitudinal follow-up of "benign" multiple sclerosis at 20 years. Neurology. 2007;68:496-500. 290. Pittock SJ. Does benign multiple sclerosis today imply benign multiple sclerosis tomorrow?: implications for treatment. Neurology. 2007;68:480-481. 291. Phillips JT. What causes multiple sclerosis to worsen? Arch Neurol. 2007;64:167-168. 292. Nortvedt MW, Riise T, Frugard J, et al. Prevalence of bladder, bowel and sexual problems among multiple sclerosis patients two to five years after diagnosis. Mult Scler. 2007;13:106-112. 293. Julian L, Merluzzi NM, Mohr DC. The relationship among depres sion, subjective cognitive impairment, and neuropsychological performance in multiple sclerosis. Mult Scler. 2007;13:81--86. 294. Korostil M, Feinstein A. Anxiety disorders and their clinical corre lates in multiple sclerosis patients. Mult Scler. 2007;13:67-72. 295. Mills R, Yap L, Young C. Treatment for ataxia in multiple sclerosis. Cochrane Database .s:vst Rev. CD005029, 2007. 296. Benedict RH, Bobholz JH. Multiple sclerosis. Semin Neurol. 2007; 27:78--85. 297. Costello F. Myasthenia gravis and multiple sclerosis: a review of the ocular manifestations. Insight. 2006;31:19-22; quiz 23-24. 298. Rajasekaran D, Chandrasekar S, Rajendran M. Drug related crisis in myasthenia gravis. ] Assoc Ph,vsicians India 2006;54:820--821. 299. Hartl DM, Leboulleux S, Klap P, et al. Myasthenia gravis mimick ing unilateral vocal fold paralysis at presentation. ] Laryngol Otol. 2007;121:174-178. 300. Conti-Fine BM, Milani M, Kaminski HJ. Myasthenia gravis: past, present, and future. ] CUn Invest. 2006;116:2843-2854. 301. Toyka KY. Ptosis in myasthenia gravis: extended fatigue and recovery bedside test. Neurology. 2006;67: 1524. 302. Meenakshisundaram S. Myasthenia gravis in older patients. Age Ageing. 2006;35:542. 303. Benatar M. A systematic review of diagnostic studies in myasthe nia gravis. Neuromuscul Disord. 2006;16:459--467. 304. Romi F, Gilhus NE, Aarli JA. Myasthenia gravis: disease severity and prognosis. Acta Neurol Scand Suppl. 2006;183:24-25. 305. Singh R, Pentland B. Myasthenia gravis masquerading as post poliomyelitis syndrome. ] Rehabil Med. 2006;38:136-137. 306. Cheesman M, Kessell G. First presentation of myasthenia gravis. Anaesthesia. 2006;61:66. 307. Budrys V. A portrait of myasthenia gravis? Eur Neurol. 2005;54: 240-241. 308. Poudel M, Angel GM, Neopane A, et al. A typical case of myas thenia gravis. Kathmandu UnivMedj. 2003;1:193-196. 309. Alarcon GS. Infections in systemic connective tissue diseases: sys temic lupus erythematosus, scleroderma, and polymyositis/ dermatomyositis. Infect Dis CUn North Am. 2006;20:849--875. 310. Yoshidome Y, Morimoto S, Tamura N, et al. A case of polymyosi tis complicated with myasthenic crisis. CUn Rheumatol. 2006;26: 1569-70.
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311. Pongratz D. Therapeutic options in autoimmune inflammatory myopathies (dermatomyositis, polymyositis, inclusion body myositis). ] Neural. 2006;253:v64-v65. 312. Lundberg IE. The heart in dermatomyositis and polymyositis. Rheumatology (Oxford). 2oo6;45(suppl 4):ivl8-iv21. 313. Senechal M, Crete M, Couture C, et al. Myocardial dysfunction in polymyositis. Can] Cardiol. 2006;22:869-871. 314. Ytterberg SR. Treatment of refractory polymyositis and dermato myositis. Curr Rheumatol Rep. 2006;8: 167-173. 315. Zampieri S, Ghirardello A, Iaccarino L, et al. Polymyositis dermatomyositis and infections. Autoimmunity. 2006;39:191-196. 316. Hui AC, Wong SM, Leung 1'. Prognosis of polymyositis and dermatomyositis. Clin Rheumatol. 2007;26:92. 317. Bronner 1M, van der Meulen MF, de Visser M, et al. Long-term out come in polymyositis and dermatomyositis. Ann Rheum Dis. 2006;65: 1456-1461. 318. Airio A, Kautiainen H, Hakala M. Prognosis and mortality of polymyositis and dermatomyositis patients. Clin Rheumatol. 2006;25:234-239. 319. Schnabel A, Hellmich B, Gross Wi. Interstitial lung disease in polymyositis and dermatomyositis. CUlT Rheumatol Rep. 2005;7: 99-105. 320. Dalakas Me. Inflammatory disorders of muscle: progress in polymyositis, dermatomyositis and inclusion body myositis. Curr apin Neural. 2004;17:561-567. 321. Strupp M. Medical and surgical treatment of epilepsy. ] Neura. 2007;254:268-70. 322. Hara H. Autism and epilepsy: A retrospective follow-up study. Brain Dev. 2007;29:486-90. 323. Regis J, Bartolomei J, Chauvel P. Epilepsy. Prog Neural Surg. 2007;20:267-278. 324. French JA. Refractory epilepsy: clinical overview. Epilepsia. 2007;48(suppl l}3-7. 325. Abou-Khalil BW. Is epilepsy intractability predetermined or acquired? Epilepsy Curro 2007;7:9-10. 326. Hermann B, Seidenberg M. Epilepsy and cognition. Epilepsy Curro 2007;7:1-6. 327. When is it epilepsy? Ham Ment Health Lett. 2006;23:5-6. 328. Haut SR, Hall CB, LeValley AJ, et al. Can patients with epilepsy predict their seizures? Neuralogy. 2007;68:262-266. 329. Beghi E, De Maria G, Gobbi G, et al. Diagnosis and treatment of the first epileptic seizure: guidelines of the Italian league against epilepsy. Epilepsia. 2006;47(suppl 5):2-8. 330. Camfield P, Camfield e. The office management of epilepsy. Semin Pediatr Neural. 2006;13:201-207. 331. Harris-Love MO, Siegel KL, Paul SM, et al. Rehabilitation manage ment of Friedreich ataxia: lower extremity force-control variability and gait performance. NeurorehahilNeuralRepair. 2004;18:117-124. 332. Voncken M, Ioannou P, Delatycki MB. Friedreich ataxia-update on pathogenesis and possible therapies. Neuragenetics. 2004;5:1-8. 333. Pandolfo M. Friedreich ataxia. Semin Pediatr Neural. 2003;10: 163-172. 334. Alldredge CD, Schlieve CR, Miller NR, et al. Pathophysiology of the optic neuropathy associated with Friedreich ataxia. Arch aphthalmol.2003;121:1582-1585.
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335. Albin RL. Dominant ataxias and Friedreich ataxia: an update. Curr Opin Neurol. 2003;16:507-514. 336. Puccio H, Koenig M. Friedreich ataxia: a paradigm for mitochon drial diseases. Curr Opin Genet Dev. 2002;12:272-277. 337. Pandolfo M. Molecular basis of Friedreich ataxia. Mov Disord. 2001;16:815-821. 338. Pandolfo M. The molecular basis of Friedreich ataxia. Neurologia. 2000; 15:325-329. 339. Delatycki MB, Williamson R, Forrest SM. Friedreich ataxia: an overview.] Med Genet. 2000;37:1-8. 340. Koenig M, Mandel J1. Deciphering the cause of Friedreich ataxia. Curr Opin Neurobiol. 1997;7:689--{)94. 341. Sloane PD, Coeytaux RR, Beck RS, et al. Dizziness: state of the sci ence. Ann Intern Med. 2001;134:823-832. 342. Smith-Wheelock M, Shepard Nf, Telian SA. Physical therapy pro gram for vestibular rehabilitation. Am] Otol. 1991;12:218-225. 343. Schubert Me. Vestibular disorders. In: O'Sullivan SB, Schmitz 1J, eds. PhysicalRehabilitation. 5th ed. Philadelphia: FA Davis; 2007:99-1029. 344. Jacobson GP, Newman CWo The development of the Dizziness Handicap Inventory. Arch Otolaryngol Head Neck Surg. 1990; 116:424-427. 345. Gacek RR. The pathology of facial and vestibular neuronitis. Am ] Otolaryngol. 1999;20:202-210. 346. Gacek RR, Gacek MR. Vestibular neuronitis. Am] Otol. 1999;20: 553-554. 347. Gacek RR, Gacek MR. Vestibular neuronitis: a viral neuropathy. Adv Otorhinolaryngol. 2002;60:54-66. 348. Imate Y, Sekitani T, Okami M, et al. Central disorders in vestibu lar neuronitis. Acta Otolaryngol Suppl. 1995;519:204-205. 349. Ishikawa K, Edo M, Togawa K. Clinical observation of 32 cases of vestibular neuronitis. Acta Otolaryngol Suppl. 1993;503:13-15. 350. Lumio JS, Aho]. Vestibular neuronitis. Ann Otol Rhinol Laryngol. 1965;74:264-270. 351. Ogata Y, Sekitani T, Shirnogori H, et al. Bilateral vestibular neu ronitis. Acta Otolaryngol Suppl. 1993;503:57---60. 352. Tahara T, Sekitani T, Imate Y, et al. Vestibular neuronitis in chil dren. Acta Otolaryngol Suppl. 1993;503:49-52. 353. Baloh RW. Differentiating between peripheral and central causes of vertigo. Otolaryngol Head Neck Surg. 1998;119:55-59. 354. Baloh RW. Differentiating between peripheral and central causes of vertigo.] Neurol Sci. 2004;221:3. 355. Buttner U, Helmchen C, Brandt T. Diagnostic criteria for central versus peripheral positioning nystagmus and vertigo: a review. Acta Otolaryngol. 1999;119:1-5. 356. Drozd CEo Acute vertigo: peripheral versus central etiology. Nurse Pract. 1999;24:147-148, 1999. 357. Frederic MW. Central vertigo. Otolaryngol Clin North Am. 1973; 6:267-285. 358. Williams D. Central vertigo. Trans Med Soc Lond. 1958;74:15-19. 359. Williams D]. Central vertigo. Proc R Soc Med. 1967;60:961-964. 360. Di Girolamo S, Ottaviani F, Scarano E, et al. Postural control in horizontal benign paroxysmal positional vertigo. Bur Arch Otorhinolaryngol. 2000;257:372-375. 361. Dornhoffer JL, Colvin GB. Benign paroxysmal positional vertigo and canalith repositioning: clinical correlations. Am] Otol. 2000; 21:230-233.
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362. FurmanJM, Cass SP. Benign paroxysmal positional vertigo. N Eng I ] Med. 1999;341:1590-1596. 363. Herdman SJ, Blatt PJ, Schubert Me. Vestibular rehabilitation of patients with vestibular hypofunction or with benign paroxysmal positional vertigo. Curr Opin Neurol. 2000;13:39-43. 364. Hilton M, Pinder D. Benign paroxysmal positional vertigo. BM]. 2003;326:673. 365. Karlberg M, Hall K, Quickert N, et al. What inner ear diseases cause benign paroxysmal positional vertigo? Acta Otolaryngol. 2000;120:380-385. 366. Kentala E, Pyykko 1. Vertigo in patients with benign paroxysmal positional vertigo. Acta Otolaryngol Suppl. 2000;543:20-22. 367. Kovar M, Jepson T, Jones S. Diagnosing and treating benign parox ysmal positional vertigo.] Gerontol Nurs. 2006;32:22-27; quiz 28-29. 368. Mosca F, Morano M. Benign paroxysmal positional vertigo, incidence and treatment. Ann Otolaryngol Chir Ceroicofac. 2001;118:95-101. 369. Solomon D. Benign paroxysmal positional vertigo. Curr Treat Options Neurol. 2000;2:417-428. 370. von Brevern M, Lempert T. Benign paroxysmal positional vertigo. Arch Neurol. 2001;58:1491-1493. 371. Gussen R. Meniere syndrome. Compensatory collateral venous drainage with endolymphatic sac fibrosis. Arch Otolaryngol. 1974; 99:414-418. 372. Haubrich WS. Meniere of Meniere's syndrome. Gastroenterology. 1998;114:1150. 373. Lee H, Yi HA, Lee SR, et al. Drop attacks in elderly patients sec ondary to otologic causes with Meniere's syndrome or non Meniere peripheral vestibulopathy.] Neurol Sci. 2005;232:71-76. 374. Karagol U, Deda G, Kukner S, et al. Early-onset Huntington chorea. Eur] Pediatr. 1995;154:752-753. 375. Lanska D]. George Huntington and hereditary chorea. ] Child Neurol. 1995;10:46-48. 376. Tolosa ES, Sparber SB. Huntington chorea. Arch Neurol. 1977;34: 58-59. 377. Patient information. Bell's palsy.] Fam Pract. 2003;52:160. 378. Managing Bell's palsy. Drug Ther Bull. 2006;44:49-53. 379. Cederwall E, Olsen MF, Hanner P, et al. Evaluation of a physio therapeutic treatment intervention in "Bell's" facial palsy. Physiother Theory Pract. 2006;22:43-52. 380. Holland]. Bell's palsy. Clin Evid. 2006;15:1745-1750. 381. Hutchinson M. The management of Bell's palsy. Ir Med]. 98:165, 2005. 382. Salinas R. Bell's palsy. Clin Evid. 2002;8:1301-1304. 383. Burnett MG, Zager EL. Pathophysiology of peripheral nerve injury: a brief review. Neurosurg Focus. 2004;16:E1. 384. CostaJ, Henriques R, Barroso C, et al. Upper limb tremor induced by peripheral nerve injury. Neurology. 2006;67:1884-1886. 385. Duff Sv. Impact of peripheral nerve injury on sensorimotor con trol.] Hand Ther. 2005;18:277-291. 386. Hirate H, Sobue K, Tsuda T, et al. Peripheral nerve injury caused by misuse of elastic stockings. Anaesth Intensive Care. 2007;35:306-307. 387. Mohler LR, Hanel DP. Closed fractures complicated by peripheral nerve injury.] Am Acad Orthop Surg. 2006;14:32-37. 388. Reyes 0, Sosa I, Kuffler DP. Promoting neurological recovery fol lowing a traumatic peripheral nerve injury. P R Health Sci]. 2005;24:215-223.
653
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389. Tomaino MM. Upper extremity peripheral nerve injury. Am] Orthop. 2005;34:60-61. 390. Winfree C]. Peripheral nerve injury evaluation and management. Cun- Surg. 2005;62:469-476. 391. Heald PW. Current treatment practice of herpes zoster. Expert Opin Pharmacother. 2001;2:1283-1287. 392. Leung AK, Robson WL, Leong AG. Herpes zoster in childhood. ] Pediatr Health Care. 2006;20:300-303. 393. Miller GG, Dummer JS. Herpes simplex and varicella zoster viruses: forgotten but not gone. Am] Transplant. 2007;7:741-747. 394. Morrow T. Herpes zoster vaccine brings relief for the elderly. Manag Care. 2006;15:57-58. 395. Raza N, Dar NR, Ejaz A. Simultaneous onset of herpes zoster in a father and son. ] Ayub Med Coli Abbottabad. 2006; 18:64-65. 396. Sauerbrei A, Wutzler P. Herpes simplex and varicella-zoster virus infections during pregnancy: current concepts of prevention, diagnosis and therapy. Part 2: varicella-zoster virus infections. Med Microbiol Immunol. 2007;196:95-102. 397. Thyregod HG, Rowbotham MC, Peters M, et al. Natural history of pain following herpes zoster. Pain. 2007;128:148-156. 398. Volpi A, Gatti A, Serafini G, et al. Clinical and psychosocial corre lates of acute pain in herpes zoster.] Clin Virol. 2007;38:275-279. 399. Bagheri SC, Farhidvash F, Perciaccante YJ. Diagnosis and treat ment of patients with trigeminal neuralgia.] Am Dent Assoc. 2004; 135:1713-1717. 400. Bennetto L, Patel NK, Fuller G. Trigeminal neuralgia and its man agement. BM]. 2007;334:201-205. 401. Cheshire WP. Trigeminal neuralgia: diagnosis and treatment. Curr Neurol Neurosci Rep. 2005;5:79-85. 402. Cheshire WP Jr. Trigeminal neuralgia. Curr Pain Headache Rep. 2007;11:69-74. 403. Ecker AD. The cause of trigeminal neuralgia. Med Hypotheses. 2004;62:1023. 404. El Gammal T, Brooks BS. Trigeminal neuralgia. Radiology. 2004; 231:284. 405. Liu JK, Apfelbaum RI. Treatment of trigeminal neuralgia. Neurosurg Clin North Am. 2004;15:319-334. 406. Rozen TD. Trigeminal neuralgia and glossopharyngeal neuralgia. Neurol Clin. 2004;22:185-206. 407. Scrivani SJ, Mehta N, Mathews ES, et al. Clinical criteria for trigem inal neuralgia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004;97:544; author reply 544-545. 408. Zakrzewska JM. Trigeminal neuralgia. Clin Evid. 2003;9: 1490-1498. 409. Zakrzewska JM, Lopez Be. Trigeminal neuralgia. Clin Evid. 2003; 9:1599-1609. 410. Briese M, Esmaeili B, Sattelle DB. Is spinal muscular atrophy the result of defects in motor neuron processes? Bioessays. 2005;27: 946-957. 411. Iannaccone ST, Smith SA, Simard LR. Spinal muscular atrophy. Curr Neurol Neurosci Rep. 2004;4:74-80. 412. Muthukrishnan J, Varadarajulu R, Mehta SR, et al. Distal spinal muscular atrophy.] Assoc Physicians India. 2003;51:1113-1115. 413. Scheffer H. Spinal muscular atrophy. Methods Mol Med. 2004;92: 343-358.
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414. Wang HY, Ju YR, Chen SM, et al. Joint range of motion limitations in children and young adults with spinal muscular atrophy. Arch Phys Med Rehabil. 2004;85:1689-1693. 415. Wirth B, Brichta L, Hahnen E. Spinal muscular atrophy and ther apeutic prospects. Prog Mol Subcell BioI. 2006;44:109-132. 416. Yap SH. Spinal muscular atrophy. Int J Obstet Anesth. 2003; 12:237. 417. Bartell JC, Hayney MS. In the spotlight: Guillain-Barre syndrome. JAm Pharm Assoc (Wash DC). 2006;46:104-106. 418. Chaudhuri A. Guillain-Barre syndrome. Lancet. 2006;367:472-473; author reply 473-474. 419. Cosi V, Versino M. Guillain-Barre syndrome. Neurol Sci. 2006;27 (suppl 1):S47-S51. 420. Douglas MR, Winer JB. Guillain-Barre syndrome and its treat ment. F-XfJert Rev Neurother. 2006;6:1569-1574. 421. Gurwood AS, Drake]. Guillain-Barre syndrome. Optometry. 2006; 77:540-546. 422. Kashyap AS, Anand KP, Kashyap S. Guillain-Barre syndrome. Lancet. 2006;367:472; author reply 473-474. 423. Kuwabara S. Guillain-Barre syndrome. Curr Neural Neurosci Rep. 2007;7:57--62. 424. Logullo F, Manicone M, Di Bella P, et al. Asymmetric Guillain Barre syndrome. Neurol Sci. 2006;27:355-359. 425. Saxena AK. Guillain-Barre syndrome. Lancet. 2006;367:472; author reply 473-474. 426. Shahar E. Current therapeutic options in severe Guillain-Barre syndrome. Clin Neuropharmacol. 2006;29:45-51. 427. Tsang RS, Valdivieso-Garcia A. Pathogenesis of Guillain-Barre syndrome. Expert Rev Anti Infect Ther. 2003;1:597--608. 428. van Doorn PA, Jacobs Be. Predicting the course of Guillain-Barre syndrome. Lancet Neural. 2006;5:991-993. 429. Logroscino G, Armon e. Amyotrophic lateral sclerosis: a global threat with a possible difference in risk across ethnicities. Neurology.2007;68:E17. 430. Kurt A, Nijboer F, Matuz T, et al. Depression and anxiety in indi viduals with amyotrophic lateral sclerosis: epidemiology and management. CNS Drugs. 2007;21:279-91. 431. Grossman AB, Woolley-Levine S, Bradley WG, et al. Detecting neurobehavioral changes in amyotrophic lateral sclerosis. Amyotroph Lateral Scler. 2007;8:56--61. 432. Hardiman 0, Greenway M. The complex genetics of amyotrophic lateral sclerosis. Lancet Neurol. 2007;6:291-2. 433. Lederer CW, Santama N. Amyotrophic lateral sclerosis-The tools of the trait. Biotechnolj. 2007;2(5):608. 434. Pozza AM, Delamura MK, Ramirez C, et al. Physiotherapeutic conduct in amyotrophic lateral sclerosis. Sao Paulo Med j. 124: 350-4, 2006. 435. Shoesmith CL, Strong M]. Amyotrophic lateral sclerosis: update for family physicians. Can Fam Physician. 2006;52:1563-9. 436. Aguilar JL, Echaniz-Laguna A, Fergani A, et al. Amyotrophic lat eral sclerosis: all roads lead to Rome. J Neurochem. 2007;101(5);1153-1160. 437. Postpolio syndrome. J Indian Med Assoc. 2000;98:24-5. 438. Carlson M, Hadlock T. Physical therapist management following rotator cuff repair for a patient with postpolio syndrome. Phys Ther.2007;87:179-92.
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439. Dalakas M. Postpolio syndrome. Curr Opin Rheumatol. 1990;2:901-7. 440. Gevirtz C. Managing postpolio syndrome pain. Nursing. 2006;36:17. 441. Hodges DL, Kumar VN. Postpolio syndrome. Orthop Rev. 1986;15:218---22. 442. Howard RS. Poliomyelitis and the postpolio syndrome. Bm}. 2005;330:131H. 443. Moskowitz E. Postpolio syndrome. Arch Phys Med Rehabil. 1987;68:322. 444. Nollet F, de Visser M. Postpolio syndrome. Arch Neurol. 2004; 61:1142-4. 445. Owen RR. Postpolio syndrome and cardiopulmonary condition ing. West] Med. 1991;154:557-8. 446. Sliwa]. Postpolio syndrome and rehabilitation. Am] Phys Med Rehabil. 2004;83:909. 447. Winters R. Postpolio syndrome. ] Am Acad Nurse Pract. 1991;3: 69-74. 448. Shumway-Cook A, Woollacott M. Motor control-Theory and practical applications. Baltimore: Williams & Wilkins, 1995. 449. O'Sullivan SB. Strategies to improve motor function, in O'Sullivan SB, Schmitz TJ (eds): Physical Rehabilitation (ed 5). Philadelphia, FA Davis; 2007:471-522. 450. Hoare B, WasiakJ, Imms C, et al. Constraint-induced movement ther apy in the treatment of the upper limb in children with hemiplegic cerebral palsy. Cochrane Database Syst Rev. 2007; 18(2):CD004149. 451. Wu CY, Chen CL, Tsai WC, et al. A randomized controlled trial of modified constraint-induced movement therapy for elderly stroke survivors: changes in motor impairment, daily functioning, and quality of life. Arch Phys Med Rehabil. 2007;88:273-8. 452. Boake C, Naser EA, Ro T, et al. Constraint-induced movement therapy during early stroke rehabilitation. Neurorehabil Neural Repair. 2007;21:14-24. 453. Mark VW, Taub E, Morris DM. Neuroplasticity and constraint induced movement therapy. Bura Medicophys. 2006;42:269-84. 454. Morris DM, Taub E, Mark VW. Constraint-induced movement ther apy: characterizing the intervention protocol. Bura Medicophys. 2006;42:257-68. 455. Smania N. Constraint-induced movement therapy: an original concept in rehabilitation. Bura Medicophys. 2006;42:239-40. 456. Clayton-Krasinski D, Klepper S. Impaired neuromotor develop ment, in Cameron MH, Monroe LG (eds): Physical Rehabilitation: Evidence-Based Examination, Evaluation, and Intervention. St Louis, WE Saunders/Elsevier; 2007:333-366. 457. Winstein C]. Motor learning considerations in stroke rehabilitation. In: Duncan PW, Badke MB (eds): Stroke Rehabilitation: the Recovery ofMotor Control. Chicago: Yearbook Medical Publishers, Inc.; 1987:109-134. 458. Unsworth CA. Cognitive and perceptual dysfunction. In O'Sullivan SB, Schmitz TJ (eds). Physical Rehabilitation. (ed 5). Philadelphia: FA Davis; 2007:1149-1188. 459. Parziale JR, Akelman E, Herz DA. Spasticity: Pathophysiology and management. Orthopedics. 1993;16:801-11. 460. Vodovnik L, Bowman BR, Hufford P. Effects of electrical stimula tion on spinal spasticity. Scand] Rehabil Med. 1984;16:29-34. 461. Goulet C, Arsenault AB, Bourbonnais D, et al. Effects of transcu taneous electrical nerve stimulation on H-reflex and spinal spas ticity. Scand] Rehabil Med. 1996;28:169-76.
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462. Marshall S, Teasell R, Bayona N, et al. Motor impairment rehabil itation post acquired brain injury. Brain In). 2007;21:133-60. 463. Booth MY, Yates CC, Edgar TS, et al. Serial Casting vs Combined Intervention with Botulinum Toxin A and Serial Casting in the Treatment of Spastic Equinus in Children. Pediatr Phys Ther. 2003; 15:216-220. 464. Westberry DE, Davids JR, Jacobs JM, et al. Effectiveness of serial stretch casting for resistant or recurrent knee flexion contractures following hamstring lengthening in children with cerebral palsy. ] Pediatr Orthop. 2006;26:109-14. 465. Singer BJ, Dunne JW, Singer KP, et al. Non-surgical management of ankle contracture following acquired brain injury. Disabil Rehabil. 2004;26:335-45. 466. Stoeckmann T. Casting for the person with spasticity. Top Stroke Rehabil. 2001 ;8:27-35. 467. Donovan E. Serial casting, in Placzek JD, Boyce DA (eds): OrthopaediC Physical Therapy Secrets. Philadelphia: Hanley & Belfus, Inc.; 2001:200-203. 468. Vanek ZF, Menkes]H. Spasticity, Available at: www.emedicine.com! neuro/topic706.htm, 2005. 469. Bauer CA, Girardi M Vestibular rehabilitation, Available at: www.emedicine.com!ent/topic666.htm. 2005.
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Comprehension Questions
j
1. A spinal cord patient has pain and stiffness in his anterior thigh. He is diagnosed as having heterotrophic bone formation. Which manual technique should the physical therapist avoid? A. Manual resistive exercises. B. Massage. C. Aggressive passive stretching. D. Muscle energy techniques. 2. In a patient with aspinal cord injury at the T12 level, which of the following would not be one of your goals for the intervention? A. Independent control of the trunk musculature above the level ofT12. B. Good sitting balance. C. Bowel and bladder control. D. Ambulation without assistive device.
3. The femoral nerve innervates all but which of the following muscles? A. Sartorius. B. Vastus lateralis. C. Adductor magnus. D. Pecti neus. 4. A patient presents with weak quadriceps muscles with adiagnosis of a lumbar disc herniation. You suspect an L3-L4 problem. What other muscle could you test to help confirm the diagnosis? A. Sartorius. B. Adductor magnus. C. Biceps femoris. D. II iopsoas.
~
.
I
5. A patient presents with ahemisection of the spinal cord (Brown-Sequard) at the T12 level. When examining the patient's right lower extremity, which of the following would you likely find? A. Muscle paralysis. B. Loss of position sense. C. Loss of pain sensation. D. Loss of vibratory sense. 6. What happens to the intracranial pressure of a patient placed in the Trendelenburg position? Does it increase or decrease? 7. Which of the following would you expect to find in a patient diagnosed with carpal tunnel syndrome? A. Tingling in the ulnar side of the hand and reports of pain in the hand with rest. B. Tingling in the radial side of the hand and pain in the hand at night. C. A loss of peripheral vision. D. Pain with elbow extension.
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8. Which of the following is characterized by a deep sleep, from which the patient cannot be aroused? A. Stupor. B. Lethargy. C. Coma. D. Obtundation. 9. All of the following are true statements with regard to epidural hematomas, except: A. They are mostly venous in origin, involving the venous dural sinuses. B. They are most commonly caused by head trauma. C. They are commonly characterized by alternating CNS depression, with lethargy and confusion. D. They are, acutely, the most serious of the intracranial hemorrhages. 10. Myasthenia gravis is an example of a myopathy due to A. Nerve injury. B. Muscle disuse. C. Metabolic abnormality. D. Myoneural junction block. 11. Which of the following would least likely be a causative agent in encephalitis? A. Polio. B. Pneumococcus. C. Measles. D. Rabies. 12. Which two cranial nerves arise from the midbrain? 13. Which four cranial nerves arise from the pons? 14. How many pairs of spinal nerves are there? A. 32. B. 31. C. 33.
D. 24. 15. Which nerve roots commonly form the cervical plexus? 16. Which nerve roots commonly form the brachial plexus? 17. What are the three divisions of the trigeminal nerve called? 18. Which two cranial nerves have distributions in other regions than to just the head and neck? 19. Which area of the brain controls the autonomic nervous system? 20. Which of the two systems, parasympathetic or sympathetic, stimulates the release of epinephrine from the adrenal medulla? 21. Which nerve innervates all but one of the intrinsic muscles of the tongue? 22. Which nerve innervates the sternocleidomastoid and the trapezius muscles? 23. Which cord of the brachial plexus supplies the radial nerve?
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24. What three arm muscles does the musculocutaneous nerve supply? 25. A lesion to which nerve results in a claw-hand deformity? 26. Which peripheral nerve is responsible for stimulating the muscles that produce dorsiflexion? 27. Which two nerves innervate the adductor magnus? 28. Which peripheral nerve can be trapped in the arcade of Frohse? 29. Which peripheral nerve can be trapped between the two heads of the pronator teres? 30. Which peripheral nerve can be trapped by the ligament of Struthers? 31. Atrophy of the hypothenar eminence could indicate a lesion to which nerve? 32. A lesion to which nerve can result in an ape-hand deformity? 33. List two special tests you could use to help diagnose carpal tunnel syndrome. 34. Which muscles does the suprascapular nerve innervate? 35. Which nerve innervates the serratus anterior? 36. Which nerve innervates the latissimus dorsi muscle? 37. Which muscles are innervated by the superior gluteal nerve? 38. A herniated disc between the (6 and (7 vertebral levels could impinge upon which nerve root level? 39. Injury to the radial nerve in the spiral groove would result in weakness of which group of muscles? 40. Which of the fol/owing muscles is not innervated by the median nerve? A. Abductor pollicis brevis. B. Flexor pol/icis longus. C. Medial heads of flexor digitorum profundus. D. Superficial head of flexor pol/icis brevis. E. Pronator quadratus.
41. Name the nerve that innervates the first lumbrical muscle in hand. 42. A patient presents with a burning sensation in the anterolateral aspect of the thigh. Dysfunction of which nerve could lead to these symptoms? A. Lateral cutaneous (femoral) nerve of the thigh. B. Femoral. C. Obturator. D. Genitofemoral. E. Ilioinguinal. 43. The saphenous nerve supplies cutaneous sensation to the medial aspect of the leg. From which nerve does the saphenous nerve arise? A. Obturator. B. Deep fibular (peroneal).
CHAPTER 9. NEUROMUSCULAR PHYSICAl THERAPY
e.
Sciatic. D. Femoral. E. The saphenous nerve arises as a direct branch from the sacral plexus.
44. An injury to the deep branch of the peroneal nerve would result in asensory deficit to which of the following locations? A. Medial side of the foot. B. Lateral side of the foot. Lateral one and one half toes. D. Medial border of the sole of the foot. E. Adjacent dorsal surfaces of the first and second toes.
e.
45. A brachial plexus injury in the upper portion of the plexus produces winging of the scapula. Weakness of which of the following muscles would produce the winging observed? A. Long head of the triceps. B. Supraspinatus. Deltoid. D. Pectoralis major. E. Serratus anterior.
e.
46. Which of the following flexor muscles is not innervated by the median nerve? A. Flexor carpi radialis. B. Flexor carpi ulnaris. Palmaris longus. D. Flexor digitorum superficial is. E. Flexor pol/icis longus.
e.
47. Which two muscles does the anterior interosseous branch of the median nerve innervate?
48. A birth injury which results in injury to the lower portion of the brachial plexus is referred to as A. Bell's palsy. B. Erb's paralysis. e. Klumpke's paralysis. D. Saturday night palsy. E. Tinel sign. 49. The axillary nerve can occasionally be injured when it passes through which muscle? 50. The lateral ventricles of the brain drain into what structure? 51. Which arteries are connected by the anterior communicating artery in the brain? 52. Name the structure that connects the anterior intercranial division and the posterior intercranial division blood supplies of the brain. 53. In the brain, what is Wernicke's area responsible for? 54. Which structure connects the two cerebral hemispheres?
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55. Which cranial nerve is responsible for chewing? 56. Which nerve supplies cutaneous sensation to the dorsum of the medial one and one half fingers? 57. Identify six impairments or functional limitations that would warrant (or indicate the need for) an examination of sensory function. 58. Define the following: arousal, attention, orientation, and cognition. 59. Saltatory conduction in a nerve fiber refers to A. Difference in nervous tissue conduction when the person is on a high-sodium diet. B. Difference in nervous tissue conduction when the person is on a low-sodium diet. C. The increased conduction velocity as the action potential jumps from node to node of Ranvier. D. The method by which pain transmissions are conducted. 60. Sensory perception of vibration is mediated through A. Pacinian corpuscles. B. Free nerve endings. C. The proprioceptive receptors. D. All the different tactile receptors.
61. Neurotransmitter substances may include all of the following except A. Prostaglandin. B. Acetylcholine. C. GABA. D. Epinephrine. 62. Areas of the body with a higher density of two-point discrimination cells include all of the following except A. Skin of the lips. B. Skin on the palm of the hand. C. Skin on the sole of the feet. D. Skin on the arms. 63. All A. B. C. D.
of the following are false about the stretch reflex except It is found only in primates. It may be either monosynaptic or polysynaptic. It is more easi Iy demonstrated than any other reflex. It is monosynaptic.
64. All of the following features may be found in muscle spindles except A. They require a change in length as well as in the rate of change in order to fire. B. They demonstrate two kinds of intrafusal fibers, nuclear bag and nuclear chain fibers. C. They are arranged in parallel with the extrafusal fibers of the muscle itself. D. They are innervated by one very large type la fiber that serves both fiber types.
1
CHAPTER 9. NEUROMUSCULAR PHYSICAL THERAPY
65. True or false: Muscle spindles, under normal conditions, emit sensory nerve impulses constantly. A. True. B. False. 66. The presence of clonus indicates A. A lesion in the muscle spindle. B. Impairment of the conduction at the myoneural junction. C. Muscle fatigue. D. A high degree of facilitation of the spinal cord. 67. The perception of the position of the extremities in space is often referred to as A. Depth perception. B. Spatial discrimination. C. Paresthesias. D. Kinesthesia. 68. The organ most concerned with detecting sensations relating to equilibrium is A. The coch lea. B. The cerebellum. C. The vestibular apparatus. D. The pinna. 69. You decide to test the integrity of the equilibrium mechanism of apatient with ahis tory of balance disturbance. You ask the individual to stand perfectly still with the eyes closed. What is the name of this test? A. The Babinski. B. The tonic neck reflex. C. Romberg's sign. D. Phalen's. 70. All of the following are examples of the simple stretch reflex, except A. Knee-jerk reflex. B. Monosynaptic reflex. C. Myotatic reflex. D. Flexor withdrawal reflex.
71. All of the following spinal functions are affected during or following spinal shock, except
A. Autonomic regulation of blood pressure. B. All skeletal muscle reflexes integrated in the spinal cord. C. The sacral reflexes for control of bladder and colon evacuation. D. The vomiting reflex. 72. The purpose of the tympanic membrane and the ossicular system in hearing is A. The location of specialized sensory receptors of sound waves. B. The modulation of incoming sound waves. C. A system for impedance matching between the sound waves in air and the sound vibrations in the cochlear fluid. D. A transducer system, changing sound to electrical impulses.
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73. The normal stimulus to the semicircular canals is a change in A. Incoming visual patterns. B. Frequency of incoming auditory impulses. C. Intensity of incoming auditory impulses. D. Movement velocity of the head around a vertical, transverse, or medial sagiltal axis.
74. The two cerebral hemispheres derive from what early embryologic portion of the neural tube? A. Metencephalon. B. Mesencephalon. C. Telencephalon. D. Diencephalon.
75. Which lobe of the brain is responsible for vision and integration of visual data? 76. Which lobe of the brain is responsible for somatic sensory perception and interpretation?
77. Which lobe of the brain is responsible for memory, hearing, and comprehension of speech? 78. Which portion of the brain regulates peripheral autonomic nervous system dis charges and is responsible for homeostatic mechanisms such as regulation of body temperature? A. Hypothalamus. B. Thymus. C. Thalamus. D. The pons.
79. Which of the following structures do not compose the limbic system? A. The parahippocampal gyrus. B. A cingulate gyrus. C. The uncus. D. The corpus callosum. 80. Functions of the "right brain" include all of the following except A. Control of the left side of the body. B. Tactile identification of objects. C. Control of the right side of the body. D. Processing of information. 81. The red nucleus is involved in all of the following except A. Motor movement. B. Postural reflex patterns. C. Blushing. D. None of the above. 82. Clinical findings in spina bifida include all of the following except A. Incomplete closure of the neural plate. B. Severe paralysis.
CHAPTER 9. NEUROMUSCULAR PHYSICAL THERAPY
C. Excretory dysfunctions. O. No sensory impairment. 83. True or false: The autonomic nervous system serves as the essential neurogenic reg ulatory system for homeostatic maintenance. 84. True or false, the sympathetic division maintains normal homeostasis during rest and prepares the body for stress; while the parasympathetic system returns func tions to normal following stress. 85. All of the following controls are affected by the ANS except A. Heart rate and blood pressure. B. Body temperature regulation. C. Fine motor control. O. Sweating and salivation. 86. Which of the following drugs or medications are adrenergic? A. Nicotine. B. Atropine. C. Epinephrine. O. Reserpine. 87. While evaluating a patient who suffered a complete spinal cord lesion, you note the following strength grades with manual muscle testing: wrist extensors =3+/5, elbow extensors = 2+/5, and intrinsic muscles of the hand = DIS. What is the highest possi ble level of this lesion?
A. C3. B. C4.
C. C5. O. C7. 88. You are examining a patient who suffered a traumatic brain injury. The patient demonstrates deficits in sensation in the right upper and lower extremities. In which of the following locations is at least part of the injury involved: A. Inferior right hemisphere of the somatosensory cortex. B. Superior right hemisphere of the somatosensory cortex. C. Inferior left hemisphere of the somatosensory cortex. O. Superior left hemisphere of the somatosensory cortex. 89. You decide to use the neurodevelopmental treatment (NOT) approach with a patient recovering from stroke. Which of the following components would not be included: A. Facilitation of early movement in synergistic patterns followed quickly by move ment patterns out-of-synergy. B. Reduction of spasticity and abnormal reflex activity through positioning and handling techniques. C. Facilitation of selective movement control out of synergistic patterns. O. Functional activities emphasizing reintegration of the hemiplegic side.
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90. A 3-year-old boy with moderate spastic diplegia is referred to physical therapy for an adaptive equipment check. Which of the following equipment is NOT indicated in this case? A. Bilateral KAFOs. B. Prone stander. C. AFOs to reduce tone. D. Posterior walker. 91. You are planning an intervention for an individual recovering from traumatic brain injury who demonstrates Rancho Level Cognitive function VII. The best intervention strategy in this case would be to A. Involve the patient in decision-making, emphasizing safety, and independent performance. B. Provide a high degree of environmental structure. C. Provide assistance for guided movements during all movement tasks. D. Provide maximum supervision to ensure successful performance. 92. When examining the gait in a patient with Parkinson's disease, you notice a prob lem of a forward festinating gait. To correct this problem, you could A. Fit the patient with a toe wedge. B. Ask the patient to increase cadence. C. Ask the patient to increase stride length. D. Fit the patient with a heel wedge. 93. A realistic functional goal for a 6-year-old child with a very high lumbar lesion myelomeningocele and minimal cognitive involvement would be A. Ambulation for exercise with a reciprocating gait orthosis and Lofstrand crutches. B. Community ambulation with HKAFOs and Lofstrand crutches. C. Community ambulation with a reciprocating gait orthosis and Lofstrand crutches. D. Physiologic ambulation with KAFOs and rollator walker. 94. In formulating a plan of care concerning an 87-year-old resident of a community nursing home diagnosed with organic brain syndrome, Alzheimer's type, it is important to understand that he A. Will likely be resistant to activity training if unfamiliar activities are used. B. Can usually be trusted to be responsible for his daily care needs. C. Is more likely to remember current experiences than past ones. D. Can usually be trusted with transfers and with appropriate positioning of the wheelchair. 95. You are testing two-point discrimination on the right hand of a patient who is sus pected of having had a stroke. The patient is unable to tell you whether you are touching him with one or two points. This could indicate impaired function in the A. Anterior spinothalamic tract or thalamus. B. Lateral spinothalamic tract or somatosensory cortex. C. Dorsal column/lemniscal pathways or somatosensory cortex. D. Spinal lemniscus or ventral posterolateral nucleus of the thalamus.
CHAPTER 9. NEUROMUSCULAR PHYSICAL THERAPY
96. You are planning an intervention for a patient who suffered a left CVA that has left him hemiparetic on the right side. During the examination, the patient demon strated strong and dominant hemiplegic synergies in his leg. Which activity would NOT be helpful to break up these synergies? A. Weight shifts in quadruped. B. Assuming the bridging position. C. Rolling from the hook-lying position using lower extremity 01 flexion PNF pattern. D. Foot tapping in a sitting position. 97. A patient with amyotrophic lateral sclerosis presents with early signs of progressive muscle weakness and muscle cramping. He also has minimal spasticity in his lower extremities. Your intervention should initially focus on A. Low-intensity general conditioning exercises. B. PROM exercise to maintain joint flexibility since active exercise is contraindi cated. C. Active exercises since resistive exercises are contraindicated. D. Maximizing exercise and activity. 98. A 72-year-old patient who suffered a cerebral thrombosis 5 days ago presents with analgesia and thermoanesthesia of the ipsi lateral face; nystagmus, vertigo, and nau sea; dysphagia and dysarthria; ipsilateral Horner's syndrome; and contralateral loss of sensations of pain and temperature of the body. Which artery would you suspect to be involved? A. Basilar. B. Anterior inferior cerebellar. C. Internal carotid. D. Posterior inferior cerebellar. 99. You are instructing the family of apatient who has a complete spinal cord injury at the level of C6. The passive range-of-motion exercises you want the family to focus on include A. Keeping all muscles fully ranged through normal ROM. B. Ranging individual muscles according to specific functional needs. C. Keeping muscles fully ranged, with hyperflexibility in the low back extensors and hamstrings. D. Limiting range of motion in the shoulders to promote stability.
100. During surgery to remove an apical lung tumor, the long thoracic nerve was injured. The muscle that is weakened (3+/5) is: A. Serratus anterior. B. Upper trapezius. C. Serratus anterior. D. Subscapularis.
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Answers 1. The answer is C. 2. The answer is C. 3. The answer is C. 4. The answer is A. 5. The answer is C. 6. Increases. 7. The answer is B. 8. The answer is C. 9. The answer is A. 10. The answer is D. 11. The answer is B. 12. Cranial nerves III and IV. 13. Cranial nerves V through VIII. 14. The answer is B.
15. Cl-C4. 16. C5-Tl. 17. Ophthalmic, maxillary, and mandibular. 18. The spinal accessory nerve (XI) and the vagus nerve (X). 19. The hypothalamus. 20. Sympathetic. 21. Hypoglossal. 22. Spinal accessory. 23. Posterior. 24. Coracobrachialis, brachialis, and biceps brachii. 25. The ulnar nerve. 26. The deep fibular (peroneal) nerve. 27. The obturator and tibial division of the sciatic. 28. The radial nerve. 29. The median nerve. 30. The median nerve. 31. The ulnar nerve.
CHAPTER 9, NEUROMUSCULAR PHYSICAL THERAPY
32. The median nerve. 33. Phalen's test and Tinel test. 34. Supraspinatus and infraspinatus. 35. Long thoracic nerve. 36. Thoracodorsal nerve. 37. Gluteus medius and minimus, and tensor fascia lata.
38. C7. 39. Wrist extensors. 40. The answer is C. 41. Median nerve. 42. The answer is A. 43. The answer is D. 44. The answer is E. 45. The answer is E. 46. The answer is B.
47. Flexor pollicis longus and pronator quadratus. 48. The answer is C. 49. Coracobrachialis. 50. The third ventricle. 51. The anterior cerebral arteries. 52. The circle of Willis. 53. The understanding of language. 54. The corpus callosum. 55. The trigeminal nerve. 56. The ulnar nerve. 57. Impairments of circulation, integumentary integrity, muscle performance, and pos ture; functional limitations in self-care, home management, and work. 58. Arousal: the physiologic readiness of the human system for activity; attention: selected awareness of the environment or responsiveness to astimulus or task with out being distracted by other stimuli; orientation: the patient's awareness of time, person, and place; cognition: the process of knowing and includes both awareness and judgment. 59. The answer is C. 60. The answer is D.
669
670
SECTION II. TESTS AND MEASURES
61. The answer is A. 62. The answer is D. 63. The answer is D. 64. The answer is D. 65. The answer is A. This statement is true. 66. The answer is D. 67. The answer is D. 68. The answer is C. 69. The answer is C. 70. The answer is D. 71. The answer is D. 72. The answer is C. 73. The answer is D. 74. The answer is C. 75. Occipital lobe. 76. Parietal lobe. 77. Temporal lobe. 78. The answer is A. 79. The answer is D. 80. The answer is C. 81. The answer is C. 82. The answer is D. 83. The answer is A. This statement is true. 84. The answer is A. This statement is true. 85. The answer is D. 86. The answer is C. 87. The answer is D. 88. The answer is D. 89. The answer is A. 90. The answer is A. 91. The answer is A.
CHAPTER 9. NEUROMUSCULAR PHYSICAL THERAPY
92. The answer is A. 93. The answer is A. 94. The answer is A. 95. The answer is C. 96. The answer is D. 97. The answer is A. 98. The answer is D. 99. The answer is B. 100. The answer is A.
671
Pulmonary Physical Therapy
ANATOMY AND PHYSIOLOGY The pulmonary or respiratory system (Fig. 10-1) is contained within a cage-like structure. The sternum, 12 pairs of ribs, the clavicle, and the vertebrae of the thoracic spine form the thoracic cage (Table 10-1). The primary function of the respiratory system is to exchange gases between tissue, the blood, and the environment so that arterial blood oxygen, carbon dioxide, and pH levels remain within specific limits throughout many different physiologic challenges. The pul monary system also plays a number of other roles including con tributing to temperature homeostasis via evaporative heat loss from the lungs; and filtering, humidifying, and warming or cooling the air to body temperature. This process protects the remainder of the res piratory system from damage caused by dry gases or harmful debris.! The respiratory system (Table 10-2) is arranged basically as an upside-down tree, which can be divided into two main portions!; • The conducting portion includes the upper airway (Table 10-3) and the lower airway (trachea, bronchi, and the bronchioles) Within this portion, air moves by bulk flow under the pressure gradients created by the respiratory muscles and the elastic recoil of the lungs. The left main bronchus branches at a more acute angle and is longer than the right main bronchus, which is more directly in line with the trachea. This relationship pre disposes to aspiration of material into the right rather than the left lung.! • The respiratory portion includes the terminal portion of the bronchial tree and alveoli, the site of gas exchange. 2 The total cross-sectional area rapidly increases at the respiratory zone. Forward velocity of air flow therefore decreases, and the gases readily move by diffusion through the alveoli into the pul monary capillaries.
I
ISfudY Pearl • External respiratiom
:~j~~sb::~en
tAeexc~ I
the atmosphere
I
• InternaJ·respiratiomthe eX€Daoge of gases between . the blood and the cellsoftMbocly.
Study Pearl • VMtilatioJ1 ; the . movement of air thrOl~ghtheconductlng airways (see Pu.lmonary System..Physiology later in this chapter}.
I
".R.thegasexchangewlthm •.e.Spirat.ioo.::ate.l'.ffi... u.. S~tO.d..e.scribe •.•· thebOdy~····
I
~--------------, I
Study Pearl
I
The.tr~J1siti{)nal·.zone'9()nSisting()fthe r~.8irat~IY bron~~i()les,separa.tes the
coo(iuctingang. r~piratoryportions.
673
674
SECTION II. TESTS AND MEASURES Primary bronchus
Conducting portion
Right lung
,
Lefllung
,
Bronchiole (1 mm or less in diameter)
Terminal bronchiole
:.~ Alveolar duct Respiratory portion
[)'h
N"."'=~ (termination of alveolar duct)
Figure 10-1. Schematic representation of the main divisions of the res piratory tract. (Reproduced, with permission, from Junqueira LC, Carneiro J. Basic Histology: Text and Atlas. 10th ed. New York: McGraw-Hili; 2003:349.)
TABLE 10-1. BONY ANATOMY OF mE mORACIC CAGE The sternum
The rib cage
Consists of three parts; the manubrium, the body, and the xiphoid process. The articulation between the manubrium and the sternum (the angle of Louis or sternal angle) is usually a symphysis. This structure serves to allow the pump-handle action of the sternal body during respiration. Formed by 12 pairs of ribs, each different from the others in size, width, and curvature, although they share some common characteristics. ~ Ribs 1 to 7 are considered to be true ribs, and have a single anterior costochondral attachment to the sternum. Approximately 32 structures attach to the first rib and body of Tl. ~ Ribs 8 to 10 are referred to as false ribs, as they share costochondral attachments before attaching anteriorly to the sternum. ~ Ribs 11 and 12 are termed floating or costovertebral ribs, as they have no anterior attachment to the sternum. Posteriorly, the 12 pairs of ribs articulate with the thoracic vertebrae. Based on the orientation of the joint axes of the thoracic vertebrae, movement of the upper ribs is primarily in an anterior and posterior direction (pump handle), whereas the transverse diameter increases for the lower ribs, allowing movement primarily in the medial-lateral direction (bucket handle). Attached to the entire interior of the thoracic cage is a thin sheet of cells, the pleura, which folds back on itself to form two completely enclosed sacs that cover the lungs.
CHAPTER 10. PULMONARY PHYSICAL THERAPY
675
TABLE 10-2. VENTILATION TERMINOLOGY TERM
DEFINITION
Air spaces Alveolar ventilation
Alveolar dead space Anatomical dead space Dead space ventilation Hyperventilation Hypoventilation Physiological dead space Pneumothorax Standard atmosphere Torr
Alveolar ducts, alveolar sacs, and alveoli The volume of gas per unit time that reaches the pulmonary alveoli; equal to the tidal volume minus the volume of dead space times the ventilation rate Represents those alveoli that are ventilated with fresh gas but not perfused by the pulmonary circulation Volume of the gas in the conducting areas of the respiratory system (eg, mouth and trachea) that does not come to the alveoli of the lungs The volume of gas per unit time that does not reach the respiratory portions, but instead remains in the airways Alveolar ventilation that is excessive in relation to metabolic rate; results in abnormally low alveolar CO2 , An alveolar ventilation that is low in relation to metabolic rate; results in abnormally high alveolar CO 2 , Combination of anatomical dead space and under ventilated or under perfused alveoli that do not contribute normally to blood-gas exchange Presence of gas in the intrapleural space (the space between the visceral and parietal pleurae), causing lung collapse A value intended to represent the mean atmospheric pressure at mean sea level at the latitude of Paris, France Unit of pressure defmed as 1/760 of an atmosphere (760 mm Hg = 760 torr)
Data from Van de Graaff KM, Fox 5I: Respiratory system, in Van de Graatl' KM, Fox 51 Ceds); Concepts ofHuman Anatomy and Physiology. New York, WeB/McGraw-Hill, 1999:72&-777.
LUNGS The lungs lie within the thoracic cavity, on either side of the medi astinum. The most superior aspect of each lung is called its apex. ~
Right lung: divided into three lobes (right superior, right mid
dle, and right inferior), separated by a series of oblique and
horizontal fissure lines. Each lobe is subdivided by connective
tissue into 10 independently functioning compartments, called
bronchopulmonary segments. 2 Each bronchopulmonary seg
ment is supplied by its own set of blood vessels and tertiary
bronchus (or segmental bronchus). Thus, if one becomes
infected or is damaged, other bronchopulmonary segments in
the same lobe may not be affected.
TABLE 10-3. STRUCTURES OF THE UPPER AIRWAY Nasal cavities
Serve as the entry point into the respiratory system. The upper airway is designed to filter and keep inspired air at 1000!o humidity and body temperature at 37 C (98.6 F). Air pockets located inside the bones that form the skull. They are located beneath the maxillary bone, the ethmoid bone, the frontal bone, and the sphenoid. The sinuses serve a number of functions induding redUcing the weight of the skull, protecting the face by deflecting the force of a direct blow to the sides, providing heat insulation for the base of the brain, creating resonance to the voice, facilitating facial growth and development, and aiding in smelling and breathing. The sinuses are lined with very fme hair-like projections called cilia, which function to move mucus (which is normally produced by the sinus) toward the ostium to allow drainage for the sinus. A fibromuscular tube that extends from the base of the skull to the lower border of the cricoid cartilage (at which point it becomes the esophagus). The pharynx serves a dual role, as it is used for both the respiratory and the digestive systems. The pharynx is divided by the soft palate into the nasopharynx, and the oropharynx. Formed by cartilage, ligaments, muscles, and mucous membrane, connects the pharynx to the trachea, and houses the vocal cords. The larynx protects the entrance to the lower respiratory passages (trachea, bronchi, and lungs) from food and foreign bodies by acting as a valve. Begins at the level of the cricoid cartilage of the larynx (approximately at the level of C6) and terminates as the carina, a ridge at the bifurcation of the trachea into left and right bronchi. Considered the differentiating structure between the upper and lower airways. Q
Sinuses
Pharynx
Larynx (voice box)
Trachea
Q
676
SECTION II. TESTS AND MEASURES
Study Pearl The lungs both secrete and absorb fluiqiR two anta.gonistic processes thatnQrmaHyleave only avery thin film offluid On the alveolar surface. SUrfa!Ce tension, created by the pres enceofthe interface between air in the ah/eol1and the watery alveolar tis SuetWhich is responsible for much of the lung's elastic recoil, is kept at an optirnallevel because ofa chemical
able.S,incesystoH\" theeprlm~l}' of'. secondary. d$ac~tands.ntl.
~ Prjlt)~ry~~~stole~g~~~~whenthe heiart'se~trIc~I.~rsternintri ns i." cally.fails.tg?en~rate
depotiarizatior)'x.
..
• •a • . vef)tfi~ular ..••.. . ••.••.•••.. . . .•.•. •. . •
~ seeon~ryasystole OCfJlr:~when
fa(j1:ors Qutside ofthe heart'selec,:. triq:lI conduction systemJesultina failt,tre to· generate anye.lectrjcal depolarization.
Study Pearl A com~nsatQry pause· i.stheduration of the.paus~ thatocCUfs,after an extrasystole.< (tI.ttectopi.cbeat that is, both prematu.rei,md cOnstantly Jelat~ to the previous, beat): ~ A. complete cOl1"lpensatqrypause" occurs when lnesum.of)thecolJ-< plinginteNaJ and .the. compensa tory pause' 15 equal to. twice the s{nus c:yCle< length. It. is. charact&is . tlcoLa.ve,ntrkular ectopic focus .thaf{ai1s it:) conduct retrogradely to tn~.atfialhence leaving the sinus nodeundistOrbed. ... }\flincomplete cOll1pensatqrypaU:~e arises. if thesi nus.oodeis dis~ha.rged early by the ectopic depolarisatj.on.. The pause "compensates" forlhepre maturity of. the extrasystol~i:mdthe. sinus rhythm resumes on schedule.
754
SECTION II. TESTS AND MEASURES
TABLE 11-6. ECG CHARACTERISTICS OF ABNORMAL CARDIAC RHYTHMS RHYTIIM
DESCRIPTION
Sinus bradycardia
A heart rate less than 60 bpm
Sinus tachycardia
A heart rate greater than 100 bpm
Premature atrial contraction (PAC)
Originate from areas of irritable, sometimes ischemic, myocardium that form the wall of the atrium. PACs are generally not as important as premature ventricular contractions: the loss of adequate filling and contraction of the atria associated with PACs are not as hemodynamically disruptive as premature contractions within the ventricles
Paroxysmal atrial tachycardia
Bouts of rapid, regular heart beats originating in the atrium that begin and end abruptly
Atrial flutter
An abnormal heart rhythm that occurs in the atria of the heart
Atrial fibrillation
Atrial fibrillation is characterized by multiple ectopic foci, or firing at random throughout the cardiac cycle with no single, unified wave of depolarization in the atria, and thus no organized myocardial contraction
Junctional rhythm
Cardiac rhythms arising from the atrioventricular (AV) junction
Accelerated junctional rhythm Ventricular tachycardia
A narrow complex rhythm that often supersedes a clinically bradycardic sinus node rate A run of three or more PVCs occurring sequentially; very rapid rate (1S0 to 200 bpm); may occur paroxysmally (abrupt onset); usually the result of an ischemic ventricle Chaotic activity of ventricle originating from multiple foci resulting in a pulseless, emergency situation reqUiring emergency medical treatment: cardiopulmonary resuscitation (CPR), defibrillation, medications A rapid heart rate for a person's age that is driven by a focus with abnormal automaticity within or immediately adjacent to the atrioventricular (AV) junction A premature beat arising from the ventricle; occurs occasionally in the majority of the normal population
Ventricular fibrillation
Junctional tachycardia
Premature ventricular contraction (PVC) Idioventricular rhythm
A slow independent ventricular rhythm under control of a ventricular center
Accelerated idioventricular rhythm
A form of ectopic or automatic ventricular arrhythmia usually noted in the acute care setting during cardiac rhythm monitoring
ECG CHARACTERISTIC P-wave rate < 60/min QRS rate < 60/min P-wave rate> 100/min QRS rate> 100/min P-QRS occurs earlier P-wave may be abnormal in shape/configuration QRS is normal P-R interval may be altered Incomplete compensatory pause P-wave rate: lSQ-2S0/min QRS rate: lSQ-2S0/min P-waves may be fused on T-waves Characterized by multiple P-waves to every QRS response P-wave rate: 2SQ-3S0/min (have a typical "sawtooth" pattern) QRS rate < P-wave rate Regular R-R interval 2:1, 3:1, 4:1 or variable AV block Absence of P-waves-fibrillatory baseline Fibrillatory rate> 3S0/min Irregular R-R interval QRS rate < P-wave rate P-wave may be inverted and before the QRS/buried in the QRS/after the QRS QRS rate: 40-60/min Regular R-R interval Findings as with junctional rhythm QRS rate: 6Q-lOO/min QRS rate> 100/min, regular (refer to ideoventricular rhythm for other characteristics) Coarse waviness of baseline Fine waviness of baseline No visible QRS complexes QRS rate: lOQ-lSO/min (See junctional rhythm characteristics earlier in this table) QRS duration> 0.10 sec T-wave is opposite polarity of QRS Complete compensatory pause No P-waves QRS rate: 20-40/min QRS duration: > 0.10 sec Regular R-R interval T-waves opposite polarity of QRS QRS rate: 4Q-lOO/min Refer to idioventricular rhythm characteristics
Data from, DeTurk WE, Cahalin LP: Electrocardiography, in DeTurk WE, Cahalin LP Ceds} Cardiovascular and pulmonary physical therapy: an eVidence-based approach. New York, McGraW-Hill, 2004:325--359.
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
Heart Blocks. Heart blocks occur when conduction from the SA node to the AV node gets altered, usually at the level of the AV node. Heart blocks are graded by levels of severity, from first-degree to third degree. A third-degree block is a complete heart block and usually requires the insertion of an artificial pacemaker. Dysrhythmias. The presence of any of the following dysrhythmias may prove potentially dangerous 9 ; ~
~ ~ ~ ~ ~ ~
~
Sinus rhythm with short episodes of ventricular tachycardia. Sinus rhythm with short episodes of paroxysmal supraventricu lar tachycardia. Accelerated junctional rhythms. Artificial pacemaker rhythm with premature ventricular con tractions that are new, multifocal, or couplets. Sinus rhythm with second-degree AV block. Atrial flutter or fibrillation with tachycardia ventricular rates. Sinus rhythm with sinus arrest. Sinus bradycardia with rates below 50 per minute.
The following dysrhythmias are associated with significantly altered hemodynamics 9 ; ~ ~
~ ~
Ventricular tachycardia (with pulses). Sinus rhythm or atrial fibrillation with complete heart block. VelY slow (40 per minute or below) sinus, junctional, or ideoventricular rhythms. Malfunctioning artificial pacemakers with ideoventricular rhythms.
Examination of Blood Pressure. The manual method of measuring blood pressure (BP) is commonly used by the phYSical therapiSt. While listening with a stethoscope placed over the brachial artery at the elbow, the clinician slowly inflates the blood pressure cuff until the sound of the artery is completely occluded. At this point, the clinician slowly releases the pressure in the cuff. At the point when the clinician begins to hear a "whooshing" or pounding sound (first Korotkoff sound-see Study Pearl) the pressure reading (systolic) is noted. The cuff pressure is further released until no sound can be heard (fifth Korotkoff sound). This is the diastolic blood pressure. Traditionally, the systolic blood pressure is taken to be the pres sure at which the first Korotkoff sound is first heard and the diastolic blood pressure reading is taken at the point at which the fourth Korotkoff sound is just barely audible. 19-24 However, there has recently been a move toward the use of the fifth Korotkoff sound (i.e., silence) as the diastolic blood pressure, as this has been felt to be more repro ducible. 25- 27 Relevance of Blood Pressure to Rehabilitation. Typically, systolic BP rises rapidly and diastolic pressure rises slightly during the first few minutes of aerobic exercise and then both level off. I •28 With resistance training, systolic BP rises more dramatically. High-level resistance training can cause rises in systolic BP that can be
755
Study Pearl ~
Bigeminy: defined as premature beats alternating regularly With nor ma.l beats. Bigeminy is either atrial or ventricular bigeminy, depending upon whether the alternating regu larpremature beats are atrial or ventricular. Bigeminy is generally considered pathologic, especially when symptomatic. Because the premature beats alternate regularly, bigeminy generally sounds like a regularly irregular heart rhythm. Bigeminy can be associated with hypoxia, ischemia, acute myocar dial infarction, and medication overdose. ~ Trigeminy; . . a type of .PVC pattern. The pvc follows very two normal QRS complexes. Possible causes are electrolyte. imbalances, hypoxia, ischemia, acute myocardial infarc tion, and medication toxicity.
756
SECTION II. TESTS AND MEASURES
Study Pearl Korotkoff sounds are the sounds that meclkal personpel listen for when they are· taking blood pressure. Korotkoff actually . described five phases of sounds: ... The first clear,· clear, rhythmic tap ping sound that gradually increases in intensity. This represents the high est . pressure in the arterial system during ventricular contraction and is recorded as the. systolic pressure (Fig. 11~3). The clinician should be alert for the presence of an auscul tatorygap, especially in patients with hypertension. 12 An ausculta tory gap is the temporary disappear ance of sound normaHy heard over the brachial artery between phase 1 and phase 2and may covera range of as much as 40 mm Hg.l'" Not identifying this gap may lead to an !,lnde.restimation of systolic pressure and overestimation of diastolic pressure. l l ... A murmur or swishing sound heard as the artery widens and more blood flows through the artery. This sound is heard for most of the time between the systolic and diastolic pressures. ... Sounds become crisp, more intense, and louder. ... The sound is distinct, abrupt muf fling; soft blowing quality. At pres sures within 10 mm Hg above the diastolic blood pressure (in children less than 13 years old, pregnant women, in patients with high car diac output or peripheral vasodila tion) the muffling sound should be used to indicate diastolic pressure, but both muffling (phase 4) and dis appearance (phase 5) should be recorded. ... The last sound that is heard.
I
harmful for individuals with pre-exIstmg hypertension or heart dis ease, and therefore loads should be kept lower in such patients. Aerobic exercise performed with the arms produces a greater rise in systolic and diastolic BP than lower-extremity exercise performed at the same intensity (as measured by percent of maximal oxygen uptake). Although exercise causes an acute increase in BP, regular sub maximal aerobic and resistance training do not cause long-term increases in resting BP but rather result in lowered BP for 2 to 3 hours after exercise, lowered resting BP, and blunting of the BP response to this form of exercise.
Exercise Tolerance Testing. Exercise tolerance testing (also known as graded [maximal or submaximal] exercise testing or stress test) is an important diagnostic and prognostic tool for assessing the ability of the cardiovascular system to accommodate increasing VOz in patients with suspected or known ischemic heart disease. The patient exercises through stages of increasing workloads, expressed in units of oxygen (Llmin, mLlkg/min), kcal, or metabolic equivalents (METs).z The two major goals of exercise testing are to detect the presence of ischemia and to determine the functional aerobic capacity of the indi viduaP Indications for this test include l ... Assessment of chest pain in patients with intermediate proba bility for coronary artery disease. ... Arrhythmia provocation. ... Assessment of symptoms (for example, presyncope) occurring during or after exercise. Contraindications for exercise tolerance testing include l ... ... ... ... ... ... ... ... ... ... ... ...
Acute myocardial infarction (within 4--6 days). Unstable angina (resting) pain in the previous 48 hours). Uncontrolled heart failure (atrial or ventricular dysrhythmias). Acute myocarditis or pericarditis. Acute systemic infection. Deep vein thrombosis. Uncontrolled hypertension (systolic blood pressure> 220 mm Hg, diastolic > 120 mm Hg). Severe aortic stenosis. Severe hypertrophic obstructive cardiomyopathy. Untreated life-threatening arrhythmia. Dissecting aneurysm. Recent aortic surgery.
Although exercise testing has been shown to have a sensitivity of 78% and a specificity of 70% for detecting coronary artery disease, it cannot be used to rule in or rule out ischemic heart disease unless the probability of coronary artery disease is taken into account. Z9- 33 In each of the following tests, the patient's pulse is recorded before and after the test to provide an estimate of oxygen consumption, the presence or absence of heart disease, or fitness level. Throughout the testing procedure the patient should be moni tored for
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY ~ ~
~
General appearance, including signs and symptoms of exercise intolerance. Unusual changes in heart rate. The heart rate should increase linearly in relation to woakload (workload is a reflection of oxygen consumption and hence energy use). During the test, an electrocardiogram machine or a halter monitor (Table 11-7) can be used to provide a continuous record of the heart rate, and the 12-lead electrocardiogram is recorded intermittently. The aim of the exercise is for the patient to achieve maximum predicted heart rate. Changes in blood pressure. Blood pressure must be measured before the exercise begins and at the end of each exercise stage. Blood pressure may fall or remain static during the initial stage of exercise. This is the result of an anxious patient relax ing. As the test progresses, however, systolic blood pressure should rise as exercise increases. A level of up to 225 mm Hg is normal in aduhs, although athletes can have higher levels. Diastolic blood pressure tends to fall slightly.
Numerous protocols for exercise tests, and other tests (Table 11-7), have been devised to assess cardiac responses to increased workloads.
Step Tests. ~
~
~
There are three traditional step tests 1 :
Master's two-step test: a test in which subjecl'i ascend and descend two steps, with specified dimensions for height and Width, in synchrony with a metronome. One-step test: consists of one step that is ascended and descended in such a way that the subject initially steps onto the step with the right foot and then brings the left foot onto the step. The right foot is then removed from the step and placed on the floor, which is followed by the left foot. The stepping sequence begins again, but the left foot is initially placed on the step followed by the right. This reciprocal sequence is per formed in synchrony with a metronome. Climbing step test: also utilizes standardized step heights in addition to standardized arm heights for climbing.
Cycle Ergometry Tests.
A number of standardized cycle ergom etry testing, with developed normal values, exist, but the most com mon appear to be the Astrand-Rhyming protocol,34-36 the YMCA pro tocol, and various ramping protocols.
Treadmill Tests. The Bruce exercise testing protocol is the most popular protocol for testing patients with known or suspected heart disease. The protocol has seven stages, each lasting 3 minutes, result ing in 21 minutes of exercise for a complete test. In clinical practice, patients rarely exercise for the full duration. However, completion of 9 to 12 minutes of exercise or reaching 85% of the maximum predicted change in heart rate is usually satisfactory.29-33 In stage 1, the patient walks at 1.7 mph (2.7 km) up a 10% incline. Energy expenditure is esti mated to be 4.8 METs (metabolic equivalents) during this stage. The speed and incline increase with each stage. A modified Bruce protocol (mini-Bruce) is used for exercise testing within 1 week of myocardial infarction.
757
Study Pearl ~ Normal adult BP:
< 120 mm Hg
systolic, < 80 mm Hg diastolic.
~ Prehypertension: 120 to 139 mm Hg
systolic, 80 to 89 mm Hg diastolic.
~ Hypertension (primary or secondary): Stage one: 140 to 159 mm Hg sys tolic, 90 to 99 mm Hg diastolic. Stage two: greater than or equal to 160 mm Hg systolic, greater than or equal to 100 mm Hg diastolic. ~ Normal pediatric BP: Infants less than 2 years: 106 to 110 mm Hgsystolic, 59 to 63 mm Hg diastolic. Chiidren 3 to 5 years: 113 to 116 mm Hg systolic, 67 to 74 mm Hg diastolic.
L
Study Pearl The symptoms of exercise intoler ance include persistent dyspnea, complaints of vertigo, chest pain, and leg cramps (claudication). ~ The signs of exercise intolerance include incoordination, ataxia, confusion, pallor, cyanosis, and abnormal diaphoresis. ~
L
758
SECTION II. TESTS AND MEASURES
TABLE 11-7. CARDIAC DIAGNOSTIC TESTING AND MONITORING TEST
~ DESCRIPTION
tic:
C(
Holter monitor
Exercise gated blood pool scan, exercise MUGA, or exercise radionuclide angiography
Event recorder
Thallium scans or myocardial perfusion scans
Positron emission tomography (PET) scan PET F-18 FDG (fluorodeoxyglucose) scan Radionuclide angiography
Technetium 99m scanning (hotspot imaging) Thallium-201 myocardial perfusion imaging (cold spot imaging) Cardiac catheterization
A small, portable, battery-powered ECG machine worn by a patient to record heartbeats on tape over a period of 24 to 48 hours during normal activities. At the end of the time period, the monitor is returned to the physician's office so the tape can be read and evaluated.
A nuclear scan to see how the heart wall moves and how much blood is expelled with each
heartbeat, just after the patient has walked on a treadmill or ridden on a stationary bike.
Resting First Pass The scan taken while the patient is at rest to measure the percentage of blood going through the heart with each beat. Exercise First Pass The scan taken while the patient is exercising to measure the percentage of blood going through the heart with each beat. A small, portable, battery-powered machine used by a patient to record ECG over a long period of time. Patients may keep the recorder for several weeks. Each time symptoms are experienced, the patient presses a button on the recorder to record the ECG sample. As soon as possible, this sample is transmitted to the physician's office by telephone hookup for evaluation.
fu 'i
s,., P
dJ
'1
d
3l
I c o
Resting SPECf Thallium Scan or Myocardial Perfusion Scan A nuclear scan given while the patient is at rest that may reveal areas of the heart muscle that are not getting enough blood.
e a II 3
Exercise Thallium Scan or Myocardial Perfusion Scan A nuclear scan given while the patient is exercising that may reveal areas of the heart muscle that are not getting enough blood.
•
Persantine Thallium Scan or Myocardial Perfusion Scan A nuclear scan given to a patient who is unable to exercise to reveal areas of the heart muscle that are not getting enough blood. Chemicals injected include dipyridamole thallium (thallium-201, a potent vasodilator) and dobutamine. A nuclear scan that gives information about the flow of blood through the coronary arteries to the heart muscle. A glucose scan sometimes done immediately after the PET scan to determine if heart muscle has permanent damage. Red blood cells tagged with a radionuclide are injected into the blood; ventricular wall motion can be evaluated and the ejection fraction determined; abnormal blood flow with valve and congenital defects can also be detected; techniques include gated-pool equilibrium studies and first-pass techniques. Technetium 99m injected into the blood is taken up by damaged myocardial tissue; this identifies and localizes acute myocardial infarctions. This radioisotope is readily available, and its short half-life reduces handling problems and patient exposure. Thallium-201 injected into the blood at peak exercise; scanning identifies ischemic and infarcted myocardium, which does not take up thallium-201; used to diagnose coronary artery disease and perfusion, particularly when ECG is equivocal. The passage of a tiny tube into heart via blood vessels with the introduction of a contrast medium into coronary arteries, which is then visualized with cinefluoroscopy to evaluate narrowing or occlusion of arteries. ~ Provides information about anatomy of heart and great vessels, ventricular function, car diac output, and abnormal wall movement. ~ Allows determination of intracardiac, transvalve, pulmonary artery pressures, ejection frac tion (EF), and blood gas pressures.
Data from Rothstein JM, Roy SH, Wolf SL: Perceptual and communication problems in hemiplegia. In The Rehabilitation Specialists Handbook. Philadelphia: FA Davis, 1991:548-550, and Warren]V and Lewis RP: Diagnostic procedures in Cardiology: A clinician's gUide. Year Book Medical Publishers, Chicago, 1985.
e
c Ii
iJ (
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
Walk Tests. Walk tests have been used extensively in the examina tion of patients with heart failure. Although the 6-minute walk test is considered submaximal, it appears to provide information about the functional status, exercise tolerance, oxygen consumption, and sur vival of persons with cardiac pump failure. Special Tests Percussion Test. The percussion test is used to determine the com petence of the greater saphenous vein. While the patient is standing, the clinician palpates one segment of the vein while percussing the vein at a point approximately 20 cm higher. If a pulse wave is felt by the lower hand, an assumption can be made that the intervening valves are incompetent.
Trendelenburg Test. The Trendelenburg test (retrograde filling test) can be used to determine the competence of the communicating veins of the saphenous system. The patient is positioned supine with the legs elevated to 60 degrees. A tourniquet is placed on the proximal thigh and the patient is then asked to stand. The clinician assesses whether the veins fill in a normal pattern. The filling should take approximately 30 seconds. Rubor of Dependency. The rubor of dependency is a test of periph eral arterial circulation patency. The clinician assesses whether changes in skin occur during elevation of foot followed by placing the limb in a position of dependency (seated, hanging position). With insufficiency, pallor develops in elevated position; relative hyperemia (rubor of dependency) develops in dependent position.
Diagnostic Tests Left Heart Catheterization/Coronary Angiogram. This proce dure involves insertion of a catheter into a major artery (often the femoral or radial artery) and advancing it retrograde through the aorta until it reaches the left ventricle. The catheter may then proceed into the LV and is used to measure hemodynamic pressures during systole and diastole to examine LV function (ejection fraction). The angiogram component involves injecting a radiopaque dye into the ostium of each coronary artery, observing blood flow through each of the arteries to determine the presence of lesions or blood flow obstructions. 2
Duplex Ultrasonography. Duplex ultrasonography is the study of choice for the evaluation of venous insufficiency syndromes. Color flow duplex imaging uses the Doppler information to color code a two dimensional sonogram. On the image, red indicates flow in one direc tion (relative to the transducer) and blue indicates flow in the other direction-the shade of the color may reflect the flow velOCity (in the Doppler mode) or the flow volume (in the power Doppler mode). Magnetic Resonance Venography. Magnetic resonance venogra phy (MRV) is the most sensitive and specific test for the assessment of deep and superficial venous disease in the lower legs and pelvis, areas not accessible with other modalities. MRV is particularly useful because it can help in the detection of previously unsuspected nonvascular causes of leg pain and edema when the clinical presentation erro neously suggests venous insufficiency or venous obstruction.
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SECTION II. TESTS AND MEASURES
Direct Contrast Venography. Direct contrast venography is a labor intensive and invasive imaging technique. In most centers, duplex sonography has replaced direct contrast venography in the routine evaluation of venous disease. Physiologic Tests of Venous Function. Physiologic tests of venous function are important in assessing the cause and severity of venous insufficiency. The physiologic parameters most often measured are the venous refilling time (VRD, maximum venous outflow (MVO), and calf muscle pump ejection fraction (MPEF). Venous Refilling Time (VRT). The VRT is the time necessary for the lower leg to become suffused with blood after the calf muscle pump has emptied the lower leg as thoroughly as possible. Maximum Venous Outflow (MVO). The MVO test is used to detect an obstruction to venous outflow from the lower leg, no matter what the cause. Its results are a measure of the speed with which blood can flow out of a maximally congested lower leg when an occluding thigh tourniquet is suddenly removed. The advantages of MVO testing are that it is a functional test rather than an anatomic test, and it is sensitive to significant intrinsic or extrinsic venous obstruction due to any cause at almost any level. Calf Muscle Pump Ejection Fraction (MPEF). The MPEF test is used to detect failure of the calf muscle pump to expel blood from the lower leg. The patient is asked to stand on his or her tiptoes 10 to 20 times or to dorsiflex the ankle. The change in a physical parameter that reflects the blood volume in the calf is recorded as the calf muscle is pumped. Doppler Ultrasound. Examination uses an ultrasonic oscillator con nected to earphones. Dependent blood flow within a vessel is meas ured, useful in both venous and arterial disease. The Doppler probe is placed over a large vessel, an ultrasound signal is given transcuta neously, and movement of blood causes an audible shift in signal frequency. The test is useful in locating nonpalpable pulses and measuring systolic BP in extremities. Air Plethysmography (APC). Pneumatic device calibrated to measure patency of venous system and volume. 1. Cuff inflated around calf, attached to a pressure transducer
and microprocessor. 2. Occludes venous return, permits arterial inflow; recorder reg isters increasing volume with cuff; time to return to baseline with cuff deflation. 3. Comparison tests performed in sitting, standing, and up on tiptoes.
Chest Radiograph. Can help to determine the presence of lung fluid abnormalities, and the overall shape and size of the heart. Myocardial Perfusion Imaging. Used to diagnose and evalu ate ischemic heart disease, myocardial infarction (Table 11-7).
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
761
Continuous Hemodynamic Monitoring (Swan-Ganz Catheter). Catheter inserted through vessels into right side of heart. Measures central venous pressure (CVP), pulmonary artery pres sure (PA), and pulmonary capillary wedge pressure (PCWP).
Echocardiography. A technique involving the use of ultrasonic sound waves to create a moving picture of the heart. Two types are commonly used: 1. Transthoracic (TfE): used to evaluate left ventricular systolic function and the structure and function of the cardiac walls, valves, and chambers. 2. Transesophageal (TEE): used in cases when the TIE image is unclear due to a barrel chest, congestive obstructive pul monary disease, or obesity. The patient's esophagus is anaesthetized and a modified gastroscopy probe is inserted. On the end of the scope is an ultrasonic device that is guided down to the lower part of the esophagus, where it is used to obtain a clear two-dimensional echocardiogram of the heart.
Electrocardiogram (ECG). A 12-lead ECG provides informa tion about rate, rhythm, conduction, areas of ischemia and infarct, hypertrophy, and electrolyte imbalances. An ECG is constructed by measuring electrical potential between 12 different points of the body using a galvanometer. The 12 leads measure the average electrical activity generated by the summation of the action potentials of the heart at a particular moment in time. Laboratory Tests and Values Enzyme Studies. Cardiac enzyme studies measure the levels of the enzymes troponin (TnI, TnT) and creatine phosphokinase (CPK, CK) in the blood. The values listed in the tables can be used as a general guide (see Tables A-4 to A-6 in the Appendix). Lipid Profile. A group of tests often ordered together to help deter mine coronary risk based on target levels. The lipid profile includes total cholesterol, HDL-cholesterol (often called good cholesterol), LDL cholesterol (often called bad cholesterol), and triglycerides. An LDL/HDL ratio is sometimes also included. The values listed below can be used as a general guide. ~ ~ ~
~
~
Cholesterol: desirable, < 200; borderline, 200 to 230; high-risk, > 240. High-density lipoprotein (HDL): low risk (negative risk factor), > 60; moderate risk, 35 to 60; high-risk, < 35. Low-density lipoprotein (LDL): < 100 with heart disease or diabetes, >100 with multiple risk factors, >160 for low-risk individuals. Triglycerides: desirable, > 165. LDL/HDL ratio: low risk, 0.5 to 3.0; moderate risk, 3.0 to 6.0; high risk, > 6.0.
Study Pearl To manuallycakulate the ventricular rate using ahECGstrip, the clinician shOUld count the number of intervals betweeoQRScomplexes itl a 6-second strip and multiply by 10. The normal sinus rhythm consists of ~ A P-waveata rate of 60 to l00/min. ~ AQRS rate of 60 to l00lmin. ~ A P-wave before every QRS complex. ~ A regular p.p interval. ~ A regular R-R interval.
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SECTION II. TESTS AND MEASURES
CARDIOVASCULAR CONDITIONS RISK FACTORS ASSOCIATED WITH CARDIOVASCULAR DYSFUNCTION Physical therapists often examine and treat patients with one or more chronic medical conditions that are the inherent causes of depend ence, dysfunction, and disability, and/or increase the risk of other pathologic conditions 37 .38 . ~
Co-morbidity: • Atherosclerosis: a major contributing factor to coronary heart disease, including angina pectoris and myocardial infarction. 39 • Hypertension: causes mechanical damage to vascular endothelium, resulting in areas that are stripped of normal endothelial cells. Associated with increased thrombus and plaque formation, intracerebral aneurysms and hemorrhage, and left ventricular hypertrophy.4o,41 • Hyperlipidemia (high blood cholesterol). 42 • Diabetes: a complex mix of physiologic abnormalities that accelerates the development of atherosclerosis and leads to many cardiovascular complications. 43--45 • Osteoporosis: can be associated with classic spinal defoffi1ities including increased kyphosis with loss of height, thoracic ver tebral body fractures, back pain, and decreased vital capacity. • Ankylosing spondylitis: pulmonary involvement including nonspecific fibrosis, dilated bronchi, stiffening and straight ening of the spine, and decreased intestinal compliance, the latter of which increases the potential for pneumothorax, atelectasis, and aspiration. • Idiopathic scoliosis: the lateral curve plus the rotation of the involved thoracic vertebrae around a vertical axis causes a decrease in lung function. • Pectus deformities: includes pectus excavatum (funnel chest) and pectus carinatum (pigeon breast). • Sarcoidosis: a systemic disease that primarily affects the lungs and the lymphatic system. • Systemic lupus erythematosus: affects the pulmonary system more frequently than any other collagen vascular disease. Can be associated with pleuritis, pneumonitis, pulmonary interstitial fibrosis, and pulmonary hypertension. • Neurologic disease: 'J Cerebrovascular accident: cardiovascular disease is the most common cause of death in long-term survivors of stroke (refer to Chapter 14).46--49 o Spinal cord injury: stimulation of the cardiopulmonary sys tem is impaired due to lack of innervation to the autonomic nervous system, thereby reducing the ability to support higher rates of aerobic metabolism. 50 ,51 o Multiple sclerosis: the loss of myelin reduces the speed of nerve conduction, thus interfering with smooth, rapid, and coordinated movement. 52 o Parkinson's c1i"ease: asscx:iated with bradykinesia, slow and shuf fling gait, freezing, kyphotic posture, and overall flexed posture.53
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY ~
~
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Medications: aspirin resistance may increase the risk of major adverse cardiac events (MACE) more than threefold in patients with stable coronary artery disease (CAD).54 Lifestyle: cigarette smoking substantially increases the risk for cardiovascular disease in addition to other diseases, notably chronic obstructive pulmonary disease and lung cancer. 55 Obesity: many of the effects of obesity appear to be medi ated through other risk factors including diabetes and hypertension. 56 Physical inactivity: physical inactivity may exert much of its influence through other risk factorsY However, numerous public health and medical associations have identified physical inactivity as a significant risk factor for cardiovascular and other diseases. 58 Race: African-American women have the highest risk of death from heart disease; Native Americans, particularly those living in North and South Dakota, also have a higher risk. 59 Gender: CAD is the number one killer of women, surpassing all forms of cancer, including breast cancer, combined. 60 At the onset of menopause, the CAD risk for women begins to approach that of men. 60 •61 Family history: family history is considered positive if myocar dial infarction or sudden cardiac death occurred in a primary male relative age 55 or less, or in a primary female relative age 65 or less. 62 Psychosocial factors: an individual's response to stress can be a determinant factor in the development of CAD. Depression, social isolation, and chronic stress have all been shown to be associated with CAD. 63
PERIPHERAL ARTERIAL AND VASCULAR DISEASE
Arterial Disease Arteriosclerosis. Arteriosclerosis is a group of diseases characterized by thickening and loss of elasticity of the arterial wall, often referred to as hardening of the arteries. Arteriosclerosis can be divided into three types: ~
~
~
Atherosclerosis: plaques of fatty deposits form in the inner layer (intima) of the arteries (see "Coronary Artery Disease" later in the chapter). Monckeberg's arteriosclerosis: involves the middle layer of the arteries with destruction of muscle and elastic fibers and for mation of calcium deposits. Arteriolosclerosis or arteriolar sclerosis: characterized by thick ening of the walls of small arteries (arterioles).
Arteriovenous Malformations. Arteriovenous malformations (AVM) are congenital vascular malformations of the cerebral vasculature-the result of localized maldevelopment of the primitive vascular plexus. AVMs vary in size and location and therefore in clinical presentation. Early diagnosis can reduce the chance of hemorrhage. Aneurysm. An aneurysm is an abnormal stretching in the wall of an artery, a vein, or the heart with a diameter that is at least 50% greater
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SECTION II. TESTS AND MEASURES
than normal. 18 Aneurysms are named according to the specific site of formation. Aortic aneurysms can form a thoracic aneurysm (involving the ascending, transverse, or first half of the descending portion of the
aorta), or an abdominal aneurysm (involving the aorta between the renal arteries and iliac branches). The underlying causes of aortic aneurysms are associated with many factors, including atherosclerosis, hypertension, medial degeneration and aging, aortitis, congenital abnormalities, trauma, smoking, cellular enzyme dysfunction, and hyperlipidemia. 64 Acute aortic dissection is characterized by the onset of intense pain, described as sharp, tearing, or stabbing. The pain occurs in the chest and spreads toward the back and into the abdomen. The pain associated with this condition is unaffected by position. Distal pulses frequently are decreased or absent. This is a potentially life-threatening condition requiring irrunediate transport of the patient to an emergency department. 64
Study Pearl The difft1rential,diagnosis of paresthe~ siasilnd peripheral neuropathyisdiffi cult. Peripheral neuropathies can be caused byentrapmenlsyndrornes, trauma,diabetes, hypothyroidism, vita min B12 defideru::¥1 alcohol ism,i(lfIam matory conditions, connective tissue disorders,toxic injury, hereditary con ditions, malignancy,.· infections,. and miscellaneous calJSeS.65 Peripheral neuropathy can also be mimicked by myelopathy, syringomyelia, or dorsal column disorders such as tabes dorsa.fis.66 Hysterical symptoms can sometimes. mimica neuropathy; Many medications can cause a peripheral heuropathy (Table 11-8}.66
Arteritis. Arteritis (giant cell arteritis, cranial or temporal arteritis) is a vasculitis primarily involving multiple sites of temporal and cranial arteries. Early diagnosis is important to prevent blindness.
Thromboangiitis Obliterans. Thromboangiitis obliterans (Buerger's disease) is a chronic, inflarrunatory vasculitis affecting the peripheral blood vessels (small arteries and veins), which occurs corrunonly in young adults, largely male, who smoke heavily. There is a risk of ulcer ation, gangrene and amputation if left untreated. The condition usually progresses proximally in both upper and lower extremities, accompa nied by a thrombus formation and vasospasm. Patients exhibit paresthesias or pain, cyanotic cold extremity, diminished temperature sensation, and fatigue (intermittent claudica tion) due to occlusion of the arteries. Intervention includes cessation of smoking and avoidance of any environmental or second-hand smoke inhalation, pharmacologic inter vention (vasodilators, pain relieD, and physical or occupational therapy. Diabetic Angiopathy. Diabetic angiopathy is an inappropriate ele vation of blood glucose levels and accelerated atherosclerosis if untreated. Complications include neuropathy and/or neurotrophic ulcers, the latter of which may lead to gangrene and amputation. Raynaud's Disease. Raynaud's disease or phenomenon results in intermittent spasms of small arteries and arterioles, causing temporary pallor and cyanosis of the digits, usually exacerbated by exposure to cold or emotional stress. .. Abnormal vasoconstrictor reflex results in pallor, cyanosis, numbness, and tingling of digits (fingertips more often than toes). .. Affects largely females. .. Occlusive disease is not usually a factor.
Hypertension. Hypertension (hypertensive vascular disease; see Chapter 14) includes, hypertensive heart disease, pulmonary hyper tension (see Chapter 10), and pulmonary heart disease.
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CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
765
TABLE 11-8. MEDICATIONS THAT MAY CAUSE NEUROPATHIES AXONAL Vincristine (Oncovin, Vincosar PFS) Paclitaxel (Taxo!) Nitrous oxide Colchicine (Probenecid, Col-Probenecid) Isoniazid (Laniazid) Hydralazine (Apresoline) Metronidazole (Flagy!) Pyridoxine (Nestrex, Beesix) Didanosine (Videx) Lithium Alfa interferon (Roferon-A, Intron A, Alferon N) Dapsone Phenytoin (Dilantin) Cimetidine (Tagamet) Disulfiram (Antabuse) Chloroquine (Aralen) Ethambutol (Myambuto!) Amitriptyline (Elavil, Endep)
DEMYELINATING
NEURONOPATHY
Amiodarone (Cordarone) Chloroquine Suramin (Fourneau 309, Bayer 205, Germanin) Gold
Thalidomide (Synovir) Cispla tin (Platino!) Pyridoxine
Data from Masson C, Boulu P, Henin D. Les neuropathies iatrogenes. Rev Med Interne ]992;]3(3):225-32.
Data from Poncelet AN: An algorithm for the evaluation of peripheral neuropathy. Am Fam Physician ]998;57:755--64.
Hypotension. Blood pressure that is too low is known as hypotension. Low blood pressure may be a sign of severe disease and requires more urgent medical attention. When blood pressure and blood flow are very low, the perfusion of the brain may be critically decreased (Le., the blood supply is not sufficient), causing light headedness, dizziness, weakness, and fainting. Sometimes the blood pressure drops significantly when a patient stands up from sitting orthostatic hypotension (see next section). Other causes of low blood pressure include ~
~
~ ~ ~
Sepsis. Hemorrhage. Toxins including toxic doses of blood pressure medicine. Hormonal abnormalities, such as Addison's disease. Shock. Shock is a complex condition that leads to critically decreased blood perfusion. The usual mechanisms are loss of blood volume, pooling of blood within the veins reducing ade quate return to the heart, and/or low effective heart pumping. Low blood pressure, especially low pulse pressure, is a sign of shock and contributes to/reflects decreased perfusion.
Orthostatic Hypotension. Orthostatic hypotension is associated with an extreme drop in blood pressure--the primary cause is a decreased compensatory vasoconstriction, especially in the large vascular beds (skeletal muscle and splanchnic regions) in association with venous pooling in the lower extremities, which reduces venous blood return, stroke volume, and blood pressure. Orthostatic hypotension can be clas sified as neurogenic (dysfunction of the autonomic nervous system, such as that which can be associated with a spinal cord injury or post cere brovascular accident), non-neurogenic (low blood volume in patients who are postoperative or dehydrated), or iatrogenic (e.g., caused by medication, such as antihypertensive medications) (Table 11_9).14
Study Pearl Activities that may increase the chanceoforthostatlc hypotension, such as application of heat modalities, hydrotherapy,. pool therapy, moderate to vigorous exerdseusing the large muscles, sudden changes of position, I :nd stationary standing,shoutd· be Lvoided in susceptible patier1ts. 14
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SECTION II. TESTS AND MEASURES
TABLE 11-9. ETIOLOGIES AND DRUGS THAT CAN CAUSE ORTIiOSTATIC HYPOTENSION NON-NEUROGENIC ETIOLOGIES Cardiac pump failure Aortic stenosis Bradyarrhythmia Myocardial infarction Myocarditis Pericarditis Tachyarrhythmia Reduced intravascular volume Adrenal insufficiency Burns Dehydration Diabetes insipidus Diarrhea Hemorrhage Salt-losing nephropathy Straining with heavy lifting, urination, or defecation
Vomiting
Venous pooling Alcohol consumption Fever Heat (e.g., hot environment, hot shower or bath) Postprandial dilation of splanchnic vessel beds Prolonged recumbency or standing Sepsis Vigorous exercise with dilation of skeletal vessel beds
NEUROGENIC ETIOLOGIES
MEDICATIONS
Spinal cord problems Syringomyelia Tabes dorsalis Transverse myelitis Tumors Peripheral nervous system problems HN/AIDS Alcoholic polyneuropathy Amyloidosis Diabetes mellitus Dopamine beta-hydroxylase deficiency Guillain-Barre syndrome Paraneoplastic syndrome Renal failure Vitamin Bll or folate deficiency Other neurogenic etiologies Brainstem lesions Brain tumors Carotid sinus hypersensitivity Cerebral vascular accidents Dysautonomias Multiple sclerosis Neurocardiogenic syncope Parkinson's disease Pure autonomic failure Sepsis syringobulbia
Alpha- and beta-blockers Antihypertensives Bromocriptine (Parlodel) Diuretics Insulin MAO inhibitors Marijuana Minor tranquilizers Narcotics/sedatives Nitrates Phenothiazines Sildenafil (Viagra) Sympatholytics Sympathomimetics (with prolonged use) Tricyclic antidepressants Vasodilators Vincristine (Oncovin)
Instances of orthostatic hypotension should be. reported to >the patient's physician because of its association with severa' diagnoses and conditions, including an increased rate of falls and a history of'myocardial infarction or transient ischemic attack; it a!~ may be predictive of ischemic stroke..
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Orthostatic hypotension has been observed in all age groups, but it occurs more frequently in the elderly, especially in persons who are sick and frail. In cases of suspected orthostatic hypotension, the clini cian should position the patient in the supine position, take a blood pressure measurement, and then repeat the blood pressure measure ment at 1 and 3 minutes after the patient assumes a standing or sitting position. Intervention strategies for orthostatic hypotension include pro gressive elevation of the head of the bed, deep breathing, dangling one extremity over the edge of the bed, progressive sitting on the edge of the bed with active lower-extremity exercise, and progressive sitting out of bed with the lower extremities progressed to a dependent posi tion. 67 Elastic stockings should be worn over the lower extremities. 67 Elevating the head of the bed by 5 to 20 degrees dUring sleep also is recommended. 67
Venous Insufficiency. Venous insufficiency syndromes are caused by valvular incompetence in the high-pressure deep venous system, low-pressure superficial venous system, or both. Physical examination alone is not a reliable means of assessing the venous sys tem--diagnostic testing nearly always is necessary to rule out deep venous obstruction, to assess the paths of reflux, and to guide treatment
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
planning. The Trendelenburg test (see "Special Tests" earlier in the chapter) is traditionally part of the physical examination and may be helpful in making the differential diagnosis.
Deep Venous Insufficiency. Deep venous insufficiency occurs when the valves of the deep veins are damaged as a result of deep venous thrombosis (DVT)-see "Deep Vein Thrombophlebitis" later in the chapter. With no valves to prevent deep system reflux, the hydro static venous pressure in the lower extremity increases dramatically. This condition is often referred to as a post-phlebitic syndrome. Superficial Venous Insufficiency. Superficial venous incompe tence is the most common form of venous disease. In superficial venous insufficiency, the venous blood escapes from a normal deep system and flows backward through dilated superficial veins in which the valves have failed after a single point of high-pressure leakage develops. High pressure causes secondary valve failure when otherwise nor mal superficial veins become so widely dilated that the thin flaps of the venous valves can no longer make contact in the lumen of the vessel. Over time, these incompetent superficial veins become visibly dilated and tortuous, at which point they are recognized as varicose veins.
Klippel-Trenaunay-Weber Syndrome. A less common cause of venous insufficiency is Klippel-Trenaunay-Weber (KTW) syn drome, which involves port-wine stains, varicose veins, and bony or soft-tissue hypertrophy. High pressure can enter the superficial veins as a result of the failure of key valves at any point of communication between the deep system and the superficial system. Patients with venous insufficiency often report subjective symp toms that are typically bothersome early in the disease, become less severe in the middle phases, and then worsen again with advancing age. Common symptoms include the following: ~
~ ~ ~
~ ~
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Burning. Swelling. Throbbing. Cramping. Aching. Heaviness. Restless legs. Leg fatigue.
Pain caused by venous insufficiency often is improved by walking or by elevating the legs.
Thrombophlebitis. Microscopic thrombosis is a normal part of the dynamic balance of hemostasis. There are two types of venous thrombosis: superficial vein thrombophlebitis and deep vein throm bophlebitis. Superficial vein thrombophlebitis and deep vein throm bophlebitis share the same pathophysiology, pathogenesis, and risk factors. Superficial Vein Thrombophlebitis. Superficial vein throm bophlebitis may occur spontaneously or as a complication of medical
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Study Pearl
I
Perthes percussive test can be used to test whether venous segments are interconnected. With the patient in a standing position, a vein segment is tapped at one location while an exam ining hand feels for a pulse wave at another location. Propagation of a pal pable pulse wave suggests that a fluid filled vessel with open or incompetent valves connects the two locations.
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Patients Who undergo total hip arthro plasty or total knee arthroplasty are at high risk for DVT. If no prophylaxis is used, DVT occurs in 40% to 80% of these... pat;ents, and the prox;mal DVT ~ccurs in 15% to 50%.73
or surgical interventions. Patients with superficial thrombophlebitis often give a history of a gradual onset of localized tenderness, followed by the appearance of an area of erythema along the path of a superfi cial vein. There may be a history of local trauma, prior similar episodes, varicose veins, prolonged travel, or enforced stasis. Swelling may result from acute venous obstruction (as in deep vein thrombosis) or from deep or superficial venous reflux, or it may be caused by an unrelated disease condition such as hepatic insufficiency, renal failure, cardiac decompensation, infection, trauma, or environmental effects. Palpation of a painful or tender area may reveal a firm, thickened, thrombosed vein. Duplex ultrasound is the initial diagnostic study of choice for most patients with signs and symptoms of phlebitis. Graduated compression stockings have been proven effective in the prophylaxis of thromboembolism and are also effective in prevent ing progression of thrombus in patients who already have superficial phlebitis or actual DVT and PE. 6&-71
Deep Vein Thrombophlebitis. Deep venous thrombosis (DVT) and its sequela, pulmonary embolism, are the leading causes of preventa ble in-hospital mortality in the United States. 72 The Virchow triad, as first formulated (i.e., venous stasis, vessel wall injury, hypercoagulable state), is still the primary mechanism for the development of venous thrombosis. 72 Hypercoagulable states include ~ ~
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No single physical finding or combi nation of symptoms and signs is suffi ciently accurate to establish the diagof DVT.72 ~
LSiS
Genetic: includes antithrombin C deficiency, protein C defi ciency, and protein S deficiency. Acquired: includes postoperative, postpartum, prolonged bed rest or immobilization, severe trauma, cancer, congestive heart failure, obesity, and prior thromboembolism.
The signs and symptoms of DVT are related to the degree of obstruction to venous outflow and inf1ammation of the vessel wall. The following is a list outlining the most sensitive and specific physical findings in DVT72.74-76: ~ ~
~
~
Edema, principally unilateral. Tenderness, if present, is usually confined to the calf muscles or over the course of the deep veins in the thigh. • Pain and/or tenderness away from these areas is not consis tent with venous thrombosis and usually indicates another diagnosis. Homans' sign. • Discomfort in the calf muscles on forced dorsiflexion of the foot with the knee straight has been a time-honored sign of DVT. However, this sign is found in more than 50% of patients without DVT and is present in less than one-third of patients with confirmed DVT, making it very nonspecific. Venous distension and prominence of the subcutaneous veins. • Patients with superficial thrombophlebitis without coexisting varicose veins and with no other obvious etiology (e.g., IV catheters, IV drug abuse, soft-tissue injury) are at high risk because associated DVT is found in as many as 40% of these patients. Patients with superficial thrombophlebitis extending to the saphenofemoral junction are also at higher risk for associated DVT.
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY ~
Fever: Patients may have a fever, usually low grade. High fever is usually indicative of an infectious process such as cellulitis or lymphangitis.
Prophylaxic treatment of DVT includes medication (heparin, war farin, aspirin, and dextran) and the use of mechanical modalities such as external pneumatic compression devices and compression stockings.
KA WASAKI
DISEASE
Kawasaki disease is an acute febrile illness associated with systemic vasculitis (see Chapter 16),77 HEART FAILURE
Heart failure is the pathophysiologic state in which the heart fails to pump blood at a rate commensurate with the requirements of the metabolizing tissues,78 In patients with heart failure, exercise tolerance is limited by an inadequate cardiac output response because of a reduction in both stroke volume and heart rate. Alterations in gas exchange also limit exercise tolerance in this patient population. Fluid accumulation in the lungs results in abnormal gas exchange and can cause shortness of breath. Patients with heart failure also have more vasoconstriction at rest because of elevated sympathetic tone, which further limits the delivery of oxygenated blood to the muscles.
Congestive Heart Failure. Congestive heart failure (CHF) can be categorized as forward or backward ventricular failure: ~ ~ ~
Forward ventricular failure is secondary to reduced forward flow into the aorta and systemic circulation. Backward failure is secondary to elevated systemic venous pressure. Heart failure can also be subdivided into systolic and diastolic dysfunction. • Systolic Cleft heart) failure: decrease in stroke volume, which leads to activation of peripheral and central baroreflexes and chemoreflexes that are capable of eliciting marked increases in sympathetic nerve activity. This in turn produces a tempo rary improvement in systolic blood pressure and tissue per fusion. Signs and symptoms of left-sided heart failure include progressive severity of (1) exertional dyspnea, (2) orthopnea, (3) paroxysmal nocturnal dyspnea, (4) dyspnea at rest, and (5) acute pulmonary edema (termed congestive heart failure).
Systolic failure can be further categorized as ischemic or non
ischemic heart failure:
Ischemic: the breakdown of the heart muscle because of lack
of blood flow to the coronary vessels that may occur with or
without myocardial infarction.
Results from any process other than coronary artery disease. (CAD).
• Diastolic (right heart) failure: a decrease in stroke volume with the same outcome as with systolic failure but through different mechanisms. The altered relaxation of the ventricle (due to delayed calcium uptake and delayed calcium efflux)
769
Study Pearl In the event of a suspected DVT, the clinician should hold the therapeutic interventions and inform the physi cian. The patient should be posi· tioned in non-weight bearing on the side of the affected lower extremity.
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SECTION II. TESTS AND MEASURES
occurs in response to an increase in ventricular afterload (pressure overload). This impaired relaxation of the ventricle leads to impaired diastolic filling of the left ventricle. Signs and symptoms of left-sided heart failure include ascites, congestive hepatomegaly, and anasarca (generalized edema). Regardless of etiology or classification, heart failure is character ized by the inability of the heart to meet the demands of the body at higher levels. This results in the hallmark symptom of heart failure: exercise intolerance. The New York Heart Association uses the follow ing functional classification: ~
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The central hemodynamic character istics of heart failure that contribute to exercise intolerance include: ~ Abnormal pressures within the heart. ~ Reduced left ventricular ejection fraction. ... Reduced cardiac output. ... Increased pulmonary capillary wedge pressure. ~ Increase production of angiotensin II, which increases heart rate, impaired cardiac filling, and increases coro na')' vasoconstddion and peripheral vascular resistance.
~
~ ~
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Class I describes a patient who is not limited with normal phys ical activity by symptoms. Class II occurs when ordinary physical activity results in fatigue, dyspnea, or other symptoms. Class III is characterized by a marked limitation in normal phys ical activity. Class IV is defined by symptoms at rest or with any physical activity.
During exercise, cardiac output should be able to increase to four to six times its resting level. Patients with heart failure can often only achieve half this normal increase in cardiac output during exercise.7'J-81 The medical intervention for heart failure focuses on improving central hemodynamics through three main goals: (1) preload reduc tion, (2) reduction of systemic vascular resistance (afterload reduction) through administration of vasodilators, and (3) inhibition of both the renin-angiotensin-aldosterone system and the vasoconstrictor neuro humoral factors (inotropic support) produced by the sympathetic nervous system in patients with heart failure.
COR PULMONALE Cor pulmonale is defined as an alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system. 82--i:l6 Pulmonary hypertension (see Chapter 10) is the common link between lung dysfunction and the heart in cor pulmonale. Cor pulmonale can develop secondary to a wide variety of cardiopul monary disease processes. Although cor pulmonale commonly has a chronic and slowly progressive course, acute onset or worsening cor pulmonale with life-threatening complications can occur. Several dif ferent pathophysiologic mechanisms can lead to pulmonary hyperten sion and, subsequently, to cor pulmonale. These pathogenetic mecha nisms include ~ ~
~
~
Pulmonary vasoconstriction due to alveolar hypoxia or blood academia (abnormally high level of acid in the blood). Anatomic compromise of the pulmonary vascular bed second ary to lung disorders such as emphysema, pulmonary throm boembolism, and interstitial lung disease. Increased blood viscosity secondary to blood disorders such as polycythemia vera, sickle-cell disease, and macroglobulinemia. Idiopathic primary pulmonary hypertension.
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
771
Clinical manifestations of cor pulmonale generally are nonspecific and may be subtle, especially in early stages of the disease. The patient may complain of fatigue, exertional dyspnea, and syncope with exer tion with a subsequent drop in the systemic arterial pressure. Exertional chest pain also can occur. Other symptoms mainly related to pulmonary artery hypertension include cough, hemoptysis, and rarely, hoarseness. In advanced stages, passive hepatic congestion secondary to severe right ventricular failure may lead to anorexia, right upper quadrant abdominal discomfort, and jaundice. Swelling of the legs also can occur. The most obvious physical findings in cor pulmonale reflect the underlying lung disease, with an increase in chest diameter, labored respiratory efforts with retractions of the chest wall, hyperres onance to percussion, diminished breath sounds, wheezing, distant heart sounds, and, rarely, c..yanosis. The medical intervention for cor pulmonale varies according to type: ~
~
Acute cor pulmonale with resultant acute right ventricular fail ure: fluid loading and vasoconstrictor (e.g., epinephrine) administration. Chronic cor pulmonale: oxygen therapy, diuretics, vasodilators, digitalis, theophylline, and anticoagulation therapy.
Phlebotomy is indicated in patients with chronic cor pulmonale and chronic hypoxia causing severe polycythemia.
CONGENITAL LESIONS The incidence of congenital cardiac anomalies is 8 per 1000 live births. The anomalies occur during the first trimester. There are two categories: ~
~
Cyanotic: result from obstruction of blood flow to the lungs, or mixing of desaturated venous blood with fully saturated arterial blood within the chambers of the heart. IS Acyanotic: usually involve left-to-right shunting through an abnormal opening.
CARDIOMYOPATHY Cardiomyopathy is part of a group of conditions affecting the heart muscle itself so that the fibers involved with contraction and relaxation of the myocardial muscle are impaired. Causes include coronary artery disease (see later), valvular disorders, hypertension, congenital defects, and pulmonary vascular disorders.
VALVULAR DISEASE Heart problems that occur secondary to impairment of the valves may be caused by infection such as endocarditis, congenital deformity, or disease. Three types of valve deformities may affect aortic, mitral, tri cuspid, or pulmonary valves: stenosis, insufficiency, or prolapse. ~
Mitral stenosis: a sequela of rheumatic heart disease that prima rily aflects women. • Mitral regurgitation: many causes, but involvement of the mitral valve accounts for approximately 50% of all cases.
Rubella is the most common infection related to congenital cardiovascular defects. 87 Other possible causes include exposure to x-rays, alcohol, infection or drugs, maternal diabetes, family history, and some hereditary dysplasia such as Down's syndrome. 18
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SECTION II. TESTS AND MEASURES
~
~
Other causes include infective endocarditis, dilated car diomyopathy, rheumatic disease, collagen vascular disease, rupture of the chordae tendineae, and rarely, cardiac tumors. 18 • Mitral valve prolapse (floppy valve syndrome, Barlow's syn drome): characterized by a slight variation in shape or struc ture of the mitral valve. Unknown etiology, although there may be a genetic component. Aortic stenosis: a disease of aging most conunonly caused by progressive valvular calcification. • Aortic regurgitation (insufficiency): used to occur secondary to rheumatic fever but antibiotics have reduced the number of rheumatic-related cases. Non-rheumatic causes include congenital defects, infective endocarditis, hypertension, and aortic dissection. Tricuspid stenosis and regurgitation: usually occurs in people with severe mitral valve disease. Unconunon.
ARRHYTHMIAS
Arrhythmias are a group of conditions that affect the cardiac nervous system. Arrhythmias are usually classified according to their origin (ventricular, or supraventricular [atrial]), pattern (fibrillation or flut ter), or the speed or rate at which they occur (tachycardia or brady cardia). Causes include congenital defects, hypertrophy of the heart muscle fibers, valvular heart disease, and degeneration of conductive tissue. CORONARY ARTERY DISEASE
Coronary artery disease (CAD) is a complex disease involving a nar rowing of the lumen of one or more of the arteries that encircle and supply the heart, resulting in ischemia to the myocardium. Injury to the endothelial lining of arteries, an inflanunatory reaction, thrombosis, calcification, and hemorrhage all contribute to arteriosclerosis or scar ring of an artery wall ATHEROSCLEROSIS
Atherosclerosis, the most conunon form of arteriosclerosis, is a chronic thickening of the arterial wall of medium- and large-sized vessels, through the accumulation of lipids, macrophages, T-lymphocytes, smooth muscle cells, extracellular matrix, calcium, and necrotic debris. Atherosclerosis primarily affects the lower extremities. When the arter ies of the heart are affected it is referred to as coronary artery disease (CAD) or coronary heart disease (CHD); when the arteries to the brain are affected, cerebrovascular disease (CVD) develops.88 Conunon symptoms of atherosclerosis include ~ ~ ~
~
Decreased or absent peripheral pulses. Skin color: pale on elevation, dusky red on dependency. Intermittent claudication (early stages): pain is described as burning, searing, aching, tightness, or cramping. In the later stages, patients exhibit ischemia and rest pain; ulcerations and gangrene, trophic changes.
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
Risk factors for CAD are classified as modifiable or unmodifiable. ~
~
Modifiable risk factors: smoking, exposure to second-hand smoke, hypertension, hyperlipidemia, high cholesterol (total or LDL-C) levels, low HDL-C) levels, high triglyceride levels, dia betes, abdominal obesity, sedentary lifestyle, high homocys teine levels, and high levels of C-reactive protein (which indi cates inflammation). Unmodifiable risk factors: age, male sex, race, and family history.
The clinical symptoms of CAD include any symptoms that may represent cardiac ischemia, such as an ache, pressure, pain, other dis comfort, or possibly just decreased activity tolerance due to fatigue, shortness of breath, or palpitations.
ANGINA PECTORIS Angina pectoris is the result of myocardial ischemia caused by an imbalance between myocardial blood supply and oxygen demand, which causes myocardial cells to switch from aerobic to anaerobic metabolism, with a progressive impairment of metabolic, mechanical, and electrical functions. 89 Most patients with angina pectoris complain of retrosternal chest discomfort rather than frank pain. The former is usually described as a pressure, heaviness, squeezing, burning, or choking sensation. Anginal pain may be localized primarily in the epigastrium, back, neck, or jaw. Typical locations for radiation of pain are the arms, shoulders, and neck (C8-T4 dermatomes). Typically, exertion, eating, and exposure to cold or emotional stress precipitate angina. Episodes typically last for approximately 1 to 5 minutes and are relieved by rest or by taking nitroglycerin. The New York Heart Association classification (see Congestive Heart Failure) may be used to quantify the functional limitation imposed by patients' symptoms. Types of angina include87 : ~
~
~
~
Chronic stable: classic exertional angina, which occurs after exercise, eating, or emotional stress and is relieved by rest, nitrates, or other coronary artery vasodilators. The discomfort is most often substernal, precordium, or epigastrium, with radia tion to the left arm, jaw, or neck. Unstable (preinfarction, crescendo angina): unstable angina can occur at rest or with activity. The pain is similar to that with typi cal stable angina but may be more intense and may last several hours; ST segment depression or elevation occurs. Pain is difficult to control. New-onset angina pectoris, which has developed for the first time within the last 60 days, is also considered unstable. Prinzmetal (vasospastic, variant): occurs principally at rest and may occur in a circadian manner, at a similar time of day, often in the early morning hours. It is more common in women (under 50). Coronary artery spasm in normal or obstructed arteries has been found with this type of angina. Syndrome X (insulin-resistant syndrome): chest pain that is seemingly ischemic in origin (microvascular) but with a normal arteriogram and normal ECG. More prevalent among women, particularly those who have undergone hysterectomy.18
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SECTION II. TESTS AND MEASURES
MYOCARDIAL INFARCTION Myocardial infarction (M!) is the rapid development of myocardial necrosis caused by a critical imbalance between the oxygen supply and demand of the myocardium. 9o This usually results from plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium. ~
~
Atherosclerotic causes: the most common cause of MI. Plaque rupture with subsequent exposure of the basement membrane results in platelet aggregation, thrombus formation, fibrin accu mulation, hemorrhage into the plaque, and varying degrees of vasospasm. MI occurs most frequently in persons older than 45 years. Nonatherosclerotic causes: include coronary vasospasm as seen in variant (Prinzmetal) angina and in patients using cocaine and amphetamines; coronary emboli from sources such as an infected heart valve; occlusion of the coronaries due to vasculitis; or other causes leading to mismatch of oxygen supply and demand, such as acute anemia from GI bleeding.
Signs and symptoms of MI include ~
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Chest pain, typically described as tightness, pressure, or squeezing, located across the anterior precordium. Pain may radiate to the jaw, neck, arms, back, and epigastrium. The left arm is affected more frequently than the right; however, pain may be felt in both arms. Dyspnea, which may accompany chest pain or occur as an iso lated complaint (especially in an elderly person or the diabetic patient). Nausea and/or abdominal pain often are present in infarcts involving the inferior or posterior wall.
Anxiety.
Light-headedness with or without syncope.
Cough.
Nausea with or without vomiting.
Diaphoresis.
WheeZing.
INFLAMMATORY CONDITIONS OF THE HEART Myocarditis, pericarditis, and infective endocarditis are all inflamma tory conditions of the heart. ~
~
Myocarditis: relatively uncommon inflammatory condition of the muscular walls of the heart (myocardium), usually the result of bacterial or viral infection. Other possible causes include chest radiation for treatment of malignancy, sarcoidosis, and drugs such as lithium and cocaine. 18 Pericarditis: most commonly drug-induced or in association with an autoimmune disease (e.g., connective tissue disorders such as SiP, rheumatoid arthritis), postmyocardial infarction, with renal failure, after open-heart surgery, and after radiation therapy. 18
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY ~
~
Infective endocarditis: an infection (frequently caused by bac teria-streptococci or staphylococci) of the endocardium, including the heart valves. Can occur at any age, but rarely occurs in children. Rheumatic fever: a form of endocarditis caused by streptococ cal group A bacteria.
HEMATOPOIETIC SYSTEM DISORDERS
Sickle-Cell Disease. A generic term for a group of inherited, autosomal recessive disorders characterized by the presence of an abnormal form of hemoglobin within the erythrocytes (crescent or sickle shape versus usual biconcave disc shape)-see Chapter 12. The Thalassemias.
A group of inherited, chronic hemolytic ane mias predominantly affecting people of Mediterranean or southern Chinese ancestry-see Chapter 12.
Fanconi's Anemia. Fanconi's anemia is an autosomal recessive inherited disease that primarily affects the bone marrow, resulting in decreased production of all types of blood cells. The lack of white blood cells predisposes the patient to infections, while the lack of platelets and red blood cells may result in bleeding, and fatigue (anemia), respectively. Gaucher's Disease. Gaucher's disease is an inherited metabolic disorder. All Gaucher's patients exhibit a deficiency of an enzyme called glucocerebrosidase, which is involved in the breakdown and recycling of glucocerebroside. The buildup of this fatty material within cells prevents the cells and organs from functioning properly, and a fatty substance called glucocerebroside accumulates in the spleen, liver, lungs, bone marrow, and sometimes in the brain. There are three types of Gaucher's disease: ~
~
~
Type 1: the most common. Patients in this group usually bruise easily, experience fatigue due to anemia and low blood plateleL'i, and have an enlarged liver and spleen, skeletal disor ders, and in some instances, lung and kidney impairment. Type 2: liver and spleen enlargement are apparent by 3 months of age. Patients have extensive and progressive brain damage and usually die by 2 years of age. Type 3: liver and spleen enlargement is variable, and signs of brain involvement such as seizures gradually become apparent.
Hemophilia. Leukemia. ~
~
Refer to Chapter 16.
Leukemia is divided into four major categories:
Acute myelogenous: a malignant disease of the bone marrow in which hematopoietic precursors are arrested in an early stage of development. Acute lymphocytic (acute lymphoblastic leukemia and acute lymphoid leukemia); most cases of acute lymphocytic leukemia (ALL) occur in children under age 10, but it can appear in all age groups. ALL is an acute leukemia of unknown etiology caused by a change in the cells in the bone marrow.
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SECTION II. TESTS AND MEASURES ~
~
Chronic myelogenous: a malignant cancer of the bone marrow, which can occur in adults (usually middle-aged) and children. It is usually associated with a chromosome abnormality called the Philadelphia chromosome. Chronic lymphocytic: a disorder of morphologically mature but immunologically less mature lymphocytes that is manifested by progressive accumulation of these cells in the blood, bone mar row, and lymphatic tissues.
LYMPHATIC DISEASE
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Lymphedema. In a diseased state, the lymphatic transport capac ity is compromised, causing the normal volume of interstitial fluid for mation to exceed the rate of lymphatic return, which results in the stagnation of high-molecular-weight proteins in the interstitium. This high oncotic pressure in the interstitium favors the accumulation of additional water. Accumulation of interstitial fluid leacl" to significant dilatation of the remaining outflow tracts and valvular incompetence, resulting in a reversal of flow from subcutaneous tissues into the der mal plexus. The protein and fluid accumulation initiates a marked inflammatory reaction. Macrophage activity is increased, resulting in destruction of elastic fibers and production of fibrosclerotic tissue. Fibroblasts migrate into the interstitium and deposit collagen. The lym phatic walls undergo fibrosis, and fibrinoid thrombi accumulate within the lumen, destroying much of the remaining lymph channels. Spontaneous lymphovenous shunts may form. Lymph nodes harden and shrink, losing their normal architecture. The overlying skin becomes thickened and displays the typical peau d'orange (orange skin) appearance of congested dermal lym phatics. The epidermis forms thick scaly deposits of keratinized debris; cracks and furrows often develop and accommodate debris and bacte ria, resulting in the leakage of lymph onto the surface of the skin. Lymphedema may be classified as primary or secondary, based on underlying etiology, although this classification usually has little signif icance in determining treatment modality. Primary Lymphedema. Primary lymphedema represents a develop mental abnormality of the lymphatic system that is present, but not always clinically evident, at birth. Thus, primary lymphedema has been further subdivided based on age of onset91 - 97 : ~
~
~
Congenital lymphedema: represents all forms that are clinically evident at birth and accounts for 10% to 25% of all primary lym phedema cases. Females are affected twice as often as males, and the lower extremity is involved three times more frequently than the upper extremity. Two-thirds of patients have bilateral lymphedema, and this form may improve spontaneously with increasing age. Lymphedema praecox: the most common form of primary lym phedema (also known as Meige's disease). It becomes clinically evident after birth and before age 35 years, most often arising during puberty. Females are affected four times as often as males. Lymphedema tarda: does not become clinically evident until age 35 years or older.
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
These conditions are most often sporadic, with no family history, and involve the lower extremity almost exclusively.
Secondary Lymphedema. Secondary lymphedema represents an acquired dysfunction of otherwise normal lymphatics that occurs as a result of obstruction of lymphatic flow by known mechanisms, includ ing filariasis (infestation of lymph nodes by the parasite Wuchereria bancrofti), silica, obstruction by a proximal mass, postsurgical mecha nisms (e.g., mastectomy, peripheral vascular surgery, lipectomy), burns, burn scar excision, insect bites, and fibrosis secondary to chronic infections. Patients with secondary lymphedema present with varying degrees of severity, from mild swelling to severe disabling enlargement with potentially life-threatening complications. This disease is often first noticed by the patient as an asymmetry or increased circumference of an extremity. If lymphedema is not treated it progresses through the following stages: ~
~
~
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Stage 0 (latency/subclinical stage): characterized by reduction of the normal lymph transport capacity, but there will be no measurable increase in volume. Stage I (reversible lymphedema): characterized by the presence of protein-rich edema and associated with a measurable increase in volume, including pitting edema. Activity, heat, and humidity may cause or increase stage I lymphedema. Stage II (spontaneously irreversible lymphedema): presents with increased volume, replacement of some of the protein rich lymphatic fluid with tissue fibrosis, and a positive Stemmer's sign (the inability to lift the thickened cutaneous folds at the dorsum of the toes or fingers). Stage III (lymphostatic elephantiasis): characterized by subcu taneous fibrosclerosis and severe skin alterations, including hyperkeratosis and papillomatosis.
SURGICAL INTERVENTIONS fOR CARDIOVASCULAR CONDITIONS
Heart Valve Surgery. Surgery on defective heart valves is some times necessary in cases of mitral valve regurgitation. Surgical options include ~
~
Mitral valve reconstruction with mitral annuloplasty, quadratic segmental resection, shortening of the elongated chordae, or posterior leaflet resection. Mitral valve replacement with either a mechanical valve (requir ing lifelong anticoagulation) or a bioprosthetic porcine valve.
Percutaneous Transluminal Coronary Angioplasty. Percutaneous transluminal coronary angioplasty (PTCA) encompasses a variety of procedures used to treat patients with diseased arteries of the heart. Typically, PTCA is performed by threading a slender balloon tipped catheter under fluoroscopy from an artery in the groin to a trou ble spot in an artery of the heart. Once positioned correctly inside the
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SECTION II. TESTS AND MEASURES
lumen, the balloon is inflated, compressing the plaque and dilating the narrowed coronary artery. There are at present no guidelines for when a patient may resume aerobic training following this procedure. Conventional wisdom, however, favors waiting approximately 2 weeks to allow the inflammatory process resulting from the intervention an appropriate time to subside. 2
Coronary Artery Bypass Graft. Coronary artery bypass graft (CABG) surgery is a procedure that allows a circumvention of an obstructed coronary artery using a healthy heart or vein taken from the patient's chest, leg, or arm (e.g., saphenous vein, internal mam mary artery). Coronary artery bypass graft surgery often is the treat ment of choice for patients with severe coronary artery disease (three or more diseased arteries with impaired function in the left ventricle). Physical therapy intervention following this procedure should address any soft-tissue impairments that may be affected by the incision to maintain appropriate flexibility and postures, with an awareness that patients often experience soreness and/or discomfort around the donor site. 2 Some surgeons choose to limit upper extremity fleXibility exercises during the 4 to 6 weeks following surgery while the sternum is healing.
Cardiac Transplantation. Cardiac transplantation, the pro cedure by which the failing heart is replaced with another heart from a suitable donor, is a widely accepted therapy for the treatment of end-stage congestive heart failureYs A ventricular assist device (VAD) is a mechanical pump that helps the heart pump blood through the body. The cardiac allograft can be sewn in a heterotopic or orthotopic position: ~
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Heterotopic: usually restricted to only those patients with severe pulmonary hypertension due to inherent problems (e.g., pulmonary compression of the recipient, difficulty obtaining endomyocardial biopsy, need for anticoagulation). Orthotopic: involves excision of the recipient's heart above the atrioventricular valves and replacement with the donor heart using either the classic Shumway-Lower technique or as a bicaval anastomosis. The graft includes the sinus node so that a sinus rhythm is possible after transplantation; however, some patients need lifelong pacing.
Immunosuppression is started soon after surgery and long-term immunosuppression usually is maintained with cyclosporine, azathio prine, and prednisone.
Transmyocardial
Revascularization. Transmyocardial revascularization (TMR) is a new laser surgery designed to improve myocardial oxygenation, eliminate or reduce angina, and improve car diovascular function in those patients who are not candidates for bypass surgery or angioplasty. The surgeon makes an incision over the left breast to expose the heart, and then, using a laser, interjects a strong energy pulse into the left ventricle, vaporizing the ventricular muscle and creating a transmural channel with a I-mm diameter. The precise physiologic mechanism for the efficacy of TMR is not thor oughly understood.
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CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
CARDIOVASCULAR PHYSICAL THERAPY Physical therapy interventions for cardiovascular conditions can be broadly classified into primary prevention and secondary intervention, although it must be remembered that both of these categories are linked by physiologic, epidemiologic, and clinical elements. ~
~
Primary prevention: the prevention of a cardiovascular disease from developing, even among individuals with risk factors Preferred Practice Pattern 6A. Secondary intervention: aimed at reducing symptoms and/or slowing the progression of a cardiovascular disease. Patients in this category have • Impaired aerobic capacity/endurance associated with decon ditioning-Preferred Practice Pattern 6B. • Impaired aerobic capacity/endurance associated with cardio vascular pump dysfunction or failure-Preferred Practice Pattern 6D. • Impaired circulation and anthropometric dimensions associated with lymphatic system disorders-Preferred Practice Pattern 6H.
(Preferred practice patterns 6c, 6E, 6F, and 6G are covered in Chapter 10).
PHYSICAL THERAPY ASSOCIATED WITH PRIMARY PREVENTION, RISK REDUCTION, AND DECONDITIONING Patients who have identifiable risk factors should be encouraged to adopt lifestyle behaviors that can modify the risk factors. These include ~ ~
~ ~ ~
Activity recommendations.
Dietary recommendations.
Smoking cessation.
Education about the effects of medications.
Importance of compliance.
Exercise Prescription. Any prescribed exercise for this popula tion must be quantified. The quantification can be expressed in a num ber of ways-total distance walked and time taken; workload expressed in watts when using an ergometer; heart rate (which is pro portional to both cardiac output and systemic oxygen consumption) and blood pressure taken at rest, during, and after the activity.99 A patient's abnormal cardiovascular response to exercise may be catego rized as dysrhythmia, ischemia, or congestive heart failure. 99
Dysrhythmia. Dysrhythmia can occur normally, but may result from premature atrial contractions (PACs), premature ventricular contrac tions (PYCs), or atrial fibrillation (refer to "Examination of the Heart Rhythm" earlier in the chapter). If PYCs exist at rest, the clinician must consider the impact that exercise might have.
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A decrease of PYCs with exercise is a good sign, as it would tend to indicate that the PYCs are suppressed by a higher-order pacemaker (overdrive suppression) as physical activity and heart rate increase.
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SECTION II. TESTS AND MEASURES ~
An increase of PVCs with exercise is a less desirable response,
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as it would tend to indicate that the PVCs are ischemic in origin. PVCs that do not change with exercise would tend to indicate that the PVCs are unrelated to exercise.
Ischemia. Ischemia occurs when the demand for oxygen by cardiac muscle outstrips the supply of oxygen available to it. This condition fre quently arises during exercise with the onset of chest pain, or angina. Congestive Heart Failure. Shortness of breath with exercise does not necessarily indicate congestive heart failure. A thorough medical history is important. ~
~
In left-sided failure, the pressure builds up in the left ventricle and is reflected backward, up through the left atrium, and into the lungs. The lungs become wet, stiff, soggy, and difficult to move-thus the feeling of shortness of breath. In right-sided failure, the cause is often the result of left-sided heart failure. Because of the restriction in forward blood flow, the pressure passes through the lungs and is reflected through the right ventricle and right atrium and into the venous circula tory system. This may result in distension of the jugular vein, organomegaly, or pitting edema in the lower extremities.
Other signs and symptoms of exercise intolerance: ~
~ ~
~ ~ ~ ~
The appearance of ST-segment elevation at rest with a signifi cant Q-wave (on ECG)--may indicate the residual effects of a myocardial infarction (e.g., an aneurysm) and should be noted as such. Heart murmur-in the setting of myocardial infarction, this murmur usually indicates papillary muscle dysfunction. A fall in systolic blood pressure with exercise that occurs beyond the early transient drop in BP (usually as a result of regional shunting of blood). Absence of a rise in systolic BP with exercise may signify growing left ventricular dysfunction. Chest pain, shortness of breath.
Reports of skipped beats or "fluttering" of the heart, especially
in the presence of dizziness, light-headedness, or syncope. Pallor, diaphoresis. Unresponsiveness to questions.
PHYSICAL THERAPY ASSOCIATED WITH IMPAIRED AEROBIC CAPACITYIfNDURANCE ASSOCIATED WITH CARDIOVASCULAR PUMP DYSfUNCTION OR FAILURE According to the APTA Guide to Physical Therapist Practice,100 the development of specific anticipated goals and expected outcomes is based on the following general goals of physical therapy intervention2 : 1. Aerobic capacity is increased. 2. Ability to perform physical tasks related to self-care, home management, community and work integration or reintegra tion, and leisure activities is increased.
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CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
3. Physiologic response to increased oxygen demand is improved. 4. Strength, power, and endurance are increased. 5. Symptoms associated with increased oxygen demand are decreased. 6. Ability to recognize a recurrence is increased, and intervention is sought in a timely manner. 7. Risk of recurrence is reduced. 8. Behaviors that foster healthy habits, wellness, and prevention are required. Rehabilitation interventions for patients with heart failure focus primarily on different types of exercise. Appropriate exercise, in com bination with optimal medical care, can improve function, symptoms, and quality of life in patients with chronic heart failure. 101- 107
Cardiac Rehabilitation. Cardiac rehabilitation provides many benefits for patients. The most important benefits are l09 ~
~ ~ ~ ~ ~
~ ~ ~ ~
~
Improved exercise tolerance. Control of symptoms. Improvement in the blood levels of lipids. Beneficial effect on body weight. Possible improvement with high blood pressure. Reduction in smoking. Improved psychosocial well-being. Reduction of stress. Enhanced social adjustment and functioning. Return to work. Reduced mortality.
Cardiac rehabilitation has to be both comprehensive and individ ualized at the same time. The goals of a cardiac rehabilitation program can be separated into short and long-term goals.
Short-Term Goals ~ ~ ~ ~
"Reconditioning" sufficient for resumption of customary activities. Limiting the physiologic and psychological effects of heart disease. Decreasing the risk of sudden cardiac arrest or reinfarction. Controlling the symptoms of cardiac disease.
Long-Term Goals ~ ~ ~
Identification and treatment of risk factors. Stabilizing or even reversing the atherosclerotic process. Enhancing the psychological status of the patients.
Phases of Cardiac Rehabilitation. Cardiac rehabilitation programs can be stratified into four phases, described in the next sections.llO.l ll Phase 1. This phase occurs in the hospital inpatient department, start ing in the CICU and continuing through the step-down phase (approxi mately 24 days). This program includes a visit by a member of the cardiac rehabilitation team (cardiac nurse, exercise specialist, physical thera pist, occupational therapist, dietitian, and social worker), education
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regarding the disease and its recovery process, personal encourage ment, and inclusion of family members in classroom group meetings. In the coronary care unit, assisted range-of-motion exercises can be initiated within the first 24 to 48 hours. Low-risk patients should be encouraged to sit in a bedside chair and begin to perform self-care activities (e.g., shaving, oral hygiene, sponge bathing). Early mobilization programs are designed for uncomplicated patients with acute MI in order to progressively increase activity levels in three areas: active exercises, activities of daily living, and educa tional activities with the goal of early return to independence. On trans fer to the step-down unit, patients should try to sit up, stand, and walk in their rooms in the beginning. Subsequently, they should start to walk in the hallway at least twice daily either for certain specific distances or as tolerated without unduly pushing them or holding them back. Standing heart rate and blood pressure should be obtained followed by 5 minutes of warm-up or stretching. Walking, often with assistance, is resumed with target heart rate of > 20 beats above the resting heart rate, and RPE under 14. Starting with 5 to 10 minutes of walking each day, exercise time gradually can be increased to up to 30 minutes daily. Team members should incorporate in the discharge planning an appropriate emphasis on secondary prevention through risk factor modification and therapeutic lifestyle changes (TLC), such as aspirin and beta-blocker use in all patients, angiotensin-converting enzyme (ACE) inhibitor use in patients with left ventricular ejection fraction of less than 40%, smoking cessation, lipid management, weight manage ment, and stress management. They must also ensure that phase 1 patients get referred to appropriate local, convenient, and comprehen sive phase 2 programs. Phase 1.5 (Postdischarge Phase). This phase begins after the patient returns home from the hospital. Team members check the patient's medical status and continuing recovery, and should offer reassurance and education about risk reduction strategies as the patient regains health and strength. This phase of recovery includes low-level exercise and physical activity and instruction about changes for resumption of an active and satisfying lifestyle. After 2 to 6 weeks of recovery at home, the patient is ready to start cardiac rehabilitation phase 2. Phase 2 (Supervised Exercise). Patients who have completed hospital ization and 2 to 6 weeks of recovery at home can begin phase 2 of their cardiac rehabilitation program. This subacute phase is designed to allow the heart muscle time to heal and to progress the patient to full resumption of activities of daily living. During this phase, patients are allowed to return to work, as appropriate, and are advised to com mence a walking or biking program. Physician and cardiac rehabilitation staff members formulate the level of exercise to meet an individual patient's needs. Exercise treat ments usually are scheduled three times a week at the rehabilitation facility. Constant medical supervision is provided, including exercise ECGs as well as supervision by a nurse and exercise specialist. Patients are gradually weaned from continuous monitoring of vital signs to spot checks and self-monitoring. Risk factor modification, activity pacing, and energy conservation are emphasized. For example, in addition to exercise, counseling and education about stress management, smoking
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
cessation, nutrition, and weight loss also are incorporated. 1bis phase of rehabilitation may last 3 to 6 months.
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of
Phase 3 (Maintenance Phase). Phase 3 of cardiac rehabilitation is a maintenance program designed to continue for the patient's lifetime. The exercise sessions usually are scheduled three times a week. ECG monitoring usually is not necessary. Activities consist of the type of exercises the patient enjoys, such as walking, bicycling, or jogging. The main goal of phase 3 is to pro mote habits that lead to a healthy and satisfying lifestyle. Phase 3 programs do not usually require medical or nursing super vision. In fact, most patients participate in "phase 3" equivalent exer cises at the exercise facilities in the community (e.g., YMCA, YWCA, Gold's gym, Life-style fitness). Entrance into this phase begins with the performance of a maximum, symptom-limited exercise test, the results of which are used to write an exercise prescription. During this phase, patients exercise at 65% to 85% of their maximum heart rate. 1bree main components of an exercise-training program are as follows: ~
~ ~
~
: 1 ~n
Frequency: the minimum frequency for exercising to improve cardiovascular fitness is three times weekly. Time: patients usually need to allow 30 to 60 minutes for each session, which includes a warm-up of at least 10 minutes. Intensity: the intensity prescribed is in relation to one's target heart rate. Aerobic conditioning is emphasized in the first few weeks of exercise. Strength training is introduced later. 1be Borg scale of Rate of Perceived Exertion (RPE) is used. Patients usually should exercise at an RPE of 13 to 15.
ent
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r at
ital heir 1 to full
PHYSICAL THERAPY ASSOCIATED WITH IMPAIRED CIRCULATION AND ANTHROPOMETRIC DIMENSIONS ASSOCIATED WITH LYMPHATIC SYSTEM DISORDERS
Lymphedema. The intervention for lymphedema is multifaceted. Patients should be encouraged to ~ ~
, are
om-
: the
reat
ltion
tcise ients spot cing,
:>n to
)king
~ ~ ~
~
Lose weight. Avoid even minor trauma. Skin care and avoidance of trauma are important to avoid lymphangitis, cellulites, and ulceration. 1be skin should be kept well lubricated and should not be exposed to strong soaps or detergents. Acute lymphangitis, which can either precede or follow chronic lymphedema, is usually treated with a combination of rest, elevation, and antibiotics. Avoid overheating local body parts or a rise in core body temperature. Avoid lifting heavy objects; no heavy handbags with over-the shoulder straps. Avoid constrictive clothing and jewelry that might have a tourniquet effect. Elevate the affected extremity whenever possible, particularly at night. For lower extremity lymphedema, this may be accom plished by elevating the foot of the bed to an appropriate level.
783
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SECTION II. TESTS AND MEASURES
In addition, patients should use compression garments. These are worn continuously during the day, but may be removed at night when the extremity is elevated in bed, and should be replaced promptly each morning. To encourage compliance, the elastic compression garments must be comfortable and fit appropriately-should be custom fit when the extremity is decompressed; have graduated compression, increas ing from distal to proximal, on the affected extremity; and should not have a tourniquet effect. Patients should exercise with compression applied to the involved extremity or area. Simple active exercises should be prescribed that require the joints to maintain range of motion and activate the muscle and joint pump. Intermittent pneumatic pump compression therapy may also be instituted on an outpatient basis or in the home (refer to Chapter 18). These devices provide sequential active compression from distal to proximal, effectively milking the lymph from the extremity. Manual lymphatic drainage (MLD) according to the Vodder and/or Leduc techniques may also be prescribed (refer to Chapter 18).112,113
Venous Insufficiency. Treatment is aimed at ameliorating the symptoms and, whenever possible, at correcting the underlying abnor mality. Deep system disease is often refractory to treatment, but super ficial system disease can usually be treated by ablating the refluxing vessels.
Study Pearl
Graduated Compression. Graduated compression is the corner stone of the modern treatment of venous insufficiency. Properly fitted gradient compression stockings provide 30 to 40, or 40 to 50 mm Hg of compression at the ankle, with gradually decreasing compression at more proXimal levels of the leg. This amount of gradient compression is sufficient to restore normal venous flow patterns in many or most patients with superficial venous reflux and to improve venous flow, even in patients with severe deep venous incompetence. The compression gradient is extremely important because non gradient stockings or high-stretch elastic bandages (e.g., ACE wraps) may cause a tourniquet effect, with worsening of the venous insufficiency. The prescription should specify one pair of gradient compression hose with a 30- to 40-mm Hg gradient that is calf-high (or thigh-high with waist attachment or panty hose style), with refills as needed. Venoablation. All methods of venoablation are effective. Once the overall volume of venous reflux is reduced below a critical threshold by any mechanism, venous ulcerations heal, and patient symptoms are resolved. Endovenous Laser Therapy. Endovenous laser therapy (EVLT), a newer procedure, is performed by passing a laser fiber from the knee to the groin and then delivering laser energy along the entire course of the veiny4-1l6 Destruction of the vascular wall is followed by fibrosis of the treated vessel. EVLT has demonstrated excellent early (4-year) results and an extremely low rate of complications, but the duration of follow-up is not yet long enough to provide information about midterm and long-term results.
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
Radiofrequency Ablation. Radiofrequency ablation (RFA) is a rela tively new procedure that has a low rate of complications. ll7 RFA is performed by passing a special radiofrequency (RF) catheter from the knee to the groin and by heating the vessel until thermal injury causes shrinkage. The process is repeated every few centimeters along the course of the vein. Initial thermal injury is followed by fibrosis of the treated vessel. MANAGEMENT OF PERIPHERAL VASCULAR DISORDERS
Patients with peripheral vascular disease (PVD) often have multiple diagnoses and may have socioeconomic constraints. The best inter vention for all forms of PVD is prevention-appropriate exercise, healthy diet, and avoidance of smoking.
Arterial Disease. When the metabolic demands of a muscle or group of muscles exceed blood flow, claudication symptoms ensue. A useful tool in assessing a patient with claudication is the ankle brachial index (ABO, which is calculated as the ratio of systolic blood pressure at the ankle to the arm. A normal ABI is 0.9 to 1.1. However, any patient with an ABI less than 0.9, by definition, has some degree of arterial disease. The physical therapy intervention for patients with arterial disease depends on the level of severity. A simple four-point functional grad ing system can be used to help select the appropriate intervention 118 : ~
~ ~ ~
Grade I: no functional limitations. Grade II: ambulatory more than 4 blocks before onset of claudication. Grade III: ambulatory less than 4 blocks before onset of claudication. Grade IV: nonambulatory because of ischemic pain at rest.
For those patients in grades I and II, exercise therapy is advised. Exercises can include ~
~ ~
Ambulation at a steady pace up to, but not beyond, the point of pain. A daily walking program of 45 to 60 minutes is recom mended. The patient is instructed to walk until claudication pain occurs, rest until the pain subsides, and repeat the cycle. A small heel lift can be used to help reduce the oxygen demand in the gastrocnemius. Modified Bueger-Allen exercises (postural exercises, active ankle plantar flexion/dorsiflexion). Resistive calf exercises.
For grade III patients who are not surgical candidates, exercises within pain-free limits are advocated. Since Grade IV patients are ischemic at rest, under no circum stances should they be put on an exercise program. For all grades, risk-factor modification should be encouraged. Medications may be prescribed to decrease blood viscosity and pre vent thrombus formation. Patients with limb-threatening ischemia or lifestyle-limiting claudication are referred to a vascular surgeon.
785
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SECTION II. TESTS AND MEASURES
Venous Disease. Acute thrombophlebitis requires only rest, ele vation, and warm soaks until symptoms subside if limited to a superfi cial vein. ~
~
~
Deep vein thrombophlebitis (DVT): associated with long-term venous insufficiency if poorly managed. In acute cases, patients are placed on bed rest and elevation of the involved extremity until signs of inflammation have subsided. Exercise therapy is contraindicated during this phase because of the potential to dislodge the clot, which can result in a pulmonary embolism, a potentially fatal condition. Once the local tenderness and swelling have resolved, passive range of motion and ambula tion, while wearing elastic stockings, is permitted. Early exer cise is thought to promote fibinolysis and maintain patency of the deep vein. Patients are advised to not wear high-heeled shoes and to stretch the heel cords regularly to lessen com pression of the deep veins. Chronic venous insufficiency (CVI): varies by severity. Patients are advised to wear well-fitted support hosiery and to perform frequent muscle pumping (using active and active resistive plantar flexion/dorsiflexion exercises), ambulation as tolerated, and extremity elevation throughout the day. Weight reduction to reduce the strain on the venous system is also indicated if the patient is obese. Patients may also benefit from intermittent pneumatic compression. Stasis ulcers: approached in a variety of ways including whirlpool, hyperbaric oxygen, electrical stimulation, and sur gery (ligation and vein stripping, vein grafts).
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CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
9. Cahalin LP. Cardiovascular evaluation. In: DeTurk WE, Cahalin LP, eds. Cardiovascular and Pulmonary Physical Therapy: An Evidence-Based Approach. New York: McGraw-Hili; 2004: 273-324. 10. Van de Graaff KM, Fox SI. Circulatory system: cardiac output and blood flow. In: Van de Graaff KM, Fox SI, eds. Concepts of Human Anatomy and Physiology. New York: WCB/McGraw-HilI; 1999:655-691. 11. Di Salvo G, Pergola V, Ratti G, et al. Atrial natriuretic factor and mitral valve prolapse syndrome. Minerva Cardioangiol. 2001;49: 317-325. 12. Schmitz T]. Vital signs. In: O'Sullivan SB, Schmitz TJ, eds. Physical Rehabilitation. 5th ed. Philadelphia: Davis; 2007:81-120. 13. Judge RD, Zuidema GD, Fitzgerald FT. Vital signs. In: Judge RD, Zuidema GD, Fitzgerald FT, eds. Clinical Diagnosis. 4th ed. Boston: Little, Brown; 1982:49-58. 14. Bailey MK. Physical examination procedures to screen for serious disorders of the low back and lower quarter. In: Wilmarth MA., ed. Medical Screening for the Physical Therapist. 011hopaedic Section Independent Study Course 14.1.1. La Crosse, WI: Orthopaedic Section, APTA; 2003:1-35. 15. Huber MA, Terezhalmy GT, Moore WS. White coat hypertension. Quintessence Int. 2004;35:678-679. 16. Chung I, Lip GY. White coat hypertension: not so benign after all? ] Hum Hypertens. 2003;17:807-809. 17. Alves LM, Nogueira MS, Veiga EV, et al. White coat hypertension and nursing care. Can] Cardiovasc Nurs. 2003;13:29-34. 18. Goodman cc. The cardiovascular system. In: Goodman CC, Boissonnault WG, Fuller KS, eds. Pathology: Implications for the Physical Therapist. 2nd ed. Philadelphia: Saunders; 2003:367---476. 19. O'Sullivan J, Allen J, Murray A. The forgotten Korotkoff phases: how often are phases II and III present, and how do they relate to the other Korotkoff phases? Am] Hypertens. 2002;15:264-268. 20. Venet R, Miric D, Pavie A, et al. Korotkoff sound: the cavitation hypothesis. Med Hypotheses. 2000;55:141-146. 21. Weber F, Anlauf M, Hirche H, et al. Differences in blood pressure values by simultaneous auscultation of Korotkoff sounds inside the cuff and in the antecubital fossa.] Hum Hypertens. 1999;13: 695-700. 22. Paskalev D, Kircheva A, Krivoshiev S. A centenary of auscultatory blood pressure measurement: a tribute to Nikolai Korotkoff. Kidney Blood Press Res. 2005;28:259-263. 23. Perloff D, Grim C, Flack J, et al. Human blood pressure determi nation by sphygmomanometry. Circulation. 1993;88:2460-2470. 24. Strugo V, Glew FJ, Davis J, et al. Update: recommendations for human blood pressure determination by sphygmomanometers. Hypertension. 1990;16:594. 25. Higgins JR, Walker SP, Brennecke SP. Re: Which Korotkoff sound should be used for diastolic blood pressure in pregnancy? Aust NZ] Obstet Gynaecol. 1998;38:480---481. 26. Likeman RK. Re: Which Korotkoff sound should be used for dias tolic blood pressure in pregnancy? Aust NZ] Obstet Gynaecol. 1998;38:479---480. 27. Franx A, Evers 1M, van der Pant KA, et al. The fourth sound of KorotkotT in pregnancy: a myth. Eur] Obstet Gynecol Reprod Bioi. 1998;76:53-59.
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28. Peterson BK. Vital signs. In: Cameron MH, Monroe LG, eels. Physical Rehabilitation: Evidence-BfL'Ied F:xamination, Evaluation, and Interoention. St. Louis: Saunders/Elsevier; 2007:598-624. 29. Fletcher GF, Mills WC, Taylor we. Update on exercise stress test ing. Am Fam Physician. 2006;74:1749-1754. 30. Kharabsheh SM, Al-Sugair A, Al-BuraikiJ, et al. Overview of exer cise stress testing. Ann Saudi Med. 2006;26:1-6. 31. Michaelides AP, Aigyprladou MN, Andrikopoulos GK, et al. The prognostic value of a QRS score during exercise testing. Clin Cardiol. 2005;28:375-380. 32. Yosefy C, Cantor A, Reisin L, et al. The diagnostic value of QRS changes for prediction of coronary artery disease during exercise testing in women: false-positive rates. Coron Arte1}' Dis. 2004; 15: 147-154. 33. Fowler-Brown A, Pignone M, Pletcher M, et al. Exercise tolerance testing to screen for coronary heart disease: a systematic review for the technical support for the U.S. Preventive Services Task Force. Ann Intern Med. 2004; 140:W9-W24. 34. Cullinane EM, Siconolfi S, Carleton RA, et al. Modification of the Astrand-Rhyming sub-maximal bicycle test for estimating VOzmax of inactive men and women. Med Sci Sports F:xerc. 1988;20:317-318. 35. Jessup GT, Riggs CE, Lambert J, et al. The effect of pedalling speed on the validity of the Astrand-Rhyming aerobic work capacity test.] Sports Med Phys Fitness. 1977;17:367-371. 36. Pollock ML, Linnerud Ae. Observations of the Astrand-Rhyming nomogram as related to the evaluation of training. Am Correct 1ber]. 1971;25:162-165. 37. Cay S, Metin F, Korkmaz S. Association of renal functional impair ment and the severity of coronary artery disease. Anadolu Kardiyol Derg. 2007;7:44-48. 38. Junnila JL, Runkle GP. Coronary artery disease screening, treat ment, and follow-up. Prim Care. 2006;33:863--885, vi. 39. Sbarsi I, Falcone C, Boiocchi C, et al. Inflammation and athero sclerosis: the role of TNF and TNF receptors' polymorphisms in coronary artery disease. Int] Immunopathol Pharmacal. 2007;20: 145-154. 40. Ask the doctors. I recently read that patients with coronary artery disease ought to have their blood pressure reduced to less than 120/80. I thought 120/80 was normal blood pressure, so why would you want blood pressure to be lower than normal? Heart Advis. 2007;10:8. 41. Dzielinska Z, Januszewicz A, Demkow M, et al. Cardiovascular risk factors in hypertensive patients with coronary artery disease and coexisting renal artery stenosis.] Hypertens. 2007;25:663-670. 42. DeFaria Yeh D, Freeman MW, Meigs JB, et al. Risk factors for coronary artery disease in patients with elevated high-density lipoprotein cholesterol. Am] Cardiol. 2007;99:1~. 43. Carneiro AV Coronary heart disease in diabetes mellitus: risk fac tors and epidemiology. Rev Port Cardiol. 2004;23:1359-1366. 44. Graner M, Syvanne M, Kahri J, et al. Insulin resistance as predic tor of the angiographic severity and extent of coronary artery dis ease. Ann Med. 2007;39:137-144. 45. Orchard TJ, Costacou T, Kretowski A, et al. Type 1 diabetes and coronary artery disease. Diabetes Care. 2006;29:2528-2538.
'"
1
r
e
'
d
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
46. Pepine C], Kowey PR, Kupfer S, et al. Predictors of adverse out come among patients with hypertension and coronary artery dis ease.] Am Coll Cardiol. 2006;47:547-551. 47. Hennessey ]V, Westrick E. Coronary artery disease and cere brovascular disease prevention in diabetes mellitus: early identi fication and aggressive modification of risk factors. Med Health RI. 1998;81:350--352. 48. Sukhija R, Aronow WS, Yalamanchili K, et al. Prevalence of coro nary artery disease, lower extremity peripheral arterial disease, and cerebrovascular disease in no men with an abdominal aor tic aneurysm. Am] Cardiol. 2004;94: 1358-1359. 49. Ness ], Aronow WS. Prevalence of coronary artery disease, ischemic stroke, peripheral arterial disease, and coronary revas cularization in older African-Americans, Asians, Hispanics, whites, men, and women. Am] Cardia!. 1999;84:932-933, A7. 50. Lee CS, Lu YH, Lee ST, et al. Evaluating the prevalence of silent coronary artery disease in asymptomatic patients with spinal cord injury. Int Heart]. 2006;47:325-330. 51. Bauman WA, Spungen AM, Raza M, et al. Coronary artery disease: metabolic risk factors and latent disease in individuals with para plegia. Mt Sinai] Med. 1992;59:163-168. 52. White L], McCoy SC, Castellano V, et al. Effect of resistance train ing on risk of coronary artery disease in women with multiple sclerosis. Scand] Clin Lab Invest. 2006;66:351-355. 53. Steffens DC, O'Connor CM, Jiang WJ, et al. The effect of major depression on functional status in patients with coronary artery disease.] Am Geriatr Soc. 1999;47:319-322. 54. Pamukcu B, Otlaz H, Onur I, et al. Clinical relevance of aspirin resistance in patients with stable coronary artery disease: a prospective follow-up study (PROSPECTAR). Blood Coagul Fibrinolysis. 2007; 18: 187-192. 55. Ludvig], Miner B, Eisenberg MJ. Smoking cessation in patients with coronary artery disease. Am Heart]. 2005;149:565-572. 56. Schooling CM, Lam TH, Leung GM. Effect of obesity in patients with coronary artery disease. Lancet. 2006;368: 1645; author reply 1645-1646. 57. Lundberg GD. A new aggressive approach to screening and early intervention to prevent death from coronary artery disease. MedGenMed. 2006;8:22. 58. Boekholdt SM, Sandhu MS, Day NE, et al. Physical activity, C reactive protein levels and the risk of future coronary artery dis ease in apparently healthy men and women: the EPIC-Norfolk prospective population study. Eur] Cardiovasc Prev Rehabil. 2006; 13:970-976. 59. Prayaga S. Asian Indians and coronary artery disease risk. Am] Med. 2007;120:e15; author reply e19. 60. Chambers TA, Bagai A, Ivascu N. Current trends in coronary artery disease in women. Curr Opin Anaesthesiol. 2007;20: 75-82. 61. Turhan S, Tulunay C, Gulec S, et al. The association between androgen levels and premature coronary artery disease in men. Co ron Artery Dis. 2007;18:159-162. 62. Saghafi H, Mahmoodi M], Fakhrzadeh H, et al. Cardiovascular risk factors in first-degree relatives of patients with premature coro nary artery disease. Acta Cardiol. 2006;61:607-613.
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63. Ahmed A, lefante CM, Alam N. Depression and nursing home admis sion among hospitalized older adults with coronary artery disease: a propensity score analysis. Am] Geriatr Cardiol. 2007;16:76-83. 64. Nauer KA. Acute dissection of the aorta: a review for nurses. Crit Care Nurs Q. 2000;23:20-27. 65. McKnight JT, Adcock BB. Paresthesias: a practical diagnostic approach. Am Fam Physician. 1997;56:2253-2260. 66. Poncelet AN. An algorithm for the evaluation of peripheral neu ropathy. Am Fam Physician. 1988;57:755-764. 67. Gillette PD. Exercise in aging and disease. In: Placzek JD, Boyce DA, eds. Orthopaedic Physical Therapy Secrets. Philadelphia: Hanley & Belfus; 2001:235-242. 68. Clarke M, Hpewell S, Juszczak E, et al. Compression stockings to prevent deep vein thrombosis in long-haul airline passengers. Int ] Epidemio!. 2006;35:1410-1411; discussion 1411. 69. Ali A, Caine MP, Snow BG. Graduated compression stockings: physiological and perceptual responses during and after exercise. ] Sports Sci. 2007;25:413-419. 70. Compression stockings. How hosiery can help circulation and leg swelling. Mayo Clin Womens Healthsource. 2006; 10:6. 71. Graduated compression stockings. Prevention of postoperative venous thromboembolism is crucial. Am ] Nurs. 2006; 106: 2AA-DD. 72. Motsch J, Walther A, Bock M, et al. Update in the prevention and treatment of deep vein thrombosis and pulmonary embolism. Curr Opin Anaesthesio!. 2006;19:52-58. 73. Garmon RG. Pulmonary embolism: incidence, diagnosis, preven tion, and treatment.] Am Osteopath Assoc. 1985;85: 176-185. 74. Bounameaux H, Reber-Wasem MA. Superficial thrombophlebitis and deep vein thrombosis: a controversial association. Arch Intern Med. 1997;157:1822-1824. 75. Gorman WP, Davis KR, Donnelly R. ABC of arterial and venous disease. Swollen lower limb-1: general assessment and deep vein thrombosis. EM]. 2000;320: 1453-1456. 76. Aschwanden M, Labs KH, Engel H, et al. Acute deep vein throm bosis: early mobilization does not increase the frequency of pul monary embolism. Thromb Haemost. 2001;85:42--46. 77. Fukazawa R, Ikegam E, Watanabe M, et al. Coronary artery aneurysm induced by kawasaki disease in children show features typical senescence. Circ]. 2007;71:709-715. 78. Zevitz ME. Heart Failure. Available at: http://www.emedicine.com/ medltopic3552.htm, 2005. 79. Rees K, Taylor RS, Singh S, et al. Exercise based rehabilitation for heart failure. Cochrane Database Syst Rev. 2004;3:CD003331. 80. Pina IL, Daoud S. Exercise and heart failure. Minerva Cardioangiol. 2004;52:537-546. 81. Pina IL, Apstein CS, Balady GJ, et al. Exercise and heart failure: A statement from the American Heart Association committee on exercise, rehabilitation, and prevention. Circulation. 2003;107: 1210-1225. 82. Budev MM, Arroliga AC, Wiedemann HP, et al. Cor pulmonale: an overview. Semin Respir Crit Care Med. 2003;24:233-244. 83. Weitzenblum E. Chronic cor pulmonale. Heart. 2003;89:225-230. 84. Lehrman S, Romano P, Frishman W, et al. Primary pulmonary hypertension and cor pulmonale. Cardiol Rev. 2002;10:265-278.
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85. Romano PM, Peterson S. The management of cor pulmonale. Heart Dis. 2000;2:431--437. 86. Missov ED, De Marco T. Cor pulmonale. Curr Treat Options Cardiovasc Med. 2000;2:149-158. 87. Rothstein ]M, Roy SH, Wolf SL. Vascular anatomy, cardiology, and cardiac rehabilitation. The Rehabilitation Specialists Handbook. Philadelphia: Davis; 1991:548--550. 88. Roffe C. Aging of the heart. BrJ Biomed Sci. 1998;55:136-148. 89. Alaeddini ], Alimohammadi B. Angina Pectoris. Available at: www.emedicine.comlmed/topic133.htm. 2006. 90. Fenton DE, Stahmer S. Myocardial infarction. Available at: www.emedicine.comlEMERG/topic327.htm. 2006. 91. Gragnani SG, Michelotti F, Rocca R, et al. Primary congenitallym phedema. A case report. Minerva Pediatr. 1999;51:217-219. 92. Wananukul S, ]ittitaworn S. Primary congenital lymphedema involving all limbs and genitalia. J Med Assoc Thai. 2005;88: 1958--1961. 93. Bauer T, Wechselberger G, Schoeller T, et al. Lymphedema prae cox of the lower extremity. Surgery. 2002;132:899-900. 94. Lewis ]M, Wald ER. Lymphedema praecox. J Pediatr. 1984;104: 641.-{)48. 95. Wheeler ES, Chan V, Wassman R, et al. Familial lymphedema praecox: Meige's disease. Plast Reconstr Surg. 1981;67: 362-364. 96. Majeski J. Lymphedema tarda. Cutis. 1986;38:105-107. 97. Saab S, Nguyen S, Collins ], et al. Lymphedema tarda after liver transplantation: a case report and review of the literature. Exp Clin Transplant. 2006;4:567-570. 98. Mancini MC, Gangahar DM. Heart Transplantation. Available at: www.emedicine.comlmed/topic3187.htm. 2006. 99. DeTurk WE. Exercise and the intolerant heart. Clin Manag. 1992;12:67-73. 100. American Physical Therapy Association. Guide to physical thera pist practice. Second edition. Phys Ther. 2001;81:1-746. 101. Laethem CV, Van De Veire N, Backer GD, et al. Response of the oxygen uptake efficiency slope to exercise training in patients with chronic heart failure. Bur J Heart Fail. 2007;7:7. 102. Klecha A, Kawecka-]aszcz K, Bacior B, et al. Physical training in patients with chronic heart failure of ischemic origin: effect on exercise capacity and left ventricular remodeling. BurJ Cardiovasc Prev Rehabil. 2007;14:85-91. 103. Maria Sarullo F, Gristina T, Brusca I, et al. Effect of physical train ing on exercise capacity, gas exchange and N-terminal pro-brain natriuretic peptide levels in patients with chronic heart failure. Bur J Cardiovasc Prev Rehabil. 2006;13:812-817. 104. van Tol BA, Huijsmans R], Kroon DW, et al. Effects of exercise training on cardiac performance, exercise capacity and quality of life in patients with heart failure: a meta-analysis. BurJ Heart Fail. 2006;8:841-850. Epub May 18, 2006. 105. Keteyian S], Brawner CA, Schairer ]R. Exercise testing and train ing of patients with heart failure due to left ventricular systolic dysfunction. J Cardiopulm Rehabil. 1997;17:19-28. 106. Keteyian S], Levine AB, Brawner CA, et al. Exercise training in patients with heart failure. A randomized, controlled trial. Ann Intern Med. 1996;124:1051-1057.
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107. McKelvie RS, Teo KK, McCartney N, et al. Effects of exercise train ing in patients with congestive heart failure: a critical review. ] Am Colt Cardiol. 1995;25:789-796. 108. Dekerlegand]. Congestive heart failure. In: Cameron MH, Monroe LG, eds. Physical Rehabilitation: Evidence-Based Examination, Evaluation, and Intervention. St. Louis: Saunders/Elsevier; 2007: 669---688. 109. de Carvalho T, Curi AL, Andrade DF, et al. Cardiovascular reha bilitation of patients with ischemic heart disease undergoing medical treatment, percutaneous transluminal coronary angio plasty, and coronary artery bypass grafting. Arq Bras Cardiol. 2007;88:72-78. 110. Certo CM, DeTurk WE, Cahalin LP. History of cardiopulmonary rehabilitation. In: DeTurk WE, Cahalin LP, eds. Cardiovascular and Pulmonary Physical Therapy: An Evidence-Based Approach. New York: McGraw-Hill; 2004:35-72. 111. Vibhuti NS, Schocken DD. Cardiac Rehabilitation. Available at: www.emedicine.com/pmr/topic180.htm. 2006. 112. Kafejian-Haddad AP, Perez JM, Castiglioni ML, et al. Lymphscintigraphic evaluation of manual lymphatic drainage for lower extremity lymphedema. Lymphology. 2006;39:41-48. 113. Williams AF, Vadgama A, Franks PJ, et al. A randomized con trolled crossover study of manual lymphatic drainage therapy in women with breast cancer-related lymphoedema. Eurj Cancer Care (Engl). 2002;11:254-26l. 114. Reijnen MM, Disselhoff BC, Zeebregts C]. Varicose vein surgery and endovenous lasertherapy. Surg TechnolInt. 2007;16:167-174. 115. Schmedt CG, Meissner GA, Hunger K, et al. Evaluation of endovenous radiofrequency ablation and laser therapy with endoluminal optical coherence tomography in an ex vivo model. ] Vasc Surg, 2007;45:1047-58. 116. Myers K, Fris R, Jolley D. Treatment of varicose veins byendove nous laser therapy: assessment of results by ultrasound surveil lance. Medj Aust. 2006;185:199-202. 117. Peden E, Lumsden A. Radiofrequency ablation of incompetent perforator veins. Perspect Vasc Surg Endovasc Ther. 2007;19: 73-77. 118. Winsor T, Hyman C. A Primer of Peripheral Vascular Diseases. Philadelphia: Lea & Febiger; 1965.
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
Comprehension Questions
1. The term "cardiac output" refers to the amount of blood pumped by the heart A. During any 24-hour period. B. Relative to body mass. Relative to respiratory rate. D. During 1 minute.
e.
2. What is the function of the pulmonary arteries?
3. Which component of blood is the primary transporter of oxygen in mammals and many other species? 4. In the heart, what is the function of the AV node? 5. On which side of the heart is the tricuspid valve? 6. From which arteries does the heart receive its own blood supply?
7. Which of the four chambers of the heart receives blood from the systemic circulation via the superior vena cavae? 8. What causes the first heart sound (Iubb)? 9. The tricuspid and mitral valves differ from the semilunar valves in that the latter A. Are subjected to more stress and pressure. B. Are located within the heart. Do not have attachments to papillary muscles. D. Have attachments to papillary muscles.
e.
10. The state of the cardiac chamber during its period of contraction is known as A. Syncope. B. Diastole. Systole. D. None of the above.
e.
11. True or false: Starling's law states that within physiologic limits, stretching of the heart muscle will increase the vigor of contractions. A. True. B. False. 12. The clinical signs and symptoms of severe heart failure include all of the following except A. Hypertrophy. B. Resultant congestive heart failure. Lower than normal cardiac output. D. Higher than normal cardiac output.
e.
793
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SECTION II. TESTS AND MEASURES
13. True or false: For any given cardiac output, the mean pressure will be controlled by the resistance factor. A. True. B. False.
14. The heart sounds heard by using a stethoscope over the anterior surface of the chest are associated primarily with A. A combination of the respiratory intake plus the heartbeat. B. The contraction of the ventricles. C. The contractions of the atria. D. The opening and closing of the four major heart valves. 15. What is the function of the chordae tendineae? 16. True or false: Cardiac tissue has the ability to depolarize spontaneously-to contract without external nervous stimulation. A. True. B. Fa/se. 17. Which of the following is the normal conduction pathway for muscular contraction of the heart to follow? A. Left ventricle, right ventricle, atrium. B. Right atrium, left atrium, ventricles. C. Left atrium, right atrium, ventricles. D. Right ventricle, left ventricle, atrium. 18. All A. B. C. D.
of the following are involved with peripheral circulation except Arteries. Capillaries. Veins. Sinuses.
19. At what part of the cardiac cycle do the coronary arteries receive the majority of their blood flow? 20. All A. B. C. D.
of the following are signs and symptoms associated with atherosclerosis except: Increase in systolic pressure. Little or no increase in diastolic pressure. Large increase in pulse pressure. No appreciable change in mean pressure.
21. The specialized receptors lying in the carotid sinus and the aortic arch involve all of the following except A. Mechanoreceptors. B. Pressoreceptors. C. Baroreceptors. D. Chemoreceptors. 22. Active forces that contribute to lymphatic flow include all of the following except A. Skeletal muscle function. B. Negative intrathoracic pressure. C. Lymphatic valves. D. Cardiac function.
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
23. What effect does the Bainbridge reflex have? 24. Factors promoting venous return to the heart during exercise include all of the followi ng except: A. Comparative ease of flow from arteries to veins through dilated skeletal muscle arterioles. B. Increase in venous tone. C. Increased respiratory movements. D. Decreased peristalsis. 25. Edema may be defined as all of the following except A. Brawny or indurated. B. Excess fluid in the interstitial space. C. Acquired or congenital. D. Excess fluid in the intercellular space. 26. Clinical signs and symptoms of congestive heart failure include A. Orthopnea. B. Cyanosis. C. Pitting edema. D. All of the above. 27. Hypertrophy of the left ventricle of the heart is associated with A. Aortic stenosis. B. Mitral stenosis. C. Pulmonary stenosis. D. None of the above. 28. The clinical features of right ventricular hypertrophy in congestive heart failure do not include which of the following? A. Cyanosis. B. Dyspnea. C. Edema of the lower extremities. D. Ascites. 29. Which of the following cardiovascular disorders causes hypertrophy of the left ventricle? A. Pulmonary hypertension. B. Systemic hypotension. C. Stenosis of the mitral valves. D. Stenosis of the aortic valves. 30. Which of the following clinical features of congestive heart failure would not be attributable to right ventricular failure? A. Pulmonary edema. B. Increase in venous pressure. C. Peripheral edema. D. Congestion of the liver.
795
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SECTION II. TESTS AND MEASURES
31. The most frequent area of involvement for myocardial infarction is in the A. Right ventricle. B. Right atrium. C. Left ventricle. D. Left atrium. 32. A disease involving the aorta and its large branches is called A. Arteriosclerosis. B. Atherosclerosis. C. Arteriolosclerosis. D. Venosclerosis. 33. The P-wave of an ECG corresponds to which of the following? A. Mitral depolarization. B. Atrial depolarization. C. Mitral repolarization. D. Atrial repolarization. 34. The T-wave of an ECG is generated by A. Atrial repolarization. B. Atrial depolarization. C. Ventricular repolarization. D. Ventricular depolarization. 35. Intermittent claudication in the lower extremities suggests A. Still's disease. B. Raynaud's disease. C. Buerger's disease. D. Pott's disease. 36. Acute bacterial endocarditis may develop from A. Gonococci. B. Pneumococci. C. Streptococci. D. All of the above. 37. The closure of the mitral valve occurs when A. Left atrial pressure equals left ventricular pressure. B. Left ventricular pressure exceeds left atrial pressure. C. Left atrial pressure exceeds aortic pressure. D. Left atrial pressure exceeds left ventricle pressure. 38. One of the early symptoms of mitral stenosis is A. Palpitations. B. Angina. C. Chest pain. D. Dyspnea with exertion.
CHAPTER 11. CARDIOVASCULAR PHYSICAL THERAPY
39. The physiologic actions of epinephrine includ A. Decreased blood pressure. B. Peripheral vasodilation. C. Increased heart rate. D. Vasoconstriction of cardiac muscle blood vessels. 40. What is the normal resting blood pressure for adults? 41. Describe the classic triad for the pathogenesis of venous thrombosis. 42. Where do most deep vein thromboses rDVT) originate? 43. When do most postoperative DVTs occur? 44. What is the most serious complication of DVT? 45. What prophylactic measures are recommended to prevent DVT? 46. What are the signs and symptoms of pulmonary thromboembolism?
Answers 1. The answer is D. 2. To carry oxygen-deficient blood that has just returned from the body to the lungs, where carbon dioxide is exchanged for oxygen. 3. Hemoglobin. 4. To delay the impulse from the SA node. 5. The right side. 6. The right and left coronary arteries. 7. Right atrium. 8. The AV valves closing. 9. The answer is C. 10. The answer is C. 11. The answer is A. This statement is true. 12. The answer is D. 13. The answer is A. This statement is true. 14. The answer is D. 15. To prevent the valves from everting when the ventricles contract, thereby stopping any backflow of blood. 16. The answer is A. This statement is true. 17. The answer is B. 18. The answer is D.
797
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SECTION II. TESTS AND MEASURES
19. During diastole. 20. The answer is D. 21. The answer is D. 22. The answer is D. 23. The reflex decreases the sympathetic input and heart rate on those occasions when the heart is beating too rapidly. 24. The answer is D. 25. The answer is D. 26. The answer is D. 27. The answer is A. 28. The answer is B. 29. The answer is D. 30. The answer is A. 31. The answer is C. 32. The answer is B. 33. The answer is B. 34. The answer is C. 35. The answer is C. 36. The answer is D. 37. The answer is B. 38. The answer is D. 39. The answer is C. 40. Systolic blood pressure < 120 mm Hg and diastolic blood pressure < 80 mm Hg. 41. Venous stasis, vascular damage, and hypercoagulabiI ity. 42. The calf veins. 43. 50% occur within the first 24 hours; 85% occur within the first 4 days. 44. Pulmonary embolism. 45. Early ambulation, extremity elevation, range-of-motion exercises, graduated elastic stockings, intermittent pneumatic compression stockings, and anticoagulation measures. 46. The clinical presentation may be variable, but most often patients have dyspnea, pleuritic chest pain, hypoxemia, and tachypnea.
Pathology, Gynecology, and Psychology
PATHOLOGY INFECTIOUS DISEASE Infection is a process in which an organism establishes a parasitic rela tionship with its host.! This invasion and multiplication of microorgan isms produces an immune response from the host and subsequent signs and symptoms. Infectious agents are now suspected in the ori gins of chronic diseases such as sarcoidosis, various forms of inflam matory bowel disease, scleroderma, rheumatoid arthritis, systemic lupus erythematosus, diabetes mellitus, Kawasaki disease, Alzheimer's disease, and many forms of cancer. All health care professionals need to have an understanding of the infectious process, the sequence of transmission, and approaches to lessen the spread of infections. A great variety of microorganisms are responsible for infectious diseases, including fungi (yeast and molds), bacteria, mycobacteria, viruses, mycoplasmas, bacteria, rickettsiae, chlamydiae, helminths (e.g., tapeworms), protozoa, and prions.
Study Pearl Nosocomiallnfections (lre those that originate oraccur • ina • hospital ·or hOsp'ltal41kesetting. Clinicians can' help:pr~"~I1~tra~$mission of nosoco." mial.·,··iilrectio·j'l:s••.,:frorn··themselves to othl§r~,· frorn'cUent to.·· dient, ana from·€li·entt~selfQyfoUowing·stan dard.p,ec.ii
• Ille~pensive a~deasy.>~(;).,obta·ii1· ai1dt.r~. .
HEMATOLOGIC (BLOOD) DISORDERS Hematology is the branch of science that studies the form and structure of blood and blood-forming tissues. Function of the hematologic system is integrated with the lymphatic and immune systems. Manifestations of hematologic system dysfunction are outlined in Table 12-1. Hematologic conditions alter the oxygen-carrying capacity of the blood and the constituents, structure, consistency, and flow of the blood. 49 These changes can contribute to hypo- or hypercoagulopathy, increased work of the heart and breathing, impaired tissue perfusion, and increased risk of thrombus. 49
Disorders of Iron Absorption Hemochromatosis. Hemochromatosis is an autosomal recessive hereditary disorder characterized by excessive iron absorption by the small intestine. 49 •55 ,56 Individuals with this condition lack an effective way to remove iron, and the iron begins to accumulate in the liver,
TABLE 12-1. MANIFESTATIONS OF HEMATOLOGIC SYSTEM DYSFUNCTION MANIFESTATION
Edema Congestion Infarction Thrombosis and embolism Lymphedema
Hypotension and shock
DESCRIPTION
Buildup of excessive fluid within the interstitial tissues or within body cavities Buildup of excess blood within the blood vessels of an organ or tissue A localized region of necrosis caused by reduction of arterial perfusion below the level required for cell viability ~ Thrombus: a solid mass of clotted blood within an intact blood vessel or chamber of the heart. ~ Embolus: a mass of solid, liquid, or gas that moves within a blood vessel to lodge at a site distant from its place of origin A chronic swelling of an area because of a buildup of interstitial fluid secondary to obstruction of lymphatiC vessels or lymph nodes. Although it presents commonly in the limbs, it can develop in other areas as well. Lymphedema is a localized and asymmetrical condition The result of reduced arterial blood circulation and thus decreased perfusion to an organ or tissue
Data from Goodman ec. The hematologic system. In: Goodman Therapist. 2nd ed. Philadelphia: Saunders; 2003:509-552.
ee, Boissonnault WG, Fuller KS, eds. Pathology: Implications for the Physical
810
SECTION II. TESTS AND MEASURES
pancreas, skin, heart, and other organs. Symptoms include weakness, fatigue, abdominal pain, arthralgia, or arthritis (40-60% of this popu lation), enlarged liver, and darkened skin. Hemochromatosis is char acterized by: ~ ~
Chronic hemolytic anemia: hemoglobin is released into plasma with resultant reduced oxygen delivery to the tissues. Vaso-occlusion because of the misshapen erythrocytes, which can result in ischemia, occlusion, and infarction of bordering tissue.
Diagnosis can be made by a simple genetic test based on family history. 49 Physical Therapy Role. Due to the fact that arthropathy occurs in 40% to 60% of individuals with hemochromatosis, therapeutic intervention is essential in providing flexibility, strength, and proper alignment to promote function and prevent the loss of independence in activities of daily living. 49 The physical therapist can be very helpful in evaluating the need for assistive devices, orthotics, and splints toward these goals. 49
Study Pearl Exercise intolerance (easy fatigability) can be expected in patients with ane mia. Vital signs should be monitored for tachycardia, which is usually accompanied by a sense of general ized weakness, loss of stamina, and exertional dyspnea. Central nervous system symptoms can develop in cases of severe pernicious anemia, whereas neuropathy is observed in the early cases of B12 deficiency, allowing for early identification.49
Disorders of Erythrocytes Anemia. Anemia, one of the more common blood disorders, is an abnormality in the quantity or quality (reduction in the oxygen-carrying capacity of erythrocytes-see Chapter 11) of the blood. Anemia is not a disease, but rather a symptom of many other disorders, including49 : ~
~
~ ~
~
Dietary deficiency (nutritional anemia): iron, vitamin B, folic acid deficiency. Decreased production of erythrocytes: chronic diseases (rheumatoid arthritis, tuberculosis, cancer), bone marrow failure (leukemia, aplasia), inborn or acquired metabolic defect. Acute or chronic blood loss (iron deficiency): trauma, bleeding peptic ulcer, excessive menstruation, bleeding hemorrhoids. Congenital defects of hemoglobin (sickle-cell diseases). Destruction of erythrocytes (mechanical or autoimmune hemolysis, enzyme defects, hypersplenism).
Treatment of anemia is directed toward alleviating or controlling the causes, relieving the symptoms, and preventing complications. 49
Physical Therapy Role. Exercise for any patient with anemia should be approved by the physician. The prevalence of iron deficiency ane mia is likely to be higher in athletic populations and groups, especially in younger female athletes, than in sedentary individuals. 49 A knowl edge of the underlying cause of the anemia may be very helpful for the physical therapist in identifying red flag symptoms, indicating the need for alteration of the program or medical referraJ.49 Examples include: ~ ~
Evidence of easy bruising in response to the slightest trauma may indicate an alteration in platelet production. Decreased oxygen delivery to the skin results in impaired healing and loss of elasticity, delaying wound healing, and the healing of other musculoskeletal injuries.
CHAPTER 12. PATHOLOGY, GYNECOLOGY, AND PSYCHOLOGY ~
~
811
Paresthesias, especially numbness mimicking carpal tunnel syndrome, gait disturbances, and extreme weakness, can all indicate anemia caused by vitamin BIZ deficiency. Tachycardia and palpitations may occur due to changes in rest ing cardiac output.
Hemostasis Disorders Sickle-Cell Disease. Sickle-cell disease refers to a group of inherited, autosomal recessive disorders in which the erythrocytes, particularly hemoglobin S, are crescent or sickle shaped instead of being bicon cavey--60 The condition is chronic and can be fatal. The two primary pathophysiologic features of sickle-cell disorders are chronic hemolytic anemia and vaso-occlusion resulting in ischemic injury. 49
Sickle-Cell Anemia. Sickle-cell anemia, a hereditary, chronic form of hemolytic anemia, is merely a result of the disease and not the disease itself. 49 In sickle-cell anemia, the erythrocytes rupture, releasing hemo globin prematurely into the plasma, thereby reducing oxygen-delivery capacity to the tissues. It is important that the physical therapist be able to recognize the signs and symptoms associated with sickle-cell ane mia and a condition called sickle-cell crisis, which is an acute episodic condition occurring in children with sickle-cell anemia (Table 12-2). It is also important for the clinician to recognize signs of complications associated with sickle-cell anemia, which include cerebrovascular acci dents, convulsions, blindness, chronic leg ulcers, avascular necrosis of the femoral head, and bone infarcts. 49
Hemophilia. Hemophilia is a bleeding disorder inherited as a sex linked autosomal recessive trait (males are affected, females are carri ers).61--65 'The condition is caused by an abnormality of plasma clotting proteins (clotting factor VIII in hemophilia A; clotting factor IX in hemophilia B or Christmas disease) necessary for blood coagulation, producing a prolonged but not faster bleeding than would occur in a normal person with the same injury. Complications include: ~ ~
~
Joint contracture(s) and deformities (especially at the hip, knee, elbow, and ankle joint"). Hemophiliac arthropathy, which may occur in severe forms: the articular cartilage softens, turns brown (due to hemo siderin), and becomes pitted and fragmented. 49 Muscle weakness and atrophy around affected joints.
TABLE 12-2. SIGNS A.ND SYMPTOMS OF SICKlE-CELL ANEMIA AND SICKLE-CELL CRISIS SICKLE-CELL CRISIS
SICKLE-CELL ANEMIA
Pain (abdOminal, chest, headache) Fatigue Weakness Dyspnea on effort Tachycardia Pallor or yellow skin
Acute and severe pain because of ischemia Recurrent joint, extremity and back pain Neurologic manifestations: dizziness, paresthesias, blindness, and cranial neNe palsies Renal compensations
Data from Goodman ec. The hematologic system. In: Goodman Therapist. 2nd ed. Philadelphia: W.B. Saunders; 2003:509-552.
ee.
Boissonnault WG, Fuller KS, eds. Pathology: Implications for the Physical
812
SECTION II. TESTS AND MEASURES ~ ~ ~ ~
Peripheral nerve compression by hematoma. Postural scoliosis. Decreased aerobic fitness. Difficulties with ADLs.
Currently, no known cure or prenatal treatment for hemophilia exists. 49
Thrombocytosis. Thrombocytosis refers to an increase in the number of circulating platelets (greater than 450,OOO/mm3), which can be primary or secondary.66-69 The high platelet count causes an increase in blood viscosity, which can cause intravascular clumping or thrombosis. Thrombocytopenia. Thrombocytopenia refers to a decrease in the number of circulating platelets (less than 150,OOO/mm3), caused by inadequate platelet production from the bone marrow, increased platelet destruction outside the bone marrow, or splenic sequestra tion,70-73 Thrombocytopenia is a common complication of leukemia or metastatic cancer. The Thalassemias. The thalassemias are a group of inherited, chronic hemolytic anemias commonly affecting people of Mediterranean or southern Chinese ancestry,74 The thalassemias are characterized by production of extremely thin, fragile erythrocytes, called target cells. 49 The onset of thalassemia is usually insidious and the symptoms resemble those of other hemolytic anemias (jaundice, leg ulcers, splenomegaly), and bony changes in older children if untreated. 49 ~ ~
Severity depends on whether the infected patient is homozy gous or heterozygous for the thalassemia trait. Diagnosis is by laboratory testing.
Histiocytosis X. Histiocytosis is a generic name for a group of syndromes characterized by an abnormal increase in the number of certain immune cells called histiocyte cells, including monocytes, macrophages, and dendritic cells,75-77 Most cases of histiocytosis X affect children between ages 1 and 15 years old. The extra immune cells may form tumors, which can affect various parts of the body. In children, histiocytosis X usually involves the bones (80%) and may consist of single or multiple sites. The skull is frequently affected. P~ysical
Disorders.
Therapy
Intervention
for
Hemostasis
It is important that the physician approve any exercise
for the patient with a hemostasis disorder. Physical therapy interven tion should be geared towards enhancing flexibility, strength, and appropriate alignment to promote function, preventiing contracture formation, preventing falls, and preventing the reduction of independ ence with ADLs.49 The physical therapist can provide methods of pain control, relaxation techniques, emotional support, patient and family education, and the provision of assistive devices, orthotics, or splints. In those patients with hemostasis disorders, physical therapists need to be able to recognize any signs of early (first 24 to 48 hours) bleeding
CHAPTER 12. PATHOLOGY, GYNECOLOGY, AND PSYCHOLOGY
episodes (warm, swollen, and painful joints with decreased range of motion, paresthesias, protective muscle spasm). and sickle-cell crisis (Table 12-2).49 Providing immediate factor replacement by medical personnel to stop the bleeding, and following the PRICE (protection, rest, ice, compression, and elevation) principle to promote comfort and healing are two goals for treating acute joint hemarthrosis or muscle bleed. 49 J
813
Study Pearl Patients withsivl ~~f1l~~~r,~~siyely·• . inc~~~~~ ~·iZ·,,:':~ ~ L~ d~ ~lfa(;tors. .
~
Increased blood volume: increases progressively from 6 to 8 weeks' gestation (pregnancy) and reaches a maximum at approximately 32 to 34 weeks with linle change thereafter. 18l The increased blood volume serves two purposes1 82 ,J83: • It facilitates maternal and fetal exchanges of respiratory gases, nutrients, and metabolites. • It reduces the impact of maternal blood loss at delivery. Typical losses of 300 to 500 mL for vaginal births and 750 to 1000 mL for cesarean sections are thus compensated with the so-called "autotransfusion" of blood from the contracting uterus. Increased plasma volume (40-50%) is relatively greater than that of red cell mass (20-30%), resulting in hemodilution and a decrease in hemoglobin concentration (intake of supplemental iron and folic acid is necessary to restore hemoglobin levels to normal, which is 12 gldL).182,J84,185 Increased cardiac output: increases to a similar degree as the blood volume. 182 ,J83 During the first trimester, cardiac output is 30% to 40% higher than in the nonpregnant state. 184 During labor, further increases are seen. The heart is enlarged by both chamber dilation and hypertrophy.
Metabolic System. Because of the increased demand for tissue growth, insulin is elevated from plasma expansion, and blood glucose is reduced for a given insulin load. Fats and minerals are stored for maternal use. The metabolic rate increases during both exercise and preg nancy, resulting in greater heat production. Fetoplacental metabolism generates additional heat, which maintains fetal temperature at O.5°C to 1.0°C (0.9°F to 1.8°F) above maternal levels. 186-188
CHAPTER 12. PATHOLOGY, GYNECOLOGY, AND PSYCHOLOGY
Renal and Urologic Systems. During pregnancy, the renal threshold for glucose drops because of an increase in the glomerular filtration rate and there is an increase in sodium and water retention. 165 Anatomic and hormonal changes during pregnancy place the pregnant woman at risk for both lower and upper urinary tract infections and for urinary incontinence. 165 As the fetus grows, stress on the mother's blad der can occur. This can result in urinary incontinence (refer to "Urinary Incontinence" earlier in the chapter). COMPLICATIONS ASSOCIATED WITH PREGNANCY
Hypertension. Hypertensive disorders complicating pregnancy are the most common medical risk factor responsible for maternal mor bidity and death related to pregnancy.165 Hypertensive disorders com plicating pregnancy have been divided into five types (Table 12-12). Symphysis Pubis Dysfunction (SPD) and Diastasis Symphysis Pubis (DSP). The symptoms of SPD and DSP vary from person to person. On examination, the patient typically demon strates an antalgic, waddling gait. 194-197 Subjectively the patient reports pain with any activity that involves lifting one leg at a time or parting the legs. Lifting the leg to put on clothes, getting out of a car, bending over, turning over in bed, sitting down or getting up, walking up stairs, standing on one leg, lifting heavy objects, and walking in general are all painful. Patients may also report that the hip joint seems stuck in place or they describe having to wait for it to "pop into place" before being able to walk. Palpation reveals anterior pubic symphyseal ten derness. Occasional clicking can be felt or heard. The findings on the physical examination include positive sacroiliac joint stress tests (com pression, distraction, and FABER tests). The range of hip movements will be limited by pain, and there is an inability to stand on one leg. Characteristic pain can often be evoked by bilateral pressure on the trochanters or by hip flexion with the legs in extension. However, such maneuvers may result in severe pain or muscle spasm and are not nec essary for diagnosis. Radiologic evaluation may occasionally be useful in confirming the diagnosis. 198 The amount of symphyseal separation does not always correlate with severity of symptoms or the degree of disability. Therefore, the intervention is based on the severity of symp toms rather than the degree of separation as measured by imaging studies. 198 Although the symptoms can be dramatically severe in presenta tion for SPD and DSP, a conservative management approach is often effective in cases of SPD. In more severe cases, the interventions can inch:de bed rest in the lateral decubitus position, pelvic support with a brace or girdle, ambulation with assistance or devices such as walkers, and graded exercise protocOIS. 198 In all cases, patient education is extremely important in terms of providing advice on how to avoid stress to the area. Suggestions to give include the following. ~ ~
Use a pillow between the legs when sleeping. Move slowly and without sudden movements. Keep the legs and hips parallel and as symmetrical as possible when moving or turning in standing, and in bed. Silk/satin sheets and night garments may make it easier to turn over in bed.
Study Pearl
841
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SECTION II. TESTS AND MEASURES
TABLE 12-12. SUMMARY OF TYPES OF HYPERTENSION DURING PREGNANCY DISORDER/INCIDENCE Gestational hypertension: affects nulliparous women most often
DEFINITION Diagnoses made retrospectively when preeclampsia does not develop and blood pressure returns to normal by the 12th week postpartum
DIAGNOSTIC CRITERIA
SIGNS/SYMPTOMS
Blood pressure 140/90 mm Hg or greater for the frrst time during pregnancy; no proteinuria; blood pressure returns to normal by 12 weeks postpartum Blood pressure 140/90 nm1 Hg or greater after 20 weeks gestation; proteinuria: 300 mg or more of urinary protein in a 24-hour period or persistent 30 mg/dL in random urine samples
Epigastric pain, thrombocytopenia, headache
A life-threatening disorder that Preeclampsia: 5% incidence influenced occurs only during pregnancy and the postpartum period (in by parity, race, etlmicity, and environmental at least 5-8% of all pregnancies) factors and atlects both the mother and the unborn baby. The syndrome involves reduced organ perfusion from vasospasm and endothelial activation Eclampsia: 1 in 3250 in Seizures in a pregnant woman Grand mal seizures appearing United States (1998) with preeclampsia not assigned before, during, or after labor; in nulliparas, seizures may to other causes develop 48 hours to 10 days after delivery
Superimposed preeclampsia on chronic hypertension
Chronic hypertensive disorders predispose the development of superimposed preeclampsia or eclampsia
Chronic hypertension: strong familial history of essential hypertension and/or multiparous women with hyperten sion complicated by a previous pregnancy beyond the first one
Hypertension that persists longer than 12 weeks after delivery
New-onset proteinuria of 300 mg or more in 24 hours in hypertensive women; no proteinuria before 20 weeks gestation Blood pressure 140/90 nm1 Hg or greater before pregnancy; hypertension 140/90 =1 Hg or greater detected before 20 weeks, gestation; persistent hypertension long after delivery
The more severe the hypertension or proteinuria, the more certain is the severity of preeclampsia; symptoms of eclampsia, such as headache, cerebral vLsual disturbance, and epigastric pain can occur Mother may develop abmptio placentae, neurological deficits, aspiration pneumonia, cardiopulpulmonary edema, cardiopulmonary arrest, acute renal failure; maternal death The risk of abmptio placentae; fetus at risk for growth restriction and death
Risk of abmptio placentae; fetus at risk for growth restriction and death; pulmonary edema; hypertensive encephalopathy; renal failure
Reproduced, with permission, from Boissonnault ]S, Stephenson R: The obstetric patient. In: Boissonnault WG, ed. Primary Care for the Physical Therapist: E>;;amination and Triage. St. Louis: Elsevier Saunders; 2005:239--270. Copyright© Elsevier.
~ ~ ~ ~
A waterbed mattress may be helpful. When standing, stand symmetrically, with the weight evenly
distributed through both legs. Avoid "straddle" movements.
Sit down to get dressed, especially when putting on underwear
or pants. An ice pack may feel soothing and help reduce inflammation in the pubic area.
Swimming may help relieve pressure on the joint (the breaststroke may prove aggravating). Deep-water aerobics or deep-water running using floatation devices may also be helpful.
CHAPTER 12. PATHOLOGY, GYNECOLOGY, AND PSYCHOLOGY
843
Resolution of symptoms in approximately 6 to 8 weeks with no lasting sequela is the most cornmon outcome in SDP and DSp. 198 Occasionally, patients report residual pain requiring several months of physical therapy but long-term impairment is unusual. Surgical inter vention is rarely required but may be utilized in cases of inadequate reduction, recurrent diastasis, or persistent symptoms.
Low Back Pain. Low back pain is said to occur in 50% to 90% of pregnant women.17°.199--206 However, it is not clear whether the low back pain is the result of the shift in the center of gravity and con comitant changes in the spinal curvature. Because the annulus is a lig amentous structure, and therefore softens with the release of relaxin, it could be postulated that the low back pain may be related to structural changes in the intervertebral disk. However, frank disc herniations are no more cornmon dUring pregnancy than at other times. Thus, the pain is likely mechanical in nature. Coccydynia. Coccygeal pain, pain in and around the region of the coccyx, is relatively cornmon postpartum. 20 7- 211 Symptoms include pain with sitting. The patient should be provided with seating adaptation (donut cushion) to lessen the weight on the coccyx and to support the lumbar lordosis. If symptoms persist for more than a few weeks, the displaced coc cyx can often be corrected manually by grasping the coccyx after inserting the index finger in the anal canal. The coccyx is distracted and pulled posteriorly, while pulling laterally on the medial surface of the ischial tuberosity. Gestational Diabetes. Gestational diabetes is detlned as carbo hydrate intolerance of variable severity, with onset or first recognition during pregnancy. After the birth, blood sugars usually return to nor mal levels; however, frank diabetes often develops later in life. Typical causes include: ~
~
Genetic predisposition. • High-risk populations include people of Hispanic, Asian, or African descent. • Family history of diabetes, gestational diabetes, or glucose intolerance. Increased tissue resistance to insulin during pregnancy, due to increased levels of estrogen and progesterone
Current risk factors include: ~ ~
~
~ ~
Maternal obesity (> 20% above ideal weight). Excessive weight gain during pregnancy. Low level of high-density-lipoprotein (HDL) cholesterol «0.9 mmol/L) or elevated fasting level of triglycerides (>2.8 mmol/o. Hypertension or preeclampsia (risk for gestational diabetes is increased to 10% to 15% when hypertension is diagnosed). Maternal age > 25 years.
Most individuals with gestational diabetes are asymptomatic. However, subjectively the patient may complain of:
I
StUdy Pe_ar_1-
It is worth remembering that complaints of low back pain in this popu I lation may be because of a kidney or I urinary tract infection.
844
SECTION II. TESTS AND MEASURES ~
~ ~ ~
Polydipsia. Polyuria. Polyphagia. Weight loss.
Diastasis Recti Abdominis. Diastasis recti abdominis is defined as a lateral separation of greater than two fingertip widths of the two bellies of the rectus abdominis at the linea alba (or linea nigra, in pregnancy) that can occur during pregnancy or delivery. To check for diastasis recti, the patient is asked to lie supine with the knees bent and feet flat on the floor. The clinician places his or her fingertips in the center of the abdomen just above the navel. The patient is then asked to perform a posterior pelvic tilt, and then exhale as she lifts the head off the floor. If a diastasis recti is present the clinician will be able to press the fingertips into the gap between the two sides of the muscle. If diastasis recti abdominis is confirmed, corrective exercises need to be performed to prevent further muscle trauma. The patient can per form any exercise that does not increase intra-abdominal pressure including partial sit-ups, posterior pelvic tilts while using hands to sup port the abdominal wall, and transversus abdominis exercises. Traditional abdominal exercises, such as full sit-ups or bilateral straight leg raises, can be resumed when the separation is less than 2 cm. Cesarean Childbirth. Cesarean delivery, also known as cesarean section, is a major abdominal surgery involving 2 incisions: ~ ~
An incision through the abdominal wall. An incision involving the uterus to deliver the baby.
Although the physical therapist is not involved in the surgical pro cedure, he or she can play an important role postoperatively: ~ ~
~
TENS can be described to decrease incisional pain (electrodes are placed parallel to the incision). Patient education: • Correct breathing and coughing to prevent postsurgical pul monary complications. • Heavy lifting precautions (4 to 6 weeks), use of pillow for incisional support. • Instruction on transverse frictional massage to prevent inci sional adhesions. • Ambulation.
Exercise:
• Postural exercises. • Pelvic floor exercises. • Gentle abdominal exercises
Hyperemesis Gravidarum. The calLses of this condition are largely unknown. Indications that the patient may have this condition include per sistent and excessive nausea and vomiting throughout the day and an inability to keep down any solids or liquids. If the condition is prolonged, the patientt may also report fatigue, lethargy, headache, and faintness. 174,m Various degrees of dehydration may be present: skin may be pale, there may be dark circles under eyes, eyes may appear sunken, mucous membranes may be dry, and skin turgor may be poor. 174,177
CHAPTER 12. PATHOlOGY, GYNECOLOGY, AND PSYCHOlOGY
Supine Hypotension. Supine hypotension (also known as infe rior vena cava syndrome) may develop in the supine position, espe cially after the first trimester. The decrease in blood pressure is thought to be caused by the occlusion of the aorta and inferior vena cava by the increased weight and size of the uterus. Spontaneous recovery usually occurs upon change of maternal position. However, patients should not be allowed to stand up quickly, to decrease the potential for hypotension. Signs and symptoms of this condition include: ~
~ ~ ~
~
~ ~ ~ ~
~
Bradycardia.
Shortness of breath.
Syncope (fainting).
Dizziness.
Nausea and vomiting.
Sweating or cold, clammy skin.
Headache.
Numbness in the extremities.
Weakness.
Restlessness.
Psychiatric Changes. Pregnancy-related depression and post partum depression may occur. Postnatal depression has been docu mented to occur in 5% to 20% of all postpartum mothers,212-214 but can also occur in fathers. 215 Depressive postpartum disorders range from "postpartum blues," which occur from 1 to 5 days after birth and last for only a few days, to postpartum depression and postpartum psy chosis, the latter two of which are more serious conditions and require medical or social intervention to avoid serious ramifications for the family unit. 165 ,216,217 PHYSICAL THERAPY EXAMINATION Special questions for the pregnant patients should include the following l65 : ~
~
~
~
Have you had any complications with the pregnancy?
Complications include uterine bleeding, premature contrac
tions, incompetent cervix, pregnancy-induced hypertension,
preeclampsia, or other need for special tests or bed rest. A pos
itive response to this question may alter the rigor of the physi
cal exam and any exercise prescribed, It may also necessitate
monitoring of vital signs and other signs and symptoms with
each visit.
Have you had any complications with a previous pregnancy or
delivery that is placing you at high risk now? For example,
preterm labor in one pregnancy places a woman at risk for sim
ilar outcome in subsequent pregnancies.
Did you have any of your current musculoskeletal symptoms
dUring a previous pregnancy, and if so, what was done for
them, and was the treatment successful?
Which medications are you currently taking and what medica
tions did you stop taking because of the pregnancy? Many pre
scription and some over-the-counter medications and herbal
remedies are contraindicated in pregnancy because of the risk
845
846
SECTION II. TESTS AND MEASURES
~
to the fetus or the mother. Medications such as nonsteroidal anti-inflammatories, antidepressants, and migraine prescrip tions are contraindicated in pregnancy. Herbal remedies con taining aloe, cascara, anthraquinone, or phenolphthalein should be avoided. Do you currently have any urinary stress incontinence? Recognition of this condition will help a physical therapist and patient with the intervention before and after delivery.
PHYSICAL THERAPY INTERVENTION Given the number of physiologic changes that occur during pregnancy and the postpartum period within the various body systems, the extent of the physical therapy intervention will depend on the findings of the examination. Therapeutic exercise plays a key role with this patient population. Objective data on the impact of exercise on the mother, the fetus, and the course of pregnancy are limited, and results of the few stud ies in humans are often equivocal or contradictory.218 Both exercise and pregnancy are associated with a high demand for energy. Caloric demands with exercise are even higher. The competing energy demands of the exercising mother and the growing fetus raise the theoretical concern that excessive exercise might adversely affect fetal development. 165 Theoretically, because of the physiologic changes associated with pregnancy, as well as the hemodynamic response to exercise, some precautions should be observed during exercise218-225: ~
~
Study Pearl Wamingsi&ns ·a~sodated .withexer dse· ouring pregnancy inc1vde: ~
~
~
Pain.
~ V~gi~ 30 Impaired mobility
Data from Fuller GF: Falls in the elderly. Am Fam Physician. 2000;61:2159-2168, 2173-2174 and from Podsiadlo D, Richardson S: The timed "Up & Go": A test of basic functional mobility for frail elderly persons. ] Am Geriatr Soc. 1991;39:142-148 and from Mathias S, Nayak US, Isaacs B: Balance in elderly patients: the "get-up and go" test. Arch Phys Med Rehabil. 1986;67:387-389.
Physical Therapy Intervention. With patients who have a his tory of falling, the intervention is directed at the underlying cause of the fall and in preventing recurrence. Interventions that may be suc cessful in reducing falls are listed in Tables 14-10 and 14-11. Functional training should include ~ ~
~
~
Sit to stand transitions. Turning. The provision of appropriate assistive devices/adaptive equipment. Patient and family/caregiver education • Identification of risks. • Safety issues. • Adequate lighting at home. • Using contrasting colors. • Reducing clutter.
POLYPHARMACY AND MEDICATION ERRORS Refer to Chapter 19.
TABLE 14-10. CRITICAL STEPS IN REDUCING THE RISK OF FALLS IN THE ELDERLY Eliminate environmental hazards. Improve home supports. Provide opportunities for socialization and encouragement. Modify medication. Provide balance training. Modify restraints. Involve the family. Provide follow-up. Data from Sloan JP: Mobility failure, in Sloan JP (ed): Protocols in primary care gen·atn'cs. New York, Springer, 1997;33-38.
956
SECTION II. TESTS AND MEASURES
TABLE 14-11. INTERVENTIONS BASED ON RISK FACTORS TO REDUCE lBE RISK OF FALLS IN lBE ELDERLY RISK FACTORS Postural hypotension: a drop in systolic blood pressure of ;:: 20 mm Hg or to < 90 mm Hg on standing
Use of a benzodiazepine or other sedative-hypnotic drug Use of four or more prescription medications Environmental hazards for falling or tripping Any impairment in gait
Any impairment in balance or transfer skills Impairment in leg or arm muscle strength or range of motion (hip, ankle, knee, shoulder, hand, or elbow)
INTERVENTIONS Behavioral recommendations, such as ankle pumps or hand clenching and elevation of the head of the bed. Decrease in the dosage of a medication that may contribute to hypotension; if neces sary, discontinuation of the drug or substitution of another medication. Pressure stockings. If indicated, fludrocortisone (FlorineD, in a dosage of 0.1 mg two or three times daily, to increase blood pressure. If indicated, midodrine (ProAmatine), in a dosage of 2.5 to 5 mg three times daily, to increase vascular tone and blood pressure. Education about appropriate use of sedative-hypnotic drugs. Nonpharmacologic treatment of sleep problems, such as sleep restriction. Tapering and discontinuation of medications. Review of medications. Home safety assessment with appropriate changes, such as removal of hazards, selection of safer furniture (correct height, more stability), and installation of structures such as grab bars in bathrooms or handrails on stairs. Gait training. Use of an appropriate assistive device.
Balance or strengthening exercises if indicated.
Balance exercises and training in transfer skills if indicated.
Environmental alterations, such as installation of grab bars or raised toilet seats.
Exercises with resistive bands and putty resistance training two or three times a week, with resistance increased when the patient is able to complete 10 repetitions through the full range of motion.
Data from Fuller GF: Falls in the elderly. Am Pam Physician. 2000;61 :2159--2168, 2173--2174 and from Tinetti ME, Baker Dr, McAvay G, et al: A mul tifactorial intervention to reduce the risk of falling among elderly people living in the community. N Engl] Med. 1994;331:821-827.
NUTRITIONAL DEFICIENCY Nutritional status is a "vital sign" of health. 69- 74 Nutrition takes on greater importance in the context of chronic illness. With increase in age, there is an increased risk of developing nutritional deficiencies that can lead to such debilitating consequences as functional dependency, morbidity, and mortality. Some older persons are at increased risk for nutritional deficiency because of multiple drug therapies, dental prob lems, economic hardship, and reduced social contacts. These problems arise from many varied environmental, social, and economic factors that are compounded by physiologic changes of aging. A statement on nutrition screening is needed in order to ~ ~
Incorporate nutritional screening in the clinical care of older persons. Heighten awareness of the multiple risk factors having an impact upon nutritional status of older persons.
The Food and Nutritional Board of the Institute of Medicine no longer uses the term Recommended Daily Allowance. Rather, they use Dietary Reference Intake (DRI). DRIs are reference values to estimate the nutrient intakes to be used for planning and assessing diets for healthy people. Many of the DRIs for older adults are not based on large studies of older people, but are derived by extrapolation from data obtained for
CHAPTER 14. GERIATRIC PHYSICAL THERAPY
957
TABLE 14-12. RDI FOR OLDER ADULTS OVER 70 REQUIREMENTS
HEALTHY ELDERLY WOMEN
Protein
1 g/kg body weight
1 g/kg body weight
Carbohydrate Fat
55--60% of total calories/day 30% of total calories/day
55--60% of total calories/day 30% of total calories/day
Water
1 mUkcal or 30 mL/kg body weight
1 mUkcal or 30 mL/kg body weight
Calories Calcium Zinc Iron Selenium Vitamin C Thiamin Folate Vitamin BIZ Vitamin D Vitamin E
1900 kcalldayor 30 kcallday 1200-1500 mg 8mg 8mg 55 Ilg 75 mg 1.1 mg 400 ug 2.4 ug 600 IU 15 IU
2300 kcallday or 30 kcallday 1200-1500 mg 11 mg 8mg 55 mcg 90 mg 1.2 mg 400 ug 2.4 ug 600 IU 15 IU
HEALTHY ELDERLY MEN
ADDITIONAL COMMENTS Acute and chronic diseases increases protein requirements. Healthy elderly in their 60s to 70s but overweight, hypercholesterolemic, and/or hypertensive, should reduce calories, fat, and, sodium under the supervision of a clinician. Aging does not alter any of the speciflc requirements for any essential lipids. Dehydration and diarrhea. The amount of fluid that is lost must be replaced, and replaced soon after the fluid loss. Patients and families must be educated to the importance of maintaining adequate fluid intake at all times, especially with acute conditions.
If no sun exposure, 800-1600 IU per day.
Data from Food and Nutrition Board, the National Academies of Sciences. Dietary Reference Intakes (DRl). Washington, DC: Institute of Medicine, :-Iational Academy of Science: 2001.
younger persons. The DRI adjustments for older adults have been made based on the reduction in physiologic function, changes in body compo sition and metabolic adaptation in adults over 51 years of age and then again over 71 years of age. Table 14-12 shows the most current DRIs.
Physical Therapy Role. A proper and continuous nutritional assessment of a patient's nutritional status is important to identify those patients who are at risk (Table 14-13 and 14-14). Although not directly involved with the patient's nutritional status, the physical therapist should attempt to ~ ~
~
~
Maintain or improve patient's physical function. Assist in the monitoring of the patient's nutritional intake by observing any physical or mental changes that could be nutri tionally related. Request nutritional consults as necessary • Communication with social worker for elderly food programs (Meals on Wheels, federal food stamp programs),
Recommendations for home health aides
• Assistance in grocery shopping. • Meal preparation.
958
SECTION II. TESTS AND MEASURES TABLE 14-13. NUTRITIONAL ASSESSMENT IN OLDER ADULTS
Past medical histOly Current symptoms History suggestive of depression Use of tobacco, alcohol, or illicit drugs Current medications including OTCs Socioeconomic status Weight loss (> 10% in 6 months or > 5% in 1 month) Alteration in functional status Comprehensive metabolic panel Serum levels of total protein, albumin, prealbumin, total cholesterol Thyroid function tests Serum vitamin and mineral levels: iron, folic acid, vitamin B I2 Daily energy intake and recent changes Anthropometries Oral/dental status Signs of vitamin or mineral deficiency Functional status
GENERAL PRINCIPLES OF GERIATRIC REHABIUTATION The following areas should be emphasized in the intervention of the elderly population ~
~
~
Safety • Level of cognition, vision, hearing, proprioception. • Appropriate and safe use of assistive devices. Home/living environment. Level of activity/exercise. The absolute contraindications for exercising older adults include, but are not limited to • Severe coronary artery disease with un.la ::la
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ith ~
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places the arms around patient's chest and clasps the hands behind the patient's back. Supporting the leg farther from the wheelchair between his or her legs, the clinician leans back, shift his or her weight, and lifts. The patient pivots toward the chair where possible, or is guided by the clinician. If the patient's legs are weak and appear to be buckling, the clinician can brace the knees against the patient's knees. Once correctly positioned, the patient bends toward the clinician, who bends his or her knees and lowers the patient into the back of the wheelchair. Level surfaces (bed to gurney). The clinician and an assistant stand on opposite sides of the bed, with the clinician on the side of the direction of the transfer. A large plastic garbage bag is placed between the sheet and the draw-sheet, beneath one edge of the patient's torso. The patient's legs are moved closer to the edge of the bed. Grasping the draw street on both sides of the bed, on a count of three the clinician leans backward and shifts his or her weight, sliding the patient to the edge of the bed, while the assistant holds the sheet to keep it from slipping. The bed is raised so that it is slightly higher than the gurney, and the head of the bed is lowered. The patient's legs are moved onto the gurney, and the assistant kneels on the bed. On the count of three, the clinician and assistant grasp the drawer sheet and slide the patient onto the gurney. This may take several attempts. Wheelchair to toilet, tub seat. The wheelchair is positioned as close to the destination as possible. The clinician locks the wheelchair and fastens the transfer belt. The clinician helps the patient slide to the edge of the wheelchair and positions the patient's feet directly under his or her body. The clinician lifts the patient, grasping the back of the transfer belt, and helps the patient pivot around in front of the toilet, keeping the patient's knees between the clinician's legs. The patient grasps each of the safety rails as he or she is slowly and gently lowered down onto the toilet.
Dependent Transfers. Assisted Transfers.
See Table 15-7.
See Table 15-8.
ASSISTIVE DEVICES The indications for using an assistive device include ll ~
~ ~ ~ ~
Decreased ability to weight bear through the lower extremities (refer to "Levels of Weight Bearing" later in the chapter). Muscle weakness or paralysis of the trunk or lower extremities. Decreased balance and proprioception in the upright posture. Joint instability and excessive skeletal loading. Fatigue or pain.
However, there are a number of energy costs associated with using various assistive devices (Table 15-9).
999
1000
SECTION II. TESTS AND MEASURES
TABLE 15-7. DEPENDENT TRANSFERS lYPE OF TRANSFER
Three-person carry/lift
Two-person lift
Dependent squat pivot transfer
Hydraulic or mechanical lift
DESCRIPTION
Used to transfer a patient from a stretcher to a bed or treatment plinth. Three clinicians carry the patient in a supine position; one clinician supports the head and upper trunk, the second clinician supports the trunk, and the third supports the lower extremities. The clinician at the head of the bed is usually the one to initiate commands. The clinicians flex their elbows and are positioned under the patient, and roll the patient on his or her side toward them. The clinicians then lift on command and move in a line to the destination surface, lower, and position the patient properly. Used to transfer patient between two surfaces of different heights or when transferring a patient to the floor. Standing behind the patient, the first clinician should place the arms underneath the patient's axilla. The clinician should grasp the patient's left forearm with the right hand and grasp the patient's right forearm with the left hand. The second clinician places one arm under the mid to distal thighs and the other arm is used to support the lower legs. The clinician at the head usually initiates the command to lift and transfer the patient out of the chair to the destination surface. Used to transfer patient who cannot stand independently, but can bear some weight through the trunk and lower extremities. The clinician should position the patient at a 45° angle to the destination surface. The patient places that upper extremities on the clinician's shoulders, but should not be allowed to pull on the clinician's neck. The clinician should position the patient at the edge of the surface, hold the patient around the hips and under the buttocks, and block the patients knees in order to avoid buckling while standing. The clinician should utilize momentum, straighten his or her legs, and raise the patient or allow the patient to remain in a squatting position. The clinician should then pivot and slowly lower the patient to the destination surface. A device required for dependent transfers when a patient is obese, there is only one clinician available to assist for the transfer, the patient has a weight-bearing restriction on bilateral lower extremities, or the patient is totally dependent. A body sling is required for the lift transfer. Two primary types of sling exist: full body, which covers the posterior surface of the patient from the shoulders to the back of the thighs/knees; and a sling that has divided legs that cross between the patient's legs and support him or her on the posterior surface of the thighs. The hydraulic lift is locked in position before the transfer. The clinician positions the sling under the patient by rolling the patient from side to side, and then attaches the S-ring to the bars on the lift. The longer length of chain is attached at the lower end of the sling to encourage a seated position. Once all attachments are checked, the clinician should pump the handle on the device in order to elevate the patient. Once the patient is elevated, the clinician can navigate the lift with the patient to the destination surface. Once transferred, the chains should be removed, however, the webbed sling should remain in place in preparation for the return transfer.
Parallel bars can be used to provide maximum stability and secu rity for patients during the beginning stages of ambulation or standing. The COrrect height of the bar should allow for 20 to 25 degrees of elbow flexion while grasping on the bars approximately 4 to 6 inches in front of the body. The goal is to progress the patient out of the bars as quickly as possible to increase overall mobility and decrease dependence on the parallel bars. There are three major categories of ambulatory assistive devices: canes, crutches, and walkers.
CANES Canes are usually made out of wood, plastic, or aluminum (adjustable with a pushpin lock). The function of a cane is to widen the base of support and improve balance. However, because canes provide mini mal stability and support for patients during ambulation activities, they are not intended for use with restricted weight-bearing gaits. Patients
CHAPTER 15. PROSTHETICS, ORTHOTICS, AND ASSISTIVE DEVICES
1001
TABLE 15-8. ASSISTED TRANSFERS lYPE OF TRANSFER
..
Sliding board
e e Ii: r. ~
II
Stand pivot
II
r
Stand step
Push up (pop-over)
DESCRIPTION Used for a patient who has some sitting balance, some upper extremity strength, and who can adequately follow directions. The patient should be positioned at the edge of the wheelchair or bed and should lean to one side while placing one end of the sliding board sufficiently under the proximal thigh. 'The other end of the sliding board should be positioned on the destination surface. The patient should not hold onto the end of the sliding board, in order to avoid pinching the fmgers. The patient should place the lead hand 4 to 6 inches away from the sliding board and use both arms to initiate a push-up and scoot across the board. The clinician should guard in front of the patient and assist as needed as the patient performs a series of push-ups across the board. Used when a patient is able to stand and bear weight through one or both of the lower extremities. The patient must possess functional balance and the ability to pivot. Patients with unilateral weight-bearing restrictions or hemiplegia may utilize this transfer and lead with the uninvolved side. The transfer may also be used therapeutically, leading with the involved side for a patient post-CVA. The patient should be positioned at the edge of the wheelchair or bed to initiate the transfer. The clinician can assist the patient to keep the feet flat on the floor while bringing the head and trunk forward. The clinician must guard or assist the patient through the transfer, and instruct the patient to reach back for the surface before they begin to sit down. Once the stand pivot is performed, the clinician should assist as needed to insure control with lowering the patient to the destination surface. Used with a patient who has the necessary strength and balance to weight shift and step during the transfer. The patient requires guiding or supervision from the clinician and performs the transfer as a stand pivot transfer except that patient actually takes a step to maneuver and reposition his or her feet instead of using a pivot. Use for patient with good sitting balance who can lift the buttocks clear of sitting surface (e.g., a patient with a complete C7-level spinal cord injury can be independent with this transfer without a sliding board). Can be used as a progression in transfer training from using a sliding board. The patient utilizes a head-hips relationship to successfully complete the transfer-movement of the head in one direction results in movement of the hips in the opposite direction/toward the support surface being transferred to.
are typically instructed to hold a cane in the hand opposite the affected lower extremity. The cane and involved lower extremity are advanced together, followed by the uninvolved lower extremity. The use of a cane in the contralateral hand helps preserve recip rocal motion and a more normal pathway for the center of gravity.12 Use of a cane in this fashion also helps in reducing forces created by the abductor muscles acting at the hip, as etimated by external kine matics and kinetics. 13--16 Use of a cane can transmit 2()O!& to 25% of body weight away from the lower extremitiesY.l8 Holding the cane in the hand opposite the affected extremity also allows widening the base of support with less lateral shifting of the center of mass.
TABLE 15-9. ENERGY COSTS ASSOCIATED WIlli VARIOUS ASSISTIVE DEVICES ASSISTIVE DEVICE Crutches Standard walker Front-wheeled walker Cain
ENERGY COST Energy demand increased 13% to 80%, in part due to increased demands placed on arms and shoulder girdle muscles Oxygen consumption increased >2000;6 Lesser impact compared with standard walker No significant contribution
Reproduced, with permission, from Burnfield ]M, Powers CM: Normal and pathologic gait, in Placzek ]D, Boyce DA (eels): OrthopaediC Physical Therapy Secrets. 2nd ed. Mosby, 5t Louis, 2006:119-125. Copyright © Elsevier.
1002
SECTION II. TESTS AND MEASURES
In measuring cane height, the cane is placed approximately 6 inches from the lateral border of the toes. 19 Two landmarks typically are used during measurement to obtain a correct fit for a cane l9 : ~ ~
Greater trochanter: the top of the cane should come to approx imately the level of the greater trochanter. Angle at the elbow: the elbow should be flexed 20 to 30 degrees.
An alternative method includes standing the cane at the patient's side and adjusting the handle to the level of the wrist crease at the ulnar styloid. A variety of cane types exist: ~ ~
~
~
~
Standard cane: straight cane with single contact point with the ground. Adjustable aluminum offset (J-shaped) or offset cane: the design of this cane allows pressure to be borne over the center of the cane for greater stability. Quad cane: four points of contact with the ground. Patients should be instructed to place all four legs of the cane on the floor simultaneously to obtain maximum stability. This type of cane provides a larger base of support than a standard cane, thereby increasing stability. However, depending on the spe cific design of the cane, the pressure exerted by the patient's hand may not be centered over the cane and may result in patient complaints of instability.19 • Small-base quad cane is useful for stairs. • Wide-base quad cane provides the largest base of support but cannot be used on stairs. Another disadvantage is that this type of cane warrants use of a slower gait pattern-faster pro gressions often cause the cane to rock from the rear legs to the front legs. Walk cane: this type of cane provides a very broad base with four points of floor contact. The legs farther from the patient's body are angled to maintain floor contact and to improve sta bility. Walk canes fold flat and are adjustable in height. However, this type of cane cannot be used on most stairs, and requires use of a slow forward progression. Rolling cane: provides a wide wheeled base allowing uninter rupted forward progression. A pressure-sensitive break is built into the handle and can be engaged using pressure from the base of the hand. This type of cane allows weight to be contin uously applied as the need to lift and place the cane forward is eliminated, allowing for a faster forward progression.
CRUTCHES
Crutches (regular or standard), which are typically made from wood or aluminum, provide an increased base of support, a moderate degree of lateral stability, and can be used with all levels of weight bearing. However, crutches require a higher level of coordination than walkers, are awkward in small areas, and can cause pressure at the radial groove (spiral groove) of the humerus, creating a situation of potential damage to the radial nerve as well as to adjacent vascular structures in the axilla. 19
CHAPTER 15. PROSTHETICS, ORTHOTICS, AND ASSISTIVE DEVICES
:>x-
The correct height for axillary crutches includes positioning the
autches 6 inches in front and 2 inches lateral to the patient with the
autch height adjusted to be no greater than three finger widths from
me axilla (the handgrip is adjusted to allow for approximately 20 to
~ degrees of elbow flexion). The crutch height can be adjusted by ,.ing nuts (push-button locks on the aluminum crutches), and the bandgrip height is adjusted by wing nuts in both types. Alternative methods of measurement include
ide
id
~
be
~
In the standing position, one can subtract 16 inches from the patient's height or measure from a point 2 inches below the axilla to a point 6 inches in front and 2 inches lateral to the foot. With the patient supine, measure from the axilla to a point 6 to 8 inches lateral to the heel.
be
ret"
Two other types of crutches are worth mentioning:
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~
Lofstrand (forearm): can be used at all levels of weight bearing, provides increased ease of movement, and because of the pres ence of a forearm cuff, allows the wearer to use the hands with out dropping the crutches. However, this type of crutch requires the highest level of coordination for proper use. Proper fit includes 20 to 25 degrees of elbow flexion while holding the handgrip with the crutches position 6 inches in front and 2 inches lateral to the patient. The arm cuff should be positioned 1 to 1 1/ 2 inches below the olecranon process so that it does not interfere with elbow flexion. Forearm platform: allow weight-bearing on the forearm and are
useful for patients who are unable to weight-bear through their
hands. However, this type of crutch provides less lateral sup
port owing to the absence of an axillary bar.
th
ts
I
WALKERS
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d
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t
Walkers can be used with all levels of weight bearing and offer a sig nificant base of support and good anterior and lateral stability. Attachments include fold-down seats, braking mechanism, platform attachments, wheel attachments, and carrying baskets. The correct height of the walker allows for 20 to 25 degrees of elbow flexion. The Slandard walker has many variations including:
is ~ ~
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{
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~
I I
~
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~
Folding (collapsible): facilitates mobility in the community, and is easier to transport in cars. Rolling (wheeled): available with either two or four wheels, the latter of which requires a hand brake to provide added stability in stopping. The advantage of this type of walker is that it facil itates walking as a continuous movement sequence. Stair climbing: fitted with two posterior extensions and addi tional handgrips off of the rear legs for use on stairs. Reciprocal: fitted with hinges that allow advancement of one side of the walker at a time, thereby facilitating any reciprocal gait pattern. Hemi: modified for use with one hand only.
1003
1004
SECTION II. TESTS AND MEASURES
Prior to initiating instruction in gait patterns using a conventional walker, several points related to the use of the walker should be emphasized to the patient 19 : ~ ~ ~
The walker should be picked up and placed down on all four legs simultaneously to achieve maximum stability. The patient should be encouraged to hold the head up and to maintain good postural alignment. The patient should be cautioned not to step too close to the front crossbar to prevent falling.
LEVELS Of WEIGHT BEARING It must be remembered that most patients have difficulty replicat ing a prescribed weight-bearing restriction, and will need constant reinforcing. 20 ~
~
~
~
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Study Pearl
Non-weight-bearing (NWB): a patient is unable to place any weight through the involved extremity and is not permitted to touch the ground or any surface-an assistive device is required. Toe-touch weight bearing (TIWB): a patient is unable to place any weight through the involved extremity, but may place the toes on the ground to assist with balance-an assistive device is required. Partial weight bearing (PWB): a patient is allowed to put a par ticular amount of weight through the involved extremity. The amount of weight bearing is expressed as allowable pounds of pressure or as a percentage of total weight. A clinician must monitor the amount of actual weight transferred through the involved foot during partial weight bearing (these patients often need the most reinforcing}-an assistive device is required. Weight bearing as tolerated (WBAT): a patient determines the proper amount of weight bearing based on comfort. The amount of weight bearing can range from minimal to full-an assistive device mayor may not be required. Full weight bearing (FWB): a patient is able to place full weight on the involved extremity-an assistive device is not required at this level, but may be used to assist with balance.
Correct fitting for an assistive device is important for the safety of the patient and to allow for minimal energy expenditure. Once fitted, the clinician should ensure that the correct walking technique with the device is taught to the patient. GAIT TRAINING WITH ASSISTIVE DEVICES The clinician must always provide adequate physical support and instruction while working with a patient using an assistive gait device. The clinician positions himself or herself on the involved side of the patient, to assist the patient on the side where the patient will most likely have difficulty. A gait belt should be fitted around the patient's waist to enable the clinician to assist the patient.
III d
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L
CHAPTER 15. PROSTHETICS, ORTHOTICS, AND ASSISTIVE DEVICES
During ambulation, the clinician's front foot should move when
me patient moves, while the back leg and the assistive device should Dance together. The selection of the proper gait pattern to instruct the patient is dependent upon the patient's balance, strength, cardiovascular status, c:nordination, functional needs, and weight-bearing status. A number d gait patterns are recognized.
Two-Point Pattern. The two-point gait pattern, which closely approximates the normal gait pattern, requires the use of an assistive pit device (canes or crutches) on each side of the body. This pattern
lrlJUires the patient to move the assistive gait device and the contralat aa1lower extremity at the same time.
Three-Point Gait Pattern. The three-point gait pattern involves the use of two crutches or a walker. This pattern is used when 6e patient is permitted to bear weight through only one lower extremity. 1be three-point gait pattern requires good upper body strength, good balance, and good cardiovascular endurance. The pattern is initiated with the forward movement of one of the assistive gait devices. Next, the involved lower extremity is advanced. 1ben the patient presses down on the assistive gait device and Dances the uninvolved lower extremity. ~
~
If the uninvolved lower extremity is advanced to where it is parallel to the involved lower extremity, then this would be a "swing to" pattern. If the uninvolved lower extremity is advanced ahead of the unin volved lower extremity, then this would be a "swing through" pattern.
Modifications of the three-point gait pattern include touchdown wright bearing (TDWB) and partial weight bearing (PWB). This pattern is initiated with the forward movement of one of the :assistive gait devices and then the involved lower extremity is Danced forward. The patient presses down on the assistive gait device and advances the uninvolved lower extremity using either a "swing to or a "swing through" pattern.
Four-Point Pattern. The four-point gait pattern, which requires
me use of an assistive gait device (canes or crutches) on each side of me body, is used when the patient requires maximum assistance with balance and stability. The pattern is initiated with the forward move ment of one of the assistive gait devices, and then the contralateral lower extremity, the other assistive gait device, and finally the oppo sire lower extremity (e.g., right crutch, then left foot; left crutch, then right foot).
Sit to Stand Transfers Using Assistive Devices.
Before begin ambulation, the patient must first learn to safely transfer from a sitting position to a standing position. The wheels of the bed or wheelchair are locked and the patient is reminded of any weight-bearing restrictions. The patient is asked to slide to the front edge of the chair or bed, and his or her weight-bearing foot is placed
me patient can
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SECTION II. TESTS AND MEASURES
underneath the body so that the patient's center of gravity is closer to the patient's base of support, which will make it easier to stand. ~
The patient is then instructed to lean forward and push up with the hands from the bed or arm rests. • If the patient is being instructed on the use of walker, the patient should grasp the handgrips of the walker, only after they have become upright, and should not be permitted to try to pull himself or herself up using the walker, as this can cause the walker to tip over and increase the potential for falls. • If the patient is using crutches, the patient is instructed to hold both crutches with the hand on the same side as the involved lower extremity. The patient then presses down on the handgrips of the crutches, the arm rest or bed, and with the uninvolved lower extremity to stand. Once standing, the patient then moves the crutches into position and begins to ambulate. • If the patient is using one or two canes, the patient is instructed to push up with the hands from the bed or arm rests. Once standing, the patient should grasp the hand gripes) of the cane(s) with the appropriate hand and begin to ambulate.
Stand to Sit Transfers Using Assistive Devices. The stand to sit transfer is essentially the reverse of the sit to stand transfer. In order to sit down using an assistive device, the patient must first back up against the front edge of the bed or chair. If the patient has dif ficulty bending the knee of the involved lower extremity, the patient is instructed to slowly advance this extremity forward. ~ ~
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Once in position, the patient using a walker reaches for the bed or arm rest with both hands and slowly sits down. Once in position, the patient using crutches moves both crutches to the hand on the side of the involved lower extrem ity. With that hand holding onto both handgrips of the crutches, the patient reaches back for the bed or arm rest with the other hand before slowly sitting down. Once in position, the patient using a cane(s) places the handgrip of the cane against the edge of the chair or bed. Next, the patient reaches back for the bed or arm rest and slowly sits down.
Stair and Curb Negotiation Ascending Stairs. A gait belt is recommended. To ascend steps, the
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patient must first move to the front edge of the step. The walker will have to be turned toward the opposite side of the handrail or wall. The clinician should remain behind the patient, usually toward the weaker side, and should place the lead foot on the same step as the patient and the other foot one step lower. To ascend stairs using a walker, the patient is instructed to grasp the stair handrail with one hand, and to turn the walker sideways so that the two front legs of the walker are placed on the first step. When ready, the patient pushes down on the walker handgrip, and the handrail, and advances the uninvolved lower extremity on to the first step. The patient then advances the uninvolved lower extremity to the
CHAPTER 15. PROSTHETICS, ORTHOTICS, AND ASSISTIVE DEVICES
first step and then moves the legs of the walker to the next step. This process is repeated as the patient moves up the steps. ~
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To ascend steps or stairs with crutches, the patient should grasp the stair handrail with one hand, and grasp both crutches by the handgrips with the other hand. If the patient is unable to grasp both crutches with one hand, or if the handrail is not stable, then the patient should use both crutches only, although this is not recommended if there are more than two to three steps. When in the correct position at the front edge of the step, the patient pushes down on the crutches and handrail, if applicable, and advances the uninvolved lower extremity to the first step. The patient then advances the involved lower extremity and finally the crutches. This process is repeated for the remaining steps. To ascend steps or stairs with one or two canes, the patient should use the handrail and the cane. If the handrail is not sta ble, then the patient should use the cane(s) only. The patient pushes down on the cane or handrail, if applicable, and advances the uninvolved lower extremity to the first step. The patient then advances the involved lower extremity. This process is repeated for the remaining steps.
Descending Stairs. A gait belt is recommended. In order to descend steps, the patient must first move to the front edge of the top step. The clinician should remain in front of the patient, usually toward the weaker side, and should place the lead foot on the step the patient will step on and the other foot one step lower. ~
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Using a walker to descend, the walker is turned sideways so that the two front legs of the walker are placed on the lower step. One hand is placed on the rear handgrip and the other hand grasps the stair handrail. When ready, the patient lowers the involved lower extremity down to the first step. Then the patient pushes down on the walker and handrail and advances the uninvolved lower extremity down the first step. This process is repeated as the patient moves down the steps. To descend steps or stairs with crutches, the patient should use one hand to grasp the stair handrail and the other to grasp both crutches and handrail. If the patient is unable to grasp both crutches with one hand, or if the handrail is not stable, then the patient should use both crutches only, although this is not rec ommended if there are more than two to three steps. When ready, the patient lowers the involved lower extremity down to the first step. Next, the patient pushes down on the crutches and handrail, if applicable, and advances the uninvolved lower extremity down to the first step. This process is repeated for the remaining steps. To descend steps or stairs with one or two canes, the patient should use the cane and handrail. If the handrail is not stable, then the patient should use cane or canes only. When ready, the patient lowers the involved lower extremity down to the first step. Next, the patient pushes down on the cane(s) and handrail, if applicable, and advances the uninvolved lower extremity down to the first step. This process is repeated for the remaining steps.
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SECTION II. TESTS AND MEASURES
Instructions. Whichever gait pattern is chosen, it is important that the patient receive verbal and illustrated instructions for use of the assistive gait device on stairs, curbs, ramps, and doors, and for transfers. These instructions should include any weight-bearing precautions the patient may have, the appropriate gait sequence, and a contact num ber to reach the clinician if any questions arise. WHEELCHAIRS
A wheelchair is a medical device that takes the form of a chair on wheels, and is used by people for whom walking is difficult or impos sible due to illness or disability. Wheelchairs are available in a variety of sizes and styles and wheelchair design continues to improve both in safety and construction. Whenever possible, every attempt should be made to reduce the amount of resistance for wheelchair propulsion. Wheelchairs can be grouped into several classes: indoor (small wheel base to allow maneuvering in confined spaces, but lacks the ability or power to negotiate obstacles), indoor/outdoor (provides mobility for those who stay on finished services, such as sidewalks, driveways, and flooring), and active indoor/outdoor (provides the ability to travel long distances, move fast, and drive over unstructured environments such as grass, gravel, and uneven terrain). Wheelchair fitting is highly indi vidualized and requires a team effort between physiatrist, neurologist or orthopedist, occupational or physical therapist, specialist in assistive technology and driver training, and rehabilitation technology providers. When helping to choose a wheelchair, a few patient consid erations must be made: ~
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Physical needs. Rental versus purchase. Seating system. Functional mobility. Physical abilities. Cognition. Coordination. Level of endurance. Manual versus power.
Wheelchair Measurements. To physically examine the patient for a wheelchair, the patient should be positioned supine on a firm surface? The range of available pelvic and hip movements as they relate to spinal and pelvic alignment should be determined. The lower extremities must be well supported by the clinician, with the knee flexed 95 to 100 degrees or as much as is needed to eliminate the influ ence of the hamstring muscle group. Range-of-motion measurements should include hip flexion, abduction, adduction, and internal and external rotation; their effect on pelvic position and general body alignment should be noted as well? Once range of motion is docu mented, a linear measurement of seat depth should be determined. Once examination in the supine position is completed, the patient should be placed in a supported sitting position with the knees flexed to 100 degrees or more to eliminate the influence of the ham string muscle group? Ideally, seated examination should be done on a simulator, a chair specifically designed for planar seated examinations.
CHAPTER 15. PROSTHETICS, ORTHOTICS, AND ASSISTIVE DEVICES
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If a simulator is not available, the measurement can be done on the map table with a thin front edge to allow 100 degrees of knee flexion (Table 15-10).7
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Wheelchair Components Frame. Whereas stainless steel used to be the only frame material available, wheelchair users today have their choice of stainless steel, chrome, aluminum, airplane aluminum, steel tubing, an alloy of chrome and lightweight materials, titanium, and other lightweight composite materials (sports chairs accommodate a tucked position, include leg straps, slanted drive wheels, and small push rims). The ultralight wheelchair is the highest-quality chair designed specifically for active people. In general, the lighter the weight of the frame, the greater the ease of use, but the lesser amount of structural strength pro vided. The level of expected activity and environment where the ~;heelchair will be used should be taken into account when deciding on frame construction.
TABLE 15-10. STANDARD WHEELCHAIR MEASUREMENTS DIMENSION
GUIDELINES
Seat height/leg length
Measurement taken from the user's heel to the popliteal fold. 2 inches is added to this measurement to allow clearance of the foot rest.
Seat depth
Measurement taken from the user's posterior bunock, along the lateral thigh to the popliteal fold. Approximately 2 inches are subtracted from this measurement to avoid pressure from the edge of the seat against the popliteal space.
Seat width
Measurement taken of the widest aspect of the user's bunocks, hips, or thighs. 2 inches is added to this measurement so as to provide space for bulky clothing, orthoses, or clearance of the trochanters from the arm rest side panel.
Back height
Measurement taken from the seat of the chair to the floor of the axilla with the user's shoulder flexed to 90 degrees. 4 inches is subtracted from this measurement to allow the final back height to be below the inferior angles of the scapulae. Note: this measurement will be affected if a seat cushion is to be used; the person should be measured while seated on the seat cushion, or the thickness of the cushion must be considered by adding that value to the actual measurement. Measurement taken from the seat of the chair to the olecranon process with the user's elbow flexed to 90 degrees. One inch is added to this measurement. Note: this measurement will be affected if a seat cushion is to be used; the person should be measured while seated on the seat cushion, or the thickness of the cushion must be considered by adding that value to the actual measurement.
Ann rest height
AVERAGE SIZE Adult: 20 inches Narrow adult: 20 inches Slim adult: 20 inches Hemi/low seat: 17.5 inches Junior: 18.5 inches Child: 18.75 inches Tiny tot: 19.5 inches Adult: 16 inches Narrow adult: 16 inches Slim adult: 16 inches Junior: 16 inches Child: 11.5 inches Tiny tot: 11.5 inches Adult: 18 inches Narrow adult: 16 inches Slim adult: 14 inches Junior: 16 inches Child: 14 inches Tiny tot: 12 inches Adult: 16 to 16.5 inches
Adult: 9 inches above the chair seat
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SECTION II. TESTS AND MEASURES
The two most common types of frames currently available are ~
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Rigid frame: the frame remains in one piece and the wheels are released for storage or travel. • Facilitates stroke efficiency. • Increases distance/stroke. Standard cross-brace frame: enables the frame to collapse or fold for transport or storage. • Facilitates mobility in the community. • The wheelchair is folded by first raising the footplates and then pulling up on the handles (located on either side of the seat), rather than pulling up on the middle of the upholstery, which can tear the upholstery.
Anti-Tipping device. These are posterior extensions attached to the low horizontal supports, which prevent the chair from tipping back ward and limit going over curbs or over doorsills. A similar device is the Hill holder, which is a mechanical break that allows the chair to go forward, but automatically applies the brakes when the chair goes into reverse.
Upholstery. Upholstery for wheelchairs must withstand daily use in all kinds of weather. Consequently, manufacturers provide a variety of options to users, ranging from cloth to new synthetic fabrics to leather. Many manufacturers also offer a selection of upholstery colors, ranging from black to neon, to allow for individual selection and differing tastes among consumers. Seating System. Many wheelchairs come with a fabric or sling seat. The disadvantages of a sling seat are that the hips tend to slide forward, the thighs tend to adduct and internally rotate, and the patient sits asymmetrically, which reinforces poor pelvic position. Because of these problems, and the fact that seating must be customized on an individual basis, seating surfaces are often purchased separately from the wheelchairs themselves. It is important when selecting a wheelchair or a seating system to ensure that the two components are compatible. ~
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Insert or contour seats: fabricated from wood or plastic and padded with foam, these seats create a stable firm sitting sur face, improved pelvic position (neutral), and reduce the ten dency for the patient to slide forward or sit with a posterior pelvic tilt. Seat cushions: function to distribute weight-bearing pressures, which assists in preventing decubitus ulcers in patients with decreased sensation and prolongs wheelchair sitting times. Pressure-relieving air cushion: these lightweight cushions accommodate moderate to severe postural deformity and improve pressure distribution. • Disadvantages: expensive, base may be unstable for some patients, and require continuous maintenance. Pressure-relieving fluid/gel or combination cushions: can be custom molded, are designed to accommodate moderate to
CHAPTER 15. PROSTHETICS, ORTHOTICS, AND ASSISTIVE DEVICES
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Backrest. The standard-height backrest provides support to the mid scapula region. A number of modifications can be made to suit the user: ~
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severe postural deformity, and are easy for caregivers to repo sition the patient. • Disadvantages: require some maintenance, heavy, and mod erately expensive. Pressure-relieving contoured foam cushions: use dense, lay ered foam. Are designed to accommodate moderate to severe postural deformity, and are easy for caregivers to reposition patient. • Disadvantages: may interfere with slide board transfers. Suspension elements: extended exposure to the vibration sus tained propelling a wheelchair in communities may lead to dis comfort and various harmful physiologic effects, such as chronic low back pain and disc degeneration. Suspension ele ments reduce the negative effects of shock and vibration.
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A lower back height may increase functional mobility-typically seen in sports chairs-but may also increase back strain. Lateral trunk supports: improved trunk alignment for patients with scoliosis or poor stability. Insert or contour backs: improve trunk extension and overall upright alignment. A high back height may be necessary for patients with poor trunk stability or with extensor spasms.
Brakes. Brakes are an important safety feature. Most brakes consist of a lever system with a cam, or a ratchet. Extensions may be added to increase the ease of both locking and unlocking. When a wheelchair ( has a reclining back, an additional brake is necessary. Brakes must be engaged for all transfers in and out of the chair.
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Wheels/Tires. Most wheelchairs use four wheels: two large wheels (standard spokes or spokeless) at the back (fitted with an outer rim that allows for hand grip and propulsion), and two smaller ones (casters) at the front. The tires used for the rear wheels may be narrow and hard rubber, pneumatic inflatable, semipneumatic, or radial tires. The pneumatic tires provide a smoother ride, and increased shock absorp tion, but require more maintenance than the solid ties. Mag wheels and off-road wheels also are options on some chairs. The standard size for the rear wheel is 24 inches. Smaller and larger wheel sizes are available. The wheels are fitted with an outer rim that enables the patient to propel himself or herself. For those patients with only one functional ann, two outer rims can be fitted on one wheel so that arm drive achieves both forward and bach,-ward propulsion. Projections (vertical, oblique, or horizontal) may be attached to the rims to facilitate with propulsion in patients with poor handgrip. However, the horizontal and oblique extensions add to the overall width of the chair and may reduce maneuverability. Casters vary in size (ranging from 6 to 8 inches in diameter) and romposition (pneumatic, solid rubber, plastic, or a combination). Caster locks can be added to f~1Cilitate wheelchair stability during transfers.
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SECTION II. TESTS AND MEASURES
Leg Rests. Leg rests come in a variety of designs. ~ ~
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Swing away: detachable leg rests that facilitate ease in transfers and a front approach to the wheelchair when ambulating. Elevating: most frequently necessary when the patient is unable to flex the knee, for postural support, or when a dependent leg contributes to lower extremity edema. The length of the leg rest is adjustable to accommodate the full length of the patient's leg, and a padded calf support is provided. The position of the leg rest is adjusted by pushing down on a lever on the side of the chair. Elevating leg rests can be released from the wheelchair or pivoted to one side during transfers. Elevated leg rests are con traindicated for patients with hypertonicity or adaptive short ening of the hamstrings. Fixed: Allow the leg rest to be positioned in automatic and per manent manner, but it can get in the way during transfers.
Foot Rests. A footrest is standard equipment on a wheelchair. For rigid-frame chairs, the footrests are usually incorporated into the frame of the chair as part of the design. Cross-brace folding chairs often have footrests that swivel, flip up, and/or can be removed. Foot plates, which can be adjusted to accommodate the patient's foot, provide a resting base for the feet, so that the feet are in neutral with a knee flexed to 90 degrees. Heel loops can be fined to help maintain the foot position and prevent posterior sliding of the foot. Ankle and calf straps can be added to stabilize the feet onto the foot plates. Toe loops may also be used when the patient has difficulty maintaining the foot on the foot plate in a forward direction. Arm Rests. Arm rests are available in several styles including desk length (to allow the user closer access to desks and tables) or full length, and both types may be flip-up, fixed, or detachable. The desk length design also allows the patient to remove and reverse the arm rest so that the higher part is closer to the front edge in order to aid in pushing to standing. Wraparound (space saver) arm rests reduce the overall width of the chair by 11/ 2 inches. The height of the arm rests can also be adjustable. Arm rests can also be fitted with upper extremity support surface trays or troughs, which are helpful if the user has difficulty with upper body balance or decreased use of the upper extremities. Many lightweight manual chairs are designed without arm rests, which makes it easier for the user to roll up to a desk or table, and to perform transfers, in addition to providing a streamlined look.
Seatbelts. Seat belts can be used for safety or for positioning: ~ ~
Restraining belts are used to prevent patients from falling out of the wheelchair. Seat belts can be fitted to grasp over the pelvis at a 45-degree angle to the seat to help position the pelvis. Correct positioning helps to provide lateral or medial support at the hip and knee to maintain alignment of the lower extremities and/or control spasticity.
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CHAPTER 15. PROSTHETICS, ORTHOTICS, AND ASSISTIVE DEVICES
Specialized Wheelchairs Pediatric Wheelchairs. Children with cerebral palsy, spina bifida, or osteogenesis imperfecta may be candidates for either manual or power wheelchairs, depending on upper extremity strength, rate of fatigue, cognitive abilities and family circumstances. Those with spinal muscu lar dystrophy, arthrogryposis, high-level spinal cord injuries, and those with progressively worsening Duchenne's muscular dystrophy are typ ically immediate candidates for powered mobility. Key decisions con cerning wheelchair design must be a team effort. Seating Specifics. A pediatric wheelchair must have approximately 4 inches of available space in the frame to accommodate growth. In addition, the seating system should be flexible enough to accommo date tonal or postural changes. Examples of flexibility in the system involve the placement of laterals, which are often attached to tracks, or the backrest can include T-nuts placed throughout the back to allow easy hardware mounting. Pediatric chairs often employ linear seating systems (to accommodate the delicate balance between providing con tours in the system and accommodating growth) versus molded seats, which are more difficult to increase in size. Similarly a contoured back rest is more accommodating and provides more contact surface and thus more comfort. Caregivers should be made aware of the proper use of all accessories, including head supports and upper chest supports. One must also always consider the esthetic appeal of the wheel chair and where possible should reflect individuality and personality. When deciding between a manual or power wheelchair, a number of considerations should be made: ~
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Power chairs are more expensive than manual chairs. Power chairs have inherent safety concerns and create issues surround ing transportation and home accessibility. Manual wheelchairs are easier to transport and lift into a nonac cessible home.
Ileclining Wheelchairs. Reclining wheelchairs are designed with an extended back and typically with elevating leg rests. The angle of the back is adjusted by releasing knobs on the side of the wheelchair. A head support is required on a reclining back wheelchair. A bar across the back of the reclining wheelchair provides support and stability. The purpose of the reclining wheelchair is to allow intermittent or constant reclined positioning. Reclining wheelchairs are indicated for patients \\nO are unable to independently maintain an upright sitting position. The chairs can be controlled either manually or electrically (if the patient cannot do active push-ups or pressure relief maneuvers). Hemi-Chair. A chair that is designed to be low to the ground (seat height of approximately 175 inches), allowing propulsion with the noninvolved upper and/or lower extremities. Tilt in Space. A chair that is designed to allow for a reclining position without losing the required 90 degrees of hip flexion and 90 degrees of knee flexion. This type of chair is indicated for patients with extensor spasms that may throw the patient out of the chair, or for pressure relief.
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SECTION II. TESTS AND MEASURES
One-Arm Drive. A chair that is designed with the drive mechanisms located on one wheel, usually with two outer rims (or push lever). The patient is able to propel the wheelchair by pushing on both rims (or lever) with one hand. Amputee Chair. A modified wheelchair where the drive wheels are placed posterior (approximately 2 inches back.vards) to the vertical back supports, so that the base of support is lengthened and posterior stability is enhanced.
Powered Chairs. This design of chair utilizes a power source (battery) that propels the wheelchair. Microprocessors allow the wheelchair to be adapted to various controls (joystick, head, breath). This type of chair is usually prescribed for patients who are not capable of self propulsion or who have very low endurance. Recent changes in the power bases have allowed for such innovations as power seat func tions (power tilt, recline, elevating leg rest, seat elevator) and control interfaces (mini-joysticks, head controls). Power wheelchair bases can be classified in one of three categories, based on the drive wheelloca tion relative to the system's center of gravity: ~
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Rear-wheel drive: drive wheels are located behind the user's center of gravity, and the casters are located in the front, pro viding predictable drive characteristics and stability. Mid-wheel drive: drive wheels are directly below the user's center of gravity and generally have a set of casters or anti-tippers in the front and rear of the drive wheels. The advantage of this system is a smaller turning radius. The disadvantage is a ten dency to rock or pitch forward, especially with sudden stops or fast turns. Front-wheel drive: drive wheels are located in front of the user's center of gravity. This design proVides stability and a tight turning radius, and the ability to climb obstacles or curbs more easily. One of the disadvantages of this design is its rear ward center of gravity, which makes it difficult to drive in a straight line, especially on uneven surfaces.
Wheelchair Training. A number of areas need to be addressed when training a patient on how to be as functionally independent as possible with a wheelchair. Posture. It is important for the patient to maintain good posture in the wheelchair. He or she should be seated well back in the chair, with the lower extremities on the footrest., or leg rests. The patient should be able to maintain a seated position when his or her balance is challenged. Wheelchair Management. The various components of the wheel chair should be reviewed with the patient, and the patient should per form all of the necessary tasks while being supervised by the clinician. Wheelchair users are susceptible to muscle imbalances. Nearly every motion and/or repetitive motion is forward, working such areas as the shoulder flexors (pectoralis major, and anterior deltoid) and shoulder internal rotators. These anterior muscles can become adaptively short ened, while the upper back muscles become weak and elongated. The typical posture of the wheelchair user is rounded shoulders with mild
CHAPTER 15. PROSTHETICS, ORTHOTICS, AND ASSISTIVE DEVICES
thoracic kyphosis and a forward head. This posture can result in impingement of the soft-tissue structures of the acromiohumeral space.
Wheelchair Mobility. Depending on functional level, the patient is instructed on how to ~
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Operate the wheel locks, foot supports, and arm rests, and to use the mechanisms safely without tipping forward or sideways out of the chair seat. Transfer in and out of the chair with the least possible assis tance. This may involve transfer training from the wheelchair to the car seat. Propel the wheelchair in all directions and around comers. Perform a wheelie. A wheelie is performed by balancing on the rear wheels of a wheelchair while the caster wheels are in the air. Wheelies are important for those patients who need to go up and down curbs independently when there are no curb ramps. Initially the clinician must be positioned behind the chair and move with the chair, with the hands held beneath the wheel chair handles, ready to catch the wheelchair if it tilts too far backward. The patient should be taught how to tuck the head into the chest, if he or she falls backward, to avoid hitting the back of the head if performing the maneuver without assistance. To perform a wheelie, the patient is asked to place the hands at 11 :00 on the wheels, then lean forward and arch the back. Initially the patient practices bouncing the body off the back of the chair and leaning back while holding the hands still-the front of the chair is raised by pushing backward on the back of the chair. The patient practices until he or she can actually bounce the front end off the ground. By changing the center of gravity (by pushing the chair forward while the body is going backward), the patient will achieve a point of equilibrium. Once the patient is able to bounce the front end off the ground and is able to find a point of equilibrium, he or she progresses to reaching back and placing the hands at about 10:00 on the wheels. From this point, the patient leans forward, arches the back, and then begins to push forward quickly while letting the body come back against the chair (when the patient's back hits the chair, the hands should be in the 12:00 position). By continuing to lean back and while pushing the chair forward, the front end should start to leave the ground, and by the time the hands get to the 2:00 position, the front end should feel weightless, as the chair balances on the rear axle. To maintain equilibrium, the patient will need to be able to move the chair forward if the front end begins to fall down, or backward if the chair begins to fall backward. This may be accomplished by sliding the hands back to about the 1:00 position, without tak ing the hands off the wheels. Once the chair is up and bal anced, the patient will need to keep just a fraction of weight on the front end, so that if balance is lost the chair will fall forward, not backward. "Pop a wheelie" and move forward and backward in the wheelie position. Once the patient is ready to try a wheelie independently, a good place to begin practicing is on carpeting, grass, or sand.
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SECTION II. TESTS AND MEASURES
REFERENCES 1. Guide to physical therapist practice. Phys Ther. 2001;81:S13-S95. 2. May B]. Amputation. In: O'Sullivan SB, Schmitz T], eds. Physical Rehabilitation. 5th ed. Philadelphia: Davis; 2007:1031-1055. 3. Gailey RS. Considerations in treating amputees. In: Prentice WE, Voight ML, eds. Techniques in Musculoskeletal Rehabilitation. New York: McGraw-Hill; 2001:715-743. 4. White sc. Health Care Financing Administration Common Procedure Coding System. Washington, DC: U.S. Government Printing Office; 2001. 5. Wu Y], Chen SY, Lin MC, et al. Energy expenditure of wheeling and walking during prosthetic rehabilitation in a woman with bilateral transfemoral amputations. Arch Phys Med Rehabil. 2001;82: 265-269. 6. Traugh GH, Corcoran P], Reyes RL. Energy expenditure of ambu lation in patients with above-knee amputations. Arch Phys Med Rehabil. 1975;56:67-71. 7. EdelsteinjE. Prosthetics. In: O'Sullivan SB, Schmitz T], eds. Physical Rehabilitation. 5th ed. Philadelphia: Davis; 2007:1251-1286. 8. Ellis W, Kishner S. Gait Analysis after Amputation. Available at: www.emedicine.com/orthoped/topic633.htm. 2004. 9. Gailey RS. Orthotics in rehabilitation. In: Prentice WE, VOight ML, eds. Techniques in Musculoskeletal Rehabilitation. New York: McGraw-Hill; 2001 :325-346. 10. Tiberio D, Hinkebein ]R. Foot orthoses and shoe design. In: Placzek ]D, Boyce DA, eds. Orthopaedic Physical Therapy Secrets. Philadelphia: Hanley & Belfus; 2001:455--462. 11. Duesterhaus MA, Duesterhaus S. Patient Care Skills. 2nd ed. East Norwalk, CT: Appleton & Lange; 1990. 12. Baxter ML, Allington RO, Koepke GH. Weight-distribution variables in the use of crutches and canes. Phys Ther. 1969;49:360-365. 13. Edwards BG. Contralateral and ipsilateral cane usage by patients with total knee or hip replacement. Arch Phys Med Rehabil. 1986; 67:734-740. 14. Oatis CA. Biomechanics of the hip. In: Echternach], ed. Clinics in Physical Therapy: Physical Therapy of the Hip. New York: Churchill Livingstone; 1990:37-50. 15. Olsson EC, Smidt GL. Assistive devices. In: Smidt G, ed. Gait in Rehabilitation. New York: Churchill Livingstone; 1990:141-155. 16. Vargo MM, Robinson LR, Nicholas ]]. Contralateral vs. ipsilateral cane use: Effects on muscles crossing the knee joint. Am J Phys Med Rehabil. 1992;71:170-176. 17. ]ebsen RH. Use and abuse of ambulation aids. JAMA. 1967;199: 5-10. 18. Kumar R, Roe MC, Scremin OU. Methods for estimating the proper length of a cane. Arch Phys Med Rehabil. 1995;76:1173-1175. 19. Schmitz T]. Locomotor training. In: O'Sullivan SB, Schmitz T], eds. Physical Rehabilitation. 5th ed. Philadelphia: Davis; 2007:523-560. 20. Li S, Armstrong CW, Cipriani D. Three-point gait crutch walking: variability in ground reaction force during weight bearing. Arch Phys Med Rehabil. 2001;82:86-92.
CHAPTER 15. PROSTHETICS, ORTHOTICS, AND ASSISTIVE DEVICES
Comprehension Questions
1. What is the difference between an amputation and a disarticulation? 2. The primary benefit of residuallirnb wrapping following lower extremity amputation is to A. Prevent lymphedema. B. Prevent contractures. C. Prepare the limb for the prosthesis. D. None of the above. 3. You are evaluating apatient for a prosthetic replacement. The patient had atranstibial amputation and has ashort residual limb. Which type of prosthesis would be best for this patient? A. Syme's suspension. B. Thigh corset. C. Supracondylar/suprapatellar suspension. D. None of the above.
4. In terms of the length of the prosthesis, what would cause the vaulting phenomenon in a patient with an above-knee prosthesis? 5. Which of the following advantages does the valve have in the anteromedial inferior aspect of the thigh portion in an above-knee prosthesis? A. It eliminates air during the swing phase. B. It eliminates air during the stance phase. C. It gains air during the swing phase. D. It gains air during the stance phase. 6. Apatient with atransfemoral amputation and an above-knee prosthesis demonstrates knee instability while standing. His knee buckles easily when he shifts his weight. What could be the cause of his problem? A. The prosthetic knee is set too far anterior to the TKA line. B. The prosthetic knee is set too far posterior to the TKA line. C. It is a problem of phantom sensation. D. None of the above. 7. In order to increase the knee stability of an above-knee prosthesis wearer, should you move the TKA line posterior to the knee joint or anterior to it? 8. You have been asked to fit a 62-year-old patient with atransfemoral amputation with a temporary prosthesis containing a SACH prosthetic foot. This prosthetic foot: A. Allows full sagittal and frontal plane motion. B. Permits sagittal plane motion only. C. Allows limited sagittal plane Illotion with asmall amount of mediolateral motion. D. Allows no motion.
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9. The following describe the characteristics of the wall-design of aquadrilateral socket except A. The anterior and lateral walls are 2 1/2 to 3 inches higher than the posterior and medial walls. B. The posterior and lateral walls are 2 inches higher than the medial and anterior walls. C. The medial wall is 2 1/2 inches higher than the posterior wall while the anterior and lateral walls are the same height. D. The height of the posterior wall is 2 inches less than all the other walls. 10. You are assessing the functional level of a patient with a unilateral transfemorall transtibial amputation using the Medicare and Medicaid classification. The patient demonstrates the ability or potential to use a prosthesis for transfer or ambulation on a level surface at a fixed cadence. What functional level does this correspond with? 11. A common above-knee amputee gait deviation is lateral trunk bending. Which of the following is not a cause? A. Weak hip abductor. B. Weak hip adductor. C. Pain of the stump. D. Abducted socket. 12. A common above-knee amputee deviation is circumduction. Which of the following is not a cause of this deviation? A. Insufficient knee flexion. B. Socket is too large. C. Excessive plantar flexion. D. Inadequate suspension. 13. A common above-knee amputee gait deviation is wide base walking. Which of the following is not a cause for this deviation? A. The prosthesis is too short. B. The mechanical hip joint is set in abduction. C. Pain in the groin area. D. None of the above. 14. The SACH prosthesis is defined as A. Solid ankle cork heel. B. Solid ankle cushioned heel. C. Soft ankle cushioned heel. D. Soft ankle custom heel. 15. Upon examining apatient's gait using his prosthetic device, you notice that the socket has a poor fit and appears to have a weak suspension system with the knee friction being too soft. Which of the following gait deviations would you likely observe? A. Lateral whip. B. Pistoning of the socket. C. Circumduction. D. None of the above.
CHAPTER 15. PROSTHETICS, ORTHOTICS, AND ASSISTIVE DEVICES
16. You have been asked to teach a patient in awheelchair how to descend from acurb. Which is the safest method? A. Tilt the trunk backward and go down backward. B. Tilt the trunk backward and go down forward. C. Tilt the trunk forward and go down forward. D. Tilt the trunk forward and go down backward. 17. A patient presents with afixed varus deformity at the foot. What type of wedge would be the most appropriate? A. A medial heel wedge. B. A lateral heel wedge. C. A medial heel and sole wedge. D. A lateral heel and sole wedge. 18. When a cane is used for ambulation, usually it is used A. Opposite the involved side. B. On the same side as the injury. C. Only during the stance phase. D. None of the above. 19. You have been referred a patient who is recovering from traumatic brain injury and who demonstrates instability during feeding while sitting in a wheelchair. Which of the following body segments would you modify/align first? A. Pelvis. B. Trunk. C. Head. D. Lower extremities. 20. You are prescribing awheelchair for apatient with right hemiplegia. The most appro priate feature to include in this prescription would be: A. Detachable arm rests. B. Elevating leg rests. C. A 17-inch seat height. D. A feeding tray.
Answers 1. Amputation refers to the cutting of a limb along the long bones axis, whereas disar ticulation refers to cutting of a limb through the joint. 2. The answer is A.
3. The answer is C. 4. A prosthesis that was too long 5. The answer is B. 6. The answer is A. 7. Posterior.
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8. The answer is C. 9. The answer is A. 10. Levell. 11. The answer is B. 12. The answer is B. 13. The answer is A. 14. The answer is C. 15. The answer is B. 16. The answer is B. 17. The answer is D. 18. The answer is A. 19. The answer is A. 20. The answer is C.
Pediatric Physical Therapy
16
Physical therapy is a profession that focuses on the diagnosis and man 3gement of dysfunctional human movement throughout the life span. Pediatric physical therapy relates to the period (0 to 21 years) dUring "..hich an individual ages, changes, evolves, and matures. Federal laws in me United States have been particularly supportive of pediatric practice: ~
The Individuals with Disabilities Education Act (IDEA). Under the requirements of this federal law, all children who have spe cial needs must be supported in access to free and appropriate public education. This provision is based on an individualized plan. The plan for children who receive services at home (usu ally through age 3 years) under Part C of IDEA is called an Individual Family Service Plan (IFSP). For all children receiving services at school (usually after age 3 years to 21) under Part B of IDEA, the plan is called an Individualized Educational Plan (IEP). • Individual Family Service Plan (IFSP). Designed to meet the needs of the family as they relate to their child's develop ment, as well as meet the needs of the child. • Individual Educational Plan (IEP): identifies the student's spe cific learning expectations and outlines how the school will address these expectations through appropriate special edu cation programs and services. o Identifies the methods by which the student's progress will be reviewed. o Covers all deficit areas, including communication, behav ior, socialization, self-help, academics, perceptual-motor and gross-motor skills, vocational skills, and transition serv ices, related services, and needed accommodations in both general (regular and vocational) and special education.
1he term "motor control" refers to processes of the brain and spinal cord lbat govern posture and movement. 1 It is the ability to regulate or direct
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on woerher changes in
motor behavior result from external influences such as physical therapy, or to maturational influences, remain unresolved.
I Study Pea'_1- - ~ The field of motor control is directed at studying the nature of movementand how the movement is controlled. .. A motor plan is defined as an idea or plan for purposeful movement that is made up of component motor programs.l .. A motor program. is defined as an abstract representation that, when initiated, results in the production of a coordinated movementsequence.3
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SECTION II. TESTS AND MEASURES
Study Pearl .. Reflexes are evoked responses, and depend on a stimulus to be initiated. They are involuntary, stereotyped, and graded responses to sensory input, and have no threshold except that the stimulus mllst be great enough to activate the relevant sensory input pathway (see Chapter 9). .. FIxed action patterns (sneezing, orgasm) are involuntary and stereo typed, but typically have a stimulus threshold that must be reached before they are triggered, and are less graded and more complex than reflexes. .. Directed movements (reaching) are voluntary and complex, but are generally neither stereotyped nor repetitive. .. Rhythmic motor patterns (walking, scratching, breathing) are complex (unlike reflexes), stereotyped (unlike directed movements), and by defini tion, repetitive (unlike fixed action patterns), but are subject to contin uous voluntary control. .. Central pattern generators (CPGs) are neural networks that can endogenously (I.e., without rhyth mic sensory or central input) pro duce rhythmic patterned outputs; these networks underlie the pro duction of most rhythmic motor patterns, such as the gait cyde. z-s
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the mechanisms essential to movement using perception and cognition. The integral elements of motor control are listed in Table 16-1. Some of the more common models of motor control are outlined in Table 16-2. Factors that govern movement include the task, the envi ronment, and the neuromotor capabilities of the individual. Multiple variables contribute to the initiation and execution of a movement (Table 16-3).
MOTOR DEVELOPMENT Motor development refers to the processes of change in motor behav ior that occur over relatively extended time periods. 1 .. Motor development is a complex process that starts in utero and has psychomotor, phYSiologic, biochemical, biomechani cal, psychosocial, and even gender considerations. 6 .. Motor development training is the process of producing any change in motor behavior that is related to the age of the individual and includes age-related changes in posture and movement.
MOTOR DEVELOPMENT THEORIES
Neural-Maturationist. The neural-maturation theory, pio neered by Gesell,9,lO Shirley,l1 and others, holds that motor patterns emerge in orderly, predetermined genetic sequences, supported but not fundamentally altered by the environment. This theory depends on the assumption of hierarchic maturation of neural control centers and results in the recognition of general developmental sequences and milestones of development 12 ; .. Cephalocaudal. Motor development occurs in a cephalocaudal sequence. .. Central-to-distal. Motor development occurs in a central-distal sequence.
TABLE 16-1. INTEGRAL ELEMENTS OF MOTOR CONTROL ~
The CNS functioning as a fundamentally active agent with the capacity to generate action.
Motor patterns, which are the fundamental unit of neuromotor behavior.
~ The 'involvement of processes of feedback and comparison of intention and result, which enable the modification of action.
• Open-loop feedback: feedback that is available to the performer but not used to control the action. • Closed-loop feedback: a decision to move is made in the motor control center (brain). Some of the information is sent to the effector organs (muscles). The rest of the information is sent during the action, and feedback monitors the effectiveness of the movement, allowing for changes to be made dUring the movement. ~ A distributed control system that delegates the control of behavior to the most appropriate subsystem. ~ Memory structures such as schema that permit transfer of skills to new situations. ~
Data from Van Sant AF. Concepts of neural organization and movement. In: Connolly BH, Montgomery PC, eds. Therapeutic Exercise in Developmental Disabilities. Thorofare, NJ: Slack; 2001:1-12.
CHAPTER 16. PEDIATRIC PHYSICAL THERAPY
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TABLE 16-2. THEORIES OF MOTOR CONTROL TIIEORY
Maturational based
DESCRIPTION
Structure-Function Organization and Reflex-Chaining Sensory inputs are a necessary prerequisite for efferent motor output (stimulus-evoked behavior} movement occurs in response to a stimulus. Movement is the result of predictable anatomic changes in neural pathways and complex movement occurs as the result of a compounding of retlex movements. Hierarchical The nervous system is organized as a hierarchy with each successively high level exerting control over the level below it. Separation between voluntary (higher-level) and retlexive (lower-level) movement. Retlexes work together, or in sequence to achieve a common purpose, and thus provide the building blocks of complex behavior. Forms the basis of most neurotherapeutic approaches used in physical therapy (Bobath, Brunnstrom). Useful for explaining spontaneous and volitional movement. Response Chaining More emphasis on the role of the environment-action not bound to a specific stimulus (neither spontaneous or volitional movements are dependent on external agents for their initiation). Environment is the controller of the automating process. Linkages exist between muscle groups that allow for movement combinations (synergies). A full complement of motor programs are available and used appropriately in functional contexts prior to birth. 2 Movement dysfunction may be due to motor program centers in the brain and motor program centers at lower levels. Adams's Closed-Loop Theory3 In a closed loop process, sensory feedback is used for the ongoing production of skilled movment. The closed loop theory of motor learning also proposed that two distinct types of memory were important in this process: ~ Memory trace: used in this election and initiation of the movement. ~ Perceptual trace: built up over a period of practice and becomes the internal reference of correctness. This theory proposes that when learning a new movement skill, an individual gradually develops a perceptual trace for the movement that serves as a guide for later movements, and that the more an individual practices the specific movement, the stronger the perceptual trace becomes. Theoretically the more time spent in practicing the movement as accurately as possible, the better the learning. Schmidt's theory emphasizes open-loop control processes and the generalized motor program concept. Three constructs: general motor programs and two types of memory traces, recall schema and recognition schema. When learning a new motor program, an individual learns a general set of rules that can be applied to a variety of contexts. The generalized motor program is considered to contain the rules for creating the spatial and temporal patterns of muscle activity needed to carry out a given movement. Seeks to address what drives skill acquisition and how an individual moves from one developmental stage of skill to another. The system is composed of a number of identifiable variables (muscle power, body mass, arousal, neural networks, motivation and environmental forces [gravity, friction, etc.]). Movement emerges due to interaction of subsystems, which work together and which change over time. Three key hypotheses: ~ A developing organism that is genetically endowed with spontaneously generated behaviors that make up the basic movement repertoire. ~ A sensory system capable of detecting and recognizing movements having adaptive value. ~ The system has the ability to select movements having adaptive value by varying synaptic strength within and between brain circuits such that successive event selections will progressively modify the movement repertoire. (Continued)
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SECTION II. TESTS AND MEASURES
TABLE 16-2. THEORIES OF MOTOR CONTROL (Continued) THEORY
DESCRIPTION
Central pattern generators (CPGS)7-1l
These are proposed to account for the basic neural organization and function required to execute coordinated, rhythmic movements, such as locomotion, chewing, grooming (e.g., scratching), and respiration. Commonly defined as inter neural networks, located in either the spinal cord or brainstem, that can order the selection and sequencing of motor neurons independent of descending or peripheral afferent neural input. Also modulate the inputs they received, gating potentially disruptive reflex actions such as nociceptive activation of the flexor withdrawal reflex when a limb is fully loaded during the stance phase of locomotion.
1. Data from Bradley NS, Westcott SL. Motor control: developmental aspects of motor control in skill acquisition. In: Campbell SK, Vander Linden DW, Palisano R], eds. Physical Therapy for Children. 3rd ed. St. Louis: W.B. Saunders; 2006:77-130. 2. Data from Comparetti AM. The neurophysiologic and clinical implications of studies on fetal motor behavior. Semin Perinatal. 1981;5:183--189. 3. Data from Shumway-Cook A, Woollacott MH. Motor learning and recovery of function. In: Shumway-Cook A, Woollacott MH, eds. Motor Control: Theory and Practical Applications. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2001:26-49. 4. Data from Schmidt RA. Motor schema theory after 27 years: reflections and implications for a new theory. Res Q Exerc Sport. 2003;74:366-375. 5. Data from Thelen E, Corbetta D. Exploration and selection in the early acquisition of skill. Int Rev Neurobiol. 1994;37:75--102. 6. Data from Thelen E. Motor development. A new synthesis. Am Psychol. 1995;50:79-95. 7. Data from Grillner S, Wallen P. Central pattern generators for locomotion, with special reference to vertebrates. Annu Rev Neurosci. 1985;8:233--261. 8. Data from Hooper SL. Central pattern generators. Curr BioI. 2000;1O:RI76. 9. Data from Marder E, Bucher D. Central pattern generators and the control of rhythmic movements. Curr BioI. 2001;1l:R986-996. 10. Data from Prosiegel M, Holing R, Heintze M, et al. The localization of central pattern generators for swallowing in humans-a clinical-anatomical study on patients with unilateral paresis of the vagal nerve, Avellis' syndrome, Wallenberg's syndrome, posterior fossa tumours and cerebellar hemorrhage. Acta Neurochir Suppl. 2005;93:85-88. 11. Data from Verdaasdonk BW, Koopman HF, Helm FC Energy efficient and robust rhythmic limb movement by central pattern generators. Neural Netw. 2006;19:388--400. Epub Dec. 13, 2005.
The neural-maturationist theorists consider the maturational state of the nervous system as the main constraint for developmental progress--basic motor skills, such as standing and walking, are not learned by experience but are the result of cerebral maturation.
Cognitive Theories Cognitive-Behavioral. Cognitive-behavioral theory believes that developmental progress occurs through Pavlovian responses to previ ous stimulation, and by operant processes in which responses are con trolled by consequences. 14 Under this theory, behavior is goal oriented, TABLE 16-3. MOTOR CONTROL VARIABLES VARIABLE
Sensorimotor
Mechanical
Cognitive
Task requirements
DESCRIPTION
Those physiologic mechanisms or processes that reside within the nervous system, such as central pattern generators (CPGs). Movement synergies and neural mechanisms that alter or regulate them. Changes in total body mass and relative distribution of mass during development are accompanied by changes in length and center of mass in the body segment, which in turn alter inertial forces due to gravity and during movement. The viscoelastic properties of musculoskeletal tissues. May include variables that are dependent on conscious and subconscious processes such as reasoning, memory, or judgment to optimize performance (arousal, motivation, anticipatory or feedforward strategies, . a selective use of feedback, practice, and memory). May include any variable that can contribute to or in some way alter movement, including biomechanical requirements, meaningfulness, predictability, or any other variable associated with a given movement context.
Data from Braclley NS, Westcott SL. Motor control: developmental aspects of motor control in skill acquisition. In: Campbell SK, Vander Linden DW, Palisano R], eds. Physical Therapy for Children. 3rd ed. St. Louis: W.B. Saunders; 2006:77-130.
CHAPTER 16. PEDIATRIC PHYSICAL THERAPY
and has both direction and purpose-actions are motivated by a desire to achieve a goal or to avoid unpleasant circumstances. Motivation has two purposes: .. To allow internal tension to create a demand for the goal. .. To establish the events that an individual will concentrate on. There are two main types of motivators: deprivation and incentives. .. Deprivation causes an internal desire to obtain the goal. .. An incentive motivates behavior based merely upon the ade quacy of the reward.
Cognitive Piagetian. Piaget 15 emphasized an interaction between maturation of cognitive-neural structures and environmental opportu nities to promote action. Piaget felt that development proceeds in an ordered series of stages and was largely the result of the individual's experience with the environment. The four stages described by Piaget are outlined in Table 16-4. Piaget describes three processes that are instru mental to adapting to the environment through learning-assimilation, accommodation, and equilibration (Table 16-5).15
Dynamic. Thelen and colleagues l 6-18 have proposed a dynamic func tional perspective on motor development. This theoryI8.19: .. Emphasizes process rather than product or hierarchically struc tured plans. .. Places neural maturation on an equal plane with other structures and processes that interact to promote motor development. .. Emphasizes that the environment is as important as the organ ism and developmental change is seen not as a series of dis crete stages, but as a series of states of stability, instability, and phase shifts in which new states becomes stable aspects of behavior. According to dynamic theory, cooperating systems, which include musculoskeletal components, sensory systems, central sensorimotor integrated mechanisms, and arousal and motivation, become progres sively integrated with the self-organized properties of the system to gradually optimize skilled function. 19 .20
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Study Pearl R.~cent motor control and develop ment theories irlch.lde1 •7,8; .. Dynamic pattern theory (motor control theory); there are general principles of motor coordination including order parameters. (vari ables that incorporatetheattlonbf manysubunits of a system and can be used to characterize coor& nated ben;lvior) and control parameters (variables that initiate change in order parameters). Same behavioral patterns are more come mon than others-attractors. .. Dyna.mic action theory (motor development theory}: movement is an. emergent property based On multiple factors (e.g.,neur;llmatu ration, muscle force, biomechanical leverages, emotional state,cogniI .;~~~~waren. es.s , constraints.•.·.O f the ~and physical environment).
Study Pearl PediatrIc physical the:ra.pyinitially developed according to the neural maturationist theoretical model, emphasLzing the assessment stages of reflex development. and. mo~ormj]e stones as reflections of increasingly higherfevelsof neural maturation. 13 l1lus, the interventiooforchildren witn CNSdysfunctionwasbased around
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.•. . s and emphasize •the fadlitationmthe ri ghtingandequ iIibriuill reactions.,l4
T.o\BLE 16-4. PIAGETS STAGES OF LEARNING SfAGE
Sensori-motor Pre-Dperational
Concrete operational Fonnal operational
DESCRIPTION
Lasting from birth to approximately 24 months. The child learns about the world primarily through sensory experiences and movement. From 2 to approximately 5 or 6 years of age. The child develops the important skill of using symbols, including pictures and spoken words, but is not yet capable of mentally manipulating them in logical order. During this stage, from approximately 6 to 11 or 12 years of age, children become capable of what Piaget refers to as mental operations and of applying logical thought to concrete situations. Beginning at approximately 11 or 12 years of age, this is the period in which the adolescent becomes capable of logical, abstract thinking. During this period, adolescents can imagine all of the possibili ties in any situation or problem and are capable of analyzing them to determine which are the best approaches.
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TABLE 16-5. PIAGETS LEARNING PROCESSES PROCESS
DESCRIPTION
Assimilation
Accommodation
Equilibration
I
This is the process through which one uses existing mental structures or schemas to take in new information. An existing schema (idea, concept)--prior knowledge-to relate to the new information is necessary to enable assimilation. Learning occurs by connecting new information to something already known. New ideas or knowledge are integrated and combined with prior knowledge, as in the case of reading. The process through which the existing mental structures or schemas change as new information is acquired. The existing schema (ideas, concepts) are revised if the new information does not fit with them, thus modifying the existing knowledge and changing the previous mental representations. This refers to internal self-efficacy (self-regulation)-the balancing between assimilation and acconuTIodation. Equilibration is the self-regulatory process through which new experiences are balanced with what is already known to achieve a state of equilibrium.
PRENATAL DEVELOPMENT
Study Pear'
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- - - - - - - -
The impact of Piagetian theory on pedi atric physical therapy is primarily due to the inclusion of problem-solving activi ties in therapeutic programs to assist in the cognitive-motivational aspects of fadl itat1ng motor development. 14
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Study_Pe_a_r_' ~
_
Menstrual age: the age of a fetus or newborn, in weeks, from the first day of the mother's last normal men strual period. ~ Gestational age: also known as fetal age: the time measured from the first day of the woman's last menstrual cycle to the current date-the time inside of the uterus. A pregnancy of normal gestation is approximately 40 weeks, with a normal range of 38 to 42 weeks (Table 16-7). ~ Preterm (premature): born before 37 weeks of gestational age. 21 ~ Post-term (postmature): born after 42 weeks. 21 ~ Conceptional age: the age of a fetus or newborn in weeks since conception. ~ Chronologie age: the time elapsed from date of birth to present day. ~ Corrected age: based on the age the child would be if the pregnancy had actually gone to term. The cor rected age, generally used for the first 2 years of life, can be calculated as the chronologie age minus the ~umber of weeks/months premature.
The prenatal period of development (Table 16-6) is also known as the gestational period. The prenatal stage of development can be divided into three dis tinct periods: ~ ~ ~
Germinal: begins at the time of fertilization and last 2 weeks. Embryonic: begins 2 weeks after conception and lasts about 6 weeks. Fetal: begins at 7 weeks of gestation and ends at birth. At 14 to 15 weeks, all the preliminary feeding movements, including mouth opening and closing, sustained lip closure, and tongue movements, are present. At 29 weeks, audible sucking can be observed.
DEVELOPMENTAL MILESTONES A milestone is a significant point in development or a significant func tional ability achieved during the developmental process. The various developmental milestones for both sensory and motor development are depicted in Tables 16-8 to 16-10. ApPROXIMATE ACES Of EPIPHYSEAL CLOSURES See Tables 16-11 and 16-12. AUTOMATIC POSTURAL RESPONSES Automatic postural responses (Table 16-13) allow an individual to restore or maintain body equilibrium and remain functionally oriented. These responses are dependent on the organization of the visual, vestibular, and somatosensory systems (see Chapter 9).
MOTOR PROGRAMMING Motor programs allow for movements to occur in the absence of sen sation or in situations in which limitations in speed processing feed back negate control. 2 Two control systems coexist:
CHAPTER 16. PEDIATRIC PHYSICAL THERAPY ~
~
Open-loop control system: occurs virtually without the influ ence of peripheral feedback or error-detection processes." Closed-loop control system: employs feedback and a reference for correctness to compute error and initiate subsequent cor rections. Together with feedback, this process plays a critical role in the learning of new motor skills and in shaping and cor recting ongoing movements. 2
lStudy Pearl
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Birth weights: Normal (appropriate for gesta tional age). ~ Large for gestational age-4000 to 4500 g (8.8 to 9.9 lbs). ~ Small for gestational age. • Low birth weight-less than 2500 g (5.5 Ibs). • Very low birth weight-less than 1500 g (3.3 lbs). ~
MOTOR LEARNING Motor learning involves a set of processes associated with the practice or experience of new strategies for sensing as well as moving, which lead to relatively permanent changes in the capability of producing skilled action (Table 16-14). The process of motor learning leads first to attainment and later to perfection of a specific motor skill. Feedback can be either intrinsic or extrinsic in origin: ~
~
Intrinsic: inherent sensory information that comes from the spe cialized receptors in muscle, joint, tendon, and skin as well as that from visual and auditory receptors either during or follow ing movement production. Extrinsic: augmented information about movement pro vided to the performer from an external source. Extrinsic feedback has been described as motivational as it relates to goal achievement. Two major types of extrinsic feedback are recognized: • Knowledge of results (KR). KR can be defined as verbal, post-response, augmented feedback about the response out come. When KR is used, subjects practice longer, try harder, and stay interested in the task longer than when KR is not used. • Knowledge of performance (KP). In contrast to KR, KP is information about the movement pattern produced, rather than the outcome of the movement.
~
~
The outcome (KR) is often obvious to the patient, while the movement response to cause the outcome is not so obvious and needs to be supplied by the clinician. There are often several components to the desired movement outcome. In some disease states, the intrinsic feedback is often distorted, or in severe cases, absent, and must be supplemented or replaced with extrinsic feedback, usually provided by the clini cian or educated family member/caregiver.
A motor program should be thought of as a structured plan that is prepared in advance of the movement, which when executed, results in a combination of muscle contraction and relaxation to cause a spe cific movement to occur without the involvement of feedback. There are four essential features related to the motor response that the per former uses when learning
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~
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Neonatal: the period from birth until 2 weeks. The posture of the neonate is characterized by flexion. Infancy: the period from birth until the child is able to stand and walk. Typically infancy lasts approxi~-I mately 1 year.
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is considered one of the most powerfu Ivariables affecti ng moto~r \
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Learning is not directly observable and can be defined as a relatively permanent change in the capability for responding that results from prac tice or experience. True motor learn ing occurs when the subject can demonstrate a performance when the extrinsic feedback is withdrawn.
In the clinical setting, KP is used more often. This is because: ~
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i:::rtant to nore that errors are
not detrimental to learning, but rather I can provide valuable information if extrinsic feedback is provided in the form of KR and/or KP. f
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~
The initial conditions before the movement. which parameters or motor commands were assigned to the generalized motor program. The actual consequences of the movement in the form of extrinsic feedback. The actual intrinsic sensory feedback from the response.
TABLE 16-6. DEVELOPMENTAL CHARACTERISTICS OF THE EMBRYO ACCORDING TO GESTATIONAL AGE GESTATIONAL AGE
DEVELOPMENTAL CHARACTERISTICS
2.5 weeks
Neural plate formation; shape and length begin to be determined.
3 weeks
Cell differentiation occurs--formation of ectoderm (nervous system, sensory systems and many other tissues), mesoderm (muscles, skeleton, and other tissues), endoderm (respiratory system, digestive system, and other tissues). Fetus reaches a length of 0.75 to 1 cm and weighs 400 mg. Spinal cord forms and fuses at the center. Lateral wings bend fOlWard meeting at the center and will eventually form the body. Head tilts fOlWard and makes up about one-third of the entire structure. The rudimentary heart beats a regular rhythm. Arms and legs have the appearance of small buds. The beginnings of eyes, ears, and a nose are evident. Embryo now a fetus. Fetus reaches a length of 1 in (2.5 cm) and weighs 20 g. The heart has a definite septum and valves. Extremities have lengthened. External genitalia are evident, but gender is not obvious. Fetus reaches a length of 2.8-3.6 in (7-9 cm) and weighs 45 g. Some movement occurring, but usually too faint for the mother to feel. Fetal heart can be heard with a Doppler. Fetus reaches a length of 4-7 in 00-17 cm) and weighs 55-120 g. Liver and pancreatic secretions are present. Fetus starts to make sucking motions with the mouth. Fetus reaches a length of 10 in (25 cm) and weighs 223 g. The mother starts to feel fetal movement. Fetal heart tones can be heard with a stethoscope. Fetus reaches a length of 11-14 in (28-36 cm) and weighs 550 g. Eyebrows and eyelashes are clearly formed. Eyelids, which fused in the 12th week, start to open. Pupils are reactive to light. Fetus could possibly be viable if born now and cared for in a neonatal intensive care unit. Surfactant is formed and excreted by cells in the alveoli. Fetus reaches a length of 14-15 in (35-38 cm) and weighs 1200 g. Testes begin descent into the scrotal sac from the lower abdominal cavity if the fetus is male. The brain is rapidly developing. Fetus reaches a length of 15-27 in (38-43 cm) and weighs 1600 g. Fetus hears sounds and responds with movement. Delivery presentation (vertex or breech) may be assumed. Iron stores begin to develop. Fetus reaches a length of 17-20 in (42-49 cm) and weighs 5-6 lbs (1900-2700 g). Soles of the feet have only one or two creases. The central nervous system has greater control over body functions. Fetus reaches a length of 19-21 in (48-52 cm) and weighs 7-7.5 lbs (3000 g). Fingernails have grown over the fingertips. There are creases covering at least two-thirds of the soles of the feet. Fetus kicks vigorously and may cause the mother discomfort.
End of 4 weeks gestation
End of 8 weeks gestation
End of 12 weeks gestation
End of 16 weeks gestation
End of 20 weeks gestation
End of 24 weeks gestation
End of 28 weeks gestation
End of 32 weeks gestation
End of 36 weeks gestation
End of 40 weeks gestation
Data from Forslund M, Bjerre 1. Neurological assessment of preterm infants at term conceptional age in comparison with normal full-term infants. Early Hum Dev. 1983;8:195-208; Piper Me, Byrne PJ, Pinnell LE. Influence of gestational age on early neuromotor development in the preterm infant. Am] Perinatal. 1989;6:405-411; and Awoust J, Levi S. Neurological maturation of the human fetus. Ultrasound Med Bioi. 1983;suppl 2:12:583-587.
CHAPTER 16. PEDIATRIC PHYSICAL THERAPY
1029
TABLE 16-7. ASSESSMENT OF GESTATIONAL AGE AT BIRTI-I EXTERNAL CHARACfERlSTIC
28 WEEKS
32 WEEKS
Ear cartilage
Pinna soft, remains folded
Pinna harder, but remains folded
Breast tissue
None
None
Male genitalia
Testes undescended, scrotal surface smooth
Testes in inguinal canal, a few scrotal rugae
Female genitalia
Prominent clitoris with small, widely separated labia Smooth, no creases
Prominent clitoris; larger, well-separated labia
Plantar surface of foot
1 or 2 anterior creases
36 WEEKS Pinna harder, springs back into place when folded Nodule 1-2 mm in diameter Testes high in scrotum, more scrotal rugae Clitoris less prominent, labia majora cover labia minora 2 or 3 anterior creases
Data from, Pediatric Clinical Practice Guidelines for Nurses in Primary Care, Health Canada, 2001. (www.hc-sc.gc.cal)
MOTOR LEARNING THEORIES 'Theories of motor learning (Table 16-15) describe hypotheses regard ing how movement is learned. Early theories believed that learning was a process of "habit" formation. 22
PRIMITIVE REFLEXES Reflexes are involuntary movements or actions that help to identify normal brain and nerve activity. As a general rule, influence of the primitive reflexes is not readily observed in the healthy, normally developing child after 6 months of age (exceptions include the sym metric tonic neck reflex and the plantar grasp reflex). Some reflexes occur only in specific periods of development and are not evident later in development as they become integrated by the eNS (Table 16-16). However, persistence of these reflexes can interfere with motor mile stone attainment.
TABLE 16-8. MAJOR MILESTONES
MILESTONE
Roll Sit independently Belly crawl Creep (quadruped) Pull to stand Cruise Walk
APPROXIMATE AGE (IN MONTI-lS) ABLE TO PERFORM
3-4 5-6 7-8 8--9 9-10 11
12
Data from van Blankenstein M, Welbergen UR, de Haas ]H. Ie Developpement du .vourrisson: Sa Premiere Annee en 130 Photographies. Paris: Presses Universitaires de France; 1962.
40 WEEKS
Pinna firm, stands erect from head Nodule 6--7 mm in diameter Testes descended, scrotum pendulous, covered in rugae Clitoris covered by labia majora Creases cover the sole
1030
SECTION II. TESTS AND MEASURES
TABLE 16-9. GROSS MOTOR CHECKLIST MONTH!YEAR
POSITION/ACTIVITY
3 months
Prone Vertical Prone Supported sitting Prone
4 months
Prone
1 month 2 months
Supine
5 months
Supported sitting Prone Supine
6 months
Supported sitting Standing Prone Sitting
7 months
Prone Sitting
8 months
9 months
10 months 12 months
Prone Sitting Standing Prone/supine Sitting Standing Sitting Locomotion Locomotion
15 months
Kneeling Locomotion
18 months
Locomotion
2 years
Locomotion
3 years
Locomotion
4 years
Locomotion
5 years
Locomotion
MILESTONE
Lifts head and turns to side Rights head Recurrently lifts head to 45 degrees Head erect and bobbing Lifts head to 45 degrees (sustained) Recurrently lifts head to 90 degrees Supports self on forearms. Rolls to side Lifts head to 90 degrees (sustained) Rolls to supine Rolls to prone Assists with head when pulled to sit Head steady, set forward Supports self on extended arms Rolls to supine segmentally Lifts head when pulled to sitting Rolls to prone segmentally Head erect and steady Takes weight on lower extremities Can lift one arm and weight bear on the other Pivots in a circle Erect for 1 minute with hands propped forward Protective extension sideways Up on all fours Progress is forward in any manner Erect without support but unsteady Protective extension forward Crawls in any manner Erect without support Pulls to stand Rotates to sitting Goes to prone Protective extension backward Pulls to standing with rotation and support Pivots Cruises Stands up without support Walks with high guard Kneels without support Walks with medium guard Can stop, start, and change directions without falling Walks with no guard carrying object Walks fast with feet flat Squats to play Goes up/down stairs on all fours Walks up/down stairs one at the time holding rail Walks with heel-total gait Runs forward well Pedals and steers tricycle well Jumps forward on both feet Alternates feet going upstairs Walks backward easily Walks downstairs with alternating feet, holding rail Gallops Able to walk long distances on toes Skips Hops forward on one foot Smooth reciprocal movements in walking and running
't'AHLH 1().1O. DEVEI.OPMENT MILESTONES ACCOIU>INti '1'0 POSITION
AGE
PRONE
SUPINE
SIlTING
Neonate: 0-14 days
Physiological flexor activity in the ankles, knees, hips, and elbows.
Lack of trunk muscular control: the back is round and the head flops forward.
Newborn (0-1 month)
Arms and hands tucked in No control of neck flexion in supine is close to the body, present, so the baby rounded shoulders, cannot maintain the elbows flexed, and head in midline, but hands are closed keeps it rotated to loosely and positioned one side. close to mouth.
Sacral sitting if supported.
1 month
Head lifting in prone may Head to one side resulting in lateral appear to be improved. vision becoming Increased cervical rotation dominant and uncon mobility. trolled, swiping at Elbows moving forward, toys at the baby's arms away from body. side is frequently observed. Wider ranges of
movement.
Heels hit surface.
STANDING Demonstrates the remarkable capabilities of primary standing-automatic walking when supported.
Positive support and primary walking reflexes in supported standing.
COMMENTS Grasp is a reflex in which the hand automatically closes on objects the baby touches due to tactile stimulation of the palm of the hand. The hands will randomly swing out wide (neonatal reaching). No organized response to postural perturbations. Period dominated by physiologic flexion. Poor head control. Very active when awake. Random wide ranging movements primarily in supine position. Soft tissue tightness holds the hips in flexion!abduction! external rotation. The baby touches and feels, and is soon sucking and learning about the hands. Vision limited to 8 to 9 feet. Skeletal characteristics include coxa valgus, genu varum, tibial varum and torsion, calcaneal varus, and occasionally, metatarsus adductus. Decreasing physiologic flexion (less "recoil"). Increasing level of arousal. Neonatal reaching. Able to visually track a moving object horizontally.
(Continued)
...o ...
"J
...o IN N
TABLE 16-10. DEVELOPMENT MILESTONES ACCORDING TO POSITION (Continued) AGE 2 months
3 months
4 months
PRONE
SUPINE
SITTING
Increased asymmetry Head lag occurs with Able to hold the head with more visual steady in all positions pull to sit. interaction. and to raise it about Begins to develop head 45 degrees due to and trunk control and more attempts at increased activity of active shoulder sustained extension. Head bobs in supported abduction. The arms and hands begin to work to sitting. support the actions of the head and trunk. Hand movements more goal directed. Beginning of symmetry Attempts pull to sit but Change occurs in the general position of the is evident: the head falls forward. is in midline with arms, from a position where the arms are chin tucking and the tucked in close to the hands are in midline body with the elbows on the chest/to near the ribs, to one in mouth. which the elbows are almost in line with the shoulders, which allows for forearm weight bearing. Legs abducted and externally rotated Face can be raised 45 to 90 degrees when prone. Able to prop up on the Can roll from prone to Assists in pull to sit by flexing elbows. Very forearms and look side and from supine around. The head and to side, although minimal head bobbing-stabilized chest are lifted and these are usually maintained in midline. accidental occurrences. through shoulder Prone pivots. elevation. Able to bring the hands together in the space Tends to sit in a above the body due slumped pOSition. to increased shoulder Protective reactions develop, first laterally, girdle control. Hands to knees. then forward, and then Active anterior and backward. posterior pelvic tilt.
STANDING
COMMENTS
May not accept weight on lower extremities (astasia-abasia). No more neonatal stepping.
Increasing asymmetry/decreased tone. Increased head and trunk control lets the baby use the arms for reaching and playing rather than for support. Holds objects placed in the hand.
Minimal weight through extended legs.
Period of controlled symmetry. The grasp becomes more controlled and voluntary and the hands can adjust to the shape of objects. Symmetry is very obvious in the lower extremities as they assume their "frog legged" position of hip abduction, external rotation and flexion, and knee flexion. The feet come together and the baby is able to take some weight with toes curled in supported standing.
Because of the increased head-neck-trunk control, the baby is able to take more of his or her weight when placed in standing, and can now be held by the hands instead of at the chest. Legs are extended and the toes are clawed.
Ulnar palmar grasp develops. Able to perform bilateral reaching with the forearm pronated when the trunk is supported. Side-lying. Starts hand to mouth activities. Emerging righting and equilibrium reactions. Findings of concern include poor midline orientation (persistent ATNR), imbalance between flexors and extensors, poor visual attention/tracking, persistent wide base of support in standing, and poor anti~ravity strcn~th.
5 months
6 months
7 months
Equlilbrlum reactions begin in prone position. Can roll from prone to supine. Able to assume and maintain a position of extended arm weight bearing in prone position, and can shift weight from one forearm to the other and reach out with one arm. Completes turning and can roll from prone to supine. Can lay prone on hands with the elbows extended and is able to shift weight on extended arms from hand to hand and to reach forward due to sufficient shoulder girdle control. Trunk and arms free. Able to achieve and maintain the quadruped position, although prone is usually the preferred position. Can pivot on belly, often moving body in a circle.
Chin tuck, downward gaze. Feet to mouth. Anterior and posterior pelvic tilt more active. Active role to sideline. Manipulation and transfer of toys.
There ill nu heud hiM when the baby is pulled from supine to sit. Assists during pull to sit with chin tuck and head lift. Able to control head in supported sitting, although still leans forward from the hips.
Active hip extension. Transfers toys. Flexes head independently.
Can sit independently, although initially uses the arms and hands for support.
Tends to avoid except for playing.
Protective reactions more Can often pull to stand from the quadruped position. consistent. Able to actively flex and Able to perform trunk extend both legs rotation in sitting. simultaneously while Can assume the sitting standing and supporting position from the independently. quadruped position.
PlndlnM ul' l'Unl'l'rn Indudl' Poor antigravity flexion. ~ Poor tolerance for prone/ inability to bear weight to extended arms/poor weight shifting.
~
In standing, is able to bear weight on both legs and bounce and can independently hold onto the support of a person due to sufficient trunk and hip control.
Uses rolling for locomotion. Findings of concern include ~ Poor tolerance for prone position. ~ Paucity of movement patterns. ~ Inability to sit independently. ~ Inability to roll or rolling with neck hyperextension.
Very active with large variety of movements and positions available. May show fear of strangers. Findings of concern include ~ Lack of weight shifting in prone position. ~ Reliance on more primitive movement patterns as compensations in order to explore. ~ Inability to assume or maintain quadruped. ~ Poor weight bearing in supported stance. (Continued)
...
Q
W W
... Q
...
TABLE 16-10. DEVELOPMENT MILESTONES ACCORDING TO POSITION (Continued)
W
AGE 8 months
9 months
10 months
11 months
12-15 months
2 years
PRONE Minimal time spent in prone-able to creep/ crawl in the quadruped position at 9 months as the primary means of locomotion.
SUPINE
SITTING
STANDING
COMMENTS
Can reach out for objects and reach across the midline of the body without losing balance. The thumb can wrap around objects--now the baby can hold two small objects, such as cubes, in one hand. Findings of concern include: ~ Poor sitting ability. ~ Unable to use hand for play. ~ Overall reliance on upper extremities. Uses arms, hands, and body Large variety of sitting The index finger starts to move separately from the rest of the together while pulling up to positions and movements. hand when poking at objects. Pivoting/long sitting. standing through half-kneel position (9 months). This leads to the pincer grasp, Sitting often used as a transitional position. Immature stepping. with the tips of the thumb and index finer meeting in a precise The sequence in rising to standing is kneeling, half pattern. kneeling, weight shift for The baby's ability to let go of ward, squat, then upright. an object smoothly has also improved. Findings of concern include: ~ Poor standing control. ~ Poor/inadequate sitting. ~ Inability to assume quadruped. Creeping/climbing. Arms reach above shoulders. Legs very active. "High guard" Active site sitting. Cruising with wide base of Rarely stationary. support. Mostly using legs. Able to play and across Very symmetrical standing with midline. a wide base of support. Able to self-feed.
Many babies are walking Can build a tower of two cubes.
unassisted. Runs well. Goes upstairs using reciprocal pattern (reciprocal stair climbing).
Full equilibrium reactions in sitting, and the beginning of equilibrium reactions in quadruped. Able to side-sit and is also able to go from sitting to quadruped. May also kneel.
Can stand by leaning on supporting surfaces. Able to pull to stand. Early walking, cruising.
Data from van Blankenstein M, Welbergen UR, de Haas ]H. Ie Developpement du Nourrisson: Sa Premiere Annee en 130 Photographies. Paris: Presses Universitaires de France; 1962; and Prechtl HF. New perspectives in early human development. Hur] Ohsfef Gynecol Re/>rod Hiul. 19H6;21 :347-3'i'i.
CHAPTER 16. PEDIATRIC PHYSICAL THERAPY
1035
TABLE 16-11. APPROXIMATE CHRONOLOGIC AGES OF EPIPHYSEAL CLOSURES OF THE LOWER EXTREMITY BODY AREA Acetabulum Femur
Tibia Fibula
AGE (YEARS) 20-25 Greater and lesser trochanters: 18 Femoral head: 18 Distal end: 20 Proximal end: 20 Distal end: 18 Proximal end: 25 Distal end: 20
Data from Pick TP, Howden R. Gray's Anatomy. 15th ed. New York: Barnes & Noble Books; 1995.
TABLE 16-12. APPROXIMATE CHRONOLOGIC AGE OF EPIPHYSEAL CLOSURES IN THE UPPER EXTREMITY AND SPINE APPROXIMATE AGE (YEARS) 15-17 18-19 20 20-25
AREA Scapular, lateral epicondyles of humerus, olecranon process of ulna. Medial epicondyle of humerus, head and shaft of radius. Humeral head, distal ends of radius and ulna. Spine: vertebrae and sacrum. Clavicle. Thorax: sternum and ribs.
Data from Pick TP, Howden R. Gray's Anatomy. 15th ed. New York: Barnes & Noble Books; 1995.
DESCRIPTION Orientation of the head in space so that the eyes and mouth are in a horizontal plane or the body parts are restored to proper alignment. Includes vertical righting (orienting head to vertical) and rotational righting (orientation following rotation of a body segment). Operates regardless of the position of the body or where body is in the environment. Normally develops during the first 6 months of life. Complex responses to changes of posture or movement that seek to restore disturbed balance when the body's base of support is subjected to perturbation (push, pull, or tilt). Develop in a position after a child has learned to assume the position (prone, supine, sitting, quadruped, and standing) independently. Response is generally in the opposite direction of the force. ~ Spinal column concavity on the uphill side on an unstable base of support. ~ Spinal column concavity on the side of the pushing force on a stable base of support. ~ Rotation of the upper trunk and head toward the midline and counter rotations of the lower trunk may occur. ~ Abduction and extension of the extremities on the downhill side or in the direction of push. Extension movements of the extremities generally in the same direction as the displacing force, which shifts the body's center of gravity. Highly context dependent. Can be backward, forward, or laterally. Develops laterally by 6-11 months, then forward, and finally back ward by 9--12 months. from Effgen SK. Developing postural control. In: Connolly BH, Montgomery PC, eds. Therapeutic Exercise in Developmental Disabilities. fare, N]: Slack; 2001:111-123; Milani-Comparetti A, Gidoni EA. Routine developmental examination in normal and retarded children. DevMed Neurol. 1967;9:631--638; and Dargassies SS. Neurodevelopmental symptoms during the first year of life. I. Essential landmarks for each key-age. Jfed Child Neural. 1972;14:235-246.
1036
SECTION II. TESTS AND MEASURES
TABLE 16-14. THE FITS AND POSNER THREE-STAGE MODEL OF MOTOR LEARNING STAGE Cognitive
Associative
Autonomous
DESCRIPTION An understanding of the task and general plan to accomplish it.
High attention demands (requires auditory, visual, kinesthetic, somatosensory cues). Approach is slow and deliberate (trial and error). Characterized by practice. Involves integration of temporal/spatial patterns. Movements develop into habit patterns. Need for external feedback decreases. Tasks become automatic. Feedback begins to be replaced by feed-forward. Can perform the task successfully in a variety of environments.
Data from Fitts PM, Posner MI. Human Performance. Belmont, CA: Brooks/Cole; 1%7.
PEDIATRIC SCREENING AND DIAGNOSTIC TOOLS Factors to be considered when assessing a child include, but are not limited t0 23 :
Study Pearl
~
~ ~
~
Current life circumstances: the child's current health, attitudes, values of the child's immediate family, and acculturation of the child. Health history: health and nutrition history, repeated hospital izations, and so forth. Developmental history: child's past rate of achievement of developmental milestones, and events that might have had pro found effects on the child either physically or psychologically. Extrapersonal interactions: the reaction of the child to the clini cian and the conditions under which the child is observed.
TABLE 16-15. THEORIES OF MOTOR LEARNING Heterarchical and distributed control Ecological perception-action
Dynamic systems
Flow of information is not top-down. Decisions based on consensus of neural systems. This theory is based on the concept of search strategies--during practice there is a search for optimal strategies to solve the task, given the task constraints. Critical to the search for optimal strategies is the exploration of the perceptual-motor workspace, which requires exploring all possible perceptual cues to identify those that are most relevant to the performance of a specific task. According to the ecological theory, perceptual information as a number of roles in motor learning ~ It relates to understanding the goal of the task and the movements to be learned. ~ It serves as a method of feedback, both during the movement (knowledge of performance) and on completion of the movement (knowledge of results). ~ It can be used to structure the search for a perceptual motor solution that is appropriate for the demands of the task. Motor behavior emerges from the dynamic cooperation of all subsystems within the context of a specific task. Patterns of movement are fleXible, adaptable, and dynamic, yet having "preferred" paths.
Data from Larin H. Motor learning: theories and strategies for the practitioner. In: Campbell SK, Vander Linden DW, Palisano RJ, eds. Physical Therapy for Children. 3rd ed. St. Louis: W.B. Saunders; 2006:131-160; and Shumway-Cook A, Woollacon MH. Motor learning and recovery of function. In: Shumway-Cook A, Woollacon MH, eds. Motor Control: Theory and Practical Applications. 2nd ed. Philadelphia: Lippincon Williams & Wilkins; 2001 :26--49.
CHAPTER 16. PEDIATRIC PHYSICAL THERAPY
1037
1i\BLE 16-16. PRIMITIVE REFLEXES DESCRIPTION
Tonic labyrinthine Asymmetric tonic neck reflex (ATNR) Babinski Symmetric tonic neck reflex (STNR) Crossed extension Proprioceptive placing
Response to light tactile stimulation near the mouth.
Infant moves head in direction of the stimulus and opens the mouth.
Usually disappears around 9 months of age.
Response to nipple or finger in mouth.
Can be assessed as to whether it is sustainable and consistent.
One hand supports the infant's head in midline, the other supports the back. The infant is raised to
45 degrees and the head is allowed to fall through 10 degrees. Mature response is abduction then adduction of the limbs. Usually disappears around 3--6 months of age. Stimulus applied to palm of hand or soles of feet. The response is a grasping of the digits. Usually disappears around 2-3 months of age. Prone position facilitates flexion. Supine position facilitates extension. Related to position of head turn: extension of extremities on face side, flexion of extremities on skull side. Usually disappears around 2-7 months of age. The foot twists in and the toes fan out in response to a stroke of the sole of the foot. Usually disappears around 6-9 months of age. Infant positioned in quadruped. Arm and head do the same thing, legs do the opposite (e.g., head is extended, arms extend, and legs flex). Pressure applied to sole of the foot produces flexion and extension of the opposite leg. Pressure applied to dorsum of the foot or hand. Response is flexion, followed by extension of the extremity to bring the foot/hand on top of the stimulating surface. Usually disappears around 1 month of age. Pressure applied to sole of the foot produces extension of the extremity for weight bearing. Also known as primary standing. Walking motion produced as the infant is moved along a surface while being held under the arms. Also known as automatic walking.
Da1a from Capute A], Palmer FB, Shapiro BK, et al. Primitive reflex profile: a quantitation of primitive reflexes in infancy. Dev Med Child Neural. 1984;26:375-383; Damasceno A, Delicio AM, Mazo DF, et al. Primitive reflexes and cognitive function. Arq Neurapsiquiatr. 2005;63:577-582. Epub 5ept. 9, 2005; Schott ]M, Rossor MN. The grasp and other primitive reflexes. ] Neural Neurasurg Psychiatry. 2003;74:558-560; and Zafeiriou DI. Primitive reflexes and postural reactions in the neurodevelopmental examination. Pediatr Neural. 2004;31:1-K
INfANT ASSESSMENT TOOLS
Brazelton Neonatal Behavioral Assessment Scale (BNBAS) I'opulation. The BNBAS is a behavioral scale for infants from birth to Ihe approximate post-term age of 1 month. 25
rurpose. The BNBAS is based on the assumption that babies com municate through their behaVior, and assesses the infant's use of his or her state of consciousness to maintain control of reactions to environ mental and internal stimuli, including: ~ ~
~ ~
Regulation of the autonomic nervous system, including breath ing and temperature regulation. Control of motor systems. Control of states or levels of consciousness. Social interaction with parents and other caregivers.
Content. The original BNBAS contained 26 biobehavioral items and 20 reflex items. The revised edition contains 27 biobehavioral items with
Study Pearl ... Norm"rererenced ,tests are'.·',stan cl~rdiz,~d on groups of ,individuals (P100 beats/min Good, crying Completely pink Active movement
Reflex irritability
Absent
Slow fnoj')ths,sofnEj .•.• infants ·i .•• may
developsighsofiroipaired respiratOry fUrlctiorl. 145
... Inspection: can reveal postural abnormalities, modifications of
breathing pattern, or signs of respiratory distress. Evidence of a
chronic productive cough may be apparent. Examination of the
comparative dimensions of the chest in the anterior-posterior
and transverse planes may reveal the barrel chest deformity
common to obstructive lung diseases. 146
... Palpation: accurate evaluation of the findings of tactile fremitus:
will feel atelectasis, pneumothorax, or large airway secretions. 1-16
... Percussion: examination of the resonance pattern of the chest.
as demonstrated by audible changes on percussion, can pro-
vide an indication of abnormally dense areas of the lungs. 146
... Auscultation: can contribute information on the quality of air
flow and evidence of obstruction in different areas of the lungs
(rales, etc.-see Chapter 10).
Physical Therapy Role. Patients with cystic fibrosis often require management by a multidisciplinary team including physicians. nurses, nutritionists, physical therapists, respiratory therapists, coun selors, and social workers. The goals of the intervention are ... ... ... ...
Maintenance of adequate nutritional status.
Prevention of pulmonary and other complications.
Encouragement of physical activity.
Provision of adequate psychosocial support.
is
CHAPTER 16. PEDIATRIC PHYSICAL THERAPY
Specific chest physical therapy techniques for the infant include, but are not limited to 145 ,147; ~
~
Postural drainage, percussion and vibrations. Timing the phys ical therapy around feeding schedules may be necessary to reduce the risk of gastroesophageal reflux. Postural drainage positions are easily achieved by arranging the infant in the required manner on the caregiver's lap. The applied force of percussion should vary with the size and condition of the infant, and conscientious monitoring of the infant's response to treatment should guide the amount of vigor used. Education for the family in the application of prescribed physi cal therapy modalities should be ongoing.
The intervention for the preschool and school age period depends on the severity of illness. The goals should encompass an improvement in exercise tolerance with continued attention to secretion clearance rechniques (postural drainage, percussion, and vibration), correction and maintenance of proper postural alignment, and continued educa tion of the caregivers. Mechanical percussors may be used to ease the work involved with manual percussion and to provide the child with an aide to self-treatment. Alternative methods for mobiliZing secretions and stimulating cough have been suggested, usually involving directed breathing techniques. These include huffing, PEP (positive expiratory pressures), oscillating PEP (Flutter and Acapella), autogenic drainage, and active cycle of breathing (formerly known as FET-forced expira tory technique) (see Chapter 10). Exercise has also been shown to be a useful therapeutic modality for secretion clearance, increases in peak oxygen consumption, increased maximal work capacity, and improved expiratory flow rates. 148,149
The term nursemaid's elbow (also referred to as pulled elbow) refers to a subluxation of the radial head in children of preschool age, caused by a sudden longitudinal traction force applied to the pronated wrist and extended elbow.150.151 These are common causes of pulled elbow 152 : ~ ~
The child's forearm or hand is being held firmly by a parent as the child attempts to walk away. The child is lifted by an adult from the ground by his hands.
The combination of patient history and limitation of motion usu ally make the diagnosis--a painful and dangling arm, which hangs limply with the elbow extended and the forearm pronated. 152 There is usually no obvious swelling or deformity. The common sites of pain are (in order of occurrence) the forearm and wrist, the wrist alone, and me elbow alone. 153 In all cases, the child resists attempted supination of the elbow. The intervention of choice is manipulation. 152 The child's attention is diverted and the forearm is forcibly supinated with one quick motion, lDgether with application of downward pressure on the radial head. A dick in the region of the radial head (palpable and sometimes audible) is indicative of a successful reduction. Soon after the manipulation, the
1067
1068
SECTION II. TESTS AND MEASURES
child usually begins to use the arm again, but sometimes there is a delay of a day or two. In such cases, a sling can be used to both give comfort and protect the arm from being pulled again.
1
5
TORSIONAL CONDITIONS These include in-toeing or out-toeing, probably the most common reason for elective referral of a child to an orthopedist. Clinical examination of the child with in-toeing or out-toeing should include documentation
of the foot progression angle in standing or walking, hip rotation range
of motion, thigh-foot axis, and alignment of the foot9 9:
~
~
~
~
Foot progression angle (FPA): also known as the angle ofgait,
is defined as the angle between the longitudinal axis of the foot
and a straight line of progression of the body in walking. 1S4
While observing gait, the clinician assigns a value to the angle
of both the right and left foot. In-toeing is expressed as a nega
tive value (e.g., -20 degrees), and out-toeing is expressed as a
positive value (e.g., +20 degrees). FPA is variable during
infancy, but during childhood and adult life it shows little
change, with a mean of + 10 degrees and a normal range of - 3 to
+ 20 degrees. 154
Hip rotation range of motion: this is measured most accurately in the prone position (or with the anxious young child being held facing the parent's chesO, with the hip in a position of neutral flexion/extension. If the hip is in anteversion (antev erted), the patient will usually have more hip internal rotation than external rotation, assuming no soft-tissue tightness (refer to the "Hip" section in Chapter 8). The sum of hip internal rota tion and external rotation is usually 120 degrees up to age 2 years; over age 2 it is 95 to 110 degrees. 155 True femoral retroversion in an infant is rare. Although many types of interventions have been tried to correct femoral anteversion, none of these has been proved effective in clinical trials. Thigh-foot axis: a reflection of the version of the tibia, which is assessed using the thigh-foot angle, the angular difference between the longitudinal axes of the thigh and the foot, as
measured in the prone position with the knee flexed. Tibial tor
sion can also be described as the angle formed by a straight-line
axis through the knee and the axis through the medial and lat
eral malleoli. By convention, internal tibial torsion is expressed
as a negative value, whereas external tibial torsion is expressed
as a positive value. Scoles156 described the following approxi mate thigh-foot normative angles: • Birth: -15 degrees (normal range, -30 to +20 degrees). • Age 3: +5 degrees (normal range, -10 to +20 degrees). • Mid-childhood to skeletal maturity: + 10 degrees (normal range, -5 to +30 degrees). Controversy exists regarding appropriate treatment of internal tibial torsion because the natural history of the condition is gradual improvement in most cases. In some cases a Friedman countersplint or a Denis Browne bar may be prescribed for night wear for approximately 6 months. Alignment of the foot: alterations in the alignment of the foot can be divided into two categories (Table 16-29):
I I I
(
4
· ~
•i I
• • :I
>1
:I
•
CHAPTER 16. PEDIATRIC PHYSICAL THERAPY
1069
TABLE 16-29. DECISION MATRIX FOR FOOT DEFORMITY
Side view (can foot dorsiflex?) Foot shape (viewed from bottom) Heel position
METATARSUS VARUS
CLUBFOOT
CALCANEOVALGUS
Yes Kidney shaped (deviated medially) Valgus
No Kidney shaped Varus
Yes Banana shaped (deviated laterally) Valgus
Reproduced, with permission, from Leach J. Orthopedic conditions. In: Campbell SK, Vander Linden DW, Palisano R], eds. Physical Therapy jor Children. 3rd ed. St. Louis: W.B. Saunders; 2006:481-515. Copyright © Elsevier.
• Positional (packaging): caused by a restricted intrauterine
environment.
Metatarsus varus, also called metatarsus adductus, is one of
the most commonly seen positional conditions in infants. The
forefoot is curved medially, the hindfoot is in the normal
slight valgus position, and there is full dorsiflexion range of
motion.
Ca1caneovalgus, a common positional foot problem in new
borns. The forefoot is curved out laterally, the hindfoot is in
valgus, and there is full or excessive dorsiflexion.
• Manufacturing: true congenital abnormalities (talipes equino
varus)--see "Conditions Related to the Neonate" later in the
chapter.
SLIPPED CAPITAL FEMORAL EPIPHYSIS
Slipped capital femoral epiphysis (SCFE) is classified as a disorder of epiphyseal growth (Table 16-30) and represents a unique type of instability of the proximal femoral growth plate due to a Salter-Harris type 1 fracture through the proximal femoral physis. 99 ,157-162 The cause of SCFE is unclear. Stress around the hip causes a shear force to be applied at the growth plate and causes the epiphysis to move posteri orly and medially. In addition, the position of the proximal physis nor mally changes from horizontal to oblique during preadolescence and adolescence, redirecting hip forces from compression forces to shear forces. 99 SCFE is associated with the following findings: ~
~ ~ ~
The patient usually has an antalgic limp and pain in the groin, often referred to the anteromedial aspect of the thigh and knee. The leg is usually held in external rotation, both when supine and when standing. There may be tenderness to palpation on the anterior and lat eral aspect of the hip. Decreased hip motion is noted in flexion, abduction, and inter nal rotation. With attempts to flex the hip, the legs move into external rotation.
Knowledge of SCFE and its manifestations will facilitate prompt referral by the physical therapist to an orthopedic surgeon. Diagnosis can be confirmed using both anteroposterior (AP) pelvis and lateral frog-leg radiographs of both hips. CT is a sensitive method of measur ing the degree of tilt and detecting early disease, but it is rarely needed. ~ depicts the slippage earliest, and MRI can demonstrate early mar row edema and slippage.
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SECTION II. TESTS AND MEASURES
TABLE 16-30. EPIPHYSEAL DISORDERS: DISORDERS OF EPIPHYSEAL GROwrn
EPIPHYSEAL DISORDER
INCIDENCE
Slipped capital femoral epiphysis (SCFE) (adolescent coxa vara) By far the most significant of the lower limb epiphyseal plate disorders. It is the most common hip disorder seen in adolescents.
Males (13-16 years of age) are 2-5 times more likely to be affected than females (11-14 years of age). 25-33% bilateral, especially with boys < 12 years. More common in blacks.
Blount's disease (tibia vara) Growth suppression with premature closure of the medial portion of the upper tibial epiphyseal plate.
Girls> boys.
Type in infants < 2-3 years
is the most common. Juvenile type: 4-10 years. Adolescent: 11 + years. Finland and Jamaica have the highest incidence of disease.
Madelung' s deformity Localized epiphyseal dysplasia on the medial (ulnar) side of the distal radial epiphysis.
Adolescent onset. Girls> boys. Usually bilateral.
CLINICAL FEATIJRES AND DIAGNOSIS
INTERVENTION AND OUTCOME
Obesity (75% of cases). Mild hip pain referred to the medial aspect of the knee. Slight limp that increases with fatigue; positive Trendelenburg sign. Posture: lower extremity unloaded into flexion, external rotation, and abduction to avoid impingement of metaphysis on the anterior lip of acetabulum. Reduced hip flexion, internal rotation, abduction. Diagnosis is confirmed with x-ray: AP and lateral views helpful, but frog view with positive Kline's line is definitive. Often seen in obese children who are early ambulators. Lateral thrust during stance. Tibial varum. Early x-ray is essential, as it displays the defective ossification on the medial side of the tibia, beaked appearance of the underlying metaphysis, and obvious longitudinal growth disturbance.
Prescription: prevent further slip, maintain range of motion, prevent osteoarthritis, immobilize via hip spica and non-weight-bearing status. If the slip is less than 1 em, screwed/pin in situ, cast, and weight bearing after surgery.
Prescription: prevent progression of the varus deformity. If unilateral infantile form « 3 years): hip, knee, ankle, foot, orthosis (HKAFO) worn 23 hr/day or night splints to correct the varus deformity. If > 4 years: splinting usually fails and osteotomy of the tibia is required. African-American girls have the worst prognosis. Insidious onset of wrist pain. Correction of the deformity Loss of wrist/forearm range of via surgical excision of motion (flexion and supination). the distal portion of the Prominence of the distal end of ulna and osteotomy of the ulna on the dorsum of the the deformed end of the radius. wrist and forward displacement of the hand in relation to the forearm.
Reproduced, with permission, from Hallisy KM. The adolescent population. In: Boissonnault
WG,
ed. Primary Care for the Physical Therapist:
Examination and Triage. St. Louis: Elsevier W.E. Saunders; 2005:175-237. Copyright © Elsevier.
Physical Therapy Role. The goals of treatment are to keep the displacement to a minimum, maintain motion, and delay or prevent premature degenerative arthritis. 99 Following surgical fixation, using one or two pins or screws, usually in situ, the physical therapist com pletes a careful and thorough examination of the motion of the hip joint, and subsequent measurements should be taken after every oper ation and removal of the cast. Range-of-motion exercises for the hip should be done in all planes, with particular emphasis on hip flexion, internal rotation, and abduction.
CHAPTER 16. PEDIATRIC PHYSICAL THERAPY
Gait training postsurgery is initiated once lower extremity strength and range of motion is adequate for ambulation skills. The weight bearing status can vary, but is usually non-weight bearing or touch down weight bearing. Full weight bearing is permitted when the growth plate has fused (within approximately 3 to 4 months).
LEGG-CALVE-PERTHES DISEASE Legg--ealve-Perthes disease (LCPD) is the name given to idiopathic osteonecrosis of the capital femoral epiphysis of the femoral head. 163--169 LCPD has an unconfirmed etiology, but may involve: 163--169 ~
An interruption of the blood supply to the capital femoral epiphysis--osteochondroses (avascular necrosis of the epiphysis). • Bone infarction occurs, especially in the subchondral cortical bone, while articular cartilage continues to grow. • Revascularization occurs, and new bone ossification starts. • At this point, a percentage of patients develop LCPD, while other patients have normal bone growth and development. • When a subchondral fracture occurs, it is usually the result of normal physical activity, not direct trauma to the area. • Changes to the epiphyseal growth plate occur secondary to the subchondral fracture.
Patients tend to have a limp and frequently have a positive Trendelenburg sign resulting from pain or hip abduction weakness. 99 Limited hip range of motion is noted, especially in hip abduction and internal rotation. The child complains of pain in the groin, hip, or knee (referred pain).99
Physical Therapy Role. Controversy exists regarding the appro priate treatment, or whether treatment is even necessary.99 The goal of treatment is to relieve pain, and to maintain the spherical shape of the femoral head and to prevent extrusion of the enlarged femoral head from the joint. Treatment methods include observation only, range-of motion exercises in all planes of hip motion (especially internal rotation and abduction), bracing, Petrie casts (two long leg cast with a bar between, holding the hips abducted and internally rotated), and sur gery,99 Specific procedural interventions can be used to relieve the forces incurred during weight bearing (crutch training, aquatic therapy). Gait training may be initiated with an orthosis or with bracing. The spe cific gait pattern and assistive devices depend on the type of orthosis. OSGOOD-SCHLATTER DISEASE Osgood-Schlatter (OS) disease (traction apophysis) is a benign, self imiting knee condition that is one of the most common causes of knee pain in the adolescent. 17o as is manifested by pain and edema with ttaetion apophysitis of the tibial tubercle. During periods of rapid growth, stress from contraction of the quadriceps is transmitted through the patellar tendon onto a small por lion of the partially developed tibial tuberosity. This may result in a partial avulsion fracture through the ossification center. Eventually, secondary heterotopic bone formation occurs in the tendon near its msertion, producing a visible lump.
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SECTION II. TESTS AND MEASURES
I:
Study Pearl "fh~sigflS
and. symptoms
of
Osg~Srn1Cll'ild abuse.233~2J9,." Sha~if'lg j;s .. usua,llyin' response toprol~~~~in¢~~~olable
crying andtne injl1ries sustaioec! area result of the combination of the mechanism "of ',. d'l~$haki!'fgitndJbe
unique anatomi¢featu~~oianinfant~
it
relatively large bead'<with weak
neckmusdes.
Three scales are commonly used to measure severity of TEl in children 149: ~ ~
~
Glasgow Coma Scale (GCS)-see Chapter 9. Rancho Los Amigos Scale-see Chapter 9. The Children's Orientation and Amnesia Test (COAT).240 Used to evaluate level of coma in children. Test questions are based on facts commonly known by children.
Study Pearl 'Fhedotati(i)n'olloss' of consciousness the severity of
can",~,',usedfograde;
'lIBl::
Medical complications after TBI arise from the concomitant injuries, alterations in neurologic function, and the effects of prolonged immobility. Cerebral swelling and increased intracranial pressure (hydrocephalus) can be life-threatening. In addition, some of the more common complications of TEl include fever and infection, fracture, posttraumatic seizures, spasticity, heterotopic ossification, deep venous thrombosis, weakness, balance and coordination problems, and cognitive and perceptual changes.
... ~Omiriutesor'less is defined 'as mildtBh' tf>~~ofconsciousness,between
3Q.minutes and 6 hoursis moder
ateraL .t~~sof consciousness of greatertnan
6 hours is consideredsevereTBI.
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SECTION II. TESTS AND MEASURES
Near-Drowning. Drowning is the fourth leading cause of fatal injuries in children between 0 and 19 years of age. 241-243 Near-drowning has been defined as an episode in which someone survives a period of underwater submersion. The most devastating outcome of near drowning is the sequelae of global hypoxic-ischemic brain injury. The magnitude of the neuronal injury that occurs is related to both the level of blood flow during the complete ischemic interval and the total dura tion of the ischemia. Brain Tumors. Primary central nervous system tumors are those that originate in the brain rather than tumors that are a result of metas tasis to the brain. Pediatric brain tumors may be generally classified into (1) infratentorial (occur in the posterior fossa, which is below the tentorium cerebelli and contains the cerebellum, brainstem, and fourth ventricle) tumors, and (2) supratentorial (occur in the cerebral hemi spheres, lateral ventricles, and third ventricle) tumors (Table 16-37). Reports or signs of any of the following should alert the clinician to the presence of a neurologic disorder and should indicate a require ment for medical referral (radiographic imaging, such as CT scan and MRI with and without contrast): ~ ~
~ ~
Altered mental status. Cognitive impairment. Headaches. Vomiting.
TABLE 16-37. PEDIATRIC BRAIN TUMORS CLASSIFICATION Infratentorial
TYPE Astrocytomas
Ependymomas
Medullablastomas
Supratentorial
Craniopharyngiomas
Optic tract gliomas Pineal
DESCRIPTION Regional effects of astrocytomas include compression, invasion, and destruction of brain parenchyma, arterial and venous hypoxia, competition for nutrients, release of metabolic end-products (e.g., free radicals, altered electrolytes, neurotransmitters), release and recmitment of cellular mediators (e.g., cytokines) that dismpt normal parenchymal function. The type of neurologic symptoms that result from astrocytoma development depends foremost on the site and extent of tumor growth in the CNS. Astrocytomas of the spinal cord or brainstem are less common and present with motor/sensory or cranial nerve deficits referable to the tumor's location. The etiology of diffuse astrocytomas has been the subject of analytic epidemiologic studies that have yielded associations with various disorders and exposures. Found in the infratentorial region about 65% of the time, and represent 10% of all childhood brain tumors. These tumors arise from ependymal cells in the ventricles and spinal column. Initial signs and symptoms relate to increased intracranial pressure in posterior fossa ependymomas. Infiltrate the floor or lateral wall of the fourth ventricle and extend into the cavity. These are fast-growing tumors and they may spread throughout the CNS via cerebrospinal fluid. Benign tumors located near the pituitary gland. Cause problems from compression rather than invasion of tissues. Progression of the tumor is related to symptoms of increasing intracranial pressure, visual complaints, and endocrine disturbances Generally slow-growing. Visual disturbances are the predominant clinical symptom. Symptoms are often related to increased intracranial pressure and include headache.
Data from Kerkering GA. Brain injuries: traumatic brain injuries, near drowning. and brain tumors. In: Campbell SK, Vander Linden OW. Palisano R], eds. Physical Therapy for Children. 3rd ed. St. Louis: W.B. Saunders; 2006:709-734.
CHAPTER 16. PEDIATRIC PHYSICAL THERAPY ~ ~ ~
~ ~
Visual disturbances.
Motor impairment.
Seizures.
Sensory anomalies.
Ataxia, dysmetria.
Physical Therapy Role. The clinician must perform a complete and thorough neurologic examination (refer to Chapter 9). The interven tion will depend on the impairments and functional limitations found in the examination (Table 16-38), but in general will involve purpose ful and skillful interactions of the clinician with the child and family to produce changes that are consistent with the diagnosis and progno sis. 241 Specific goals for the intervention may include ~
~
~ ~ ~ ~
Maintain or improve joint range of motion (positioning, casting,
passive range of motion).
Maximize functional mobility. Intervention is directed at assist
ing the child in the achievement of the highest possible levels
of independent functioning in his or her home, school, and res
idential community.
Maximize strength and postural control.
Stimulate/arouse level of consciousness.
Facilitate gross and fine motor development through appropri
ate positioning, postures, and movements.
Maximize patient/caregiver competence with
• Therapeutic positioning and handling. • Home program.
SEIZURE DISORDERS Seizures can be defined as neurologic manifestations of involuntary and excessive neuronal discharge. 244-246 The symptom'> depend on the part of brain that is involved and may include altered level of con sciousness; tonic-clonic movements of some or all body parts; or visual, auditory or olfactory disturbance. Differential diagnosis includes epilepsy, drugs (noncompliance with prescription, withdrawal syn drome, overdose, multiple drug abuse), hypoxia, brain tumor, infection
TABLE 16-38. COMMON IMPAIRMENTS, ACTIVITY LIMITATIONS, AND PARTICIPATION RESTRICTIONS IN CHILDREN WITH BRAIN INJURIES IMPAIRMENTS
Abnormal muscle tone Postural asymmetry Decreased muscle strength Loss of range of motion Ataxia Poor balance Behavior state changes Poor motor planning Poor visual perceptual skills Impaired cognition
ACTIVITY LIMITATIONS
Decreased age-appropriate mobility Delayed gross motor skills Poor school performance Decreased attention to environment
PARTICIPATION RESTRICTIONS
Dependent mobility Dependent self-help skills Social isolation Limited play with peers
Reproduced, with permission, from Kerkering GA. Brain injuries: traumatic brain injuries, near drowning, and brain tumors. In: Campbell SK, Vander linden DW, Palisano RJ, eds. Physical Therapy for Children. 3rd ed. St. Louis: W.B. Saunders; 2006:709--734. Copyright © Elsevier.
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SECTION II. TESTS AND MEASURES
TABLE 16-39. SEIZURE DISORDERS TYPE Generalized
Simple partial
Complex partial Febrile
DESCRIPTION Affects both hemispheres Characterized by change in level of consciousness Bilateral motor involvement Affects only part of brain (focal, motor, or sensory) Formerly called focal seizures May progress to generalized seizures Partial seizure with affective or behavioral changes Associated with temperature> 38°C and tonic-clonic movements Occurs in children < 6 years old (prevalence is 2-4% among children < 5 years old) No signs or history of underlying seizure disorder Often familial Uncomplicated and benign if seizure is of short duration « 5 minutes)
Data from Camfield P, Camfield C. Advances in the diagnosis and management of pediatric seizure disorders in the twentieth century. J Pedialr.
2000;136:847-849; Nelson LP, Ureles SD, Holmes G. An update in pediatric seizure disorders. Pediatr Dent. 1991;13:128-135; Sanger MS, Perrin EC, Sandler HM. Development in children's causal theories of their seizure disorders. J Dev Bebav Pediatr. 1993;14:88-93; and Tharp BR. An overviev.'
of pediatric seizure disorders and epileptic syndromes. Epilepsia. 1987;28Csuppl 1):536--545.
4 .I
I
~
C
(e.g., meningitis), metabolic disturbances (e.g., hypoglycemia, uremia, liver failure, electrolyte disturbance), and head injury.244-246 Most seizures in children involve loss of consciousness and tonic clonic movements, but auditory, visual, or olfactory disturbances; behavioral change; or absences in attention may also occur. The vari ous types of seizures are outlined in Table 16-39.
DUCHfNNf MUSCULAR DYSTROPHY
TABLE 16-40. TYPES AND SUBTYPES OF MUSCULAR DYSTROPHY TYPE X-linked recessive Autosomal recessive
Facioscapulohumeral
SUBTYPE Duchenne Becker Limb girdle Congenital Others Distal Ocular Charcot-Marie-Tooth Werndig-Hoffman
The muscular dystrophies (MDs) associated with defects in dystrophin (dystrophin is integral to the structural stability of the myofiber) range greatly from the very severe Duchenne muscular dystrophy (DMD) to the far milder Becker muscular dystrophy (BMD).247-256 The types and subtypes of MD include those listed in Table 16-40. Duchenne muscular dystrophy (DMD), the best-known form of muscular dystrophy, is due to a mutation in a gene on the X chromo some that prevents the production of dystrophin, a normal protein in muscle. DMD affects boys and, very rarely, girls. DMD typically mani fests with weakness in the pelvis and upper limbs, resulting in clumsi ness, frequent falling, and inability to keep up with peers while playing, and an unusual gait (lateral trunk sway-waddling). Around the age of 8 years, most patients notice difficulty climbing stairs or rising from the ground. Because of this proximal lower back and extremity weakness, parents often note that the child pushes on his knees in order to stand (Gower sign). The posterior calf is usually enlarged as a result of fatty and connective tissue infiltration, or by compensatory hypertrophy of the calves secondary to weak tibialis anterior muscles. Respiratory muscle strength begins a slow but steady decline. The forced vital capacity gradually wanes, leading to symptoms of nocturnal hypox emia such as lethargy and early morning headaches. As DMD progresses, a wheelchair may be needed. Most patients with Duchenne MD die in their early twenties because of muscle-based breathing and heart problems.
01
m
st
a.r
la
ci:
.sJ::
pi
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he: de:
CHAPTER 16. PEDIATRIC PHYSICAL THERAPY
Physical Therapy Role. The role of exercise in the treatment of MD is controversial. One of the primary considerations in the early management program of the young school-age child is to retard the development of contractures. This can be achieved through correct positioning, range-of-motion exercises; stretching of the iliotibial band/tensor fascia latae, iliopsoas, hamstrings, and Achilles tendon; and use of night splints. Braces, such as ankle-foot orthoses and knee ankle-foot orthoses, are important adjuncts in prolonging the period of ambulation/mobility and delaying wheelchair dependency, which usu ally occurs during adolescence. However, the use of orthoses for a standing program or continuation of supported walking is not appro priate for all individuals; in fact, it should be considered a personal rather than therapeutic decision. 257 However, a standing program may help address the issue of decreased bone mineral density and subse quent increased risk of fracture. 257 Independent walking usually ceases by age 10 to 12. A power scooter should be considered for the child who is hesitant to use a power wheelchair when walking is no longer possible. 257 If a power scooter is initially used, transition to a power wheelchair will be necessary when the adolescent is seen propping on the arm rest for trunk controL257 Once wheelchair dependency becomes ineVitable, attention should shift to prophylaxis against the deleterious consequences of immobility: ~
~
~
The chair should be customized to the patient's needs. Eventually, a power wheelchair is necessary because upper extremity and truncal weakness will typically not allow use of a motorized scooter. 257 The fit of the wheelchair must be closely monitored to provide adequate support. Strategic cushioning and supports can help maintain alignment of the spine and pelvis, and reduces the incidence of pressure sores with attendant skin breakdown, which often occur in the sacral and coccygeal regions. The footrests should be modified to support the ankle in a neutral position. A reclining back will allow a position change while sitting in a wheelchair and will help deter flexion contracture formation at the hip. 257 Adaptive devices, such as specially designed wheelchair tables and ball-bearing splints, maximize upper extremity mobility in muscles that cannot resist gravity.
In addition, the emphasis should shift toward an exercise program of active assistive and active exercises of the upper extremities. Key muscle groups for maintenance of strength for transfers include the shoulder depressors and triceps.257 The shoulder flexor and abductor, and elbow flexor muscle groups, are key areas for exercises to main tain routine ADL such as self-feeding and hygiene. 257 Breathing exer cises, postural drainage, or intermittent pressure breathing treatments should be included in the management program based on results of pulmonary evaluation.
SPINAL MUSCULAR ATROPHY The spinal muscular atrophies (SMAs) are a clinically and genetically heterogeneous group of disorders. They are characterized by primary degeneration of the anterior horn cells of the spinal cord and often of
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SECTION II. TESTS AND MEASURES
the bulbar motor nuclei without evidence of primary peripheral nerve or long-tract involvement. Classification of SMA in the pediatric population (an adult-onset form of the disease exists) is into three groups is based on clinical presentation and progression (Table 16-41). SMA is typically inherited as autosomal recessive. 257 No cure or treat ment is currently available for SMA, but physical therapy is com monly advocated. 257 Patients with disorders of the motor unit present with predominantly lower motor neuron signs that include hypotonia, flaccid weakness, decreased or absent deep tendon reflexes, fasciculations, and atrophy.
Physical Therapy Role. The primary impairment in all forms tt SMA is muscle weakness. Secondary impairments include postural compensations resulting from muscle weakness, contractures, and occasionally scoliosis. 257 Respiratory distress is present early in acute childhood SMA.257 The goals of physical therapy are to improve the quality of life and to minimize disability. A background knowledge tt therapeutic exercise, functional use of orthoses and adaptive equip ment, and strategies to minimize disabilities secondary to the impair ments, allows the clinician to proVide a comprehensive intervention. bONCOLOGY
I
Study Pearl
~
Common signs and symptoms of cancer in children can include fever, pain, a mass or swelling, bruising, pal lor, headaches, neurologic changes, and visual disturbances. _
I
Cancer is the chief cause of death by disease and the second-leading cause of death overall, following trauma, in children aged 1 to 14 years.
Leukemia. Acute lymphoblastic leukemia (ALL) is a malignant dis ease of the bone marrow in which early lymphoid precursors (i.e., lynr phoblasts) proliferate and replace the normal hematopoietic cells tt the marrow. This results in a marked decrease in the production of nor mal blood cells. The lymphoblasts also proliferate in organs other than the marrow, particularly the liver, spleen, and lymph nodes. Neuroblastoma. Neuroblastoma, an embryonal malignancy tt the sympathetic nervous system, is the most common extracranial childhood cancer and the most common tumor occurring during infancy.258 Most patients present with signs and symptoms related to tumor growth, although small tumors have been detected in infants 00 prenatal ultrasound. 258 Large abdominal tumors often result in increased abdominal girth and other local symptoms (e.g., pain). Generally, symptoms include abdominal pain, emesis, weight loss. anorexia, fatigue, bone pain, and chronic diarrhea. 258 Because more
TABLE 16-41. CLASSIFICATION OF SPINAL MUSCLE ATROPHY IN PEDIATRICS TYPE
Childhood-onset, type I, Werdnig-Hoffman (acute) Childhood-onset, type II, Werdnig-Hoffman (chronic) Juvenile-onset, type III, Kugelberg-Welander
ONSET
COURSE
o to 3 months
Rapidly progressive, severe hypotonia, death within first year
3 months to 4 years
Rapid progression, then stabilizes; moderate to severe hypotonia; shortened lifespan Slowly progressive; mild impairment
5 to 10 years
Reproduced, with permission, from Stuberg WA. Muscular dystrophy and spinal muscular atrophy. In: Campbell SK, Vander Linden DW, Palisano RJ. eds. Physical Therapy for Children. SI. Louis: W.B. Saunders; 2006:421-451. Copyright © Elsevier.
CHAPTER 16. PEDIATRIC PHYSICAL THERAPY
than 50% of patients present with advanced-stage disease (usually to the bone and bone marrow), the most common presentation includes bone pain and a limp. 258
Lymphomas Hodgkin's Lymphoma. Hodgkin's lymphoma (HL), formerly known as Hodgkin's disease, is a malignant disorder that arises primarily in peripheral lymph nodes and is most common in young adults in the 20 and 30-year age range. 2W- 261 The etiology of HL is unknown. Signs and symptoms include2w-261 ~ ~
~ ~ ~
Constitutional symptoms (e.g., unexplained weight loss, fever, night sweats). Chest pain, cough, and/or shortness of breath (if there is a large mediastinal mass or lung involvement). Back or bone pain occurs rarely. Splenomegaly and/or hepatomegaly may be present. Central nervous system (CNS) symptoms or signs may be due to paraneoplastic syndromes.
Clinical staging occurs through assessment of the disease extent by clinical examination and imaging techniques. For staging classifica tions, the spleen is considered a lymph node area. The Ann Arbor clas sification is used most commonly (Table 16_42).262,263 The medical options for HL, which are based on the stage, include: ~
~ ~
Radiation therapy. The involved field encompasses the involved lymph node area plus one contiguous region. Chemotherapy (nonleukemogenic chemotherapy [ABVD1.) High-dose chemotherapy with transplantation. High-dose chemotherapy (HDC) at doses that ablate the bone marrow is fea sible with reinfusion of the patient's previously collected hematopoietic stem cells (autologous transplantation) or infusion of stem cells from a donor source (allogeneic transplantation).
Non-Hodgkin's Lymphoma. The non-Hodgkin's lymphomas (NHLs) constitute a heterogeneous group of lymphoid system neoplasms with
TABLE 16-42. ANN ARBOR CLASSIFICATION OF HODGKIN'S LYMPHOMA STAGE
Stage I Stage II Stage III Stage IV
CRITERIA
A single lymph node area or single extranodal site Two or more lymph node areas on the same side of the diaphragm Lymph node areas on both sides of the diaphragm Disseminated or multiple involvement of extranodal organs. Involvement of the liver or the bone marrow is considered stage IV disease
A or B designations denote the presence or absence of B symptoms.
B designation: includes the presence of one or more of the following: (1) fever (temperature> 38°C), (2) drenching
night sweats, and 0) unexplained loss of more than 10% of body weight within the preceding 6 months.
A designation: the absence of the above
Data from Rosenberg SA. Validity of the Ann Arbor staging classification for the non-Hodgkin's lymphomas.
Cancer Treat Rep. 1977;61:1023-1027: and Ultmann JE, Moran EM. Diagnostic evaluation and clinical staging in
Hodgkin's disease: usefulness and problems of the Ann Arbor staging classification in primary staging and staging
in relapse. Natl Cancer Inst Monogr. 1973;36:333-345.
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SECTION II. TESTS AND MEASURES
varying presentation, natural history, and response to therapy.264-268 Presentation of NHL in children is acute or subacute. The clinical man ifestations are diverse and depend on the site of disease involvement. In general, patients often appear mildly to moderately iII and occasionally have a low-grade fever. They may present with pallor, res piratory distress, pain, and discomfort. Staging of NHL is shown in Table 16-43. The intensity of current treatment regimens, particularly for advanced stages of disease, dictates inpatient administration of chemotherapy, as well as aggressive support by a team experienced in the care of immunosuppressed children.
3l
b
t
to study clinical decision making: referral to physical ther apy of children with cerebral palsy. Phys Ther. 1989;69:61().-{)15. 204. Bower E. The effects of physical therapy on cerebral palsy. Dev Med Child Neural. 1989;31:266. 205. Harris SR. Commentary on "The effects of physical therapy on cerebral palsy: a controlled trial in infants with spastic diplegia." Phys Occup Ther Pediatr. 1989;9:1-4.
~
11
].I
21
1
2
2
.2
.2
.2
..
.2
1
CHAPTER 16. PEDIATRIC PHYSICAL THERAPY
206. Horton SV, Taylor DC. The use of behavior therapy and physical therapy to promote independent ambulation in a preschooler with mental retardation and cerebral palsy. Res Dev Disabil. 1989; 10:363-375. 207. Physical therapy for cerebral palsy. N Engl]Med. 1988;319:796-797. 208. Palmer FB, Shapiro BK, Wachtel RC, et al. The effects of physical therapy on cerebral palsy. A controlled trial in infants with spas tic diplegia. N Engl] Med. 1988;318:803--808. 209. Sommerfeld D, Fraser BA, Hensinger RN, et al. Evaluation of physical therapy service for severely mentally impaired students with cerebral palsy. Phys Tber. 1981;61:338-344. 210. Sussman MD, Cusick B. Preliminary report: the role of short-leg, tone-reducing casts as an adjunct to physical therapy of patients with cerebral palsy. Johns Hopkins Med]. 1979;145:112-114. 211. Abdel-Salam E, Maraghi S, Tawfik M. Evaluation of physical ther apy techniques in the management of cerebral palsy.] Egypt Med Assoc. 1978;61:531-541. 212. Marx M. Integrating physical therapy into a cerebral palsy early education program. Phys Tber. 1973;53:512-514. 213. Mathias A. Management of cerebral palsy. Physical therapy in relation to orthopedic surgery. Phys Tber. 1967;47:473--482. 214. Stroumbou-Alamani S. Current concepts in the medical treatment of cerebral palsy. Physical therapy. Arch Ital Pediatr Pueric. 1967;25:113-120. 215. D'Wolf N, Donnelly E. Physical therapy and cerebral palsy. Clin Pediatr (Phila). 1966;5:351-355. 216. Footh WK, Kogan KL. Measuring the effectiveness of physical therapy in the treatment of cerebral palsy.] Appl Toxicol. 1963;43: 867-873. 217. Paine RS. Physical therapy in the management of cerebral palsy. Dev Med Child Neural. 1963;5:193. 218. Gelperin A, Payton O. Evaluation of equanil as adjunct to physi cal therapy for children with severe cerebral palsy. Phys Tber Rev. 195;39:383-388. 219. Schwartz FE Physical therapy for children with cerebral palsy. ] Int Call Surg. 1954;21:84--87. 220. Brooks W, Callahan M, Schleich-Korn]. Physical therapy and the adult with cerebral palsy; report of a conference on vocational guidance. Phys Tber Rev. 1953;33:426--428. 221. Bailey LA. Physical therapy in the treatment of cerebral palsy. Phys Tber Rev. 1950;30:230-231. 222. Grogan DP, Lundy MS, Ogden]A. A method for early postopera tive mobilization of the cerebral palsy patient using a removable abduction bar.] Pediatr Orthop. 1987;7:338-340. 223. Katz K, Arbel N, Apter N, et aL Early mobilization after sliding achilles tendon lengthening in children with spastic cerebral palsy. Foot Ankle Int. 2000;21:1011-1014. 224. Palisano R, Rosenbaum P, Walter S, et aL Development and relia bility of a system to claSSify gross motor function in children with cerebral palsy. Dev Med Child Neural. 1997;39:214-223. 225. Olney S], Wright M]. Cerebral palsy. In: Campbell SK, Vander Linden DW, Palisano R], eds. Physical Therapy for Children. St. Louis: Saunders; 2006:625-664. 226. Rosenbaum P. Cerebral palsy: what parents and doctors want to know. EM]. 2003;326:970-974.
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227. Lepage C, Noreau L, Bernard PM. Association between character istics of locomotion and accomplishment of life habits in children with cerebral palsy. Phys Ther. 1998;78:458-469. 228. Westberry DE, Davids JR, Jacobs JM, et al. Effectiveness of serial stretch casting for resistant or recurrent knee flexion contractures following hamstring lengthening in children with cerebral palsy. j Pediatr Orthop. 2006;26: 109-114. 229. Hoare B, Wasiak J, Imms C, et al. Constraint-induced movement therapy in the treatment of the upper limb in children with hemi plegic cerebral palsy. Cochrane Database Syst Rev. 2007;CD004149. 230. Clayton-Krasinski D, Klepper S. Impaired neuromotor develop ment. In: Cameron MH, Monroe LG, eds. Physical Rehabilitation: Evidence-Based Examination, Evaluation, and Interoention. St. Louis: Saunders/Elsevier; 2007:333-366. 231. Hinderer KA, Hinderer SR, Shurtleff DB. Myelodysplasia. In: Campbell SK, Vander Linden DW, Palisano RJ, eds. Physical Therapy for Children. 3rd ed. St. Louis: Saunders; 2006:735-799. 232. Hoffer MM, Feiwell E, Perry R, et al. Functional ambulation in patients with myelomeningocele. j Bone joint Surg Am. 1973;55: 137-148. 233. Douglas M, Archer P. Shaken baby syndrome-related traumatic brain injuries: statewide surveillance findings. j Okla State Med Assoc. 2004;97:487--490. 234. Clemetson CA. Shaken baby syndrome: a medicolegal problem. NZ Medj. 2004;117:154-160. 235. Smith J. Shaken baby syndrome. Orthop Nurs. 2003;22: 196-203; quiz, 204-205. 236. Geddes JF, Whitwell HL, Tasker RC. Shaken baby syndrome. Br j Neurosurg. 2003;17:18. 237. Levin AY. Shaken baby syndrome. Brj Neurosurg. 2003;17:15-16. 238. Stephenson JB. Shaken baby syndrome. j R Soc Med. 2003;96: 102-103; author reply, 103. 239. Blumenthal 1. Shaken baby syndrome. Postgrad Med j. 2002;78: 732-735. 240. Ewing-Cobbs L, Levin HS, Fletcher JM, et al. The Children's Orientation and Amnesia Test: relationship to severity of acute head injury and to recovery of memory. Neurosurgery. 1990;27: 683-691; discussion, 691. 241. Kerkering GA. Brain injuries: traumatic brain injuries, near drowning, and brain tumors. In: Campbell SK, Vander Linden DW, Palisano RJ, eds. Physical Therapy for Children. 3rd ed. St. Louis: Saunders; 2006:709-734. 242. Hwang V, Shafer FS, Durbin DR, et al. Prevalence of traumatic injuries in drowning and near drowning in children and adoles cents. Arch Pediatr Adolesc Med. 2003;157:50-53. 243. Fisher DH. Near-drowning. Pediatr Rev. 1993;14:148-151. 244. Camfield P, Camfield C. Advances in the diagnosis and man agement of pediatric seizure disorders in the twentieth century. j Pediatr. 2000;136:847-849. 245. Tharp BR. An overview of pediatric seizure disorders and epilep tic syndromes. Epilepsia. 1987;28(suppl l):S36-S45. 246. Nelson LP, Ureles SD, Holmes G. An update in pediatric seizure disorders. Pediatr Dent. 1991;13:128-135.
CHAPTER 16. PEDIATRIC PHYSICAL THERAPY
247. Eagle M, Bourke J, Bullock R, et al. Managing Duchenne muscu lar dystrophy-the additive effect of spinal surgery and home nocturnal ventilation in improving survival. Neuromuscul Disord. 2007;17:47~75.
248. King WM, Runencuner R, Nagaraja HN, et al. Orthopedic out comes of long-term daily corticosteroid treatment in Duchenne muscular dystrophy. Neurology. 2007;68:1607-1613. 249. Freund AA, Scola RH, Arndt RC, et al. Duchenne and Becker mus cular dystrophy: a molecular and immunohistochemical approach. Arq Neuropsiquiatr. 2007;65:73-76. 250. Zhang S, Xie H, Zhou G, et al. Development of therapy for Duchenne muscular dystrophy. Zhongguo Xiu Fu Chong jian Wai Ke Za Zhi. 2007;21:194-203. 251. Velasco MY, Colin AA, Zurakowski D, et al. Posterior spinal fusion for scoliosis in duchenne muscular dystrophy diminishes the rate of respiratory decline. Spine. 2007;32:459-465. 252. Main M, Mercuri E, Haliloglu G, et al. Serial casting of the ankles in Duchenne muscular dystrophy: can it be an alternative to sur gery? Neuromuscul Disord. 2007;17:227-230. 253. Karol LA. Scoliosis in patients with Duchenne muscular dystro phy. j Bonejoint Surg Am. 2007;89Csuppl 1):155-162. 254. Grange RW, Call JA. Recommendations to define exercise pre scription for Duchenne muscular dystrophy. Exerc Sport Sci Rev. 2007;35:12-17. 255. Deconinck N, Dan B. Pathophysiology of duchenne muscular dystrophy: current hypotheses. Pediatr Neurol. 2007;36:1-7. 256. Wagner KR, Lechtzin N, Judge DP. Current treatment of adult Duchenne muscular dystrophy. Biochim Biophys Acta. 2007;1772: 229-237. 257. Stuberg WA. Muscular dystrophy and spinal muscular atrophy. In: Campbell SK, Vander Linden DW, Palisano RJ, eds. Physical Therapy for Children. St. Louis: Saunders; 2006:421-451. 258. Kim S, Chung DH. Pediatric solid malignancies: neuroblastoma and Wilms' tumor. Surg Clin North Am. 2006;86:469-487, xi. 259. Roman E, Ansell P, Bull D. Leukaemia and non-Hodgkin's lym phoma in children and young adult'>: are prenatal and neonatal factors important determinant,> of disease? Br j Cancer. 1997;76: 406-415. Fiorillo A, Migliorati R, Fiore M, et al. Non-Hodgkin's lymphoma in childhood presenting as thyroid enlargement. Clin Pediatr (Phila). 1987;26:152-154. Brecher ML, Sinks LF, Thomas RR, et al. Non-Hodgkin's lym
phoma in children. Cancer. 1978;41:1997-2001.
Rosenberg SA. Validity of the Ann Arbor staging classification for
the non-Hodgkin's lymphomas. Cancer Treat Rep. 1977;61:
1023-1027.
LIItmann JE, Moran EM. Diagnostic evaluation and clinical staging
in Hodgkin's disease: usefulness and problems of the Ann Arbor
staging classification in primary staging and staging in relapse.
Nat! Cancer Inst Monogr. 1973;36:333-345. Medina-Sanson A, Chico-Ponce de Leon F, Cabrera-Munoz Mde L, et al. Primary central nervous system non-Hodgkin lymphoma in childhood presenting as bilateral optic neuritis. Childs Nero Syst. 2006;22: 1364-1368.
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265. Cairo MS, Raetz E, Lim MS, et al. Childhood and adolescent non Hodgkin lymphoma: new insights in biology and critical chal lenges for the future. Pediatr Blood Cancer. 2005;45:753-769. 266. Sandlund JT, Santana V, Abromowitch M, et al. Large cell non Hodgkin lymphoma of childhood: clinical characteristics and out come. Leukemia. 1994;8:30-34. 267. Traggis D, Jaffe N, Vawter G, et al. Non-Hodgkin lymphoma of the head and neck in childhood. j Pediatr. 1975;87:933-936. 268. Crist WM, Mahmoud H, Pickert CB, et al. Biology and staging of childhood non-Hodgkin lymphoma. An Esp Pediatr. 1988;29 (suppI34):104-109. 269. Nathan PC, Ness KK, Greenberg ML, et al. Health-related quality of life in adult survivors of childhood wilms tumor or neuroblas toma: a report from the childhood cancer survivor study. Pediatr Blood Cancer 2006;49:704-15. 270. Kutluk T, Varan A, Buyukpamukcu N, et al. Improved survival of children with wilms tumor. j Pediatr Hematol Oncol. 2006;28: 423-426. 271. Breslow NE, Beckwith JB, Perlman EJ, et al. Age distributions, birth weights, nephrogenic rests, and heterogeneity in the patho genesis of WillR" later in tne chapter). Water provid~s res.istance proportional to the . Jelativ~.speed offl1ovefi1ent .• of tnep~tient • an? the .'vVater.. t;\Jld . t~
cross.. sectionaJ area ofthe .patientln· . (;onta"t with the warer;49
1136
SECTION III. PROCEDURAL INTERVENTIONS
metabolites. 50 Each progression is made more challenging by altering one of the parameters of exercise (type/mode of exercise, intensity, duration, and frequency), which are modified according to patient response.
TYPE OF EXERCISE Type of exercise relates to the specific activity being performed, including the mode of resistance (see "Types of Resistance" earlier in the chapter) and type of activity being performed (see "Types of Exercise" earlier in the chapter).
INTENSITY Intensity refers to how much effort is required to perform the exercise. For aerobic activities, the exercise intensity should be at a level that is 4()OAJ to 85% maximal aerobic power (V0 2 max) or 55% to 9()OAJ of max imal heart rateY It is now recognized that an individual's perception of effort (relative perceived exertion, or RPE) is closely related to the level of physiologic effort (Table 11_10),52,53 It is important, therefore, to closely monitor the patient's response to exercise. Any discomfort or reproduction of symptoms that lasts more than 1 to 2 hours after the intervention is unacceptable. Patient responses that can modify the intensity include increases in pain level, muscle fatigue, time taken to recover from fatigue, car diovascular response, compensatory movements, insufficient balance, level of motivation, and degree of comprehension.
DURATION Duration refers to the length of the exercise session. In most functional exercises, fatigue must be considered when doing exercises so that the patient's tolerance is not exceeded. The exercise should be performed in a pain-free range until fatigue occurs. Fatigue may also occur as a lack of coordination observed by the clinician but not perceived by the patient. Physical conditioning occurs over a period of 15 to 60 minutes depending on the level of intensity. Average conditioning time is 20 to 30 minutes for moderate-intensity exercise. However, individuals who are severely compromised are more likely to benefit from a series of short exercise sessions (3-10 minutes) spaced throughout the day.
FREQUENCY Frequency refers to how often the exercise is performed. Frequency of activity is dependent upon intensity and duration; the lower the inten sity, the shorter the duration, the greater the frequency. The recom mended frequency is 3 to 5 sessions per week at moderate intensities and duration (> 5 METs).
,
I
I
CHAPTER 17, THERAPEUTIC EXERCISE
Exercise progression in the following populations is determined by a number of factors, including the general health of the patient, the stage of healing, the degree of irritability of the structure, and the patient's response to exercise: ... ... ... ...
Patients with an acute illness/fever. Patients with an acute injury. Postsurgical patients. Patients with cardiac disease---edema, weight gain, unstable angina. ... Patients who are obese.
DELAYED-ONSET MUSCLE SORENESS
1137
Study Pearl ... If pain is reported by the patient before a resistive activity or before the end-feel during passive range of motion, the patient's symptoms are considered irritable. The inter vention in the presence of irritabil ity should not be aggressive. 14 ... If pain occurs after resistance, then the patient's symptoms are not considered irritable and exercise, particularly stretching, can be more aggressive.
Muscular soreness may result from all forms of exercise. Acute mus cle soreness develops during or directly after strenuous and aerobic exercise performed to the point of fatigue. The soreness is theoreti cally related to the decreased blood flow and reduced oxygen that creates a temporary buildup of lactic acid and potassium. Using a cool-down period of low intensity exercise that facilitates the return of oxygen to the muscle can minimize the adverse effects of this type of soreness. A type of soreness that is related to eccentric exercise is delayed onset muscle soreness (DOMS).35 This type of soreness, which occurs between 48 and 72 hours after exercise, may last for up to 10 days. Prevention of this type of muscle soreness involves careful design of the eccentric program including prepatory techniques, accurate train ing variables, and appropriate aftercare. 35 The intervention for DOMS includes aerobic submaximal exercise with no eccentric component (swimming, biking, or stepper machines), pain-free flexibility exer cises, and high-speed (300 degrees/second) concentric-only isokinetic training. 35 ,54
EXERCISE HIERARCHY A hierarchy exists for ROM and resistive exercises during the subacute (neovascularization) stage of healing, to ensure that any progression is done in a safe and controlled fashion, The hierarchy for the ROM exercises is outlined in Table 17-3, The hierarchy for the progression of resistive exercises is outlined in Table 17-4. Gentle resistance exer cises can be introduced very early in the rehabilitative process, Although some soreness can be expected, sharp pain should not be provoked. At regular intervals, the clinician should ensure that: ... The patient is adherent with the exercise program at home, ... The patient is aware as to the rationale behind the exercise program, ... The patient is performing the exercise program correctly and at the appropriate intensity. ... The patient's exercise program is being updated appropriately based on clinical findings and patient response.
Study Pearl Neuromusculareleddf!alst~ml::lJatloll
(NMES) can bean~ff~ctiv~.compo-, nent of a rehabill~tloi'liprt)gralrtfor muscle weakness(seeC:h~pt~r18).
1138
SECTION III. PROCEDURAL INTERVENTIONS
EXERCISE PRESCRIPTIONS The greatest amount of tension the muscle can achieve is a 20% increase in fiber length, measured from the resting length. 55 The clini cal implications for this are that the patient can tolerate less resistance in the beginning of range, and at the end of range, of contraction, but can overcome more resistance at a point in the range 20% beyond rest ing contraction. 50 A number of precautions must be observed with patients who are performing strength training: ~
~
~
Substitute motions: muscles that are weak or fatigued rely on other muscles to produce the movement if the resistance is too high. This results in incorrect stabilization and poor form. Overworking of the muscles: this can occur if the exercise parameters (frequency, intensity, duration) are advanced too quickly. Adequate rest must be provided C3 to 4 minutes are needed to return the muscle to 90% to 95% of pre-exercise capacity, with the most rapid recovery occurring in the first minute) after each vigorous exercise.
The rest period between sets can be determined by the time the breathing rate, or pulse, of the patient returns to the steady state. Caution must be taken with patients diagnosed with osteoporosis, whose bones are unable to withstand normal stresses and are higWy susceptible to pathologic fracture. Osteoporotic fractures may also occur as a result of prolonged immobilization, bed rest, the inability to bear weight on an extremity, and as a result of nutritional or hormonal factors. A number of programs have been designed for the progression of exercise programs (Table 17-6). It is important to remember that any
TABLE 17-6. EXERCISE PROGRESSIONS SET(S) OF 10 DeLorme program
I
2
3 Oxford technique
1 2
3 MacQueen technique
3 (beginning/intermediate)
Sander program
4-5 (advanced)
Total of 4 sets (3 times per week)
Knight DAPRE program
Day 1: 4 sets
Day 2: 4 sets
Day 3: 1 set
2 sets 2 sets 1 2
3 4 DAPRE, daily adjusrable progressive resistive exercist:; RM, repetition maximum.
AMOUNT OF WEIGHT
REPETITIONS
50% of 10 RM 75% of 10 RM 100% of 10 RM 100% of 10 RM 75% of 10 RM 50% of 10 RM 100% of 10 RM 100% of 2-3 RM 100% of 5 RM 100% of 5 RM 100% of 3 RM 100% of 5 RM 100% of 3 RM 100% of 2 RM 50% of RM 75°;\) of RM 100% of RM Adjusted working weight
10 10 10 10 10 10 10 2-3
5
5
5
5
5
5
10
6
Maximum
Maximum
CHAPTER 17. THERAPEUTIC EXERCISE
exercise progression should always be based on sound rationale (opti mal resistance, the number of repetitions, the number of sets, and the frequency of training) and the symptomatic response.
WARM-UP AND COOL-DOWN PERIODS Each exercise session should include a S- to IS-minute warm-up and a S- to IS-minute cool-down period. The length of the warm-up and cool-down sessions may need to be longer for deconditioned or older individuals.
Warm-up ~ ~
Includes low-intensity cardiorespiratory activities. Serves to prepare the heart and circulatory system from being suddenly overloaded.
Cool-down ~ ~
Includes low-intensity cardiorespiratory activities and flexibility exercises. Helps prevent abrupt physiologic alterations that can occur with sudden cessation of strenuous exercise, such as adaptive shortening and lactic acid buildup.
OVERLOAD PRINCIPLE The principle of overload states that a greater than normal stress or load on the body is required for training adaptation to take place. To increase strength, the muscle must be challenged at a greater level than it is accustomed to. High levels of tension will produce adapta tions in the form of hypertrophy and recruitment of more muscle fibers.
SPECIFICITY OF TRAINING Specificity of training is an accepted concept in rehabilitation. This concept involves the principle of the specific adaptation to imposed demand (SAlD). Thus, the focus of the exercise prescription should be to improve the strength and coordination of functional or sports specific movements with exercises that approximate the desired activity. For example, resistance training performed concentrically improves concentric muscle strength and eccentric training improves eccentric muscle strength. The SAID principle can be applied by exercising the muscles along each extremity and within the trunk in functional patterns. 56 The exercise component of the intervention should be as specific as the manual technique used in the clinic.
PROGRESSIVE RESISTIVE EXERCISE (PRE) Progressive resistive exercises use the repetition maximum (RM) or the greatest amount of weight a muscle can move through the range of motion a specific number of times (resistance maximal; Table 17-6).
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SECTION III. PROCEDURAL INTERVENTIONS
REPETITION MAXIMUM (RM) This is based on the premise that whatever exercise progression is used to achieve an increase in the total number of repetitions while main taining a sufficient effort, the number of sets must also be increased. This increase in sets must occur in conjunction with a reduction in the number of repetitions per set by 10% to 20%,50 or a reduction in the resistance.
RESISTANCE MAXIMAL A concept introduced by DeLorme and Watkins42 that refers to the amount of resistance a group of muscles can overcome exactly ten times. This amount of resistance is then used for exercise. The various programs are summarized in Table 17-6 and Table 17-7.
CIRCUIT TRAINING Circuit training or cross-training incorporates a wide variety of modes of training and uses high repetitions and low weight to provide a more general conditioning program aimed at improving body composition, muscular strength, and some cardiovascular fitness.
INTERVAL TRAINING Interval training includes an exercise period followed by a prescribed rest interval. This type of training tends to improve strength and power more than endurance. With appropriate spacing of work and rest intervals, a significant amount of high-intensity work can be achieved and is greater than the amount of work accomplished with continuous training. The longer the work interval, the more the anaerobic system is stressed and the duration of the rest period is not important. In a short work interval, a work recovery ratio of 1: 1 or 1:5 is appropriate to stress the aerobic system.
MAINTAINING STRENGTH In order to maintain the benefits of training, exercise must be main tained. Based on studies of isokinetic and concentric exercise57 ,58:
TABLE 17-7. ADJUSTMENT SEQUENCE FOR DAPRE ISOTONIC PROGRAM NUMBER OF REPS PERFORMED DURING SET
0-2 3--4
5-6 7-10 11
ADJUSTED WORKING WEIGHT FORFOURTH SET
NEXT EXERCISE SESSION
-5-10 Ib -0-51b Same weight +5-10Ib +10-201b
-5-10Ib Same weight +5-10Ib +5-15Ib +10-201b
CHAPTER 17. THERAPEUTIC EXERCISE ~ ~
Muscle strength recovery follows a steady, nonlinear, and pre dictable increase over time. 35 Reversibility: a lack of training results in decreased muscle recruitment and muscle fiber atrophy.
If an injured patient can maintain some form of strength training, even once per week, their strength can be fairly well maintained over a 3-month period. 59 When expressed as a weekly percentage, the Albert 5% rule states that a 5% strength increase in a given week can be maintained for many weeks of resistive training, provided that the patient trains 3 times a week at a minimum resistance load of 70% of maximal voluntary mus cle contractile force. 35 While seemingly esoteric, the 5% rule can be used in determining the prognosis. For example, a patient with a 40% deficit in strength of the biceps can be assumed to take approximately 8 weeks to recover, barring any illness or disease states. 35
THE KINETIC CHAIN The expression kinetic chain is used to describe the function or activ ity of an extremity and/or trunk in terms of a series of linked chains. According to kinetic chain theory, each of the joint segments of the body involved in a particular movement constitutes a link along one of these kinetic chains. As each motion of a joint is often a function of other joint motions, the efficiency of an activity can be dependent on how well these chain-links work together. 60
CLOSED KINETIC CHAIN (CKC) A variety of definitions for a CKC activity have been proposed: ~
Palmitier and associates defined an activity as "closed" if both ends of the kinetic chain are connected to an immovable frame work, thus preventing translation of either the proximal or dis tal joint center, and creating a situation where movement at one joint produces a predictable movement at all other joints. 56 ~ Gray 61 considered a closed-chain activity to involve fixation of the distal segment so that joint motion takes place in multiple planes, and the limb is supporting weight. ~ Dillman and associates62 described the characteristics of closed chain activities to include relatively small joint movements, low joint accelerations, greater joint compressive forces, greater joint congruity, decreased shear, stimulation of joint proprio ception, and enhanced dynamic stabilization through muscle co-activation. 63 ~ Kibler6 3 defines a closed-chain activity as a sequential combi nation of joint motions that have the following characteristics: • The distal segment of the kinetic chain meets considerable resistance. • The movement of the individual joints, and translation of their instant centers of rotation, occurs in a predictable man ner that is secondary to the distribution of forces from each end of the chain.
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SECTION III. PROCEDURAL INTERVENTIONS
Examples of a closed kinetic chain exercise (CKCE) involving the lower extremities include the squat and the leg press. The activities of walking, running, jumping, climbing, and rising from the floor all incorporate closed kinetic chain components. Examples of a CKCE for the upper extremities include the push-up and using the arms to rise out of a chair.
OPEN KINETIC CHAIN (OKC) It is generally accepted that the movement of the end segment deter
mines the difference between OKC and CKC activities. The traditional definition for an "open"-chain activity included all activities that involved the end segment of an extremity moving freely through space, resulting in isolated movement of a joint. Examples of an open kinetic chain activity include lifting a drink ing glass and kicking a soccer ball. Open kinetic chain exercises (OKCE) involving the lower extremity include the seated knee exten sion and prone knee flexion. Upper extremity examples of OKCE include the biceps curl and the military press. Open-chain exercises have traditionally been deemed to be less functional in terms of many athletic movements, primarily serving as a supportive role in strength and conditioning programs. As a result, the use of OKCE in clinical settings declined, and there has been a shift in emphasis toward the use of CKCE, although evidence supports the skillful use of both.
CONTRAINDICATIONS OF STRENGTH TRAINING Absolute contraindications to strength training include unstable angina, uncontrolled hypertension, uncontrolled dysrhythmias, hypertrophic cardiomyopathy, and certain stages of retinopathy. Patients with con gestive heart failure, myocardial ischemia, poor left ventricular function, or autonomic neuropathies must be carefully evaluated before initiat ing a strength-training program.
IMPROVING MUSCULAR ENDURANCE MUSCLE ENDURANCE To increase muscle endurance, exercises are performed against light resistance for many repetitions, so that the amount of energy expanded is equal to the amount of energy supplied. This phenomenon called steady state occurs after some 5 to 6 minutes of exercise at a constant intensity level. Working at a level to which the muscle is accustomed improves the endurance of that muscle, but does not increase its strength. However, exercise programs that increase strength also increase mus cular endurance. Muscular endurance programs are typically indicated early in a strengthening program as the high-repetition and low-load exercises are more comfortable, enhance the vascular supply to muscle, cause less muscle soreness and joint irritation, and reduce the risk of muscle injury.
.
CHAPTER 17. THERAPEUTIC EXERCISE
AEROBIC CAPACITY AND CARDIORESPIRATORY ENDURANCE
By definition, cardiorespiratory endurance is the ability to perform whole-body activities (walking, jogging, biking, swimming, etc.) for extended periods of time without undue fatigue. A number of train ing adaptations occur within the circulatory system in response to exercise: ~
~
~
~
~
~
Heart rate: as the body begins to exercise, the oxygen demand of the muscles increases, so the heart must pump more oxy genated blood to meet this increased demand. Monitoring heart rate is an indirect method of estimating oxygen consumption, because in general these two factors have a linear relationship. Stroke volume: the volume of blood being pumped out with each beat (see Chapter 11) increases with exercise, but only to the point when there is enough time between beats for the heart to fill up. Cardiac output: cardiac output, calculated by multiplying stroke volume and heart rate (see Chapter 11), increases with exer cise. A training effect that occurs with regard to cardiac output of the heart is that the stroke volume increases while the exer cise heart rate is reduced at a given standard exercise load. Blood pressure: during exercise, there is a decrease in total peripheral vascular resistance and an increase in cardiac out put. Systolic pressure increases in proportion to oxygen con sumption and cardiac output, while diastolic pressure shows little or no increase (see Chapter 11). Hemoglobin concentration: the concentration of hemoglobin in circulating blood does not change with training (unless alti tude training); it may actually decrease slightly. Lung changes that occur due to exercise: • An increase in the volume of air that can be inspired in a sin gle maximal ventilation. • An increase in the diffusing capacity of the lungs. • Oxygen consumption rises rapidly during the first minutes of exercise and levels off as the aerobic metabolism supplies the energy required by the working muscles. • Fitter individuals have a respiratory system that is more capa ble of delivering oxygen to sustain aerobic energy production at increasingly higher levels of intensity. • In cases of severe pulmonary disease, the cost of breathing can reach 40% of the total exercise oxygen consumption, thereby decreasing the amount of oxygen available for the exercising muscles. • A decrease in pulmonary resistance to airflow. • Exercise-induced asthma can occur when the normal initial bronchodilation is followed by bronchoconstriction.
The maximal amount of oxygen that can be used during exercise is referred to as maximal aerobic capacity (VO z max)-refer to
Chapter 10. A number of precautions need to be taken when exerCising patients who have a compromised cardiovascular or pulmonary sys tem. An appropriate level of intensity must be chosen:
1143
1144
SECTION III. PROCEDURAL INTERVENTIONS ~ ~
Too high a level can overload the cardiorespiratory and mus cular systems and potentially cause injuries. Exercising at a level that is too high causes the cardiorespiratory system to work anaerobically, not aerobically.
A sufficient period of time should be allowed for warm-up and cool-down to permit adequate cardiorespiratory and muscular adaptation.
T~chniques for Improving or Maintaining Cardiores
piratory Endurance. The detraining effects of cardiorespiratory endurance occur rapidly, after only 2 weeks when a person stops exer cising. Several different training factors must be considered when attempting to maintain or improve cardiorespiratory endurance. Continuous training-the FIlT principle: ~
~
~
~
Frequency: to see at least minimal improvement in cardiorespi ratory endurance, it is necessary for the average person to engage in no less than 3 sessions per week. • If the intensity is kept constant, there appears to be no addi tional benefit from 2 times a week versus 4 times, or 3 times a week versus 5 times. • If the goal is weight loss, 5 to 7 days per week increase the caloric expenditure more than 2 days per week. Intensity: recommendations regarding training intensity (over load) vary. Relative intensity for an individual is calculated as a percentage of the maximum function, using V0 2 max or maximum heart rate (HR max). To see minimal improvement in cardiorespiratory endurance, the average person must train with a heart rate elevated to at least 60% of its maximal rate. Three common methods of monitoring intensity are employed: • Monitoring heart rate-two formulas are commonly used: Karvonen equation: target training HR = resting HR + (0.6 [maximum HR - resting HR]). Maximum heart rate: 220 - age. • Rating of perceived exertion (RPE)-.Table 11-10. A car diorespiratory training effect can be achieved at a rating of "somewhat hard" or "hard" 03 to 16). • Calculating the V0 2 max or HR directly or indirectly: a 3-minute step test. a 12-minute run. o I-mile walk test. Type of exercise: the type of actlVlty chosen in continuous training must be aerobic-involving large muscle groups acti vated in a rhythmic manner. Time (duration): duration is increased when intensity is limited, for example, by initial fitness level. For minimal improvement to occur, the patient must participate in continuous activity with a heart rate elevated to its working level. In poorly conditioned individuals, 3 to 5 minutes per day produces a training effect, whereas 20 to 30 minutes, 3 to 5 times a week is optimal for conditioned people.
..
CHAPTER 17. THERAPEUTIC EXERCISE ~
~
Continuous training at a submaximal energy requirement can be prolonged for 20 to 60 minutes without exhausting the oxygen transport system. A number of pieces of exercise equipment can be used to improve aerobic capacity and endurance: • Treadmill walking: progressing from slow to fast and short distances to longer distances with or without an incline. • Ergometers: these come in a variety of forms for both the upper extremities and the lower extremities. The pace pro gression is from slow to fast, and the goal is to increase the time spent exercising. • Free weights and elastic resistance: the use of low resistance and high repetitions can produce an aerobic effect. Obese individuals should exercise at longer durations and lower intensities-able to exercise while maintaining a conver sation (talk test).
IMPROVING MUSCLE POWER It has been demonstrated that when a concentric contraction is pre ceded by a phase of active or passive stretching, elastic energy is stored in the muscle. This stored energy is then used in the following con tractile phase. For example, during functional activities, the muscles operate with a strong concentric action, which is usually preceded by a passive eccentric loading, as part of a stretch shortening cycle. 44 The stretch shortening cycle includes the ability of the muscle to absorb or dissipate shock, while also preparing the stretched muscle for response. 64 Plyometric exercises, described next, are used to improve the ability of the muscles to perform these actions, by enhancing their power, speed, and agility. Having a muscle work dynamically against resistance within a specified period increases power.
PLYOMETRICS The traditional definition of plyometrics was associated with quick rapid movement involving a prestretch of the contracting muscle, which stores elastic energy in the muscle, and activates the myotatic reflex. 66-71 The muscle's ability to use the stored elastic energy is affected by time, the magnitude of the stretch, and the velocity of the stretch. 72 The nerve receptors involved in plyometrics are the muscle spin dle, the Golgi tendon organ, and the joint capsule/ligamentous recep tors (see Chapter 9). Acceleration and deceleration are the most important components of all task-specific activities. 50 These activities utilize variable speed and resistance throughout the range of contraction, stimulating neurologic receptors and increasing their excitability. These neurologic receptors play an important role in fiber recruitment and physiologic coordina tion. Plyometrics serve to improve the reactivity of these receptors by involving muscle stretch-shortening exercises, which consist of three distinct phases:
Study Pearl
1145
1146
SECTION III. PROCEDURAL INTERVENTIONS ~
~
~
A setting or eccentric phase in which the muscle is eccentrically stretched and slowly loaded. This phase begins when the ath lete mentally prepares for the activity, and lasts until the stretch stimulus is initiated. 72 A rapid amortization (reversal) phase. This phase is the amount of time between undergoing the yielding eccentric contraction and the initiation of a concentric force. 72 If the amortization phase is slow, elastic energy is wasted as heat, and the stretch reflex is not activated. 72 A concentric response contraction to develop a large amount of momentum and force.
By reproducing these stretch-shortening cycles at posltlons of physiologic function, plyometric activities stimulate proprioceptive feedback to fine-tune muscle activity patterns. Stretch-shortening exer cise trains the neuromuscular system by exposing it to increased strength loads and improving the stretch reflex (see Chapter 9).72 The goal of plyometric training is to decrease the amount of time required between the yielding eccentric contraction and the initiation of the overcoming concentric contraction. This is particularly useful in activities that require a maximum amount of muscular force in a mini mum amount of time. These parameters are difficult to imitate using traditional exercise tools, but are nonetheless a very important compo nent of the rehabilitative process in order for the patient to make a safe return to sport. Before initiating plyometric exercises, the clinician must ensure that the patient has an adequate strength and physical condition base.7 2 Minimal performance criteria for safe plyometrics include the ability to perform one repetition of a parallel squat with a load of body weight on the subject's back (for jumps over 12 inches) for the lower extrem ity, and a bench press with one-third body weight for the upper extremity.6S In addition, success in the static stability tests 6S and dynamic stability tests (vertical jump for the lower extremities and medicine ball throw for the upper extremities) may be used as a meas ure of preparation. 3S Many different activities and devices can be utilized in plyometric exercises. Plyometric exercises may include diagonal and multiplanar motions with tubing or isokinetic machines. These exercises may be used to mimic any of the needed motions, and can be performed in the standing, sitting, or supine positions.
LOWER EXTREMITY PLYOMETRIC EXERCISES
Lower extremity plyometric exercises involve the manipulation of the role of gravity to vary the intensity of the exercise. Thus plyometric exercises can be performed horizontally or vertically: ~
Horizontal plyometrics are performed perpendicular to the line of gravity. These exercises are preferable for most initial clini cal rehabilitation plans as the concentric force is reduced, and the eccentric phase is not facilitated. oS Examples of these types of exercises include pushing a sled against resistance and a modified leg press that allows the subject to push off and land on the footplate.
..
CHAPTER 17. THERAPEUTIC EXERCISE ~
1147
Vertical plyometric exercises (against or with gravitational forces) are more advanced. These exercises require a greater level of controJ.35 The drop jump is an example: the subject steps off a box, lands, and immediately executes a vertical jump.
The footwear and landing surfaces used in plyometric drills must have shock-absorbing qualities, and the protocol should allow suffi cient recovery time between sets to prevent fatigue of the muscle groups being trained.73
UPPER EXTREMITY PLYOMETRIC EXERCISES Plyometric exercises for the upper extremity involve relatively rapid movements in planes that approximate normal joint function. For example, at the shoulder this would include 90 degrees abduction in shoulder, trunk rotation, and diagonal arm motions, and rapid external! internal rotation exercises. Plyometrics should be done for all body segments involved in the activity. Hip rotation, knee flexion/extension, and trunk rotation are power activities that require plyometric activation. Plyometric exercises for the upper extremity include wall push-offs, corner pushups, box push-otIs, the rebounder, and weighted ball throws using medicine and other weighted balls (the weight of the ball creates a prestretch and an eccentric load when it is caught, creating resistance and demanding a powerful agonist contraction to propel it forward again). The exercises can be performed using one arm or both arms at the same time. The former emphasizes trunk rotation and the latter emphasizes trunk extension and flexion as well as shoulder motion. While force-dependent motor firing patterns should be re established, special care must be taken to completely integrate all of the components of the kinetic chain to generate and funnel the proper forces to the appropriate joint.
IMPROVING JOINT MOBILITY AND RANGE OF MOTION Normal mobility includes osteokinematic motion, arthrokinematic motion, and neuromuscular coordination (see Chapter 8). This control is a factor of muscle flexibility, joint stability, and central neurophysio logic mechanisms. These factors are highly specific in the body.7 6 A loss of motion at one joint may not prevent the performance of a func tional task, although it may result in the task being performed in an abnormal manner. For example, the act of walking can still be accom plished in the presence of a knee joint that has been fused into exten sion. Because the essential mechanisms of knee flexion in the stance period and foot clearance in the swing period are absent, the patient compensates for these losses by hiking the hip on the involved side, side-bending the lumbar spine to the involved side, and through exces sive motion of the foot. The amount of available joint motion is based on a number of fac tors, including: ~ ~
Integrity of the joint surfaces and the amount of joint motion. Mobility and pliability of the soft tissues that surround a joint.
~
Study Pearl In general, tonic muscles function as endurance (postural) muscles, whereas phasic muscles function as the power muscles. 74 ,75
1148
SECTION III. PROCEDURAL INTERVENTIONS ~ ~
~ ~
Degree of soft-tissue approximation that occurs. Amount of scarring that is present. 77 Interstitial scarring or fibro sis can occur in and around the joint capsules, within the mus cles, and within the ligaments as a result of previous trauma. Age. Joint motion tends to decrease with increasing age. Gender. In general, females have more joint motion than males.
m
ell
in po It
VI
d4 Joint mobility and range of motion can be improved using a num ber of techniques including flexibility training and joint mobilizations (see Chapter 18). Flexibility training has long been recognized as an essential com ponent of any conditioning program as a means to prevent injury and improve performance. Optimal flexibility is based on physiologic, anatomic, and biomechanical considerations. However, whether mus cle flexibility or stretching before activity results in a decrease in mus cle injuries has yet to be proven. The techniques of stretching all involve the stretch reflex (refer to Chapter 9). A reflex is a programmed unit of behavior in which a certain type of stimulus from a receptor automatically leads to the response of an effector. The elasticity of a muscle diminishes with cooling. To stretch a muscle appropriately, the stretch must be applied parallel to the mus cle fibers. The orientation of the fibers can be determined by palpation. Typically, in the extremities, the muscle fibers run parallel to the bone. The viscoelastic changes are not permanent, whereas plasticity changes, which are more difficult to achieve, result in a residual or per
manent change in length. Frequent stretching ensures that the length
ening is maintained before the muscle has the opportunity to recoil to its shortened state.78 It is important for the patient to realize that the initial session of stretching may increase symptoms in the stretched muscle.79 However, this increase in symptoms should only be temporary, lasting for a couple of hours at most. 78,80 The stretch should be performed at the point just shy of the pain, although some discomfort may be necessary to achieve results. 81 The muscle usually requires a greater stretching force initially, possibly to break up adhesions or cross-linkages and to allow for vis coelastic and plastiC changes to occur in the collagen and elastin fibers. 81
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Static flexibility is defmed as the passive ROM available to a joint or series of joints.77,82 Increased static flexibility should not be confused with joint hypermobility, or laxity, which is a function of the joint capsule and lig aments. Decreased static flexibility indicates a loss of motion. The end feel encountered may help differentiate between adaptive shortening of the muscle (muscle stretch) versus a tight joint capsule (capsular), or arthritic joint (hard). Static flexibility can be measured by a goniometer, or by a number of tests such as the toe-touch and the sit and reach, all of which have been found to be valid and reliable. 83,84
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DYNAMIC FLEXIBILITY Dynamic flexibility refers to the ease of movement within the obtain able ROM. Dynamic flexibility is measured actively. The important
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CHAPTER 17. THERAPEUTIC EXERCISE
1149
measurement in dynamic flexibility is stiffness, a mechanical term defined as the resistance of a structure to deformation. 85 .86 An increase in ROM around a joint does not necessarily equate to a decrease in the passive stiffness of a muscle. 87--B9 However, strength training, immobi lization, and aging have been shown to increase stiffness. 90-93 The con verse of stiffness is pliability. When a soft tissue demonstrates a decrease in pliability, it has usually undergone an adaptive shortening, or an increase in tone, termed hypertonus.
METHODS OF STRETCH ING A variety of stretching techniques can be used to increase the extensi
bility of the soft tissues. PASSIVE STRETCHING
The clinician or another individual partner can perform passive stretch ing. Because of the higher risk of injury with this type of stretching with an unskilled operator, it should only be administered after close super vision, and with the assurance that there is excellent communication between the operator and the patient. Ideally, the passive stretch should involve a gentle, controlled, lOW-intensity, and prolonged elongation of the tissues. STATIC STRETCHING
Static stretching involves the application of a steady force for a sus tained period (Table 17-8). Small loads applied for long periods produce greater residual lengthening than heavy loads applied for short periods. 95 Weighted traction, specific low-load braces, or pulley systems may be modified accordingly to provide this type of stretching. BALLISTIC STRETCHING
This technique of stretching uses bouncing movements to stretch a par ticular muscle. In comparisons of the ballistic and static methods, two studies96 ,97 have found that both produce similar improvements in flex ibility. However, this method appears to cause more residual muscle soreness or muscle strain than those techniques that incorporate relax ation into the technique. 9B-IOO
TABLE 17-8. PROGRESSIVE VELOCI1Y FLEXIBILI1Y PROGRAM Static stretching .L. SSER (slow, short-end-range stretching) .L. FSER (fast, short-end-range stretching) .L. FFR (fast, full-range stretching) Data tram ZachazewskiJE. Flexibility for sports. In: Sanders B, ed. Sports Physical Therapy. Norwalk, CT: Appleton & Lange; 1990:201-238.
Study Pearl Applying small loads to the musculo tendinous unit for 20 minutes or more :in an e.xercise session is necessary for adequate soft-tissue lengthen ing to occur.94•95
l
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SECTION III. PROCEDURAL INTERVENTIONS
CLINICAL ApPLICATION Restoration of normal length of the muscles may be accomplished using the following guidelines: ~
~
~
~
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Effective stretching,in. the ~arly phase, should be performed every hOur, but with each session lasting only a few minutes.
~
The muscle activity is inhibited and in the inhibitory period, the muscle should be stretched. With true muscle shortness, stronger resistance is used to acti vate the maximum number of motor unit,>, followed by vigorous stretching of the muscle. Stretching should be performed at least 3 times a week using: • Low force, avoiding pain. • Prolonged duration. Heat should be applied to increase intramuscular temperature prior to, and during, stretching. 101, 102 This heat can be achieved with either through low-intensity warm-up exercise using rele vant muscle groups, or through the use of thermal modalities. 102 Post-isometric relaxation techniques are advocated. Rapid cooling of the muscle while it is maintained in the stretched position. The application of a cold pack following the stretch is used to take advantage of the thermal characteristics of connective tissue, by lowering its temperature and thereby theoretically prolonging the length changes. 103
Some areas of the body are difficult to stretch adequately using a lengthening technique. In these instances, techniques of localized, manual release, using varying degrees of manual pressure along the length of the muscle and myofascial tissue, may be used. 104
NEUROMUSCULAR FACILITATION The PNF techniques of "hold-relax," "stretch-relax," and "agonist contract relax" can be used to actively stretch the soft tissues. ~
~
~
Hold-relax (HR)-autogenic inhibition: a relaxation technique usually performed at the point of limited range of motion in the agonist pattern: • An isometric contraction of the range-limiting antagonist is performed against slowly increasing resistance. • This is followed by a voluntaly relaxation by the patient and then passive movement of the extremity by the clinician into the newly gained range of the agonist pattern. Hold-relax-active (HRA)-reciprocal inhibition: follOWing application of the hold-relax technique, the patient performs an active contraction into the newly gained range of the agonisl: pattern. Contract-relax (C-R): a relaxation technique usually per formed at the point of limited range of motion in the agonisl: pattern: • An isotonic movement in rotation is performed followed by an isometric hold of the range-limiting muscles in the antagonist pattern against slowly increasing resistance, voluntary relax ation, and active movement into the new range of the agonist pattern.
CHAPTER 17, THERAPEUTIC EXERCISE
1151
A majority of studies have shown the PNF technique to be the most effective stretching technique for increasing ROM through muscle lengthening when compared to the static or slow sustained, and the ballistic or bounce techniques, 105-109
DETRIMENTAL EFFECTS OF IMMOBILIZATION Continuous immobilization of skeletal muscle tissues can cause some undesirable consequences. These include weakness or atrophy of mus cles (Table 17-9).110 Muscle atrophy is an imbalance between protein synthesis and degradation. After modest trauma, there is a decrease in whole-body protein synthesis 11l rather than increased breakdown. With more severe trauma, major surgery, or multiple organ failure, both syn thesis and degradation increase, the latter being more enhanced. 112,113 The cause of muscle damage during exercised recovery from atrophy involves an altered ability of the muscle fibers to bear the mechanical stress of external loads (weight bearing) and movement associated with exercise. Strenuous exercise can result in primary or secondary sarcolemma disruption, swelling or disruption of the sarco tubular system, distortion of the myofibrils' contractile components, cytoskeletal damage, and extracellular myofiber matrix abnormali tiesy4 These pathologic changes are similar to those seen in healthy young adults after sprint running or resistance training. 114 It appears that the act of contracting while the muscle is in a stretched or length ened position, is responsible for these injuries. 115
Study Pearl Disuse atrophy . ofmuscl~~~gins wit~in4h0l.Jrs~fthestar1ofOedrElst resu Iting)n.decreasElsio91uscle masS, muscle ceHdiamete~and then~mber of muscle fibers. However,strern.Jous exercise of.atrophic musdEl can Jei:ld. to musdedamage in~JHdingsi:lr colemmal disruption, distortion oithe myofi bri Is'contractile components, and cytosKeletaldarnage,Thus, a bal,· anee musfbe found.
TABLE 17-9. STRUCTURAL CHANGES IN THE VARIOUS TYPES OF MUSCLE FOLLOWING IMMOBILIZATION IN A SHORTENED POSITION MUSCLE FIBER TYPE AND CHANGES STRUCTURAL CHARACTERISTICS
SLOW OXIDATIVE
Number of fibers Diameter of fibers Fiber fragmentation Myofibrils Nuclei Mitochondria
Moderate decrease Significant decrease Minimal increase Minimal decrease and disoriented Degenerated and rounded Moderate decrease, degenerated
Sarcoplasmic reticulum Myofilaments Z-band Vesicles Basement membrane Register of sarcomeres Fatty infiltration Collagen Macrophages Satellite cells Target cells
Minimal decrease, orderly arrangement Minimal decrease, disorganized Moderate decrease Abnormal configuration Minimal increase Irregular projections, shifted with time Minimal increase Minimal increase between fibers Minimal increased invasion Minimal increase Minimal increase
FAST OXIDATIVE GLYCOLYTIC Minimal increase Moderate decrease Minimal increase Degenerated and rounded Moderate decrease, degenerated Minimal decrease Moderate decrease
Minimal increased invasion
FAST GLYCOLYTIC Minimal increase Moderate decrease Significant increase Wavy Degenerated and rounded Minimal decrease, degenerated, swollen Minimal decrease Minimal decrease, wavy Faint or absent
Minimal increased invasion
Data from Gossman MR, Sahrmann SA, Rose SJ Review of length-associated changes in muscle. Phys 1ber. 1982;62:1799-1808.
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SECTION III. PROCEDURAL INTERVENTIONS
The clinician must remember that the restoration of full strength and range of motion may prove difficult if muscles are allowed to heal without early active motion, or in a shortened position, and that the patient may be vulnerable to repeated strains. 116 Thus, range-of-motion exercises should be started once swelling and tenderness have sub sided to the point that the exercises are not unduly painful. 116
IMPROVI NG BALANCE Balance, or postural equilibrium, is the single most important factor dictating movement strategies, especially in the closed kinetic chain environment. Postural equilibrium involves synchronization between the neurologic system and the musculoskeletal system in order to maintain a stable weight-bearing and antigravity position for a pro longed period of time. In order for balance to be effective, an individ ual must be able to maintain his or her center of gravity (COG), which is located just above the pelvis, within the body's base of support. A wide base of support provides the best balance. Balance training involving a change in the base of support can be performed with the patient lying, sitting, or standing, depending on the ability of the patient and the goals of the intervention. The usual pro gression employed involves narrowing of the base of support, raising the center of gravity (COG), and changing the weight-bearing surface from hard to soft, or from flat to uneven, while increasing the pertur bation. Challenges to the patient's position can be added in a variety of ways (Table 17-10).
Study Pearl
MOVEMENT STRATEGIES The coordination of the body's postural equilibrium is determined by a number of factors:
TABLE 17-10. PROGRESSIVE CHALLENGES FOR BALANCE TRAINING POSITION (IN ORDER OF INCREASING DIFFICULTY)
Supine/Prone
Quadruped
Kneeling
Sitting
Standing
TARGET MUSCLE GROUPS
EXAMPLES OF ACTIVITIES
Trunk (all muscles) Neck muscles Trunk (extensors) Upper extremities Proximal lower extremities Trunk Lower extremities (except the foot and ankle) Trunk Lower extremities (hips)
Rolling to increase segmentation (a hook-lying position is used) Reaching from Side-lying Static holding with applied challenges Creeping on all fours
Trunk Lower extremities
Half-kneeling Tall-kneeling Decreasing upper extremity support Reaching activities Static challenges Static standing Gait: ~ Bilateral support: parallel bars, > walker ~ Single-hand support: quad cane> straight cane ~ Narrowing the base of support as with tandem walking
CHAPTER 17. THERAPEUTIC EXERCISE ~
~
Joint position strategies: three principal joint systems (hip, knee, and ankle) are located between the base of support and the COG. • Hip: through initiation of large and rapid motions--stepping/ stumbling. • Knee: flexes or extends according to need. • Ankle: contracting the anterior tibialis (posterior sway) or gastrocnemius (anterior sway). The primary method of stabi lization under normal circumstances. The health of the somatosensory, visual, and vestibular systems (see Chapter 9).
BALANCE ASSESSMENT A number of methods, ranging from simple to complex and expensive, can be used to assess balance (see Chapter 9): ~
~
~ ~
Standard Romberg test: standing feet together, arms by the side, and eyes closed. An inability to maintain this position without sway or falling is considered a positive test. BESS test. 118
Computerized force plate/force platform.
BERG balance test.
RESTORING POSTURAL EQUILIBRIUM When restoring postural equilibrium, it is important to follow a struc tured sequence: ~
~
~
Static control of trunk without extremity movement: stable base provided by proXimal segments and trunk to allow functional movements. • Manual perturbation to stable trunk. • Weight shifting while maintaining postural equilibrium. Dynamic control of trunk without extremity movement. • Fixation of distal segments while proximal segments are moved. • Gradual increase of range of motion from small range to large. • Reverse applies to those patients who have hyperkinetic movement disorders (ataxia) where the goal is to work from large ranges to small. Static control of trunk with extremity movement. • Maintenance of trunk stability with increasingly ballistic extremity movements. • Exercises to increase strength, endurance, flexibility, and coordination are prescribed in conjunction with equilibrium exercises. • Exercises that challenge the endurance capabilities of the core muscles. • Progress from extremity exercises with the spine in neutral to extremity exercises with the spine in a variety of functional positions. • Education of the patient about the awareness of how normal alignment of the spine feels in a variety of positions, and how muscles can be used to control those positions.
1153
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SECTION III. PROCEDURAL INTERVENTIONS ~ ~
The clinician should provide verbal, visual, tactile, and propri oceptive cues to enhance learning. Emphasize exercises that involve maintaining functional posi tions to work the correct muscle grou ps.
The clinician can employ PNF techniques to enhance training: ~
~
~ ~
~
Alternating isometrics applied in a variety of directions: unipla nar (anterior-posterior, medial-lateraD initially, and then three dimensionally. Rhythmic stabilization: produces co-contractions of opposing muscle groups.
Dynamic control of tnmk with extremity movement.
Functional activity progression:
• Simple patterns of movements that encourage safe body mechanics are taught initially, before progressing to more challenging movements. • Closed-chain activities should be initiated first (wall squats, lunges), then open-chain activities, while maintaining trunk control (add extremity motions to the squats and lunges). • Uniplanar trunk motions are performed first, before progress ing to three-dimensional trunk motions, such as PNF rotations, in a variety of positions of lumbar flexion and extension. Sport specific progressions as appropriate.
It is important to progress each patient based on the following criteria: ~
~
The required level of strength/endurance is available to per form the activities without fatigue and while maintaining good trunk control. The patient has adequate flexibility in those muscles that allow the correct pelvic tilt to occur (adaptively shortened hamstrings can hold the pelvis in a posteriorly rotated position; adaptively shortened hip flexors can hold the pelvis in an anteriorly rotated position) so that a stable base can be created.
IMPROVING BALANCE THROUGH EXERCISE AND FUNCTIONAL TRAINING Exercises to improve range of motion, strength, and synergistic responses: ~
~ ~ ~ ~ ~
~ ~ ~
~ ~
Stretches of major muscles.
Partial wall squats.
Marching in place.
Single leg kicks.
Shoulder circles.
Head and trunk rotations.
Weight shifts (ankle strategies, hip strategies).
Stepping activities (forward, backward, sideways).
Reaching activities.
Practicing of protective fall mechanisms.
Postural awareness training within limits of stability.
.
CHAPTER 17. THERAPEUTIC EXERCISE
Functional training activities: ~
~ ~ ~
~ ~ ~
~
~
~
~
~
~
Sit-stand-sit activities focusing on moving the body mass for ward over the base of support, extending the lower extremities and raising the body mass over the feet, and then reversing the procedure. Stand to sit transitions: focusing on balance control while piv oting and changing direction. Floor to standing raises: using progression of side-sit to quadruped to kneeling to half kneeling to standing. Gait activities: ambulating forward, backward, sideward at varying speeds and base of support widths (narrow to wide). Can progress to: • Cross-step walking and braiding, 360-degree turns, obstacle courses. • Lateral step-ups, stair climbing, walking up and down ramps. Performing simultaneous activities with the upper extremities (throwing or bouncing a ball, kicking a ball). Getting on and off escalators, elevators. Community integration: • Ambulating in open enVironments, grocery shopping, car transfers, and so forth. Perturbation activities: • Initiate with manual perturbations with the patient in supine, then sitting, and finally in the standing position. • Perturbations should be graded carefully in terms of force and speed. Use of stability equipment (Swiss/physio ball, wobble board, etc.): • The patient performs active weight shifts, upper extremity reaching activities, lower extremity movements such as step ping and marching, and trunk movements with body weight applied through a variety of surfaces. • Challenges can be added by increasing the range of motion of the movements and by increasing the speed of the movements. Sensory training: • The degree of sensory training will depend on the deficits noted during the examination. Ultimately, the clinician should be able to introduce sensory conflict situations (walk ing from a cement floor to a carpeted floor while turning the head to the right and left). Visual deficits: • The patient should practice standing and walking initially with the eyes open and then progressing to eyes closed. • Can be made more challenging by reducing the amount of light. Vestibular deficits: • The patient should practice standing and walking while mov ing head side to side, up and down, on both a stationary and moving surface (see Chapter 9). Somatosensory deficits: • The patient should practice standing and walking on a tile floor transitioning to a carpet. • A variety of under-the-foot surfaces can be used including differing thicknesses of carpet, dense foam, and uneven ter rain outside.
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SECTION III. PROCEDURAL INTERVENTIONS
IMPROVING JOINT STABILIZATION Instability implies that a person has increased joint range of motion but does not have the ability to stabilize and control movement of that joint. Stabilization exercises are dynamic activities that attempt to limit and control any excessive movement. Stabilization activities include patient education, mobility exercises for stiff or hypomobile joints, strengthening exercises in the shortened range for hypermobile seg ments, and neuromuscular re-education (NMR). NMR has been defined as a method of training the enhancement of unconscious motor responses by stimulating both afferent signals and central mechanisms responsible for dynamic joint controlY9 The objective in NMR is to restore proximal stability, muscle control, and flexibility through a balance of proprioceptive retraining and strength ening. NMR attempts to improve the nervous system's ability to gener ate a fast and optimal muscle-firing pattern, to increase joint stability, to decrease joint forces, and to relearn movement patterns and skills. 1l9 NMR is initiated with simple activities and progresses to more complex activities requiring proprioceptive and kinesthetic awareness, once the neuromuscular deficits are minimized. 120,121 It is recom mended that NMR be initiated as early as possible in the rehabilitative processy7 The purpose of NMR is to: ~
~ ~ ~ ~
Decrease pain and spasm by reducing the tone.
Restore mobility and control along the functional kinetic chain.
Restore force couple mechanisms to optimal efficiency.
Restore functional movements away from the base of support. Restore functional movements against gravity.
Neuromuscular control is governed by the central nervous system via the integration of information from the vestibular, vision, and pro prioceptive systems (refer to Chapter 9). According to Voight and associates,117,122 the standard progression for neuromuscular re-education involves: ~
~
Static stabilization exercises with closed-chain loading and unloading (weight shifting), This phase initially employs iso metric exercises around the involved joint on solid and even surfaces, before progressing to unstable surfaces. The early training involves balance training and joint repositioning exer cises, and is usually initiated (in the lower extremities) by hav ing the patient placing the involved extremity on a 6- to 8-inch stool, so that the amount of weight bearing can be controlled more easily. The proprioceptive awareness of a joint can also be enhanced by using an elastic bandage, orthotic, or through taping. 123- 128 As full weight bearing through the extremity is restored, a number of devices such as a mini-trampoline, bal ance board, Swiss ball, and wobble board can be introduced. Exercises on these devices are progressed from double limb support, to single leg support, to support while performing functional skills, Transitional stabilization exercises. The exercises during this phase involve conscious control of motion without impact, and
TABLE 18-9. POLAR EFFECTS PRODUCED BY THE CATHODE AND THE ANODE WITH DIRECT CURRENT NEGATIVE (CATHODE)
Depolarizes nelVe fibers Reduces pain in chronic conditions Attracts bases Increases the potential for hemorrhage Stimulates Softens tissues
POSITIVE (ANODE)
Hyperpolarizes nelVe fibers Reduces pain in acute conditions Repels bases Prevents hemorrhage Sedates Hardens tissues
Reproduced, with permission, from Pociask FD, Fleck TM. Electrotherapy. In: Placzek JD, Boyce DA, eels. Orthopaedic Physical Therapy Secrets. 2nd ed. St Louis, Mosby; 2006:75--89. Copyright © Elsevier.
These waveforms may take on a sine, rectangular, or triangular configuration (Fig. 18-2). An individual waveform is referred to as a pulse. A pulse may contain either one or two phases, which are that portion of the pulse that rises above or below the baseline displayed on an oscilloscope. .. Monophasic: a unidirectional flow of charged particles that occurs over a finite period of time (phase), which have only a single phase in each pulse. .. Biphasic waveforms have two separate phases during each individual pulse. The waveforms may be symmetrical or asym metrical. They may also be balanced or unbalanced. .. Pulsed: these waveforms are called polyphasic and consist of three or more phases in a single pulse.
Pulse Charge. The term "pulse charge" refers to the total amount of electricity being delivered to the patient during each pulse: .. Monophasic current: the phase charge and the pulse charge are the same and always greater than zero. .. Biphasic current: the pulse charge is equal to the sum of the phase charges, unless unbalanced in which case there is a net charge.
Pulse Duration. The duration of each pulse indicates the length of time the current is flowing in one cycle. .. Monophasic: the phase duration is the same as the pulsed duration. .. Biphasic: the pulse duration is determined by the combined phase durations.
Pulse Frequency. Pulse frequency indicates the pulse rate or number of pulses per second (Hz). Frequency contributes to the type of contraction (Table 18-10) as well as theorized opiate-mediated effects. 62
CHAPTER 18. ADJUNGIVE INTERVENTIONS Rate
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Conductance is a term that defines the ease with which current flows along a conducting medium. .. Metals are good conductors of electricity. . . Air, wood, and glass are all considered to be poor conductors (insulators).
Study Pearl The opposition to electron flow in a conducting material is referred to as resistance or electrical impedance, and is measured in a unit known as an ohm. Factors that can typically increase skin impedance include cooler skin temperature, the presence of hair and 6tH increased skin dryness, and increasedskin thickness.
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Current Modulation. Modulation refers to any alteration or any variation of the pulses of various waveforms (duration, width, fre quency). For example, ramp-up time is the time it takes to reach the peak amplitude. This can be used to improve the patient's tolerance to the stimulation.
An analogy'can be used to clarify the relationship betWeen current flow, voltage, and resistance; .. In order fot water to flow,some type of pump must create a force to produce movement. With elec tricity, the volt is the pump that produces the electron flow. .. The resistance to water flow is dependent on the length, diameter, and smoothness ofthe water pipe. The resistance t6 electrkal flow (ohms) depends on the characteris" tits of theconduetor (pipe). "" The.amount of water flowing is measured In gallons. Theamoullt of electricity flowing is measured in arnpereS. ~ The amount of energy produced by the flowing water is determined by two factors: • The number of gallons flowing per unit of time. • The pressure created in the pipe. • Electrkal energy is a· product of the voltage or electrornotive force and the amount of current flowi ng.
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1196
SECTION III. PROCEDURAl INTERVENTIONS +
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Figure 18-2. Waveforms of AC, DC, or pulsed current. (Reproduced, with permission, from Prentice WE. Therapeutic Modalities for Allied Health Professionals. New York: McGraw-Hili; 1998:57.)
CHAPTER 18. ADJUNCTIVE INTERVENTIONS +
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Physiologic Responses to Electrical Current. Electrical current tends to choose the path of the least resistance to flow. Electricity has an effect on each cell and tissue that it passes through. The type and extent of the response are dependent on the type of tis sue and its response characteristics. Typically, tissue that is highest in water content and consequently highest in ion content is the best con ductor of electricity. ~
~ ~ ~ ~ ~
Skin: offers the primary resistance to current flow and is con sidered an insulator. The greater the impedance of the skin, the higher the voltage of the electrical current needed to stimulate underlying nerve and muscle. Blood: composed largely of water and ions and is consequently the best electrical conductor of all tissues. Muscle: composed of about 75% water and is therefore a rela tively good conductor. Tendons: denser than muscle and contain relatively little water-poor conductors. Fat: only about 14% water-poor conductor. Bone: extremely dense, contains only about 5% water-the poorest biological conductor.
AB electricity moves through the body, changes in physiologic functioning occur at the various levels of the system (Table 18-11).
TABLE 18-10. FREQUENCY AND 1YPE OF CONTRACTION FREQUENCY (Hz)
1-10 >30
30-70
100-1000
1YPE OF CONTRACTION
Twitch contraction Tetanic contraction Nonfatiguing tetanic contraction Fatiguing tetanic contraction
Reproduced, with permission, from Pociask FD, Fleck TM. Electrotherapy. In: Placzek )D, Boyce DA, eds. Orthopaedic Physical Therapy Secrets. 2nd ed. St Louis, Mosby; 2006:75--89. Copyright © Elsevier.
1197
1198
SECTION III. PROCEDURAL INTERVENTIONS
TABLE 18-11. CHANGES IN PHYSIOLOGIC FUNCTIONING THAT OCCUR AT THE VARIOUS LEVELS OF THE BODY SYSTEM DUE TO ELECTRICITY BODY SYSTEM LEVEL Cellular level
Tissue level
Segmental level
Systematic effects
CHANGES Excitation of nerve cells Changes in cell membrane permeability Protein synthesis Stimulation of fibroblasts, osteoblasts. Modification of microcirculation Skeletal muscle contraction Smooth muscle contraction Tissue regeneration Modification of joint mobility Muscle pumping action to change circulation and lymphatic activity An alteration of the microvascular system not associated with muscle pumping An increased movement of charged proteins into the lymphatic channels with subsequent oncotic force bringing increases in fluid to the lymph system Note: transcutaneous electrical stimulation cannot directly stimulate lymph smooth muscle or the autonomic nervous system without also stimulating a motor nerve Analgesic effects as endogenous pain suppressors are released and act at different levels to control pain Analgesic effects from the stimulation of certain neurotransmitters to control neural activity in the presence of pain stimuli
MUSCLE AND NERVE PHYSIOLOGY RELATED TO ~
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Rheobase: the minimum intensity of current required to pro duce a minimum muscle contraction when applied for a maxi mum duration. Chronaxie: the length of time (pulse duration) for a CUrrent of twice the intensity of the rheobase current to produce tissue excitation.
A graphic illustration of this threshold and propagation and con traction is the strength-duration curve (Fig. 18-3). The strength-duration curves for different classes of nerve and muscle tissue illustrate different thresholds of excitability of these tissues (Fig. 18-4).
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Elimination half-life: • The time in which the concentration of the drug in the plasma falls to one-half of its original amount. • A drug's rate of disappearance from the body, whether by metabolism, excretion or a combination of both. Biologic half-life: • The time in which the duration of action falls to one-half of its original duration. • The time of the drug's response rather than its plasma concentration.
The dosage interval (time between administrations of the drug) is equal to the half-life of a particular drug. The shorter the half-life, the more often the patient must take the medication. Theoretically, a steady state will be reached when the amount of the drug taken will equal the amount that is excreted. A steady state is usually reached after five half-lives of the drug have occurred. Thus, drugs with long half-lives may take several days to weeks to reach a steady state.
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DRUG ALLERGY AND DRUG-INDUCED ILLNESSES
Drugs: pain al drugs t abseno associal physici efit and
Drug allergies or hypersensitivities range from mild presentations to very severe life-threatening events. For a drug to produce a reaction, it must have antigenic effects and stimulate antibody formation or the formation of sensitized T-Iymphocytes, which is immune-related. Drug allergies are generally classified into four types:
referre< synthet (propo: dine). I
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Type I (anaphylactic reactions): anaphylaxis is the most severe allergic reaction and involves the skin, pulmonary, and cardiovascular systems. The signs and symptoms associated with anaphylactic shock, which usually occur within minutes
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CHAPTER 19. PHARMACOLOGY FOR THE PHYSICAL THERAPIST
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after antigen exposure but may still occur up to 1 hour later, include • Neurologic: dizziness, weakness, and seizures. • Ocular: pruritus, lacrimation, edema around the eyes. • Respiratory: nasal congestion, hoarseness, stridor, cough, dyspnea, tachypnea, bronchospasm, and respiratory arrest. • Cardiac: tachycardia, hypotension, arrhythmias, myocardial infarction. • Integumentary: flushing, erythema, urticaria. • Gastrointestinal: nausea, vomiting, and diarrhea. Type II (cytotoxic reaction): the antigens adhere to the target cell and begin to destroy the target tissue. The clinical manifes tations include • Fever. • Arthralgia. • Rash. • Splenomegaly. • Lymph node enlargement. Type III (autoimmune reaction): a complex-mediated hyper sensitivity reaction in which the body has difficulty eliminat ing antigen-antibody complexes. Manifestations include serum sickness, glomerulonephritis, vasculitis, and pulmonary disorders. Type IV (cell-mediated hypersensitivity): this type of reaction is mediated through T-lymphocytes as opposed to antibodies. Manifestations include local or tissue reaction.
PHARMACOTHERAPY Although physical therapists are not permitted by law to prescribe or dispense prescription drugs, an understanding of the potential effects of certain types of drugs commonly encountered during the rehabilita tion process is essential. 33 MUSCULOSKELETAL PHARMACOLOGY
Drugs are widely used in the management of both acute and chronic pain and inflammation. The following discussion focuses on those drugs that are prescribed to control pain and/or inflammation. In the absence of data supporting a therapeutic benefit for a drug, toxicity associated with the drug can still occur. It is critical, therefore, for physicians to continually assess the balance between therapeutic ben efit and safety.
Opioid Analgesics. Most of the narcotics used in medicine are referred to as opioids, as they are derived directly from opium or are synthetic opiates. Examples of these opioids include codeine, Darvon (propoxyphene hydrochloride), morphine, and Demerol (meperi dine). Refer to "Narcotic Analgesics" later in the chapter. Non-Opioid Analgesics. Non-opioid analgesics comprise a heterogeneous class of drugs including the salicyclates (aspirin and diflunisal), para-aminophenol derivatives (primarily acetaminophen), and the NSAIDs (Ibuprofen, Voltaren, Relafen, Naprosyn, Motrin,
1249
-TION III. PROCEDURAL INTERVENTIONS
/
Indocin, Feldene, Lodine, Celebrex, and many others). Despite their diverse structures, non-opioid analgesics have similar therapeutic effects, oral efficacy, and similar side effect profiles. Non-opioid anal gesics are better tolerated than opioids by ambulatory patients, have fewer sedative effects, and are much less likely to produce tolerance or dependence. Conversely, the hazards of long-term administration of these drugs are recognized. NSAlDs have antipyretic, analgesic, and antiint1ammatory effects. The analgesic and antiinflammatory activity of NSAIDs is primarily due to the inhibition of arachidonic acid metabolism. 54 NSAlDs also seem to promote the inhibition of the release of cyclooxygenase-l (Cox-I) and cyclooxygenase-2 (Cox-2) and the synthesis of prostaglandins at an injury site. 54 Inhibition of Cox-l can also produce gastrointestinal toxicity including inflammation, ulceration, and bleeding, and can lead to perforation. 55 Suppression of prostaglandins is not limited to the site of injury and may result in alteration of normal function in the gas trointestinal mucosa and kidney blood flow. NSAlDs may also alter kidney blood t10w by interfering with the synthesis of prostaglandins in the kidney involved in the autoregulation of blood t10w and glomerular filtration. 36 Cox-2 inhibitors do not produce the same gastrointestinal effects as Cox-l inhibitors; therefore, they are safer to use in patients who are predisposed to gastric or kidney malfunctions. Cox-2 drugs only block the Cox-2 enzyme, which is responsible for triggering pain and inflam mation. 54 Because Cox-l is not affected, the patient's stomach lining is protected and bleeding tendencies are avoided.
Corticosteroids.
Corticosteroids are natural antiint1ammatory hormones produced by the adrenal glands under the control of the hypothalamus. Synthetic corticosteroids (cortisone, dexamethasone) are commonly used to treat a range of immunologic and int1ammatory musculoskeletal conditions. Corticosteroids exert their antiinflammatory effects by binding to a high-affinity intracellular cytoplasmic receptor present in all human cells. 37 As a result, these agent') are capable of producing undesirable and sometimes severe systemic adverse effects that may offset clinical gains in many patients. The side effects from corticosteroids emulate from exogenous hypercortisolism, which is similar to the clinical syndrome of Cushing's disease. These side effects include 38 ~
~
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Cutaneous manifestations. Cutaneous manifestations of hyper cortisolism include delayed wound healing, acanthosis nigri cans (a velvety, thickened, hyperpigmented plaque that usually occurs on the neck or in the axillary region), acne, ecchymoses after minor trauma, hyperpigmentation, hirsutism, petechia. and striae. Hypokalemia. Hypokalemia is a well-recognized side effect of corticosteroid therapy and is probably related to the mineralo corticoid effect of hydrocortisone, prednisone, and pred nisolone. Dexamethasone has no mineralocorticoid effect. Myopathy. There are two recognized forms of corticosteroid induced myopathy: acute and chronic. Acute myopathy may in part be caused by hypokalemia, although corticosteroids (espe cially massive dosages) may have a direct affect on skeletal muscle. Both proximal and distal muscle weakness occur
CHAPTER 19. PHARMACOlOGY FOR THE PHYSICAL THERAPIST
~
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acutely, usually with an associated and significant elevation in serum creatinine phosphokinase, which is indicative of focal and diffuse muscle necrosis. In the more chronic form of myopathy, weakness is more insidious in onset and primarily involves proximal muscle groups. Hyperglycemia. Although it is not clear how corticosteroid use causes hyperglycemia, hyperglycemia, especially when com bined with the immunosuppressive effect of corticosteroids, may significantly increase the risk for infection. Neurological impairments. These can include vertigo, headache, convulsions, and benign intracranial hypertension. Osteoporosis. Corticosteroids inhibit bone formation directly via inhibition of osteoblast differentiation and type I collagen synthesis, and indirectly by inhibition of calcium absorption and enhancement of urinary calcium excretion. Ophthalmologic side effects. Corticosteroids increase the risk of glaucoma by increasing intraocular pressure, regardless of whether administered intranasally, topically, periocularly, or systemically. Growth suppression. Corticosteroids interfere with bone for mation, nitrogen retention, and collagen formation, all of which are necessary for anabolism and growth.
Muscle Relaxants. Muscle relaxants are thought to decrease muscle tone without impairment in motor function by acting centrally to depress polysynaptic reflexes. As muscle guarding and spasm accompany many musculoskeletal injuries, it was originally thought that these drugs, by eliminating the spasm and guarding, would facili tate the progression of a rehabilitation program. However, other drugs with sedative properties, such as barbiturates, also depress polysynap tic reflexes, making it difficult to assess if centrally acting skeletal mus cle relaxants actually are muscle relaxants as opposed to nonspecific sedatives. 39 There presently exists a discrepancy between the common clinical use of skeletal muscle relaxants and the results of controlled clinical trials evaluating their efficacy in comparison with placebo. Supporting evidence does not exist for their efficacy in pain of myo genic origin, nor is it clear if they provide an additive effect with exer cises aimed at muscle relaxation. NEUROLOGIC SYSTEM PHARMACOLOGY
Antianxiety Medications Selective Serotonin Reuptake Inhibitors (SSRls). Selective sero tonin reuptake inhibitors (SSRIs) are commonly prescribed psy chotherapeutic agents. The most serious drug-related adverse effect of SSRIs is the potential to produce serotonin syndrome (SS). Serotonin synthesis is necessary in both the central and peripheral nervous sys tems because serotonin cannot cross the blood-brain barrier. Once synthesized, serotonin is either stored in neuronal vesicles or metabo lized. SS, characterized by mental status changes, neuromuscular dys function, and autonomic instability, is thought to be secondary to excessive serotonin activity in the spinal cord and brain. Symptoms attributed to serotonin excess may include restlessness, hallucinations, shivering, diaphoresis, nausea, diarrhea, and headache.
1251
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SECTION III. PROCEDURAL INTERVENTIONS
Common currently prescribed SSRls include sertraline (Zoloft), fluoxetine (Prozac), paroxetine (Paxil), and fluvoxamine (Luvox). Monoamine Oxidase Inhibitors (MAO/s). Neurotransmitters are generally monoamines. When released into the synaptic space, neuro transmitters are either reabsorbed into the proximal nerve or destroyed by monoamine oxidase (MAO) in the synaptic cleft. The two types of MAO are MAO-A and MAO-B. MAO-A is found primarily in the liver and gastrointestinal tract, with some found in the monoaminergic neurons. MAO-A present in the liver is involved in the elimination of ingested monoamines such as dietary tyramine. Circulating monoamines such as epinephrine, norepinephrine, and dopamine are inactivated when they pass through a liver rich in MAO-A. MAO-B, on the other hand, is found primarily in the brain and in platelets. MAOIs indirectly degrade the monamines and inhibit breakdown of the neurotransmitters norepinephrine, serotonin, and dopamine, resulting in hypertension, tachycardia, tremors, seizures, and hyper thermia, thereby increasing the available monamines available within the CNS. The MAOI agents currently available in the United States include phenelzine sulfate (Nardil), tranylcypromine sulfate (Parnate), isocar boxazid (Marplan), and selegiline (specific for the MAO-B enzyme), all of which irreversibly bind to MAO. Benzodiazepines. Benzodiazepines (BZDs) are sedative-hypnotic agents that are used for a variety of situations including seizure control, anxiety, alcohol withdrawal, insomnia, control of drug-associated agi tation, as muscle relaxants (antispasticity agents), and as preanesthetic agents. They also are combined frequently with other medications for conscious sedation before procedures or interventions. Gamma-aminobutyric acid (GABA) is the principal inhibitory neu rotransmitter in the CNS. BZDs exert their action by potentiating the activity of GABA. Enhanced GABA neurotransmission results in sedation, striated muscle relaxation, and anticonvulsant effects. Stimulation of peripheral nervous system (PNS) GABA receptors may cause decreased cardiac contractility, vasodilation, and enhanced perfusion. Beta-Blockers. Beta-blockers (e.g., propranolol) have been used to block the autonomic response in people with social phobia.
Sedatives/Hypnotics. Sedative-hypnotics are a group of drugs that cause CNS depression. Benzodiazepines (see above) and barbitu rates are the most commonly used agents in this class. Other agents include the nonbarbiturate nonbenzodiazepine sedative-hypnotics, such as buspirone, zolpidem, ethchlorvynol, glutethimide, chloral hydrate, meprobamate, methaqualone, methyprylon, carisoprodol, and gamma-butyrolactone (GBL). Most sedative-hypnotics stimulate the activity of GABA. Mild toxicity resembles ethanol intoxication. Moderate poisoning leads to respiratory depression and hyporeflexia. Severe poisoning leads to flaccid areflexic coma, apnea, and hypotension. Generally, ten times the hypnotiC dose produces severe toxicity.
CHAPTER 19. PHARMACOlOGY FOR THE PHYSICAL THERAPIST
1253
.. Occasionally, hyperreflexia, rigidity, clonus, and Babinski signs are present. .. Miosis is common, but mydriasis may be present with certain agents. • The nonbarbiturates, such as methyprylon and glutethimide, more commonly present with mydriasis. .. Hypotension is usually secondary to vasodilation and negative cardiac inotropic effects.
Narcotic Analgesics. The term "narcotic" specifically refers to any substance that induces sleep. In current practice, narcotic refers to any of the many opioids or opioid derivatives. Activation of the opiate receptors results in the inhibition of synap tic neurotransmission in the central nervous system (CNS) and periph eral nervous system (PNS). Opioids bind to and enhance neurotrans mission at opiate receptors. The opiate antagonists (e.g., naloxone, nalmefene, naltrexone) antagonize the effects of all opiate receptors. Opioids decrease the perception of pain, by inducing slight euphoria, rather than eliminating or reducing the painful stimulus. The GI tract and the respiratory mucosa provide easy absorption for most opioids. Following therapeutic doses, most absorption occurs in the small intestine. Toxic doses may have delayed absorption because of delayed gastric emptying and slowed gut motility. Certain opiates (e.g., propoxyphene, fentanyl, and buprenorphine) are more lipid soluble and can be stored in the fatty tissues of the body. As opiate metabolites are excreted in the urine, renal failure also leads to toxic effects from accumulated drug or active metabolites (e.g., normeperidine). Examples of commonly prescribed opioids include codeine phos phate, Demerol, Dilaudid, Empirin with codeine, Sublimaze, Synalgos DC, Talwin 50, propoxyphene, morphine, Hydrocodone, Lorcet, Lortab, Zydone, Hydrocet, Oxycontin (Oxycodone), Percodan (Percocet), Darvon (Darvocet), and Vicodin (Vicoprofen). Antidepressants Tricyclic Antidepressants (TeAs). Tricyclic antidepressants (TCAs) are used in the treatment of depression, chronic pain, and enuresis (involuntary discharge of urine, especially while asleep). Patients with depression and those with chronic pain are at high risk for abuse, mis use, and overdosing of these drugs. TCAs affect the cardiovascular, central nervous, pulmonary, and gastrointestinal systems. The toxic effects on the myocardium are related to the blocking of fast sodium channels, which involves the same mechanism as type IA antiarrhythmics (e.g., quinidine). The result is a slowing of myocardium depolarization that leads to arrhythmia, myocardial depression, and hypotension. Hypotension also results from peripheral alpha-adrenergic blockade, which causes vascular dilatation. Inhibition of norepinephrine reuptake and subsequent depletion causes further hypotension. CNS toxicity, manifested as confusion, hallucinations, ataXia, seizures, and coma, results from the anticholinergic effects and direct inhibition of biogenic amine reuptake. The effects on the pulmonary system include pulmonary edema, respiratory distress syndrome (RDS), and aspiration pneumonitis.
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SECTION III. PROCEDURAL INTERVENTIONS
The anticholinergic effects of TCAs cause a slowing of the gas trointestinal (GI) system, which results in delayed gastric emptying, decreased motility, and prolonged transit time. Examples of commonly prescribed TCAs include amitriptyline, clomipramine, doxepin, trimipramine, desipramine, nortriptyline, pro triptyline, imipramine, amoxapine (dibenzoxipine), and maprotiline (tetracyclic antidepressant).
Parkinson's Disease and Parkinsonian Syndrome. The basal ganglia motor circuit modulates cortical output necessary for nor mal movement. Levodopa, coupled with a peripheral decarboxylase inhibitor (PDI), remains the criterion standard of symptomatic treat ment for PD. It provides the greatest antiparkinsonian benefit with the fewest adverse effects. Dopamine agonists provide symptomatic bene fit comparable to levodopa/PDI in early disease but lack sufficient effi cacy to control signs and symptoms by themselves in later disease.40-46 Medications for Parkinson's usually provide good symptomatic control for 4 to 6 years. Whether levodopa has a toxic or protective effect in the brain with PD is unknown. As PD progresses, fewer dopamine neurons are available to store and release levodopa-derived dopamine. The patient's clinical status fluctuates in concert with plasma levodopa levels. Fluctuating levodopa-derived dopamine con centrations in association with advancing disease therefore may be responsible for development of motor fluctuations and dyskinesia. In contrast to levodopa, the long-acting dopamine agonists (bromocriptine, pergolide, pramipexole, ropinirole, cabergoline) pro vide relatively smooth and sustained receptor stimulation. The selection of medication depends in part on the nature and cause of the disability. If disability is due solely to tremor, a tremor-specific medication, such as an anticholinergic agent, is usually prescribed. Anticholinergic medications provide good tremor relief in approximately 50% of patients but do not improve bradykinesia or rigidity. Because tremor may respond to one anticholinergic medication and not another, a sec ond anticholinergic usually is tried if the first is not successful. These medications should be introduced at a low dose and escalated slowly to minimize adverse effects, which include memory difficulty, confu sion, and hallucinations. Adverse cognitive effects are relatively com mon, especially in the elderly. If disability is due to a dopamine-responsive symptom such as bradykinesia, rigidity, decreased dexterity, slow speech, or shuffling gait, a dopaminergic medication (dopamine agonist or levodopa/PDI) is typically introduced. Symptomatic medications are started at a low dose, escalated slowly, and titrated to control symptoms. Most patients require symptomatic dopaminergic therapy to ameliorate bradykinesia and rigidity within 1 to 2 years after diagnosis. For patients younger than 65 years, symptomatic therapy is initi ated with a dopamine agonist, adding levodopa/PDI when the dopamine agonist alone no longer controls symptoms adequately. For patients aged 65 to 70 years, a judgment is made based on general health and cognitive status. For patients who are demented or those older than 70 years, who may be prone to adverse effects from dopamine agonists, and for those likely to require treatment for only a few years, physicians may elect not to use a dopamine agonist and depend on levodopa/PDI as primary symptomatic therapy.47
CHAPTER 19. PHARMACOLOGY FOR THE PHYSICAL THERAPIST
Antiepileptic Drugs (AED). Many structures and processes are involved in the development of a seizure, including neurons, ion channels, receptors, glia, and inhibitory and excitatory synapses. The AEDs are designed to modify these processes to favor inhibition over excitation in order to stop or prevent seizure activity. The AEDs can be grouped according to their main mechanism of action, although many of them have several actions and others have unknown mechanisms of action. Side Effects and Toxicity. AEDs can produce dose-related adverse effects, which include dizziness, diplopia, nausea, ataxia, and blurred vision.
GABA Receptor Agonists. GABA has two types of receptors. ~
~
When the GABA-A receptor is stimulated, chloride channels open to allow the influx of negative ions (chloride) into the neuron and cause hyperpolarization, moving the membrane potential further from the cell-firing threshold. The GABA-A receptors have multiple binding sites for benzodiazepines, bar biturates, and others substances such as picrotoxins, bicuculline, and neurosteroids. The GABA-B receptor is linked to a potassium channel.
Direct binding to GABA-A receptors can enhance the GABA sys tem by blocking presynaptic GABA uptake, by inhibiting the metabo lism of GABA by GABA transaminase, and by increasing the synthesis of GABA. The benzodiazepines most commonly used for treatment of epilepsy are lorazepam, diazepam, clonazepam, and clobazam. The two barbiturates mostly commonly used in the treatment of epilepsy are phenobarbital and primidone. Side Effects and Toxicity. The most common effect is sedation. Other adverse effects include dizziness, ataxia, blurred vision, diplopia, irritability, depression, muscle fatigue, and weakness. Idiosyncratic reactions are very rare and no fatal reactions have been reported so far.
GABA Reuptake Inhibitors. At least four specific GABA transporting compounds help in the reuptake of GABA; these carry GABA from the synaptic space into neurons and glial cells, where it is metabolized. Nipecotic acid and tiagabine (TGB) are inhibitors of these transporters; this inhibition makes increased amounts of GABA avail able in the synaptic cleft. GABA prolongs inhibitory postsynaptic potentials (IPSPs). Side Effects and Toxicity. The most common adverse effects include dizziness, asthenia, nervousness, tremor, depressed mood, and emotional lability. Other adverse effects include somnolence, headaches, abnormal thinking, abdominal pain, pharyngitis, ataxia, confusion, psychosis, and skin rash.
GABA Transaminase Inhibitors. GABA is metabolized by transamination in the extracellular compartment by GABA-transaminase (GABA-T). Inhibition of this enzymatic process leads to an increase in
Study Pearl
1255
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SECTION III. PROCEDURAL INTERVENTIONS
the extracellular concentration of GABA. Vigabatrin (VGB) inhibits the enzyme GABA- T.
Side Effects and Toxicity. The most common adverse effect is drowsiness. Other important adverse effects include neuropsychiatric symptoms such as depression, agitation, confusion, and rarely, psy chosis. Minor adverse effects, usually at the onset of therapy, include fatigue, headache, dizziness, increase in weight, tremor, double vision, and abnormal vision.
Glutamate Blockers. Glutamate and aspartate are the two most important excitatory neurotransmitters in the brain. The glutamate sys tem is a complex system with macromolecular receptors with different binding sites (AMPA, kainate, NMDA, glycine, and metabotropic sites). Glutamate is responsible for sending signals between nerve cells, and under normal conditions it plays an important role in learning and memory. Glutamate blockers are prescribed for a wide variety of con ditions, including epilepsy, Huntington's disease, Alzheimer's disease, Amyotrophic Lateral Sclerosis (ALS) , and Parkinson's disease. Examples of glutamate blockers include topiramate and felbamate. Side Effects and Toxicity. Common adverse effects include insom nia, weight loss, nausea, decreased appetite, dizziness, fatigue, ataxia, and lethargy. Polytherapy is associated with increases in adverse effects.
Neuroleptics (Anti psychotics) . The term "neuroleptic" refers to the effects on cognition and behavior of antipsychotic drugs that reduce confusion, delusions, hallucinations, and psychomotor agi tation in patients with psychoses. The adverse effects of neuroleptics are not confined to psychiatric patients. Neuroleptics also are used as sedatives, for their antiemetic properties, to control hiccups, to treat migraine headaches, as antidotes for drug-induced psychosis, and in conjunction with opioid analgesia. Any of the acute adverse effects of neuroleptics may occur in these settings. Neuroleptics are also utilized in conjunction with antidepressants or mood stabilizers when psy chotic symptoms are present, or to enhance the effect of other med ications when attempting to control mania. Although all antipsychotic preparations share some toxic charac teristics, the relative intensity of these effects varies greatly, depending on the individual drug. Generally, all neuroleptic medications are capa ble of causing the following symptoms: ~
~
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Hypotension: phenothiazines are potent alpha-adrenergic blockers that result in significant orthostatic hypotension, even in therapeutic doses for some patients. In overdose, hypoten sion may be severe. Anticholinergic effects: neuroleptic agent toxicity can result in tachycardia, hyperthermia, urinary retention, ileus, mydriasis, toxic psychosis, and hot dry flushed skin. Extrapyramidal symptoms: alteration in the normal balance between central acetylcholine and dopamine transmission can produce dystonia, oculogyric crisis, torticollis, acute parkinson ism, akathisia, and other movement disorders. Chronic use of major tranquilizers is associated with buccolingual dysplasia (tardive dyskinesia), parkinsonism, and akathisia.
CHAPTER 19. PHARMACOLOGY FOR THE PHYSICAL THERAPIST ~
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Neuroleptic malignant syndrome: all of the major tranquilizers have been implicated in the development of neuroleptic malig nant syndrome (NMS), a life-threatening derangement that affects multiple organ systems and results in significant mortality. Seizures: most major tranquilizers lower the seizure threshold and can result in seizures at high doses and in susceptible indi viduals. With loxapine, seizures may be recurrent. Hypothermia: certain major tranquilizers prevent shivering, limiting the body's ability to generate heat. Cardiac effects: prolongation of the QT interval and QRS can . result in arrhythmias. Respiratory depression: hypoxia and aspiration of gastric con tents can occur in children and in mixed overdose.
SPASTICITY The use of oral medications for the treatment of spasticity may be very effective. 48 At high dosages, however, oral medications can cause unwanted adverse effects that include sedation as well as changes in mood and cognition. These adverse effects preclude their extensive use in children, since the intellectual function of the majority of chil dren with spasticity is at best precarious, and sedation inevitably results in some degree of impaired learning or school performance.
Benzodiazepines-Diazepam and Clonazepam. The benzodiazepines bind in the brainstem and at the spinal cord level and increase the affinity of GABA to the GABA-A receptor complex. This results in an increase in presynaptic inhibition and then reduction of monosynaptic and polysynaptic reflexes. These drugs may improve passive range of motion and reduce hyperreflexia, painful spasms, and anxiety. Diazepam has a half-life of 20 to 80 hours and forms active metabolites that prolong its effectiveness. The half-life of clonazepam ranges from 18 to 28 hours. Sedation, weakness, hypotension, adverse gastrointestinal effects, memory impairment, incoordination, confusion, depression, and ataxia may occur. Tolerance and dependency can occur, and with drawal phenomena-notably seizures-have been associated with abrupt cessation of therapy. Patients who are taking benzodiazepines with agents such as baclofen or tizanidine that potentiate sedation and have central depressant properties should be monitored carefully. Baclofen-Oral and Intrathecal Pump. Baclofen is a GABA agonist, and its primary site of action is the spinal cord, where it reduces the release of excitatory neurotransmitters and substance P by binding to the GABA-B receptor. Baclofen improves clonus, flexor spasm frequency, and joint range of motion, resulting in improved functional status. Baclofen must be used with care in patients with renal insuffi ciency, as its clearance is primarily renal. Adverse effects include seda tion, ataxia, weakness, and fatigue. When used in combination with tizanidine or benzodiazepines, the patient should be monitored for unwanted depressant effects. Adverse effects of baclofen can be minimized by intrathecal infu sion of the drug, because the concentration gradient favors higher levels at the spinal cord versus the brain.
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Dantrolene Sodium. Dantrolene sodium is useful for spasticity of supraspinal origin, particularly in patients with cerebral palsy or traumatic brain injury. It decreases muscle tone, clonus, and muscle spasm. It acts at the level of the muscle fiber, affecting the release of calcium from the sarcoplasmic reticulum of skeletal muscle and thus reducing muscle contraction. It is therefore less likely than the other agents to cause adverse cognitive effects. Its peak effect is at 4 to 6 hours, with a half-life of 6 to 9 hours. Adverse effects include generalized weakness, including weak ness of the respiratory muscles, drowsiness, dizziness, weakness, fatigue, and diarrhea. Tizanidine. Tizanidine (Zanaflex) is a new and effective therapeu tic option for the management of spasticity due to cerebral or spinal damage. The antispasticity effects of tizanidine are the probable result of inhibition of the H-reflex. It also may facilitate inhibitory actions of glycine and reduce release of excitatory amino acids and substance P, and may have analgesic effects. Dry mouth, somnolence, asthenia, and dizziness are the most common adverse events associated with tizanidine. Liver function problems, orthostasis, and hallucinations are rare tizanidine-related adverse events.
Other Oral Agents. Other agents that may be beneficial in selected patients include the following: ~
~
~ ~ ~
Clonidine is a selective alphaz-receptor agonist and may inhibit presynaptic sensory afferents. Hypotension is the main adverse effect. Gabapentin is a GABA analog that modulates enzymes that metabolize glutamate. Lamotrigine blocks sodium channels and reduces the release of glutamate and other excitatory amino acids. Cyproheptadine is a 5-HT antagonist that may neutralize sero tonergic inputs. Cannabinoid-like compounds (dronabinol, nabilone) that act on the cannabinoid receptors (CBl and CB2) may be useful in muscle spasms and spasticity.
CARDIOVASCULAR SYSTEM PHARMACOLOGY
Alpha-Adrenergic Blocking Drugs (Alpha-Blockers). These drugs work through the autonomic nervous system (ANS) by blocking nerve receptors that are called alpha-receptors. Alpha receptors normally promote constriction of the arterioles. Blocking constriction promotes dilation of vessels and lowers blood pressure as well as reducing the work of the heart in some situations. Alpha-blocking drugs also inhibit the actions of one of the adrenal hormones, norepi nephrine, that raises blood pressure as part of the fight-or-flight response. Alpha-blockers are usually prescribed along with other blood-pressure-lowering drugs, such as a beta-blocking drug and/or a diuretic. There are now several medications available that combine the effects of blocking both the beta- and alpha-receptors, such as Iabetolol (Normodyne, Trandate).
CHAPTER 19. PHARMACOLOGY FOR THE PHYSICAL THERAPIST
Examples of alpha-blockers include doxazosin (Cardura), pra zosin (Minipress), and terazosin (Hytrin).
Possible Adverse Side Effects. Nausea and indigestion; these usu ally subside with long-term use. Less frequent effects are cold hands and feet, temporary impotence, and nightmares. Dizziness may occur initially or as dosage is increased.
Angiotensin-Converting Enzyme (ACE) Inhibitors. These drugs act to prevent production of a hormone, angiotensin II, which constricts blood vessels. They belong to the class of drugs called vasodilators-drugs that dilate blood vessels, an effective way to lower blood pressure and increase the supply of blood and oxy gen to the heart and various other organs. In addition to dilating blood vessels, ACE-inhibiting medications may produce some bene ficial effects indirectly by preventing the abnormal rise in hormones associated with heart disease, such as aldosterone. ACE inhibitors are widely used to treat hypertension, a major risk factor for cardiovas cular disease. Used alone or in combination with other drugs, ACE inhibitors have also proved effective in the treatment of congestive heart failure. Examples include benazepril (Lotensin), captopril (Capoten), enalapril (Vasotec), fosinopril (MonopriD, lisinopril (Prinivil, ZestriD, moexipril (Univasc), quinapril (AccupriD, ramipril (Altace), and tran dolapril (Mavik).
Possible Adverse Side Effects. Common side effects are dizziness or weakness, loss of appetite, rash, itching, a hacking, unpredictable cough, and swelling.
Antiarrhythmic Drugs. These drugs are designed to correct arrhythmias and tachycardia. Although the vast majority of patients benefit from antiarrhythmic drugs, heart arrhythmias may paradoxically worsen in 5% to 10% of patients. Examples include amiodarone (Cordarone), digoxin (Lanoxin), disopyramide phosphate (Norpace), flecainide (Tambocor), propafenone (RhythmoD, lidocaine (Xylocaine), mexiletine (MexitiD, procainamide (Procan SR, Pronestyl, Pronestyl SR), quinidine gluconate (Duraquin, Quinaglute Dura-Tabs, Quinalan Sustained-Release), quini dine sulfate (Quinidex Extentabs), and tocainide (Tonocard).
Possible Side Effects. Most significant common side effects are weakening of heart contractions, worsening of some arrhythmias, weight loss, nausea, and tremors. Other less common effects are fever, rash, dry mouth, depressed white blood cell count, liver inflammation, confusion, loss of concentration, dizziness, and disturbances in vision.
Anticoagulants, Antiplatelets, and Thrombolytics. Anticoagulants, antiplatelet agents, and thrombolytics each have spe cific indications and uses. These drugs are sometimes referred to as "blood thinners," but this term is not truly accurate. They inhibit the ability of the blood to clot. Under a number of different circumstances, preventing clot formation is necessary.
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Study Pearl
Patients who develop atrial fibrillation may require anticoagulants; clot formation in the left atrium is a potential hazard of this rhythmic dis turbance. Oral anticoagulants are prescribed for patients who develop thrombopWebitis. One of the dangers of this condition is the develop ment of pulmonary emboli. Lastly, some patients who have a heart attack are prescribed an anticoagulant to prevent clots from forming on the inner lining of the scar. Heparin is an anticoagulant that is administered intravenously when rapid anticoagulation is necessary. Aspirin, which inhibits the clotting action of platelets, it is desig nated as an antiplatelet. It is frequently prescribed in patients who have recovered from a heart attack, in order to prevent clots from forming in the veins used for coronary bypass surgery. Thrombolytic drugs are given intravenously to help prevent clotting of the coronary arteries, and prevent permanent, debilitating damage. The three most commonly used thrombolytics are t-PA, streptokinase, and APSAC.
Possible Side Effects. Adverse effects are rare, but may include nau sea, headache, flushing, dizziness or faintness, or rash.
Beta-Adrenergic Blockers. These drugs probably reduce blood pressure by reducing the output of blood from the heart (or per haps by blocking the production of angiotensin). Beta-blockers are also used to treat hypertension. Specifically, they block responses from the beta-nerve receptors. This serves to slow down the heart rate and to lower blood pressure. Beta-blockers also block the effects of some of the hormones that regulate blood pressure. During exercise or emo tional stress, adrenaline and norepinephrine are released and normally stimulate the beta-receptors--sensors that transmit messages to the heart to speed up and pump harder. By blocking the receptors, beta blockers act to reduce heart muscle oxygen demands during physical activity or excitement, thus reducing the possibility of angina caused by oxygen deprivation. Beta-blockers also dampen heart rate increases caused by stress, exercise, or anxiety. Examples include acebutolol (Sectral), atenolol (Tenormin), betaxolol (Betoptic, Betoptic S, Kerlone), bisoprolol (Zebeta), meto prolol (Lopressor), carteolol (Cartrol Oral, Ocupress Ophthalmic), labetalol (Normodyne, Trandate), levobetaxolol, levobunolol, meto prolol (Lopressor, Toprol XL), nadolol (Corgard), penbutolol (LevatoD, pindolol (Visken), propranolol CInderal), sotalol (Betapace AF, Betapace), timolol (Betimol, Blocadren, Timoptic-XE, Timoptic, Timoptic, OcuDose). Possible Side Effects. Lethargy and cold hands and feet because of reduced circulation may occur. Also may cause nausea, nightmares or vivid dreams, and impotence. May also precipitate asthmatic attack.
Calcium-Channel Blockers. Calcium plays a central role in the electrical stimulation of cardiac cells and in the mechanical con traction of smooth muscle cells in the walls of arteries. Calcium-channel blockers are relatively new synthetic drugs that work by blocking the passage of calcium into the muscle cells that control the size of blood vessels, thereby preventing the muscles of the arteries from constricting.
CHAPTER 19. PHARMACOLOGY FOR THE PHYSICAL THERAPIST
Examples include diltiazem (Cardizem), nicardipine (Cardene), nifedipine (Procardia, Procardia XL), nimodipine (Nimotop), and vera pamil (Calan, Isoptin, Verelan)
Possible Side Effects. Excessively slow heart rate, low blood pres sure, headache, swelling of ankle/feet, constipation, nausea, tiredness, dizziness, redness of face and neck, palpitations, and rash.
Digitalis Drugs. Like many drugs, digitalis was originally derived from a plant, in this case the foxglove. Digitalis has the primary effect of strengthening the force of contractions in weakened hearts, but it is not a cardiac vitamin that can make a strong heart stronger. It is also used in the control of atrial fibrillation. The most conunonly used digi talis products are digoxin (Lanoxicaps, Lanoxin) and digitoxin. The drug penetrates all body tissues and reaches a high concentration in the muscle of the heart. Its molecules bind with cell receptors that reg ulate the concentration of sodium and potassium in the spaces between tissue cells and in the bloodstream. Digitalis preparations act by increasing the amount of calcium supplied to the heart muscle, thus enhancing its contractions. By increasing the force of heart contrac tions, there is an increase in stroke volume. Digitalis drugs also affect electrical activity in cardiac tissues. They control the rate at which electric impulses are released and the speed of their conduction through the chamber walls. These two actions determine the two major uses of dig italis drugs in heart disease-treatment of heart failure and control of abnormal heart rhythms. Possible Side Effects. Some side effects include tiredness, nausea, loss of appetite, and disturbances in vision.
Diuretics. Diuretics, conunonly referred to as water pills, lower blood pressure by increasing the kidney's excretion of sodium and water, which in turn reduces the volume of blood. There are several types of diuretics, which are classified according to their site of action in the kidney. Possible Side Effects. Although unconunon, lethargy, cramps, rash, or impotence may occur. Some of these effects may be caused by loss of potassium and may be avoided by including a potassium supple ment or potassium-sparing agent in the regimen.
Nitrates. The oldest and most frequently used coronary artery medications are the nitrates. Nitrates are potent vein and artery dilators, causing blood to pool in the veins and the arteries to dilate, thus reduc ing the amount of blood returning to the heart. This has the effect of decreasing the work of the left ventricle and lowering the blood pres sure. Nitrates may also increase the supply of oxygenated blood by causing the coronary arteries to open more fully, thus improving coro nary blood flow. Nitrates effectively relieve coronary artery spasm. They do not, however, appear to affect the heart's contractions. Examples include nitroglycerin (Deponit NTG, Minitran, Nitro Bid, Nitrogard, Nitroglyn, Nitrol, Nitrolingual, Nitrong, Nitrostat, Transderm-Nitro, Tridil) and isosorbide dinitrate (Dilatrate-SR, Iso-Bid, Isordil, Sorbitrate, Sorbitrate SA)
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Possible Side Effects. Headaches, flushing, and dizziness. PULMONARY SYSTEM PHARMACOLOGY The delivery of a drug to the lungs allows the medication to interact directly with the diseased tissue and reduces the risk of adverse effects, specifically systemic reactions, and allows for the reduction of dose compared to oral administration. Most of the inhaled drugs are admin istered through a pressurized metered-dose inhaler. Dry powder inhalers or breath-activated devices are delivery devices that scatter a fine powder into the lungs by means of a brisk inhalation. The other major drug delivery system for pulmonary problems is the nebulizer, a device that dispenses liqUid medications as a mist of extremely fine particles in oxygen or room air for inhalation.
Bronchodilator Agents. Bronchodilator agents are a group of medications that produce an expansion of the lumina of the airway passages of the lungs. Bronchodilator agents are central to the symp tomatic management of chronic obstructive pulmonary disease (COPD) and asthma. ~
~
~
Beta z agonists: mimic the activity of the sympathetic nervous system (sympathomimetics), thereby producing relaxation of airway smooth muscle, bronchodilation. In addition, these medications inhibit inflammatory mediator release from mast cells and enhance mucociliary clearance. They are the most commonly prescribed drugs for the treatment of asthma. Beta z agonists can be categorized into short-acting (rescue drugs) and longer-acting agents. Examples of the short-acting types, which are used primarily for immediate release of break through symptoms of chest tightness, wheeZing, and short ness of breath, include Ventolin, Alupent, Maxair, albuterol, salbutamol, and terbutaline. Salmeterol, Serevent, and for moterol are examples of the longer-acting agents. Side effects of Beta z agonists include tremor, tachycardia, hypokalemia, and hyperglycemia. Anticholinergic agents: these drugs are primarily used in the treatment of COPD and asthma. The muscarinic receptor antag onists cause bronchodilation by blocking the action of acetyl choline on airway smooth muscle (inhibit the parasympathetic nervous system). Although these medications do not prevent all types of bronchospasm, they are effective against asthma produced by irritant stimuli. In general, dry mouth and pharyn geal irritation are the major side effects, but tachycardia may occur with excessive dosing. Theophylline: a methylxanthine, a substance found in coffee, tea, and chocolate, that acts as a phosphodiesterase inhibitor, which in turn increases intracellular cyclic adenosine monophosphate, resulting in relaxation of smooth muscle. The drug is used for patients who do not respond to the standard asthma agents, and is occasionally used in the treatment of spinal cord injury. Adverse side effects of this drug include nau sea, increased blood pressure, arrhythmias, tachycardia, nerv ousness, headaches, and seizures.
I f
CHAPTER 19. PHARMACOLOGY FOR THE PHYSICAL THERAPIST
Antiinflammatory Agents • Corticosteroids: steroids block the release of arachidonic acid from airway epithelial cells, which in turn blocks production of prostaglandins and leukotrienes. These drugs can be adminis tered systemically or topically (MDI). Inhaled steroids have been the drugs of choice for reducing the number of asthmatic attacks in patients who have mild to moderate persistent asthma and for those who require beta z inhalers more than once a day. Examples of inhaled steroids include beclometha sone, budesonide, and fluticasone. The side effects of systemic administration are increased blood pressure, glaucoma, sodium retention, muscle wasting, osteoporosis, and dyphonia. The main side effect of inhaled steroids is oral candidiasis, although the use of the spacer device and diligent rinsing of the mouth of the inhalation can decrease the effects. Examples of these medications include Vanceril (MDI) and Azmacort (MDI). • Leukotriene receptor antagonists: act by blocking the actions of leukotrienes that are released in an allergic reaction, decreasing the migration of eosinophils, production of mucus, and bron choconstriction. Examples of these drugs include montelukast and zafirlukast. Leukotriene receptor antagonists have demon strated few adverse drug reactions. • Cromolyn and nedocromil: act by inhibiting mast cell degranu lation (i.e., histamine) after exposure to allergens, thereby blocking the release of inflammatory mediators and thus decreasing airway hyperresponsiveness. These drugs are used prophylactically to prevent exercise-induced bronchospasm and severe bronchial asthma via oral inhalation. A benefit of these drugs is that they have relatively few side effects with the exception of a bitter taste. Frequent inhalation can result in hoarseness, cough, dry mouth, and bronchial irritation.
Antitussives. Antitussives are drugs that suppress coughing by decreasing the activity of the afferent nerves or decreasing the sensi tivity of the cough center. The stimulus to cough is relayed to the cough center in the medulla and then to the respiratory muscles via the phrenic nerve. Antibiotics.
Cultures and sensitivity results are used to prescribe the most effective antibiotic.
METABOLIC AND ENDOCRINE SYSTEM
Diabetes. Because patients with type II diabetes have both insulin resistance and beta-cell dysfunction, oral medication to increase insulin sensitivity (for example, metformin, a thiazolidine dione [TZDJ) is often given with an intermediate-acting insulin (for example, neutral protamine Hagedorn 49) at bedtime or a long-acting insulin (for example, glargine [Lantus] insulin, insulin detemir [LevemirJ) given in the morning or evening. Medications for diabetes are typically prescribed based on their mode of action. Examples include
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.. Exenatide (Byetta): incretin mimetic agent that mimics glucose dependent insulin secretion and several other antihyperglycemic actions of incretins. .. Chlorpropamide (Diabinese): may increase insulin secretion from pancreatic beta cells. .. Tolbutamide (Orinase): increases insulin secretion from pan creatic beta cells. .. Tolazamide (Tolinase): increases insulin secretion from pancre atic beta cells. .. Acetohexamide (Dymelor): increases insulin secretion from pancreatic beta cells. .. Glyburide (DiaBeta, Micronase, PresTab, Glynase): increases insulin secretion from pancreatic beta cells. .. Glipizide (Glucotrol, Glucotrol XL): second-generation sulfony
lurea; stimulates insulin release from pancreatic beta cells.
.. Repaglinide (Prandin): stimulates insulin release from pancre
atic beta cells. .. Metformin (Glucophage): monotherapy or with sulfony lurea, TZD, or insulin. Taken with food to reduce adverse GI effects. .. Acarbose (Precose): delays hydrolysis of ingested complex car bohydrates and disaccharides and absorption of glucose. Inhibits metabolism of sucrose to glucose and fructose. .. Miglitol (Glyset): delays glucose absorption in small intestine; lowers after-dinner hyperglycemia. .. Pioglitazone (Actas): improves target cell response to insulin without increasing insulin secretion from pancreas. .. Rosiglitazone (Avandia): insulin sensitizer; major effect in stim ulating glucose uptake in skeletal muscle and adipose tissue. .. Pramlintide acetate (Symlin): synthetic analog of human amylin, hormone made in beta cells. Slows gastric emptying, suppresses after-dinner glucagon secretion, and regulates food intake.
POLYPHARMACY AND MEDICATION ERRORS Polypharmacy is defined here as the long-term use of two or more medications. Many medications are absorbed, distributed, metabo lized, and excreted differently in the elderly. The presence of multiple diagnoses, particularly in the elderly, leads to multiple drug and nutri ent interactions and complex medical management, with the resulting side effects of progressive loss of functional reserve and physiologic homeostasis. 50 The National Coordinating Council for Medication Error Reporting and Prevention (NCC MERP) defines a medication error as "any pre ventable event that may cause or lead to inappropriate medication use or patient harm while the medication is in the control of the health care professional, patient, or consumer. Such events may be related to pro fessional practice, health care products, procedures, and systems, including prescribing; order communication; product labeling, pack aging, and nomenclature; compounding; dispensing; distribution; administration; education; monitoring; and use." The American Hospital Association lists the following as some common types of medication errors:
CHAPTER 19. PHARMACOLOGY FOR THE PHYSICAL THERAPIST ~
~ ~
~
~
~ ~ ~
~
Incomplete patient information (not knowing about patients' allergies, other medicines they are taking, previous diagnoses, and lab results, for example). Unavailable drug information (such as lack of up-to-date warnings). Miscommunication of drug orders, which can involve poor handwriting, confusion between drugs with similar names, mis use of zeros and decimal points, confusion of metric and other dosing units, and inappropriate abbreviations. Multiple providers often are unaware of one another's new prescriptions or medication changes, especially after hospitalization. Lack of appropriate labeling as a drug is prepared and repack aged into smaller units; and environmental factors such as light ing, heat, noise, and interruptions, that can distract health care professionals from their medical tasks. Drug name confusion. Examples of drug name confusion reported to the FDA include • Serzone (nefazodone) for depression and Seroquel (quetiap ine) for schizophrenia. • Lamictal (lamotrigine) for epilepsy, Lamisil (terbinafine) for nail infections, Ludiomil (maprotiline) for depression, and Lomotil (diphenoxylate) for diarrhea. • Taxotere (docetaxel) and Taxol (paclitaxel), both for chemotherapy. • Zantac (ranitidine) for heartburn, Zyrtec (cetirizine) for aller gies, and Zyprexa (olanzapine) for mental conditions. • Celebrex (celecoxib) for arthritis and Celexa (citalopram) for depression. Older patients often have visual or cognitive impairment (or both) that leads to errors in self administration. Older patients are often on fixed incomes and may cut doses down to save money. Cultural diversity can affect the perspective about the value of taking a certain medication when some natural alternative has been used for centuries in a culture to treat the same condition. Many older patients self-prescribe.
PHYSICAL THERAPY ROLE Assist in adequate monitoring of drug therapy through ~ ~
~ ~
Scheduling physical therapy to coincide with drug schedule to maximize the effects of the drug. Recognition of drug-related side effects/adverse reactions. This includes the interaction effects of modalities and certain med ications (the use of heat with patients on vasodilators). Being aware of potential drug interactions in the elderly. Monitoring of patient responses to medications relative to exer cise and activity.
Patient and family education/compliance ~ ~
Encourage centralization of medications through one pharmacy. Safe administration of drugs.
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Medication schedule, daily pillbox. Appropriate dosage and frequency.
AMPHETAMINES The phenylethylamine structure of amphetamines is similar to that of catecholaminergic, dopaminergic, and serotonergic agonists (biogenic amines), which may explain their actions, which are similar to those of cocaine; however, while effects of cocaine last for 10 to 20 minutes, duration of amphetamine action is much longer, lasting as long as 10 to 12 hours. The routes of amphetamine administration may be oral (ingestion), inhalation (smoke), or injection (IV). Patients with amphetamine intoxication often are identified by a change of mental status alone or associated with another injury and/or illness. ~
~
~
~ ~
~
Central nervous system: • Change of mental status, disorientation, and headache. • Dyskinesias. • Agitation. • Formication. • Symptoms of stroke. Cardiovascular: • Chest pain.
• Palpitations.
Gastrointestinal:
• Dry mouth. • Nausea and vomiting. • Diarrhea. Genitourinary (GU): difficult micturition. Skin/cutaneous: .t • Diaphoresis. • Erythematous painful rashes, needle marks. • Infected deep ulcerations (ecthyma). Ocular: mydriasis.
VITAMINS Vitamins are organic substances that must be provided in small quanti ties in the diet for the synthesis of cofactors, which are essential for metabolic function and cannot be manufactured by the body. Populations at risk for vitamin deficiency include ~ ~ ~ ~ ~
Infants and preschoolers.
Pregnant and lactating women.
The elderly.
People of a low socioeconomic status.
People with chronic disease states.
FAT-SOLUBLE VITAMINS Fat-soluble vitamins include vitamins A, D, E, and K. After being absorbed by the intestinal tract, these vitamins are stored in the liver
CHAPTER 19. PHARMACOLOGY FOR THE PHYSICAL THERAPIST
and fatty tissues. Fat-soluble vitamins require protein carriers to move through body fluids, and excesses of these vitamins are stored in the body. As these vitamins are not water-soluble, it is possible for them to reach toxic levels.
Vitamin A. Vitamin A helps prevent retardation of growth, protect skin integrity, and is essential to the eyes, epithelial tissue, and repro duction. Common food sources include green, orange, and yellow veg etables, liver, butter, eggs yolks, and fortified margarine. Signs and Symptoms of Deficiency ~ ~ ~ ~ ~
Keratomalacia (softening and subsequent ulceration and perfo ration of the cornea). Xerophthalmia (dryness and ulceration of the conjunctiva and cornea). Nyctalopia (night blindness). Growth failure. Rough and dry skin.
Signs and Symptoms of Toxicity ~ ~
~
Appetite loss. Hair loss. Enlarged liver and spleen.
Vitamin D. Vitamin D stimulates calcium absorption from the small intestine. It also increases the blood flow levels of minerals such as phosphorus. Common food sources include fortified milk, fish oils, and fortified margarine. Signs and Symptoms of Deficiency ~ ~ ~ ~ ~ ~
Rickets (in children of underdeveloped countries). Impaired growth. Skeletal abnormalities. Osteomalacia. Spontaneous fractures. Muscular tetany.
Signs and Symptoms of Toxicity ~
Calcification of soft tissues and other forms of hypercalcemia.
Vitamin E. Vitamin E functions as an antioxidant with exact mech anisms not clearly defined, but is said to stabilize cell membranes and preserve red blood cells, especially those that are constantly exposed to high levels of oxygen such as in the lungs. Common food sources include vegetable oils, wheat germ, nuts, and fish. Signs and Symptoms of Deficiency ~ ~
Abnormal red blood cell hemolysis (breakdown). Edema.
Signs and Symptoms of Toxicity ~. ~
Decreased thyroid hormone levels. Increased triglycerides.
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Vitamin K. Vitamin K is necessary for the synthesis of at least two of the proteins involved in blood clotting. Common food sources· include dark green leafy vegetables, cheese, egg yolks, and liver. Signs and Symptoms of Deficiency ~ Hemorrhage. ~ Defective blood clotting. Signs and Symptoms of Toxicity. Anemia.
WATER-SOLUBLE VITAMINS
Water-soluble vitamins include the B complex, vitamin C, biotin, choline, and folacin (folic acid). Water-soluble vitamins are not stored in the body in any significant amount, which significantly reduces the incidences of toxicity, but requires that they be included in the diet on a daily basis.
Thiamine (8 1), Thiamine metabolizes carbohydrates and has
been found to prevent beriberi and diseases of the nervous system. Common food sources include grains, meat, and yeast. Signs and Symptoms of Deficiency ~ Neurologic symptoms. ~ Cardiovascular symptoms. ~ Beriberi (in underdeveloped countries).
Riboflavin (8 2 ), Riboflavin facilitates selected enzymes involved in carbohydrate, protein, and fat metabolism. Common food sources include milk, green leafy vegetables, eggs, and peanuts. Signs and Symptoms of Deficiency ~ Angular stomatitis (inflammation at the corners of the mouth, associated with a wrinkled or fissured epithelium that does not involve the mucosa). ~ Inflammation of the tongue. ~ Photophobia with lacrimation. ~ Scaling of the skin.
Niacin (8 3 ), Niacin facilitates several enzymes that regulate energy metabolism. Common food sources include meats, whole grains, and white flour. Signs and Symptoms of Deficiency ~ Pellagra. ~ Diarrhea. ~ Dementia. ~ Dermatitis.
Pantothenic Acid (8 5 ), Pantothenic acid is found in living tis sue, and is essential for the metabolism of fatty acids and for the growth of some animals. Common food sources include liver, eggs, and whole grains.
CHAPTER 19. PHARMACOlOGY FOR THE PHYSICAL THERAPIST
Signs and Symptoms of Deficiency ~ ~
~ ~
Headache. Fatigue. Poor muscle coordination. Burning feet syndrome.
Pyridoxine (B 6 ). Pyridoxine is essential in the metabolism of pro teins, amino acids, carbohydrates, and fat. Common food sources include liver, red meats, whole grains, and potatoes. Signs and Symptoms of Deficiency ~ ~
~ ~
Peripheral neuropathy. Convulsions. Hyperirritability. Depression.
Cyanocobalamin (B 12 ). Cyanocobalamin is essential for the
functioning of all cells and aids in hemoglobin synthesis. Common food sources include meats, whole eggs, and egg yolks.
Signs and Symptoms of Deficiency ~
~
Pernicious anemia. Various psychological disorders.
Ascorbic acid (Vitamin C). Vitamin C performs many functions: ~ ~
~
Assists the body to combat infections. Facilitates wound healing. Necessary for the development and maintenance of bones, car tilage, connective tissue, and blood vessels.
Common food sources include citrus fruits, tomatoes, and cantaloupe.
Signs and Symptoms of Deficiency ~.
~
Anemia. Scurvy (spongy gums, loosening of the teeth, and bleeding into the skin and mucous membranes).
Biotin. Biotin is necessary for the action of many enzyme systems. Common food sources include liver, meats, and milk. Signs and Symptoms of Deficiency ~
~
~ ~ ~
Anemia. Depression. Muscle pain. Anorexia. Dermatitis.
Choline. Choline is a soluble ammonia derivative (amine) that is found in animal and plant tissue and is synthesized from methionine, which is an amino acid. Choline is an important component of com pounds necessary for nerve function and helps to prevent fat from being deposited in the liver.
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Folacin (Folic Acid). Folacin is involved in the formation of red blood cells and in the functioning of the gastrointestinal tract. Common food sources include yeast, dark green leafy vegetables, and whole grains. Signs and Symptoms of Deficiency ~
~
Impaired cell division. Alteration of protein synthesis.
MINERALS Minerals, like vitamins, are important nutrients found in foods. The main difference is that vitamins are organic substances (meaning that they contain the element carbon) and minerals are inorganic sub stances. There are two groups of minerals, major minerals and trace minerals (Tables 19-3 and 19-4).
DIETARY AND NUTRITIONAL SUPPLEMENTS CHONDROITIN SULFATE Chondroitin sulphate is a sulphur-containing polysaccharide found naturally in the body, and which is reportedly essential for joint cartilage healthy-54 Glucosamine is an amino-add-containing monosaccharide,
TABLE 19-3. MINERALS: SOURCES AND FUNCTIONS MINERAL
FUNCTION
COMMON FOOD SOURCES
S~ofM~orMme~
Calcium (Ca)
Phosphorus (P)
Magnesium (Mg)
Aids in formation of bones and teeth, normal blood clotting, muscle contraction and relaxation, heart function, and nerve function. Aids in formation of bones and teeth. Regulates release and use of body energy. Helps carry fat in the body as a part of phospholipids. Helps maintain normal acid-base balance in the body. Necessary for muscle contraction and nerve function.
Sodium (Na)
Important component of body fluids, mostly outside cells.
Potassium (K)
Important component of body flUids, mostly inside cells.
of Some Trace Mme~ Found in hemoglobin in red blood cells and myoglobin in muscle cells. Needed to carry oxygen. Iodine CO Part of thyroid hormones (thyroxin and triiodothyronine). Selenium (Se) Acts as an antioxidant. Zinc (Zn) Part of important enzyme systems. Found in the hormone insulin. Chromium (Cr) Helps body use insulin. Copper (Cu) Part of many enzymes. Fluoride (Fl) Part of teeth and bone. Helps prevent cavities in teeth.
Milk and other dairy products, greens broccoli, salmon, sardines, legumes. Meat, fish, poultry, eggs, milk, cereal products.
Meat, seafood, nuts, legumes, dairy products, whole grains. Table salt, meat, seafood, milk, cheese, eggs, baking soda, baking powder, bread, vegetables, processed foods. Potatoes, melons, citrus fruit, banana, and most fruits and vegetables, meat, milk, and legumes.
S~
Iron (Fe)
Liver, meats, egg yolks, nuts, enriched or whole grains, legumes. Seafood, iodized salt. Grains, meat, poultry, fish, dairy products. Meat, seafood, whole grains. Liver, brewer's yeast, whole grains, nuts, cheeses. Legumes, grains, nuts, seeds, organ meat. Fluoridated drinking water, fish, tea.
CHAPTER 19. PHARMACOLOGY FOR THE PHYSICAL THERAPIST TABLE 19-4. MINERALS SUPPLIED BY FOOD GROUPS FOOD GROUP
Milk Meats Fruits Vegetables Bread, cereals, and grains
MINERALS SUPPLIED
Calcium, phosphorus, and potassium Iron, copper, zinc, chromium, phosphorus, and sulfur Magnesium, manganese, potassium, and iron Potassium, magnesium, iodine, and selenium Iron, copper, zinc, manganese, magnesium, molybdenum, chromium, and phosphorus
concentrated in joint cartilage, which is used to synthesise cartilage gly cosaminoglycan (GAG). GAGs are large molecules comprising long branched chains of sugars and smaller nitrogen-containing molecules known as amino-sugars. The action of orally administered chondroitin sulfate has yet to be clarified. Possible actions include promotion and maintenance of the structure and function of cartilage (referred to as chondroprotection), pain relief of osteoarthritic joints, and antiinflammatory activity.
GLUCOSAMINE SULPHATE Glucosamine is used in the manufacture of very large molecules found in cartilage, called proteoglycans. 55- 58 These are large linear chains of repeating polysaccharide units (GAGs), which radiate out from a pro tein core like the bristles of a bottlebrush and can attract and hold water like a sponge. When compressed, this bound water helps to absorb force and distribute it equally, which explains the ability of car tilage to protect the joints under load and during movement. In the body, these GAG chains are synthesized from glucose, the amino acid glutamine, and sulphate, but there is plenty of evidence that additional supplementation not only increases GAG significantly but can also relieve the pain and inflammation associated with osteoarthritis.
REFERENCES 1. Brookfield WP. Pharmacologic considerations for the physical therapist. In: Boissonnault WG, ed. Primary Care/or the Physical Tberapist: Examination and Triage. St. Louis: Elsevier Saunders; 2005:309-322. 2. Brodie BB. Displacement of one drug by another from carrier or receptor sites. Proc R Soc Med. 1965;58:946-955. 3. Donne-Op den Kelder GM. Distance geometry analysis of ligand binding to drug receptor sites. ] Comput Aided Mol Des. 1987;1: 257-264. 4. Glossmann H, Striessnig], Hymel L, et al. Purification and recon stitution of calcium channel drug-receptor sites. Ann NY Acad Sci. 1988;522:150-161. 5. Schou ]S. Drug interactions at (pharmacodynamically active) receptor sites. PharmacolTber. 1982;17:199-210. 6. Watson PJ. Drug receptor sites in the isolated superior cervical gan glion of the rat. Bur] Pharmacol. 1970;12:183-193. 7. Ayrton A, Morgan P. Role of transport proteins in drug absorption, distribution and excretion. Xenobiotica. 2001;31:469-497.
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8. Davis SS, Wilding IR. Oral drug absorption studies: the best model for man is man! Drug Discov Today. 2001;6:127-130. 9. Fu XC, Liang WQ, Yu QS. Correlation of drug absorption with molecular charge distribution. Pharmazie. 2001;56:267-268. 10. Idkaidek NM, Abdel-Jabbar N. A novel approach to increase oral drug absorption. Pharm Dev Technol. 2001;6:167-171. 11. Jackson K, Young D, Pant S. Drug-excipient interactions and their affect on absorption. Pharm Sci Technol Today. 2000;3:336-345. 12. Kimura T, Higaki K. Gastrointestinal transit and drug absorption. Bioi Pharm Bull. 2002;25:149-164. 13. LinJ, Sahakian DC, de Morais SM, et al. The role of absorption, dis tribution, metabolism, excretion and toxicity in drug discovery. Curr TopMed Chem. 2003;3:1125-1154. 14. Stenberg P, Bergstrom CA, Luthman K, et al. Theoretical predic tions of drug absorption in drug discovery and development. Clin Pharmacokinet. 2002;41:877-899. 15. Kennedy JM, van Rij AM. Drug absorption from the small intestine in immediate postoperative patients. Br] Anaesth. 2006;97: 171-180. 16. Taki Y, Sakane T, Nadai T, et al. Gastrointestinal absorption of pep tide drug: quantitative evaluation of the degradation and the per meation of metkephamid in rat small intestine.] Pharmacol Exp Tber. 1995;274:373-377. 17. Bartal C, Danon A, Schlaeffer F, et al. Pharmacokinetic dosing of aminoglycosides: a controlled trial. Am] Med. 2003;114:194-198. 18. Davies JE. Aminoglycosides: ancient and modern. ] Antibiot (Tokyo). 2006;59:529-532. 19. Turnidge J. Pharmacodynamics and dosing of aminoglycosides. Infect Dis Clin North Am. 2003; 17:503-528. 20. Gouda MW, Khalafalah N, Khalil SA. Effect of surfactants on absorption through membranes V: concentration-dependent effect of a bile salt (sodium deoxycholate) on absorption of a poorly absorbable drug, phenolsulfonphthalein, in humans. ] Pharm Sci. 1977;66:727-728. 21. Riegelman S. The effect of surfactants on drug stability. 1. ] Am Pharm Assoc. 1960;49:339-343. 22. Utsumi I, Kono K, Takeuchi Y. Effect of surfactants on drug absorption. N. Mechanism of the action of sodium glycocholate on the absorption of benzoylthiamine disulfide in the presence of sodium laurylsulfate and polysorbate 80. Chem Pharm Bull (Tokyo). 1973;21:2161-2167. 23. Adams JF. The effect of some drugs and of differing routes of administration on the urinary excretion of parenteral vitamin B12. Clin Sci. 1963;24:431--435. 24. Benini A, Bertazzoni Minelli E. Parenteral administration of antimi crobial drugs can affect the intestinal microflora of rat. Pharmacal Res. 1992;25(suppl 1):75-76. 25. Collomp K, Anselme F, Audran M, et al. Effects of moderate exer cise on the pharmacokinetics of caffeine. Eur] Clin Pharmacol. 1991;40:279-282. 26. Jessup JV, Lowenthal DT, Pollock ML, et al. The effects of exercise training on the pharmacokinetics of digoxin. ] Cardiopulm Rehabil. 2000;20:89-95. 27. Khazaeinia T, Ramsey AA, Tam YK. The effects of exercise on the pharmacokinetics of drugs. ] Pharm Sci. 2000;3:292-302.
r' r
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CHAPTER 19, PHARMACOLOGY FOR THE PHYSICAL THERAPIST
28. Kim HJ, Lee AK, Kim YG, et al. Influence of 4-week and 8-week exercise training on the pharmacokinetics and pharmacodynam ics of intravenous and oral azosemide in rats. Life Sci. 2002;70: 2299-2319. 29. Persky AM, Eddington ND, Derendorf H. A review of the effects of chronic exercise and physical fitness level on resting pharmacoki netics. Int] Clin Pharmacol Ther. 2003;41:504-516. 30. Ylitalo P. Effect of exercise on pharmacokinetics. Ann Med. 1991; 23:289-294. 31. Frank S, Somani SM, Kohnle M. Effect of exercise on propranolol pharmacokinetics. Eur] Clin Pharmacol. 1990;39:391-394. 32. van Baak MA. Influence of exercise on the pharmacokinetics of drugs. Clin Pharmacokinet. 1990;19:32-43. 33. Dionne RA. Pharmacologic treatments for temporomandibular dis orders. Surg Oral Med Pathol Radiol Endodont. 1997;83:134-142. 34. Sperling RL. NSAIDs. Home Healthcare Nurse. 2001;19:687-689. 35. Holvoet J, Terriere L, Van Hee W, et al. Relation of upper gastroin testinal bleeding to nonsteroidal antiinflammatory drugs and aspirin: a case-control study. Gut. 1991;32:730-734. 36. Clive DM, Stoff JS. Renal syndromes associated with nonsteroidal antiinflammatory drugs. N Engl] Med. 1984;310:563-572. 37. Brattsand R, Linden M. Cytokine modulation by glucocorticoids: mechanisms and actions in cellular studies. Aliment Pharmacol Ther. 1996;1O(suppl 2);81-90; discussion, 1-2. 38. Buchman AL. Side effects of corticosteroid therapy. ] Clin Gastraenterol. 2001 ;33:289-294. 39. Elenbaas JK. Centrally acting oral skeletal muscle relaxants. Am] Hosp Pharm. 1980;37:1313-1323. 40. Charles PD, Davis n. Drug therapy for Parkinson's disease. South Medj. 1996;89:851-856. 41. Hagan JJ, Middlemiss DN, Sharpe PC, et al. Parkinson's disease: prospects for improved drug therapy. Trends Pharmacol Sci. 1997;18:156-163. 42. Hermanowicz N. Drug therapy for Parkinson's disease. Semin Neural. 2007;27:97-105. 43. Mizuno Y. Drug therapy of Parkinson's disease. An overview. Eur Neurol. 1992;32(suppl 1);3-8. 44. Oertel WH, Quinn NP. Parkinson's disease: drug therapy. Baillieres Clin Neurol. 1997;6:89-108. 45. Robertson DR, George CF. Drug therapy for Parkinson's disease in the elderly. Br Med Bull. 1990;46:124-146. 46. Stevenson T. Drug therapy in the management of Parkinson's dis ease. Br] Nurs. 1997;6:144. 47. Caird FI. Non-drug therapy of Parkinson's disease. Scott Med j. 1986;31:129-132. 48. Vanek ZF, Menkes JH. Spasticity. Available at: http://www.emedi cine. com/neuro/topic706. htm, 2005. 49. Spitzer G, Adkins D, Mathews M, et al. Randomized comparison of G-CSF + GM-CSF vs G-CSF alone for mobilization of periph eral blood stem cells: effects on hematopoietic recovery after high-dose chemotherapy. Bone Marrow Transplant. 1997;20: 921-930. 50. Bottomley JM. The geriatric population. In: Boissonnault WG, ed. Primary Care for the Physical Therapist: Examination and Triage. St. Louis: Elsevier Saunders; 2005:28&-306.
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51. Bana G, Jamard B, Verrouil E, et al. Chondroitin sulfate in the man agement of hip and knee osteoarthritis: an ovetview. Adv Pharmacal. 2006;53:507-522. 52. Sakai S, Otake E, Toida T, et al. Identification of the origin of chon droitin sulfate in "health foods." Chem Pharm Bull (Tokyo). 2007; 55:299-303. 53. Uebe1hart D, Knols R, de Bruin ED, et al. Treatment of knee osteoarthritis with oral chondroitin sulfate. Adv Pharmacal. 2006; 53:523-539. 54. Verbruggen G. Chondroitin sulfate in the management of erosive osteoarthritis of the interphalangeal finger joints. Adv Pharmacal. 2006;53:491-505. 55. Christgau S, Hemotin Y, Tanko LB, et al. Osteoarthritic patients with high cartilage turnover show increased responsiveness to the cartilage protecting effects of glucosamine sulphate. Cltn Exp Rheumatol. 2004;22:36-42. 56. Payne RB. Glucosamine sulphate and osteoarthritis. Lancet. 2001; 357:1617; author reply, 1618. 57. Rozendaal RM, Koes BW, Weinans H, et al. The effect of glu cosamine sulphate on osteoarthritis: design of a long-term ran domised clinical trial [ISRCTN54513166J. BMC Musculoskelet Disord. 2005;6:20. 58. Swinburne LM. Glucosamine sulphate and osteoarthritis. Lancet. 2001;357:1617; author reply, 1618.
CHAPTER 19. PHARMACOLOGY FOR THE PHYSICAL THERAPIST
Comprehension Questions
1. Which federally regulated agency directs the drug development process, and gives approval for the marketing of a new drug? 2. Under the Controlled Substances Act, which schedule of drugs includes those that can be abused and can result in some physical and psychological dependence?
3. What are the three types of drug names? 4. What is the study of how the body absorbs, distributes, metabolizes, and eliminates a drug called? 5. Movement across the cell membrane of various chemical substances occurs through which process? A. Diffusion, osmosis, active transport, pinocytosis, phagocytosis, exocytosis, and endocytosis. B. Passive transport. C. Cell membrane permeability. D. An interrelation between molecular and ionic particles. 6. Which of the following statements refers to membrane transport of uncharged mole cules in simple diffusion? A. An equilibrium results when opposite unidirectional fluxes are equal. B. The permeability coefficient varies directly with molecular size. C. If molecular concentration on either side is the same, no molecules can move across the membrane. D. Net diffusion occurs down a concentration gradient.
7. What are the primary routes of drug administration? 8. True or false: Routes of drug administration can include topical, transdermal, and inhalational. A. True. B. False. 9. True or false: Absorption of virtually all drugs is faster from the stomach than from the small intestine. A. True. B. False. 10. After entering the blood vessels of the intestinal tract, where does an absorbed drug go?
11. In which three ways can the absorption rate of a drug be manipulated? 12. True or false: According to the lirnited information available, exercise has asubstantial effect on the absorption of orally given drugs. A. True. B. False.
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13. Drug elimination can be broken down into which two major physiologic components? 14. What is adrug half-life? 15. Why is knowledge of the half-life of a drug critical? 16. Which of the two NSAID types, Cox-lor Cox-2, are safer to use in patients who are predisposed to gastric or kidney malfunctions? 17. You are treating a 72-year-old woman with a diagnosis of Parkinson's disease. You notice that the patient performs well on certain days and poorly on others. Which of the following ways can you possibly improve the patient's performance on the days when she performs poorly? A. Schedule the patient's sessions so that there are fewer sessions on the days the patient usually performs poorly. B. Call the physician and recommend another medication. C. Encourage the patient to decrease her daily dosage of medication to 400 mglday on the days she usually performs poorly. D. None of the above. 18. You are examining a 58-year-old man with Parkinson's disease. The patient reports that he is taking a medication for the disease but cannot remember its name. Which of the following medications is the patient probably taking? A. Levodopa. B. Cortisone. C. Beta-blocker. D. Glutamate blocker. 19. A patient asks you to explain the function of his medication Cardizem (a calcium channel blocker). Which of the following points should be included in your explanation? A. Cardizem causes decreased contractility of the heart and vasodilation of the coronary arteries. B. Cardizem causes decreased contractility of the heart and vasoconstriction of the coronary arteries. C. Cardizem causes increased contractility of the heart and vasodilation of the coro nary arteries. D. Cardizem causes increased contractility of the heart and vasoconstriction of the coronary arteries. 20. Following a myocardial infarction, a patient was placed on medications that included abeta-adrenergic blocking agent. When monitoring this patient's response to exercise, you would expect this drug to: A. Cause the heart rate to be low at rest, and to increase very little with exercise. B. Cause the heart rate to be low at rest, and to increase linearly with exercise intensity. C. Increase proportionally to changes in systolic blood pressure. D. Increase proportionally to changes in diastolic blood pressure.
CHAPTER 19. PHARMACOlOGY FOR THE PHYSICAL THERAPIST
Answers
1. The Food and Drug Administration (FDA). 2. Schedule III. 3. Chemical, generic, and trade/brand. 4. Pharmacokinetics. 5. The answer is A. 6. The answer is D. 7. Oral (enteral), including buccal and sublingual; rectal; and parenteral (intravenous, intramuscular, subcutaneous, and intra-articular). 8. The answer is A. This statement is true. 9. The answer is B. This statement is false. 10. To the liver. 11. Reducing the particle size of the drug, coupling the drug with a timed-release or sustained-release formulation, or coupling the drug with an enteric-coated (delayed release) formulation. 12. The answer is B. This statement is false. Exercise has no substantial effect. 13. Metabolism and elimination. 14. The rate at which a drug disappears from the body, through metabolism, excretion, or acombination. 15. To determine how often and in what dosage adrug must be administered to achieve and maintain therapeutic levels of concentration. 16. Cox-2. 17. The answer is A. 18. The answer is A. 19. The answer is A. 20. The answer is A.
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section
Appendix
1279
l
Appendix APPENDIX TABLE 1. INTERVENTION CATEGORIES
Therapeutic exercise may include perfonning: A. Aerobic capacity/endurance conditioning or reconditioning: (1) Gait and locomotor training. (2) Increased workload over time (modify workload progression). (3) Movement efficiency and energy conservation training. (4) Walking and wheelchair propulsion programs. (5) Cardiovascular conditioning programs. B. Balance, coordination, and agility training: (1) Developmental activities training. (2) Motor function (motor control and motor learning) training or retraining. (3) Neuromuscular education or reeducation. (4) Perceptual training. (5) Posture awareness training. (6) Sensol)' training or retraining. (7) Standardized, programmatic approaches. (8) Task-specific performance training. C. Body mechanics and postural stabilization: (1) Body mechanics training. (2) Postural control training. (3) Postural stabilization activities. (4) Posture awareness training. D. Flexibility exercises: (1) Muscle lengthening. (2) Range of motion. (3) Stretching. E. Gait and locomotion training: (1) Developmental activities training. (2) Gait training. (3) Device training. (4) Perceptual training. (5) Basic wheelchair training. F. Neuromotor development training: (1) Developmental activities training. (2) Motor training. (3) Movement pattern training. (4) Neuromuscular education or reeducation. G. Relaxation: (1) Breathing strategies. (2) Movement strategies. (3) Relaxation techniques. H. Strength, power, and endurance training for head, neck, limb, and trunk: (1) Active assistive, active, and resistive exercises (including concentric, dynamic/isotonic, eccentric, isokinetic, isometric, and plyometric exercises). (2) Aquatic programs. (3) Task-specific performance training. (Continued)
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APPENDIX TABLE 1. INTERVENTION CATEGORIES (Continued) 1. Strength, power, and endurance training for pelvic floor: (1) Active (Kegel).
J. Strength, power, and endurance training for ventilatory muscles: (1) Active and resistive.
Functional training in self-care and home management may include A. Activities of daily living (ADL) training: (1) Bed mobility and transfer training. (2) Age appropriate functional skills. B. Barrier accommodations or modifications. C. Device and equipment use and training: (1) Assistive and adaptive device or equipment training during ADLs (specifically for bed mobility and transfer training, gait and locomotion, and dressing). (2) Orthotic, protective, or supportive device or equipment training dUring self-care and home management. (3) Prosthetic device or equipment training during ADLs (specifically for bed mobility and transfer training, gait and locomotion, and dressing). D. Functional training programs: (1) Simulated environments and tasks. (2) Task adaptation. E. Injury prevention or reduction: (1) Safety awareness training during self-care and home management. (2) Injury prevention education during self-care and home management. (3) Injury prevention or reduction with use of devices and equipment. Functional training in work (job/schooVpIay), community, and leIsure integration or reintegration may include A. Barrier accommodations or modifications. B. Device and equipment use and training: (1) Assistive and adaptive device or equipment training during instrumental activities of daily living (IADLs). (2) Orthotic, protective, or supportive device or equipment training during IADLs for work. (3) Prosthetic device or equipment training during IADLs. C. Functional training programs: (1) Simulated environments and tasks. (2) Task adaptation. (3) Task training. D. Injury prevention or reduction: (1) Injury prevention education during work (job/schooVplay), community, and leisure integration or reintegration. (2) Injury prevention education with use of devices and equipment. (3) Safety awareness training during work (job/schooVplay), community, and leisure integration or reintegration. (4) Training for leisure and play activities. Manual therapy techniques may include A. Passive range of motion. B. Massage: (1) Connective tissue massage. (2) Therapeutic massage. C. Manual traction. D. Mobilization/manipulation: (1) Soft tissue (thrust and nonthrust). (2) Spinal and peripheral joints (thrust and nonthrust). Prescription, application, and, as appropriate, fabrication of devices and equipment may include A. Adaptive devices: (1) Hospital beds. (2) Raised toilet seats. (3) Seating systems-prefabricated. B. Assistive devices: (1) Canes. (2) Crutches. (3) Long-handled reachers. (4) Static and dynamic splints-prefabricated. (5) Walkers. (6) Wheelchairs.
SECTION IV. APPENDIX
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APPENDIX TABLE 1. INTERVENTION CATEGORIES (Continued) C. Orthotic devices: (1) Prefabricated braces.
(2) Prefabricated shoe inserts. (3) Prefabricated splints. D. Prosthetic devices (lower-extremity). E. Protective devices: (1) Braces. (2) Cushions. (3) Helmets. (4) Protective taping. F. Supportive devices: (1) Prefabricated compression garments. (2) Corsets. (3) Elastic wraps. (4) Neck collars. (5) Slings. (6) Supplemental oxygen-apply and adjust. (7) Supportive taping.
Airway clearance techniques may include A. Breathing strategies: (1) Active cycle of breathing or forced expiratory techniques. (2) Assisted cough/huff techniques. (3) Paced breathing. (4) Pursed lip breathing. (5) Techniques to maximize ventilation (e.g., maximum inspiratory hold, staircase breathing, manual hyperinflation). B. Manual/mechanical techniques: (1) Assistive devices. C. Positioning: (1) Positioning to alter work of breathing. (2) Positioning to maximize ventilation and perfusion. Integumentary repair and protection techniques may include A. Debridement-nonselective: (1) Enzymatic debridement. (2) Wet dressings. (3) Wet-to-dry dressings. (4) Wet-to-moist dressings. B. Dressings: (1) Hydrogels. (2) Wound coverings. C. Topical agents': (1) Cleansers. (2) Creams.
0) Moisturizers.
(4) Ointments. (5) Sealants. Electrotherapeutic modalities may include A. Biofeedback. B. Electrotherapeutic delivery of medications (e.g., iontophoresis). C. Electrical stimulation: (1) Electrical muscle stimulation (EMS). (2) Functional electrical stimulation (FES). (3) High-voltage pulsed current (HYPe). (4) Neuromuscular electrical stimulation (NMES). (5) Transcutaneous electrical nerve stimulation (TENS). (Continued)
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APPENDIX TABLE 1. INTERVENTION CATEGORIES (Continued)
Physical agents and mechanical modalities may include Physical agents: A. Cryotherapy: (1) Cold packs. (2) Ice massage. (3) Vapocoolant spray. B. Hydrotherapy: (2) Pools. (3) Whirlpool tanks: C. Sound agents: (1) Phonophoresis. (2) Ultrasound. D. Thermotherapy: (1) Dry heat. (2) Hot packs. (3) Paraffin baths. Mechanical modalities: A. Compression therapies (prefabricated): (1) Compression garments.
(2) Vasopneumatic compression devices. (3) Taping. (4) Compression bandaging (excluding lymphedema). B. Gravity-assisted compression devices: (1) Standing frame. (2) Tilt table. C. Mechanical motion devices: (1) Continuous passive motion (CPM). D. Traction devices: (1) Intermittent. (2) Positional. (3) Sustained. Data from Guide to physical therapist practice: Phys Ther. 2001;81:513-595.
SECTION IV. APPENDIX
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APPENDIX TABLE 2. GUIDE FOR CONDucr OF lliE PHYSICAL lliERAPIST ASSISTANT A. Purpose.
1. This Guide for Conduct of the Physical Therapist Assistant (Guide) is intended to serve physical therapist assistant in inter preting The Standards of Ethical Conductfor a Physical Therapist Assistant (Standards) of the American Physical Therapy Association (APTA). The Guide provides guidelines by which physical therapist assistants may determine the propriety of their conduct. It is also intended to guide the development of physical therapist assistant students. The Standards and Guide apply to all physical therapist assistants. These guides are subject to change as the dynamics of the profession change and as new patterns of health-care delivery are developed and accepted by the professional community and the public. This Guide is sub ject to monitoring and timely revision by the Ethics and Judicial Committee of the Association. B. Interpreting standards. 1. The interpretations expressed in this Guide reflect the opinions, decisions, and advice of the Ethics and Judicial Committee. These interpretations are intended to guide a physical therapist assistant in applying general ethical principles to specific situ ations. They should not be considered inclusive of all situations at a physical therapist assistant may encounter.
Standard 1 1. A physical therapist assistant shall respect the rights and dignity of all individuals and shall provide compassionate care. a. Attitude of a physical therapist assistant. 1) A physical therapist assistant shall recognize, respect and respond to individual and cultural difference with compassion and sensitivity. 2) A physical therapist assistant shall be guided at all times by concern for the physical and psychological welfare of patients/clients. 3) A physical therapist assistant shall not harass, abuse, or discriminate against others. Standard 2 1. A physical therapist assistant shall act in a trustworthy manner toward patients/clients. a. Trustworthiness. 1) A physical therapist assistant shall always place the patient's/client's interest(s) above those of the physical therapist assis tant. Working in the patients/client's best interests requires sensitivity to the patient's/client's and vulnerability and an effec tive working relationship between a physical therapist and a physical therapist assistant. 2) A physical therapist assistant shall not explOit any aspect of the physical therapist assistant-patient/client relationship. 3) A physical therapist assistant shall clearly identify him/herself as a physical therapist assistant to patients/clients. 4) A physical therapist assistant shall conduct him/herself in a manner that supports the physical therapist-patient/client rela tionship. 5) A physical therapist assistant shall not engage in any sexual relationship or activity, whether consensual or nonconsensual, with any patient/client entrusted to his/her care. 6) A physical therapist assistant shall not inVite, accept, or offer gifts or other considerations that affect or give an appearance of affecting his/her provision of phYSical therapy interventions. b. Exploitation of patients. 1) A physical therapist assistant shall not participate in any arrangements in which patients/clients are exploited. Such arrange ments include situations where referring sources enhance their personal incomes by referring to or recommending physical therapy services. c. Truthfulness. 1) A physical therapist assistant shall not make statements that he/she knows or should know are false, deceptive, fraudulent, or misleading. 2) Although it cannot be considered unethical for a physical therapist assistant to own or have a financial interest in the pro duction, sale, or distribution of products/services, he/she must act in accordance with law and make full disclosure of his/her interest to patients/clients. d. Confidential information. 1) Information relating to the patient/client is confidential and shall not be communicated to a third-party not involved in that patient's/client's care without the prior consent of the patient/client, subject to applicable law. 2) A physical therapist assistant shall refer all requests for release of confidential information to the supervising physical therapist. Standard 3 1. A physical therapist assistant shall provide selected physical therapy interventions only under the supervision and direction of a physical therapist. a. Supervisory relationship. 1) A physical therapist assistant shall proVide interventions only under the supervision and direction of a physical therapist. 2) A physical therapist assistant shall provide only those interventions that have been selected by the physical therapist. (Continued)
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APPENDIX TABLE 2. GUIDE FOR CONDUCT OF TIlE PHYSICAL TIlERAPIST ASSISTANT (Continued) 3) A physical therapist assistant shall not provide any interventions that are outside his/her education, training, experience, or
skill, and shall notify the responsible physical therapist of his/her inability to carry out the intervention. 4) A physical therapist assistant may modify specific interventions within the plan of care established by the physical therapist
in response to changes in the patient's/client's status. 5) A physical therapist assistant shall not perform examinations and evaluations, determine diagnoses and prognoses, or estab
lish or change a plan of care. 6) Consistent with a physical therapist assistant education, training, knowledge, and experience, he/she may respond to the
patient's/client's inquiries regarding interventions that are within the established plan of care. 7) A physical therapist assistant shall have regular and ongoing communication with a physical therapist regarding the
patienfs/client 's status.
Standard 4 1. A physical therapist assistant shall comply with laws and regulations governing physical therapy. a. Supervision. 1) A physical therapist assistant shall know and comply with applicable law. Regardless of the content of any law, a physical therapist assistant shall provide services only under the supervision and direction of a physical therapiSt. b. Representation.
1) A physical therapist assistant shall not hold him/herself out as a physical therapiSt.
Standard 5 1. A physical therapist assistant shall achieve and maintain competence in the provision of selected physical therapy interventions. a. Competence. 1) A physical therapist assistant shall provide interventions consistent with his/her level of education, training, experience, and skill. b. Self-assessment.
1) A physical therapist assistant shall engage in self-assessment in order to maintain competence.
c. Development. 1) A physical therapist assistant shall participate in educational activities that enhance his/her basic knowledge and skills. Standard 6 1. A physical therapist assistant shall make judgments that are commensurate with their educational and legal qualifications as a physical therapist assistant. a. Patient safety. 1) A physical therapist assistant shall discontinue immediately any intervention(s) that, in his/her judgment, may be harmful to the patient/client and shall discuss his/her concerns with the physical therapist. 2) A physical therapist assistant shall not provide any interventions that are outside his/her education, training, experience, or skill and shall notify the responsible physical therapist of his/her inability to carry out the intervention.
3) A physical therapist assistant shall not perform interventions while his/her ability to do so safely is impaired.
b. Judgments of patients/client status. 1) If in a judgment of the physical therapist assistant, there is a change in the patient/client status he/she shall report this to the responsible physical therapist c. Gifts and other considerations. 1) A physical therapist assistant shall not inVite, except, or offer gifts, monetary incentives, or other consideration that affect or give an appearance of affecting his/her provision of physical therapy interventions. Standard 7 1. A phYSical therapist assistant shall protect the public and the confession from unethical, incompetent, and illegal acts. a. Consumer protection.
1) A physical therapist assistant shall report any conduct that appears to be unethical or illegal.
b. Organizational employment. 1) A physical therapist assistant shall inform his/her employerCs) and/or appropriate physical therapist of any employer prac tice that causes him or her to be in conflict with the Standards of Ethical Conduct of the Physical Therapist Assistant. 2) A physical therapist assistant shall not engage in any activity that puts him or her in conflict with the Standards of Ethical Conduct for the Physical Therapist Assistant, regardless of directives from a physical therapist or employer. Data from the Ethics and Judicial Committee, American Physical Therapy Association, October 1981-Last Amended February 2004.
APPENDIX TABLE 3. ACID-BASE STATIJS TESTS TEST Arterial POz Arterial PCO z Arterial pH
Oxygen saturation
RELATED PHYSIOLOGY
REFERENCE RANGE EXAMPlE
Reflects the dissolved oxygen level based on the pressure it exerts on the bloodstream. Reflects the dissolved carbon dioxide level based on the pressure it exerts on the bloodstream. Reflects the free hydrogen ion concentration; collectively this test and the arterial POz and arterial PCO z tests help reveal the acid-base status and how well oxygen is being delivered to the body. Usually a bedside technique (pulse oximetry) to indicate the level of oxygen transport.
80-100 rom Hg 36--44 mm Hg 7.35-7.45
95-100%
Reproduced, with permission, from Wall LJ. Laboratory tests and values. In: Boissonnault WG, ed. Primary Care for the Physical Therapist: Examination and Triage. St. Louis: Elsevier Saunders; 2005:348-367. Copyright © Elsevier.
APPENDIX TABLE 4. TROPONIN LAB VALUES Normal Abnormal
Troponin I (TnI): Less than 0.3 IJglL Troponin T (TnT): Less than 0.1 IJglL Elevated troponin may be present with an injury to the myocardium. Blood levels of troponin typically rise within 4 to 6 hours after a heart attack, reach their highest levels within 10 to 24 hOUrs, and fall to normal levels within 10 days.
APPENDIX TABLE 5. TOTAL CREATINE PHOSPHOKINASE (CPK) Normal Abnormal
Men 55-170 lUlL Women 30-135 lUlL CPK levels generally rise within 4 to 8 hours after a myocardial infarction, peak within 12 to 24 hours, then return to normal within 3 to 4 days.
APPENDIX TABLE 6. CPK-MB LAB VALUES Normal Abnormal
Less than 3.0 nglmL (00;6 of total CPK) CPK-MB is found in large amounts in the myocardium. A CPK-MB level greater than 3.0 nglmL may be present with muscle damage as a result of a myocardial infarction. Blood levels of CPK-MB typically rise within 2 to 6 hours after a heart attack, reach their highest levels within 12 to 24 hours, and fall to normal levels within 3 days. An ongoing high level of CPK-MB levels after 3 days may mean that a heart attack is progressing and more heart muscle is being damaged.
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APPENDIX TABLE 7. SUMMARY OF CPR GUIDELINES
00 00
Lone Rescuer
Compression-to-ventilation ratio of 30:2 to be used for all victims from infants (excluding newborns) through adults. Rescuers may use 1 or 2 hands to give chest compressions for children.
All rescuers should take a normal breath (not a deep breath) before giv ing mouth-to mouth or mouth to-barrier device rescue breaths Each rescue breath should be given over 1 second.
Rescuers should press on the breastbone at about the nip ple line. For compressions for infants, rescuers should press on the breastbone just below the nipple line.
This recommendation applies to all rescuers.
Compression-to-ventilation ratio is 15:2 for 2-rescuer scenario
Each rescue breath should make the chest rise
When attempting defibrillation, all rescuers should deliver 1 shock followed by immediate CPR, beginning with chest compressions. All rescuers should check the victim's rhythm after giving about 5 cycles (about 2 minutes) of CPR.
Automated external defibrillators (AED) are recom mended for use in children 1 year of age and older. The evidence is insufficient to recommend for or against the use of AEDs in infants under 1 year of age
When more than 1 rescuer is present, rescuers should change "compressor" roles about every 2 minutes or 5 cycles of CPR (l cycle of CPR = 30 compressions and 2 rescue breaths). Rescuers should try to com plete the switch in 5 seconds or less
Further details can be accessed at http://www.americanheart.org/down]oadable/heart/1132621842912Winter2005.pdf
If the lay rescuer finds an unresponsive adult victim, the lay rescuer should open the airway and take 5 to 10 seconds (but no more than 10 seconds) to check for normall adequate breathing. If no normal! adequate breathing is present, the rescuer should give 2 rescue breaths. After delivering the first 2 rescue breaths, the lay rescuer should immediately begin cycles of 30 chest compressions and 2 rescue breaths. The lay rescuer should continue compressions and rescue breaths until an AED arrives, the victim begins to move, or professional responders take over. The healthcare provider will deliver 10 to 12 breaths per minute for an adult (approximately 1 breath every 5 or 6 seconds) and 12 to 20 breaths per minute for an infant or child (approxi mately 1 breath every 3 to 5 seconds). If despite adequate oxygenation and ventilation (or delivery of the 2 rescue breaths to the unresponsive victim) the heart rate of the infant or child is