Advances in Psychology Volume 67 Left-Handedness Behavioral Implications and Anomalies

ADVANCES IN PSYCHOLOGY 67 Editors: G. E. STELMACH P. A. VROON NORTH-HOLLAND AMSTEKDAM NEW YOKK OXFORD 'TOKYO LEFT-...

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ADVANCES IN PSYCHOLOGY

67 Editors:

G. E. STELMACH P. A. VROON

NORTH-HOLLAND AMSTEKDAM NEW YOKK OXFORD 'TOKYO

LEFT-HANDEDNESS Behavioral Implications and Anomalies

LEFT-HANDEDNESS Behavioral Implications and Anomalies

NORTI-I-l-1OL.I.AND AMSTERDAM NEW YORK OXFORD 'TOKYO

N OHTH -H( )I, 1, A N I) LLSEVIER SCIENCE PUBLISHERS B V Sara Burgerhartwaat 25 P.0 B o x 21 I 1000 A E Am\terdam. The Netherland\

L)i\trihutor\ for the United States and Canada: ELSEVIER SCIENCE PUBL.ISHING COMPANY, INC. 655 Avenue o f the Americas New York. N.Y. 10010. U.S.A.

L l b r a r y o f Congress C a t a l o g i n g - I n - P u b l i c a t i o n Data

Left-handedness S t a n l e y Coren.

b e h a v i o r a l i n p l ~ c a t i o n sand anomalies

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e d i t e d by

p. cm. -- (Advances i n psychology ; 6 7 ) I n c l u d e s b i b l i o g r a p h i c a l r e f e r e n c e s and indexes. ISBN 0-444-88438-6 1 . L e f t - a n d right-handedness. 2. L e f t and r i g h t ( P s y c h o l o g y ) I. Coren. S t a n l e y . 11. S e r i e s Advances l n psychology (Amsterdam. Netherlands) , 67. PP335.L44 1990 152.3'35--dc20 90-35954

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ISBN: 0 444 XX43X h @'

ELSEVIER SCIENCE PUBLISHERS B.V., I990

A l l rights reserved. N o part of this publication may he reproduced. stored i n :I retrieval system. or Iranamitted. in any forni or by any means. electronic. mechanical. photocopying. recording or otherwise. without tlie prior written permission o f the puhlisher. Elsevier Science Publishers B.V./ Physical Sciences and Engineering Division. P.O. Box 1991, 1000 B% Amsterdam. The Netherlands. Special regulations for readers iii tlie U.S.A. - This publication has heen I-egisteretl with the Copyright Clearance Cenier Inc. (CCC). Salem. M chusetts. Inlormation can he obtained from the CCC about conditions under which photocopies of parts of this publication nay be made i n the U.S.A. A l l other copyright questions. including photocopying ourside o f the U.S.A.. should hc referred to the copyright owner. Elsevier Science Publishers B.V.. unless otherwise specified. N o responsibility i s n\sumetl by the Publisher for any injury and/or damage to persons or property as a matter o f products liability. negligence or otherwise. or from any use or operation of any methods. products. instructions or ideas contained i n the materi;il herein. Printed in The Netherlands

V

Table of Contents Preface

xiii

Contributors

xvii

SECTION I: BIRTH STRESS AND INTRAUTERINE FACTORS

1. Birth Stress and Left-Handedness: The Rare Trait Marker Model Stanley Coreit and AIari Searlenian

3

Rare Traits and Pathological Conditions 7 Left-Handedness and the Rare Trait Marker Model 9 Factors that Influence the Association between Pathology and the Rare Trait 14 Experimental Assessment of Birth Risk Factors and Handedness 17 Application of the Rare Trait Marker Model 18 Is Left-Handedness a Good Marker for Pathology? 25 Conclusions and Future Directions 27 Acknowledgements 30 References 30

2. NonRight-Handedness and the Continuurn of Reproductive Casualty Paul Bakari The Continuum of Reproductive Casualty 33 Implications of the Reproductive Casualty Context for NRH 35 Historical Approaches to Reproductive Casualty 35 Recent Approaches to NRH and Pathology 45 The Comorbidity Factor 52 The Hypoxia Connection 59

33

vi

Contents NRH and Reproductive Casualty: Small Effects and Negative Results 61 Summary 63 References 64

3. Left-Handedness and Prenatal Complications Murray Schwartz Genetic Theories of Handedness 77 Environmental/Cultural Theories of Handedness Prenatal Hormonal Theory 79 Prenatal Pathological Theory 79 Summary 92 References 93

75

78

4. Intrauterine Factors in Sinistrality: A Review Michel Habib. Florence Tome and Albert M. Galaburda

99

Geschwind's Theories of Handedness and Origins of Sinistrality (1982-1985) 100 Anatomical Observations 102 Hormonal Influences on the Development of Asymmetry 106 Pathological Associations of Left-Handedness 115 Fetal Position, Birth Circumstances, and Handedness 118 Acknowledgements 122 References 122

SECTION 11: PHYSIOLOGICAL AND GENETIC FACTORS

5. Laterality in Hemiplegic Children: Implications for the Concept of Pathological Left-Handedness Mem'll Hiscock arid Cheyl K. Hiscock

131

Contents Background 131 Objectives 134 The Study 134 Implications for Pathological Left-Handedness Hypothetical Characteristics of Pathological Left-Handers 148 Conclusions 149 Acknowledgements 150 References 150

144

6. The Neuroanatomy of Atypical Handedness in Schizophrenia Paul Satz, Michael Foster Green, Steven Ganzell, George Bartzokis, Anthony Bledin, and Joseph F. Vaclav Introduction 153 Method 156 Results 159 Discussion 161 Acknowledgements References 163

vii

153

163

7. Phenotype in Normal Left-Handers: An Understanding of Phenotype is the Basis for Understanding Mechanism and Inheritance of Handedness Michael Peters 167 Pathology as Basis for a Phenotypical Distinction? 170 Phenotype as Established by Questionnaire 173 Subclassification of Left-Handers by Preference and Performance A Meaningful Subclassification of Nonpathological Left-Handers? Summary and Conclusions 189 References 190

177 185

viii

Contents

SECTION 111: ENVIRONMENTAL FACTORS

8. Cultural Influences on Handedness: Historical and Contemporary Theory and Evidence Lauren Julius Ham's

195

Historical Evidence 197 Current Evidence 217 Further Questions 231 References 245

9. Switching Hands: A Place for Left Hand Use in a Right Hand World Clare Porac, Laura Rees arid Tern. Buller

Switching Hands: Who, How, When and Why Summary and Conclusions 276 Acknowledgements 285 References 286

259

266

SECTION N: COGNITIVE, SPATIAL AND LANGUAGE ABILITY IMPLICATIONS

10. Mental Retardation and Left-Handedness: Evidence and Theories Margaret-Elleii Pipe

Left-Handedness in Retarded Groups Theoretical Accounts 302 Conclusion 313 Acknowledgements 314 References 314

294

293

Contents

ix

11. Handedness, Sex, and Spatial Ability

Richard S. Lewis arid Lauren Julius Harris Left-Handedness and Spatial Skill Spatial Ability in Left- and Right-Handed "High Reasoners" Conclusions 335 References 336

319

320

328

12. Handedness and Its Relationship to Ability and Talent Michael W. O'Boyle and Camilla Persson Benbow

343

The Left Hand Deficit Hypothesis 343 Factors Moderating Relations of Handedness with Ability 346 Strength of Handedness, Familial Sinistrality and Sex 346 Familial Sinistrality and Brain Lateralization 350 Immune Disorders 353 Age and Hand Consistency 354 Reasoning Ability Level 355 Handedness and Talent 356 Mathematical Precocity 358 A Reanalysis of Benbow (1986) 360 Concluding Comment 364 References 365

13. Familial Sinistrality and Cerebral Organization

Walter F. McKeever Clinical Studies 375 Experimental Studies of Normal Subjects 381 Summary of Demonstrated and Suggested Correlates of FS The Difficulty of Assessing FS Influences: Suggested Strategies 402 References 407

373

401

x

Contents

SECTION V: PSYCHOLOGICAL AND SPATIAL IMPLICATIONS

14. Sinistrality and Psychopathology

Pierre Flor-Henry

415

Sinistrality and Psychosis 417 Sinistrality in Autism and Childhood Schizophrenia Sinistrality in Monozygotic and Dizygotic Twins with Schizophrenia 423 Sinistrality and Mood 426 Conclusion 431 References 435

423

15. Autism and Anomalous Handedness

Susan E. Byson Chapter Overview 441 Current Thought on Autism 442 Handedness and Autism 444 Theoretical Accounts 446 The Geschwind-Galaburda Hypothesis Summary and Conclusions 450 Directions for Future Research 450 Acknowledgemenl 453 References 453

441

448

16. Left-Handedness and Alcoholism

Wayne P. London Increased Frequency of Left-Handedness in Alcoholic Men Left-Handedness and Treatment Outcome 459 Left-Handedness and Having an Alcoholic Father 460 Cerebral Laterality and the Study of Alcoholism 462 Alcoholism and Thyroid Disorders 464 Prenatal Environmental Effects 465

457 458

Contents

Season of Birth 466 Correlations with Latitude 469 Left-Handedness and Seasonal Sensitivity 471 Left-Handedness and Light Pigment 472 Left-Handedness and Life Expectancy 473 Alcoholism and Creativity 474 Alcoholism and Other Neurological Phenomena Issues of Methodology 477 Conclusions 480 Acknowledgement 480 References 480

xi

475

17. Left- and Mixed-Handedness and Criminality: Explanations for a Probable Relationship Lee Ellis

485

A Review of Evidence for an Association between Criminality and Sidedness 486 Possible Explanations for HandednessCriminality Associations 488 A Model of How Sex Hormones Influence Hemispheric Functioning in Ways that May Influence Handedness and Criminality 497 Discussion and Conclusions 498 Acknowledgement 500 References 500

18. Laterality and Longevity: Is Left-Handedness Associated with a Younger Age at Death? Diane F. Halpeni arid Stanley Coren

Right-Handedness as the Human Norm 510 Why Left-Handedness? 511 Is Left-Handedness Genetic? 512 Is Left-Handedness Learned? 513 Is Left-Handedness the Result of Pathology? 517 Prenatal and Perinatal Stressors and Sinistrality 518

509

xii

Contents

Variability in Cognitive Functioning 521 Immune System Disorders 523 Alcoholism and Smoking 527 The Alinormal Syndrome 528 Left-Handedness and Mortality Risk 530 Left-Handedness and Environmental Risk Factors Sinistrality and Longevity: Archival Data 533 Left-Handedness and Mortality: Next of Kin Data Are Left-Handers at Increased Risk of Mortality? Acknowledgements 541 References 541

531

537 540

Name Index

547

Subject Index

563

xiii

Preface There is a long history of fascination with handedness. Early references to it can be found in the Bible and appears in some Egyptian tomb writings. The problem of hand preference has caught the attention of many historical thinkers and scientists including Charles Darwin,Benjamin Franklin and Thomas Carlyle. Several early psychologists, such as G. Stanley Hall, James Mark Baldwin, William James and John Watson, have written on the subject. Many of these writings have included speculation about differences between left-and righthanders that transcend the simple asymmetry in manual skill, and suggest that sinistral individuals have psychological and physiologicalcharacteristicsthat make them quite different from their dextral counterparts. Advocates of this viewpoint have pointed to examples from numerous disparate cultures that have associated left-handednesswith evil, weakness, disease, and treachery. In fact the very word lejl comes from the Celtic Lyft, meaning we& or broken. The French word for left is guuclie, which has been adopted in Engllsh with the meaning of uwkward or guwky, while the Latin word for left, sinister, has come to mean evil or unfomtnate, and these examples could be multiplied many times. These traditions reflect the underlying presumption that right-handedness is associated with nonnaiity as opposed to the abnonalify or pathology of left-handedness. Such traditions and linguistic conventions, of course, do not constitute real evidence that there is something different, or anomalous, about left-handers. They do, however, define the context in which investigatorsbegan to consider the possibility that left-handedness might be due to some form of pathological intervention, or perhaps u markerfor some underlying pathology. Over the past several decades, a vast amount of data has been collected on this issue. Some of this data has suggested that left-handedness may be due to birth traumas or intrauterine hormonal imbalances. Other researchers have found linkages between sinistrality and sleep disturbances, retardation, autism, schizophrenia, dyslexia, criminality, alcoholism, homosexuality, bedwetting, verbal and spatial ability, cerebral organization, creativity, minor brain damage, level of neural maturation, and even reduced longevity. This book gathers together a number of researchers who will present evidence and evaluate whether there are actually differences between left- and right-handers, which extend into the broader psychological and physiological realms. The book is divided into five major sections, each of which deals with a different aspect of the problem. The first section deals with some recent suggestions that, for a large segment of left-handers, their sinistrality is due to some forms of pathological factors

xiv

Preface

associated with pregnancy and birth, with particular emphasis being placed upon the conditions surrounding the actual delivery and the intrauterine environment. The chapter by Coren and Searleman, proposes a general model, which explains why one might expect that a higher proportion of pathological conditions would be found to be associated with left-handedness. The chapter by Bakan explores the specifics of the perinatal and birth circumstances to show how lefthandedness can result from pathological factors, although Schwartz, in his chapter, sounds a warning that the association between pathology and sinistrality may not always be very marked. Finally, Habib, Touze and Galaburda describe the effects of hormonal factors and other factors during gestation, that may serve to shift handedness away from the right-handed norm. The second section presents three chapters that use different techniques to study the brain organization and implications of left-handedness. AU three suggest that there may be several subgroups of left-handers. The specific techniques used to reach this conclusion are quite different, ranging from Hiscock and Hiscock’s study of hemiplegiacs, through Satz, Green., Ganzell, Bartzokis, Bledin, and Vaclav‘s use of magnetic resonance imagery to Peters’ use of some clever behavioural indexes. The third section of this volume provides an exploration of the question of whether cultural, environmental or learning factors can alter manifest handedness. In his chapter, Harris presents an historical and cross-cultural discussion of the various pressures that have been placed on left-handers to become right-handed. Porac, Rees and Buller review some cross-cultural differences in the distribution of handedness and also provide some direct empirical evidence of the effectiveness of trying to change handedness through direct intervention. The fourth section of the book discusses the possibility that left-handedness may be a marker that predicts aspects of an individual‘s cognitive abilities. Pipe opens this discussion with a review of the relationship between retardation and an elevated incidence of left-handedness. In their chapter, Lewis and Harris suggest that the relationship between handedness and spatial ability may be clarified if more is known about cerebral laterality. O’Boyle and Benbow go on to demonstrate that left-handedness may be over-represented in both extremes of cognitive ability, both the cognitively impaired and the precocious. In his chapter, McKeever looks at the cerebral organization of language processing in individuals that have a familial history of left-handedness. The fmal section of the book contains some of the most diverse and controversial material in this volume. It looks at some of the psychological and

Preface

xv

physical factors that have been shown to be associated with left-handedness. In his chapter Flor-Henry explores the possibility that left-handedness may be elevated in groups of patients with clinical depression and other forms of psychopathology.Bryson’s contribution extends this discussion into the realm of autism. In the next chapter, London suggests that left-handers may have an increased susceptibility to alcoholism. Ellis returns us to a more behavioural level when he attempts to tease apart the suggestion that there may be an association between criminality and increased incidence of left-handedness. In the fmal chapter, Halpern and Coren attempt to tie together many of these fmdings. Following a consideration of some of the behavioural and physiological differences between left- and right-handers, and with the introduction of some new data, they reach the startling conclusion that left-handers may actually have a shorter life span than their right-handed contemporaries. My hope in collecting all of this material together in one place, is that we will now be better able to assess whether handedness is an indicator of psychological and physiological predispositions that have consequences for our understanding of broader aspects of behaviour. In so doing, I hope that we are closer to learning whether left-handers are indeed different, pathological, or disadvantaged, or whether they are merely a misunderstood and maligned minority.

Acknowledgements During the preparation of this book, my research has been supported by grants from the Medical Research Council of Canada, the Natural Sciences and Engineering Research Council of Canada, and the British Columbia Health Care Research Fund. Finally, let me acknowledge the assistance of Tania Jackson, without whose efforts this book would not have been completed, and also the assistance of David Wong and Wayne Wong who have run my laboratory in a manner that allowed me the time to finish this task. I also must acknowledge Joan, Flint and Wiz, who keep that other portion of my life in working order. Stanley Coren Vancouver, 1990

This Page Intentionally Left Blank

xvii

Contributors Paul Bakan Department of Psychology Simon Fraser Uniwrsity George Barnoliis Department of Psychiatry and Biobehavioral Sclenccs University of California, Los h g e l e s Camilla P e w n Bcnbow Department of Psychology Iowa State University Anthony Bledin Medical Diagnostic Imaghg Thousand Oaks, C X Susan E. Bryson

Department of Psychology Unive rsity of G uelph Terri Buller Department of Psychology University of Bntsh Columbia Stanley Corm Department of Psychology University of British Columbia Lee Ellis Department of Sociology Minot State Uniwnity Pierre nor-Henry Department of Psychiatry University of Alberta

Michael Foster Green Department of Psychiatry and Biobehavioral Sciences University of California, LQS h g e l e s Michel H. Habib Department of Neuropsychology Centre Hospitalier University d e Marseille Diane F. Halpcrn Department of Psychology California State University, San Bcmardino Lauren Julius Harris Department of Psychology Michigan State Univenity Cheryl K. Hiscock

The Methodist Hospital Houston, TX Menill Hiscock Department of Psychology University of Houston Richard S. Lewis Department of Psychology Pomona College Wayne P. London Dartmouth Medical School Walter F. McKeever Department of Psychology Northern Arizona University

Albert M. Galabunla Hanard Medical School

Michael W. O'Boyle Department of Psychology Iowa State University

Steven Ganzell Department of Psychiatry and Biobehavioral Sctences University of California, Los Angeles

Michael Peters Department of Psychology University of Guelph

xviii Margaret-Ellen Pipe Department of Psychology University of Otago

Alan Searleman Department of Psychology St. Lawrence University

Clare Porac Department of Psychology University of Victoria

Florence Touze Department of Neuropsychology Centre Hospitalier University de Marseille

Laura Rees Department of Psychology Carleton University Paul Satz Department of Psychiatry and Biobehavioral Sciences University of California, Lw Angeles Murray Schwam Department of Psychology Victoria General Hospital, Halifax

Joseph F. Vaclav Department of Psychiatry and Biobehavioral Sciences University of California, Los Angeles

SECTION I: BIRTH STRESS AND INTRAUTERINE FACTORS

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LEFT-HANDEDNESS Behavioral Implications and Anomalies, S. Coren (Editor) 0 Elsevier Science Publishers B.V. (North-Holland), 1990

3

Chapter 1

Birth Stress and Left-Handedness The Rare Trait Marker Model Stanley Coren University of British Columbia and Alan Searleman St. Lawrence University Given the fact that approximately nine out of every ten individuals is right-handed, it is understandable that left-handers have often been viewed as, not just a minority, but as if they were "different" or "strange." Perhaps it is this attitude that explains why there is such a long history of attempts to explain why some individuals deviate from the dextral norm. For instance, one philosophical note, dated 1686, refers to left-handedness as a "digression or aberration from the way which nature generally intendeth (quoted in Wile, 1934, p.92). Around the turn of the century, a series of experimental studies began to show that left-handedness was more prevalent in selected "non-normal" populations such as retardates, criminals, epileptics etc. (Lombroso, 1903; Redlich, 1908; Woodruff, 1909). This rapidly led to the hypothesis that left-handedness might be more than a marker for other deficits, but rather that left-handedness itself may be an aberration. The general tone of this early theorizing about the pathological genesis of left-handedness is well summarized by Brewster (1913) who noted:

4

Coren and Searleman A sound and capable stock, like a right-handed one, breeds true generation after generation. Then something slips a cog, and there appears a left-handed child, a black sheep, or an imbecile. (p. 183)

He makes it clear that slipping a cog refers to some form of damage or insult that results in the left-handed tendencies when he continues: An adult brain, wrecked on the educated side by accident or disease, commonly never learns to do its work on the other; the victim remains crippled for the rest of his days. But a child in whom the thinking area on the other side is still uncultivated, hurt on one side, can usually start over again with the other. A shift of this sort carries the body with it, and the child, instead of being permanently disabled, becomes left handed. (p. 179) Wilhelm Fliess, who, in addition to being a physician and a biologist, was Sigmund Freud’s closest friend, associated left-handedness with several pathological conditions, including homosexuality. In 1906 he wrote: Where lefthandedness is present, the character pertaining to the opposite sex seems more pronounced ... Since degeneracy consists in a displacement of the male and female qualities, we can understand why so many left-handed people are involved in prostitution and criminal activities. (quoted in English by Fritsch, 1968, p. 133) Other deviations in personality, cognitive ability or character were also often associated with left-handedness. In his book, The Backward Child, Cyril Burt (1937) notes:

if it is even safe to treat left-handedness as a sign or symptom, it should be regarded rather as a mark of an ill-organized nervous system. (p. 287) While Blau (1946) also wants to use sinistrality as a pathological marker, but for psychopathology:

Rare Trait Marker Model

5

Sinistrality thus can be used a cue by the psychiatrist in his studies of people with personality difficulties... Sinistrality may then be regarded not only as a neurotic symptom but as one of the signs of an infantile psychoneurosis. (p. 96 and 115) Most of these theorists suggest that there is something congenital about the pathological condition that leads to left-handedness. The congenital aspect refers either to some form of genetic malfunction (e.g., a chromosomal abnormality) or to damage during pregnancy or delivery. Gordon (1921), who looked at handedness in 3,298 normal children, compared to 4,620 children in schools for the retarded, provides a good example of this early theoretical presumption of an association between left-handedness and pathological birth processes. After concluding that there was a higher percentage of left-handed children in "mental defective" as opposed to normal elementary schools, Gordon proposed: It also seems probable that the percentage of naturally left-handed in mental defective schools may be no higher than that in ordinary schools, the increased percentage being due to some cause that has brought about the change, before birth, at birth, or at some subsequent date. (p. 334, emphasis added) Harris and Carlson (1988) make a distinction between a one-type model of left-handedness, that maintains that all left-handedness is pathological, and a two-type model, that maintains that there are two types of left-handedness, one of which is pathological in origin and one that is not. Although most of the researchers discussed above seem to have adopted the one-type (all pathological) model, some other theorists were hesitant to claim that all left-handers were to be regarded as being pathological in some way. Thus, contemporary with some of the earlier researchers mentioned above, was the geneticist H. E. Jordan (1922) who maintained that left-handedness "is not necessarily a stigma of inferiority" (p. 379). He wanted to distinguish between "pure" (presumably genetically based) left-handedness "which constitutes the bulk of the left-handed population" and the subset of anomalous left-handedness that marks some neurological or psychological problem. His viewpoint has generally been accepted by modern theorists, since today it is common to distinguish between presumably genetic left-handers and an additional group commonly designated

6

Coren and Searleman

as pathological left-handers (Satz, 1972, 1973; Satz, Orsini, Saslow, and Henry, 1985; Silva and Satz, 1979). However, this distinction still recognizes the other side of the coin, in other words, that left-handedness may come about through some form of neurological insult or genetic damage. Why is left-handedness often perceived as not merely an indication that the individual displaying the trait is different, but also that the individual is somehow inferior, or damaged? It is easy to demonstrate that the left side in general, and the left hand in particular, has come to be associated with something impure, imperfect, or even evil. This shows itself in many ways. For example, Wile (1934) found some 80 references in the Bible to the right hand, each according to it honours, virtues, and powers. However, Wile reports that "there is not one honourable reference to the left hand." Such negative and disparaging attitudes have found their way into the language as well. For instance, the French word gauche means both left and also clumsy, and has been adopted into English as the word gawky. The German word for left is links, and carries a strong negative connotation that is used pejoratively in forms such as linkisch, meaning clumsy. The word "left" itself comes from a similar negative source, namely the Celtic lyjt meaning weak or broken. In Spanish there is an idiom no ser mrdo that has come to mean "to be very clever," however, the literal translation of the phrase is "not to be left-handed." The Italian word ritancino not only means a left-handed man, but also a dishonest one as well. As a final example, in Australia, a slang term for left-hander is mol$-dooker, where "dook or "duke" is slang for hand, while "molly" is an effeminate man. The reason for all of this bad press for left-handers may not simply be due to the attitude that "different is bad," but may actually have some basis in fact. A number of researchers have reported that increased proportions of left-handers are found in a variety of groups with special problems (Molfese & Segalowitz, 1988; Porac & Coren, 1981; and of course this volume itself, all contain several chapters reviewing these sometimes controversial data). Some of the problems or conditions that have been positively correlated with lefthandedness include: 1) 2) 3) 4) 5)

brain damage epilepsy reading disability neuroticism alcoholism


7

drug abuse homosexuality aggression criminality mental retardation allergies autoimmune disorders migraines emotionality birth stress chromosomal damage poor spatial ability poor verbal ability school failure attempted suicide autism psychosis vegetarianism sleep difficulty slow maturation

Rare Traits and Pathological Conditions There's an interesting observation, that rare traits are often markers for neurological, physical, or genetic deficits. While, at first blush, this seems inexplicable, it is, nonetheless, a valid observation. For instance, rare coloured animals, whether it be a "blue-marl" collie or an albino human, often have major sensory deficits affecting their vision or hearing. Rare physical markers or characteristics, even though their only apparent effects are cosmetic, often show an association with various physical deficits. Consider the following list of relatively rare physical characteristics. 1) 2)

3) 4)

two or more whorls in the hair low seated ears asymmetrical ear heights adherent ear lobes

8

Coren and Searlernan

fifth finger curved third toe as long or longer than the second toe webbing or partial adhesion between the two middle toes overly large gap between first and second toe tongue furrows one lateral flexion crease across the palm instead of two lower lateral flexion crease continues to the edge of the hand fine "electric" uncombable hair many radial loops in the fingerprint patterns The interesting parallel to our discussion of left-handedness is that these so called "minor physical anomalies," which, of themselves, seem to have no particular linkage to psychological or neurological status, have, in fact been associated with a number of problems (see, for example, Bell & Waldrop, 1982; Campbell, Geller, Small, Petti & Ferris, 1978; Krouse & Kauffman, 1982). Some of the problems or conditions that have been associated with these rare features are: attention deficits hyperactivity aggression impulsivity emotionality mental retardation brain damage autism neuroticism low spatial ability low verbal ability psychosis learning disability delinquency

One might notice a degree of overlap between this list and the list previously mentioned as being associated with left-handedness. Is there something in


9

common between left-handedness and a curved fifth finger, an overly long third toe, or the existence of two hair whorls? Yes there is. The common factor, however, is a statistical one. The crucial similarity is that left-handedness and all of these other features that we have mentioned are relatively rare. We believe that such rare features (defined as statistically uncommon or infrequently occurring in the population) will often be associated with "problems" of a psychological or a physiological nature. This association between rare traits and pathological conditions is not capricious, but can be shown to be theoretically predictable, as we shall see below.

Left-Handedness and the Rare Trait Marker Model Since left-handedness is only present in about one out of every ten individuals, it may be classified as a relatively rare behavioural trait. Based simply on statistical considerations, it is possible to predict (even in the absence of any specific physiological mechanism) that left-handedness will be associated with an increased degree of pathology. The theoretical framework that we will use to make this prediction we will call the Rare Trait Marker Model. In describing the assumptions and mechanics of the Rare Trait Marker Model, it should be clear that although we will be concentrating upon left-handedness as the rare trait that we are interested in (cf. Satz, 1972, 1973), we actually could be dealing with any rare trait. We could have chosen any of those minor physical abnormalities that were listed earlier, or many other physiological or behavioural traits that we have not listed. Basically, the model has only two requirements that must be fulfilled. The first is that we have a dominant trait in the population and an alternative trait that may occur in its stead, but is relatively rare. The second requirement is that there should exist some form of pathology that can disrupt the development or emergence of the dominant or common trait. Suppose, for example, that we consider handedness in light of the model that we are going to present. For purposes of analysis, let us suggest some plausible, but hypothetical numbers. First, let us begin with a population in which the natural distribution of handedness is 90% right and 10% left if development proceeds normally. For sake of argument, let's assume that human laterality and lateral preferences are normally under the control of a some form of genetic mechanism or some form of maturational gradient (e.g., Corballis, 1983; Corballis and Morgan, 1978; Morgan and Corballis, 1978). Accordingly, if the genotype expresses itself normally, there may be an asymmetry in growth

10

Coren and Searleman

rate that will result in more rapid development on the left side of the human brain. Because of the contralateral neural link between brain and limb control, this maturational gradient could result in the emergence of a preference for the right hand in 90% of the population. The remaining 10% of the population might have a reversed maturational gradient due to genetic factors and become left-handed. The reader should not get too involved with the specifics of the theory outlined above, since it is merely an example, and we will show that the specific mechanisms involved make little difference for the model we are proposing. The important point to note is that, through some mechanism, if development proceeded normally, the population would contain a majority of right-handers (!lo% in this hypothetical example) and left-handedness would be the relatively rare trait (10%). If we can assume that this is the case, then we have fulfilled our first requirement, namely, the existence of a rare trait in the normal, undisturbed, population. To meet our second requirement we must next suppose that there is some pathological intervention that interrupts this normal maturational process, which, in turn, causes (for argument's sake) 10% of the population to switch their hand preference to the side opposite their natural, physiologically determined side of preference. In this hypothetical example let us assume that the pathology is a chromosomal abnormality of some sort. Again, it is not necessary to be very specific about the mechanism involved, all that is required is that, under appropriate circumstances, this pathology will result in a failure in some individuals to develop the genetically programmed right-handedness, resulting in a "pathological" left-hander, or conversely, that a genetically programmed left-handed individual might have normal development disrupted resulting in a "pathological" right-hander. If some pathology causes a 10% shift away from the genetically programmed handedness, this process would then cause 10% of the natural right-handers (9% of the population) to switch to left hand preference, and 10% of the natural left-handers (1%of the population) to switch to right hand preference. This model is illustrated in Figure 1, where the circles represent individuals with naturally determined, nonpathological preference, and the squares represent the


RIGHT

11

LEFT

Starting Population Prior to Pathological Insult

(A)

RIGHT

LEFT

Resultant Population After Pathological Shift of 10%

(B)

Figure 1:

Diagrammatic representation of the Rare Trait Marker Model applied to Handedness. Circles represent percentages of normal individuals and squares represent percentages of pathologically affected individuals.

12

Coren and Searleman

pathological members of the population. In this arbitrary example, the resultant population contains a distribution of 82% right-handers and 18% left-handers after the effects of the pathological insult are included. Before we go any further in this discussion it may be worthwhile to notice, that in terms of our presuppositions, we are adopting what Harris and Carlson (1988) called a two-type model since we assume that any given handedness pattern may be the result of either natural or pathological factors. In order to describe the population that we have just created we now would benefit from the use of some quantitative indexes. For this purpose we will borrow some measures from the field of epidemiology. In the epidemiological literature the concept of risk is used when describing outcomes in a population. In its simplest form the risk is much the same as rate of an outcome. Thus, the incidence of the outcome in a population is equivalent to an individual member’s risk, or probability of developing the outcome. For any targeted population and any given outcome, this is simply defined as: Percentage o f Population w i t h t h e Outcome

(1) Outcome Risk = T o t a l Target Population

Since this is equivalent to the incidence rate, we would then say that the risk of left-handedness in the population shown in Figure 1 is 0.18. At this level we have not added anything very much to a simple description of incidence, however, the concept of risk becomes more useful when we want to compare the incidence of an outcome in various groups, such as a group with a particular marker and one without. This is usually done by using the ratio of two risks, which is called the relative risk. For any given outcome, then, the relative risk would be defined as: Risk i n p o p u l a t i o n w i t h marker

(2)

Relative r i s k = Risk i n p o p u l a t i o n w i t h o u t marker

Each of the individual risk factors is estimated by Equation 1, and the percentage of individuals in that group actually having the outcome under investigation. Now returning to our hypothetical example, the outcome that we are interested in is for an individual to be affected by some form of pathology (of sufficient severity to affect the natural course of the development of handedness). The marker that we are considering is, of course, left-handedness.


13

When we look at the risk of pathology in each hand preference type, we find that the risk for left-handers is 0.5 or 50% (9/18), but only 0.122 or 1.22% (1/82) for the right-handers. If we now compute the relative risk from Equation 2, in order to compare the two handedness groups, we find that the relative risk is 40.98 (50/1.22). Simply put this means that the probability of finding a pathological individual in the left-handed group is nearly 41 times greater than the probability of finding one in the right-handed group in the example diagrammed in Figure 1. Now the reader might be quite skeptical at this point, since we seem to have made many assumptions about the causes of natural left-handedness (genetic predisposition) and the nature of the pathological intervention (chromosomal abnormality) that we postulated to work out this example. Recall, however, that we indicated we were not too concerned as to the actual mechanism or the nature of the actual pathology involved. In fact, these mechanisms can be considered to be completely hypothetical themselves, with the cause of natural handedness designated as merely Mechanism X , while the nature of the pathology could by Mecliartisni Y. The relative risk of pathology is always higher in the left-handed (rare trait) group regardless of the mechanism(s) causing either the original population distribution differences or the pathological shift to the other side. This occurs because of the statistical considerations from which the Rare Trait Marker Model is derived. All that is required is an asymmetrical population distribution for a given trait and a risk factor that can thwart the development of the targeted trait resulting in a shift in the phenotype. If the normal development of handedness were determined by intrauterine factors, such as the position in which the baby rested (rather than the genetically programmed maturational gradient that we suggested earlier) and the pathological intervention were due to the intervention of some maleficent deity (rather than a neurological insult or chromosomal abnormality) it would make no difference at all. As long as the initial population split was 90% vs 10% and the incidence of pathological shift away from the normal phenotype was lo%, the results would be the same. Any stressor that disrupts the normal development of lateral preference, regardless of mechanism, would be expected to show itself in higher relative proportion in the lower frequency pattern due to the initial skew in the population distribution of the preference pattern and the proportional nature of the pathological change. Although mechanisms and causes are not important in the Rare Trait Model, there are some characteristics of the population and the probability of pathology that do affect the association between pathology and the rare trait, as we will see in the following section.

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Coren and Searleman

Factors that Influence the Association between Pathology and the Rare Trait Although the pattern of results obtained from the rare trait marker model is completely insensitive to the nieciianisnis that cause the original population asymmetry or the pathological shift, the results are very sensitive to the initial population dislribufiort of the trait. The rarer the trait, the higher the likelihood (relative risk) that it will be found in association with pathology. This can be seen in Table 1 for a number of different initial population distributions. Notice that for our original example, the population distribution of 90% for the common trait (right-handedness) and 10% for the rare trait (left-handedness) resulted in a relative risk (likelihood of pathology) that was 40.98 times higher for the left-handers. If the starting population was split 95% for the common trait and 5% for the rare trait, the relative risk of pathology for individuals with the rare trait jumps to 117 times higher than for individuals with the common trait. If the original population was split 80% for the common trait and 20% for the rare trait, the relative risk is still high, but is now considerably less with pathology 11.40 times more likely for the rare trait group. The relative risk continues to drop as the initial difference in the percentage of subjects with the rare and common traits lessens until it disappears completely when the initial population is split evenly between the two traits. Thus we can conclude that the usefulness of a rare trait as a marker for pathology increases when the rare trait becomes rarer. The sensitivity of the Rare Trait Model to the asymmetry of the trait in the population, as shown in Table 1, makes it clear why handedness might prove to be such a good marker for pathology. The usual 90% vs 10% split in favour of dextrality which is normally found in most surveys, provides powerful statistical pressure toward increased likelihood of pathology in the left-handed population. Other aspects of laterality (ix., footedness, eyedness, and earedness) will simply not provide as much resolution since the split between right and left side preference is not as great as it is for handedness. Thus the percentage of the population that is left-footed is 19%, left-eyed 29% and left-eared 40% (Porac & Coren, 1981), which produce considerably lower relative risk values than the 10% associated with left-handedness. Up to now we have only considered the effect of the distribution of the rare and common trait as a factor. The model also incorporates another


15

Table 1: Variations in the distribution of the rare and common traits as a function of the initial population distribution, given a 10% likelihood of a pathological switch.

I n i t i a l Population Distribution ( X )

-r Percent p a t h o l o g i c a l i n F i n a l Population

Relative Risk

Conon

Rare T r a i t

Trait

Trait

Conon T r a i t

5

95

67.86

0.58

117.00

10

90

50.00

1.22

40.98

20

80

30.77

2.70

11.40

30

70

20.59

4.55

4.53

40

60

14.29

6.90

2.07

50

50

10.00

10.00

1.oo

I

quantity, namely the percentage of pathological shift. In our original hypothetical example we selected a value of 10% for this parameter. The assumption that 10% of the population is shifted away from its "natural" handedness by some form of pathological intervention may seem rather arbitrary, and possibly too large of a figure. What would happen if the rate of pathological shift were lower? Changing the rate of pathological shift does have an effect on the rare trait marker model of handedness. The effect, however, is somewhat counterintuitive in terms of likelihood of pathology. If, for example,the rate of pathological shift in the example shown in Figure 1 had been 1% instead of lo%, then out of a hypothetical sample of lo00 subjects, only 1 of the 100 natural left-handers would become a pathological right-hander, whereas 9 of the natural right-handers would become pathological left-handers. This has the effect, of course, of reducing the overall percentage of pathological individuals.

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Coren and Searleman

Table 2: Variations in the distribution of rare and common traits as a function of the percentage of shift due to pathological intervention and the initial population distribution of traits.

Percent Shift

Initial Population D i s t r i b u t i o n (%:

Percent patho log i c a 1 in Final Population

Relative Risk

Oue

To

Rare

Comnon

Rare

Comnon

Rare T r a i t

Patho log)

Trait

Trait

Trait

Trait

Comnon T r a i t

1

95

16.10

0.05

322.00

10

95

67.86

0.58

117.00

20

95

82.61

1.30

63.55

1

10

90

8.33

0.11

75.76

10

10

90

50.00

1.22

40.98

20

10

90

69.23

2.70

25.64

1

20

80

3.88

0.25

15.52

10

20

80

30.77

2.70

11.40

20

20

80

50.00

5.88

8.50

Instead of the pathological left-handers comprising 50% of the full sample of left-handers, they now make up only 8.33%, while the percentage of pathological right-handers falls from 1.22% to 0.11%. Although the incidence of pathological individuals is proportionally less in the left-handed group, the relative risk of pathology is now actually greater. With a 10% shift in handedness a left-hander was 40.98 times more likely to be pathological than was a right-hander, but with a shift of only 1%, the relative risk rises to 75.76 times.


17

Table 2 illustrates the relative risk of pathology for some different starting populations and for different percentages of pathological shift. Notice, that as the rate of pathological shift increases, so does the proportion of pathological individuals in both the rare and common trait groups. However, the risk of pathology in the rare trait group is proportionally less when compared to the common trait group. 7 7 1 ~the s usefulness of a rare trait as a niarker forpossible pathology diminishes if the rate of pathology is high.

Experimental Assessment of Birth Risk Factors and Handedness In our brief historical review, it was noted that some early researchers had suggested that pathology due to birth stress could be a cause of left-handedness. Curiously, despite the early interest in this issue, research on the relationship between hand preference, pathology, and the birth process virtually disappeared during an interval that went from the 1940’s to the early 1970’s. The reemergence of interest was not rekindled until the publication of a one page article by Paul Bakan in 1971. Bakan reported that a sample of male (but not female) left-handed college students were more likely than their right-handed counterparts to have been born in what he claimed was a “high risk birth order. According to Bakan, one would be classified as having a high risk birth order if they were either first born or fourth or later born, on the assumption that individuals born in these birth positions are more likely to suffer from perinatal complications. Largely due to the interest engendered by Bakan’s publication, the last two decades have produced a substantial number of studies that have attempted to find a relationship between left-handedness and indicators of possible birth stress. These studies have not only looked at birth order, but have also monitored several more direct measures of birth stress, in both clinical and nonclinical populations. A recent article by Searleman, Porac, and Coren (1989) has reviewed this literature for the nonclinical samples incorporating meta-analytic techniques. To briefly summarize the results of their review and analysis, it was found that there was no reasonable evidence to indicate that birth order is related to increases in deviations from right-handedness (or from right-sidedness in general) for either males or females. However, when more direct measures of birth stress were used, there was evidence that certain specific birth stressors

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Coren and Searleman

were significantly related to increases in nonright-handedness, particularly for male subjects. Although the size of the effect was quite small for any individual birth stressor, accounting for less than 1% of the variance in handedness, there was evidence of considerable consistency in the overall pattern. Using 10 different indices of birth stress and a composite index (subjects being classified as having had a stressful birth if any of several different birth stressors were present at birth), separate analyses were performed for males only, females only, and collapsed across sex. It was found that 30 of the 33 possible comparisons were in the direction that suggested a positive relationship between increases in the incidence of nonright-handedness and birth stress. This is a much higher proportion than would be expected by chance (p c 0.001), and indicates that when birth stressors are considered collectively, there is some validity to the hypothesis that birth stress is correlated with deviations from right- handedness. In their article, Searleman et al. (1989) drew attention to a number of methodological and theoretical problems that exist in the literature and offered suggestions to help alleviate these problems for future researchers. Specifically, they suggested: examining the variables in question in the context of family studies; decreasing reliance on questionnaire methods and increasing reliance on the use of archival records; conducting longitudinal, prospective studies instead of retrospective studies; using adequately sized samples of birth-stressed individuals; using continuous rather than dichotomous measures of lateral preference; and finally, obtaining a more complete profile of sidedness by examining all four lateral preferences. Until future research adheres to these suggestions, it will be impossible to make final definitive statements concerning the relationships between specific birth stressors and the development of particular patterns of lateral preference among normal individuals. (pp 406-407)

Application of the Rare Trait Marker Model Up to now we have been fairly non-specific in our discussion of the Rare Trait Marker Model. We have only applied it to general cases and hypothetical data. Let us now apply the model to an actual data set. As will be shown below, this will, not only illustrate the model in action, but will also show the kinds of information that the model can extract from empirical data banks. Specifically,


19

application of the model to a particular stressor will allow us to not only calculate the strength of the effect of that particular stressor (in terms of the degree of increased risk of pathology associated with left-handedness) but to also describe the “natural”(genetic?) distribution that would be expected if there were no pathological intervention. For the purposes of demonstrating the application of the rare trait marker model, we will examine the relationship between advanced maternal age at the time of birth and the subsequent incidence of left-handedness in the male and female offspring. Advanced maternal age was selected for several reasons. To begin with, births associated with older mothers seem to be subject to a variety of additional risks across a broad spectrum of birth stressors. For example, if we eliminate the maternal age groups below 16 years, the incidence of congenital malformations, prematurity, miscarriages and still births, increases steadily with increasing maternal age (Montagu, 1962). Lesinski (1975) reviewed 22 studies on birth risk and concluded that all mothers above 30 years of age were above the median risk, and that increasing age beyond this value increased the risk further. Broman, Nichols and Kennedy (1975) conducted a mammoth study that reached the same conclusion. These investigators used data from 169 variables measured on a sample of 26,760 women and found that increasing maternal age produced increasing numbers of sub-optimal births. Maternal age may also operate to produce problems at the genetic level. Many studies have shown that there is a significant correlation between aging and chromosomal changes in normal individuals drawn from populations that are unselected for any disease, disorder, or defect (Court-Brown, Jacobs and Tough, 1967). As a consequence, abnormalities in offspring caused by chromosomal factors increase in incidence as a function of increasing maternal age (Leviton and Montagu, 1971; Matsunaga, 1973; Polednak, 1976; Selvin and Garfinkel, 1972). Another good reason to use advanced maternal age is that it’s typically a much more reliably obtained value than is the case for many other birth stressors. Although it is impossible for a given individual to know, first hand, whether his or her birth was difficult, most individuals can report the current age of their mother (or, if now deceased, the age that their mother would currently be if she were alive today) as well as their own age. This means that the age of the mother at the time of the individual’s birth is usually quite reliable. We can contrast this to asking individuals if they have any knowledge of particular birth stressors associated with their own delivery. This information is, of course, always second hand, and can only be obtained by the individual concerned if it

20

Coren and Searleman

is volunteered by the mother or other members of the family at some time in the past. Over a period of approximately five years, 2,188 freshmen enrolled at the University of British Columbia (1,323 female and 865 male with a mean age of 18.5 years) have been surveyed to obtain medical and demographic information. Patterns of lateral preferences were determined for each individual using the Lateral Preference Inventory. This is a behaviourally validated self-report inventory that is designed to measure hand, eye, foot, and ear preferences. The version used contained four questions to ascertain hand preference based upon items selected from Coren and Porac (1978) and Coren, Porac and Duncan (1979). This self-report battery, which has been extensively used in studies of lateral preference, has been behaviourally validated and the handedness scale has a 98% concordance with individual behavioural testing (see Porac and Coren, 1981 for a full discussion). The questions were presented in a mixed order, and subjects responded "left," "right" or "both to each one. Data on handedness was scored using a dichotomous measure. A continuous measure of handedness was first obtained by transforming the data into an index that incorporates both the direction and consistency of sidedness, using the formula (R-L)/N, where "R"is the number of ''right" responses, " L is the number of "left" responses, and " N is the total number of questions presented. This procedure produces a range of scores from -1 (consistent left-handedness) to t 1 (consistent right-handedness). We could, of course, use this continuous measure to assess whether or not the effects of birth stress is to reduce the strength of dextrality, rather than effecting a shift from right- to left-handedness. However, we need a dichotomous measure of handedness if we are to apply the rare trait marker model that we described in Figure 1 in its simplest and most conceptual form. Therefore, all scores greater than zero (balanced ambidexterity) were classified as right-handed,while scores less than or equal to zero were classified as left-handed, following the format suggested by Porac and Coren (1981). A series of dichotomous classifications were created for advanced maternal age at the time that the offspring was born. In each instance a cut point was used. Thus we can tabulate the percentage of left- and right- handers born to mothers 29 years of age and less and compare that with the handedness distribution for mothers over 29 first, then move the cut point to age 30,and so forth. In this manner we can use advanced maternal age as the risk factor and for each age cutoff we can compute the relative risk of the offspring manifesting left-handedness. These relative risk scores are plotted in Figure 2.


21

Relative Risk of Left-Handedness as a Function of Maternal Age in Years

Lana than

29

30

31

32

33

34

35

30

or Mom

Mother's Age at Time of Subject's Birth

Figure 2:

The likelihood of being phenotypicallyleft-handed as a function of advanced maternal age when the offspring is delivered, based upon data from 2,188 subjects.

First, look at the pattern of results for the total sample. Remember that a relative risk of 1 means that there is no contribution of the particular marker in predicting the specific outcome. In this case, a relative risk of 1would indicate no effect of advanced maternal age on the incidence of left-handedness. Notice that for cut points set at ages 29 and 30 the likelihood of left-handedness in the offspring is not affected by the mother's age. With increasing maternal age, however, there is a gradual increase in the incidence of left-handedness. This is consistent with the supposition that older mothers have more stressful deliveries and gestation periods and that pre- and peri-natal stressors contribute to the appearance of left-handedness. When males and females are considered separately, we find that the pattern of the increase in left-handedness differs as a function of gender. Let us use a relative risk of 1.5 as an arbitrary set point. This is equivalent to a 50% increase

22

Coren and Searleman

in the likelihood of becoming left-handed. This point is reached much earlier for males than for females. For males, a 1.5 relative risk of left-handedness is reached when we consider mothers between the ages of 32 and 33 years of age. For the females, however, this value is not reached until the mother is between 35 and 36 years of age. This suggests that males are more susceptible to the effects of advanced maternal age than are females. This previously unpublished set of data is, of course, another entry into the literature suggesting that birth stress may be associated with an increased incidence of left-handedness. The data presented above are consistent with the hypothesis that we are dealing with the rare trait marker effect, since a presumed set of stressors or pathological interventions (for which advanced maternal age is an indicator) has resulted in the increase in the rare trait (left-handedness). Turning back to the model illustrated in Figure 1,we note two parameters of particular interest. The first is the proportion of individuals whose handedness is pathologically shifted, while the second is the distribution of handedness if no pathology were present in the system. We can use the advanced maternal age data just described to estimate both of these parameters. Before doing this, it might be useful to agree upon some common nomenclature. We will use the term ittherent proportion to represent the proportion of the population who would show a particular handedness if their natural predispositions expressed themselves without disturbance in the targeted phenotype. By pathological proportion we will mean that segment of the population who expresses a particular phenotypic handedness that has been shifted from the naturally encoded side to the other side due to pathological factors. Now, if we represent the inherent proportion of right-handers (i.e., original proportion before it is distorted by pathology) as R, and the proportion of individuals who will be pathologically shifted in their handedness as S, then by working through the model in Figure 1, it’s quite easy to show that the proportion of left-handers with the pathological marker (which we will call PL) is (3)

P L = RS

The value Pu at least for advanced maternal age as the indicator of probable pathology, is known to us from the data set previously presented. It is simply the number of individuals with older mothers who are left-handed. If we want to solve for R and S (to determine the inherent population distribution and the pathological shift proportion) we have two unknowns, and therefore we need another equation. The present data give us a total number of left-handers in the


23

present population (i.e., pathological plus normal left-handers) that we will represent as TL‘This value is the natural proportion of left-handers (I - R) from which we subtract the number of pathological right-handers, (I - R)S, and to which we add the number of pathological left-handers (which is just RS, from equation 3 above). Thus we get T,

(4)

=

1 - R - S + 2RS

With two equations and two unknowns this set of simultaneous equations can be solved. When we do, we get the following solution for the proportion of inherent right-handers: K + (K2 - 4P,)’D

(5) I\

2

where: K = 1 - (T,

-

2PL)

and for the pathological shift factor we get:

There is a long history of empirical work that suggests that males and females differ in susceptibility to birth stress, with males typically faring worse (see Gualtieri and Hicks, 1985 for a review). Combined with the finding that males are more likely to be pathological left-handers (Searleman et al., 1989), the implication is that the pathological shift factor S should differ as a function of gender. There is another reason why we should consider the application of the model separately for males and females. Many investigators have looked at the distribution of handedness as a function of gender. In general, the existing literature suggests that when sex differences for handedness are found they usually indicate a higher percentage of left-handed males than females (e.g., Bryden, 1977; Clark, 1957; Enstrom, 1962; Hardyck, Goldman and Petronovich, 1975; Levy, 1976; Le Roux, 1979; Oldfield, 1971). Estimates of the size of the difference typically vary from 1 to 5 percent. Using the same measure of

24

Coren and Searleman

handedness that was employed in the advanced maternal age study reported above, Porac and Coren (1981) assessed the handedness of 5,147 individuals and discovered that 3.6% more of the females were right-handed than were the males. This suggests that the original proportion of natural right-handers (R in our terminology) may be different for males and females. In the advanced maternal age data it was observed that the percentage of left-handed males was 11.1% as compared to 9.5% for females, giving us 1.6% more dextral females. For all of these reasons, a separate analysis was conducted for each gender to solve for the parameters S and R using the rare trait marker model equations that were derived earlier. We must make a decision as to which set of data to apply the model to, since, as one can see from Figure 2, the risk of pathological shift seems to be changing in a continuous fashion as the mother’s age increases. Perhaps the simplest method of comparing the sexes is to select a maternal age and then calculate the theoretical values. For example, at maternal age of 35 years, 14.6% of the male left-handers had mothers over 35 years of age at the time of their birth as compared to only 8.8% of the male right-handers. For females the difference is smaller, with 11.1% of the left- handers having older mothers and only 8.1% of the right-handers. Applying Equations 5 and 6 to these data, we find that for the males the pathological shift percentage S amounts to 1.8% while for the females it is 1.2%. Note that the values produced by the equations are actually proportions, however for consistency with our previous discussions we will continue to convert the results to percentages when presenting the final product of our calculations. One advantage of presenting these values as percentages is that the value S itself is a risk factor indicating the percentage of the population that should show a pathological shift. Since S is a risk factor, it can be used to estimate the relative risk of a pathological shift in handedness for males and females separately. In this case, the relative risk is 1.5 (1.8%/1.2%) indicating that males are 50% more likely to be pathological left-handers than females. An alternative way to analyze these data would be to decide on a risk value as a threshold, and then compare males and females as soon as they surpass this threshold level. For example, if we select a likelihood value of pathological left-handedness of 1.5, and use it as the threshold level, we find that males first surpass this value when maternal age exceeds 33 years (although there’s a drop below this level at age 36 that we attribute to sampling error), while females don’t surpass this threshold until maternal age exceeds 36 years. At maternal age of 33 years, 24.0% of the left-handed males have the pathological marker (an older mother) while only 15.2% of the right-handed males do. At age 36, 11.1%


25

of the female left-handers have an older mother compared with only 5.9% of the female right-handers. Calculating the pathological shift percentage S produces a value of 3.0% for males and 1.2% for females. Thus the relative risk of pathological shift for males is actually greater, with a value of 2.5 (3.0%/1.2%), than in our previous calculations. Averaging the results of the two calculations of S for each gender reveals that the average shift factor for males is 2.4% and for females 1.2%. For the present data, this indicates that males are approximately twice as likely as females to be pathologically shifted to left-handedness. Until now we have only focused on the likelihood of pathology. Recall, however, that Equations 5 and 6 also permit calculation of the proportion of inherent right-handers (R)if there is no pathological intervention. This is an estimate of the initial population distribution depicted in Figure 1. The original percentage of male right-handers is estimated to be 91.3% and 90.3% respectively, basing our estimates upon data from the maternal ages 33 and 35 that were used in the earlier computations. This provides a mean estimate of 90.8% inherent right-handed males. For females, both computations produce the same estimate, namely 91.4%. This means that females are only 0.6% more right-handed than males. This value is considerably less than one might expect on the basis of simple consideration of the empirical data. For instance, it is only about one third the 1.6% difference found in the raw distributional data from this sample, and one sixth the 3.6% reported by Porac and Coren (1981) using the same measurement scale on a larger, more age heterogeneous sample. The finding of little difference in R as a function of gender has theoretical importance. It suggests that females are just slightly more biased towards dextrality than males, perhaps due to genetics or to the fact that females are somewhat more susceptible to cultural pressures to change handedness (Porac, Coren, and Searleman, 1986). If males and females were to develop without any pathological interventions, the distribution of handedness for the two sexes would be roughly equivalent. We believe that it’s primarily the occurrence of pathological insult that significantly shifts the final phenotype toward increased sinistrality in males.

Is Left-Handedness a Good Marker for Pathology? We have seen that left-handedness does seem to be a reasonable marker for pathology, simply based upon the operation of the statistical mechanisms

26

Coren and Searleman

associated with the rare trait marker model. Are there any other reasons, other than the population split of roughly 90% to lo%, as to why left-handedness might be a useful marker for various psychological and neurological differences? We think the answer is yes. Left-handedness is also particularly useful as a neurological and psychological marker because the control of handedness is neurologically complex, involving a number of brain sites and neural control systems. Discussions of upper limb control by Brodal(1981), Harris and Carlson (1988), and Kupyers (1985) indicate that a variety of different neurological systems are involved. These include three motor systems that originate in the cerebral cortex, several subcortical sites, a sensory system, and several commissural systems. In the cortex, Brodman’s areas 1,2,3,4,5, and 6 have all been implicated in upper limb control. The corticospinal or pyramidal tract, the ventromedial brain stem system (including the reticule-spinal tract) and the lateral brain stem system (including the rubrospinal pathway) all play roles in manual control. Among the subcortical sites mentioned as playing a role in the control of hand use are the basal ganglia structures. The corpus callosum, which transfers information between the two cerebral hemispheres, also seems to play a role in hand control. Sensory systems include, at the minimum, proprioceptive and kinesthetic systems in the postcentral cortex. The interesting issue for left-handedness as a marker for pathology is that pathological insult or malfunctions that affect any of these sites or systems also seem to affect the natural development of handedness. In other words, pathological left-handedness may arise from damage to the cortex, motor systems, sensory systems, or commissural pathways. This suggests that left-handedness is of particular interest because the genesis of pathological shifts in hand dominance may occur due to insult to many different neural centers and systems. This would, of course, increase the sensitivity of left-handedness as a marker for minor neurological damage, that might, in turn, contribute to a number of different behavioural problems. The same minor pathology that causes left-handedness might also interfere with normal learning or language processes, produce emotional, neurotic, or psychotic symptoms, or reduce adaptive and survival ability in a number of different ways. Of course, the large number of possible sites for pathology does have a negative component, in that it also means that there is little specificity (in terms of indicating locus of any lesion) in left-handedness when it is used as a marker for pathology. While the above discussion suggests that left-handedness might be particularly useful as a generalized indication of increased risk for pathology, the


27

actual mechanism that makes it likely that a higher proportion of left-handers will show such effects remains the original asymmetrical distribution of handedness in the population. Thus, the complex neural control associated with handedness makes it highly vulnerable to pathological interventions, however, the fact that it is originally a relatively rare trait is what makes it useful to serve as a marker for increased risk.

Conclusions and Future Directions In this chapter we have presented the Rare Trait Marker Model to illustrate its operation in the context of the relationship between birth stressors and the appearance of left-handedness. The Rare Trait Marker Model is a statistical model that does not rely upon any particular mechanism but simply operates upon a population in which there is an asymmetrical distribution of traits, with one trait or set of traits rarer than the others. The rarer the trait the more strongly it will serve as a potential marker for pathology, where pathology is defined as any situation, condition or intervention that 'will prevent the development of the naturally (genetically) targeted trait, hence resulting in the appearance of its counterpart. To demonstrate the operation of this model, we made a few simplifymg assumptions. To begin with, we presumed that there were only two phenotypically visible traits (in this case, left- and right-handedness). We further simplified by assuming that the traits were dichotomous rather than continuous. In addition, it was presumed that the pathological intervention was either present or absent, and we did not view it as being a continuous variable. All of these assumptions make the computations and the illustration of the operation of the model easier. It should, however, be possible to work out a continuous variable version of the model in which the common trait would be "strong right-handedness" and the stressors would be graded in intensity with stronger stressors producing a larger percentage of shift. If such were the case, the model would have to be changed somewhat to present the pathological shift factor (S) in our model's equations as a function, rather than as a constant. For the purposes of working out our example, we used only one indicator of elevated risk of birth stress, namely advanced maternal age. We are not, of course, arguing that this is the only pathological risk marker that is important in shifting handedness. It is merely a convenient data base that allows us to

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illustrate the operation of the model and also gives us the opportunity to present some hitherto unpublished data that also serve to link birth stress factors with handedness. Presumably, some composite index of birth stressors, incorporating a number of different stressors, would produce a more stable estimate of the total pathological shift factor in the population. This means that our computations of S are most assuredly underestimates of the population value of S, although they would likely be a good indicator of the salience of advanced maternal age as a single risk factor. To that extent, the computational procedures might prove to be a good means for estimating the likelihood that left-handedness would result from other manifestations of birth stress. Each potential risk factor would then produce a particular S value, indicating the influence it would have in shifting the subject’s handedness. The use of the rare trait marker model produced other outcomes of theoretical interest. To begin with, we expected, and the computations confirmed, that males are more susceptible to pathological interventions than are females. In fact, based on the present data set, the relative risk of left-handedness as a function of increasing maternal age is twice as large for males as for females. The data that was presented in Figure 2, however, could indicate that males and females do not differ qualitatively in terms of their susceptibility to stressors, but may differ only in threshold, with females requiring a greater “dose” to trigger the effects. Thus females, just like males, do show elevated risk with increasing maternal age, however the effect requires an older mother (increased stress risk). One unexpected finding of theoretical interest was that the original distribution of right-handedness (R) was very similar for males and females. The usually observed population differences showing significantlymore right- handed females may not be primarily a function of genetic endowment or to greater susceptibility to social/cultural pressures to switch from left-handedness to right-handedness. Instead, much of the difference in the incidence of right-handedness between the sexes could be due to the fact that males have an increased risk for becoming pathological left-handers. Let us conclude by noting that the operation of birth stressors upon the development of handedness does appear to be reasonably established. If one uses the Rare Trait Marker Model, one need not look for specific mechanisms to establish how handedness shifts as a function of the pathological intervention. Simple disruption or retardation of the normal, genotypically programmed, maturational pattern could account for the shift in hand dominance; alternatively, any of a variety of diverse lesions or malfunctions in the complex of systems


29

associated with manual control would work just as well. In any event, we have demonstrated that application of this model allows the assessment of the likelihood of developing left-handedness for any specific stressor, and allows us to estimate the initial proportion of left- and right-handedness in a target population prior to the intervention of any pathological factor.

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Acknowledgements This research was supported in part by grants from the British Columbia Health Care Research Foundation and the Natural Sciences and Engineering Research Council of Canada. The authors would like to acknowledge the assistance of Wayne Wong, Joan Donelly, Geof Donelly and Dereck Atha, who assisted in the collection of these data. We would also like to acknowledge the mathematical assistance of Dr. Lawrence M. Ward of the Psychology Department of the University of British Columbia.

References Bakan, P. (1971). Handedness and birth order. Nature, 229, 195. Bell, R.Q, & Waldrop, M.F. (1982). Temperament and minor physical anomalies. In Porter, R. & Collins, G.M. (eds). Temperamental differences in infants and young children (pp. 206-219). London: Pitman. Blau, A. (1946). The master hand. New York: American Orthospychiatric Association. Brewster, E.T. (1913). The ways of the left hand. McClure’s Magazine, 168-183. Brodal, A. (1981). Neurological anatomy in relation to clinical medicine (3rd edition). New York: Oxford University Press. Broman, S.H., Nichols, P.L. & Kennedy, WA. (1975). Pre-school ZQ: Prenatal and early developmental correlates. Hillsdale, NJ: Erlbaum. Bryden, M.P. (1977). Measuring handedness with questionnaires. Neuropsychologia, 15, 617-624. Burt, C. (1937). The backward child. London: London University Press Campbell, M., Geller, B. Small, A.M., Petti, T.A. & Ferris, S.H. (1978). Minor physical anomalies in young psychotic children. American Journal of Psychiatry, 135, 573-575. Clark, M.M. (1957). Left handedness: Laterality characteristics and their education implications. London: University of London Press. Corballis, M. (1983). Human laterality. New York: Academic Press. Corballis, M.C., & Morgan, M.J. (1978). On the biological basis of human laterality, I: Evidence for a maturational left-right gradient. The Behavioral and Brain Sciences, 2, 261-336. Coren, S., Porac, C., & Duncan, P. (1979) A behaviorally validated self- reported inventory to assess four types of lateral preference. Journal of Clinical Neuropsychology, 1, 55-64. Coren, S., & Porac, C. (1978) The validity and reliability of self-report items for the measurement of lateral preference. British Jounial of Psychology, 69, 207-211. Court-Brown, W.M., Jacobs, PA. & Tough, I.M. (1967). Some types of information obtainable from chromosome studies on defined population


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groups. In Human Radiation Cytogenics: Proceedings of an International Sytnposiuni (pp. 115-121). New York: Wiley. Enstrom, EA. (1962). The extent of the use of the left hand in handwriting. Journal of Educational Research, 5.5, 234-235. Fliess, W. (1906). Der Ablauf des Lebens. Vienna: Deuticke. Gordon, H. (1921). Left-handedness and mirror writing, especially among defective children. Brain, 43, 313-368. Gualtieri, T., & Hicks, R.E. (1985). An immunoreactive theory of selective male affliction. The Behavioral and Brain Sciences, 8, 427-441. Hardyck, C., Goldman, R., & Petrinovich, L. (1975). Handedness and sex, race, and age. Human Biology, 47, 369-375. Harris, L.J. & Carlson, D.F. (1988). Pathological left-handedness:An analysis of theories and evidence. In. Molfese, D.L. & Segalowitz, S.J. (eds.) Brain lateralization in children: Developntental iniplications (pp. 289- 372). New York: Guilford Press. Jordan, H.E. (1922). The crime against left-handedness. Good Health, 57, 378383. Krouse, J.P. & Kauffman, J.M. (1982). Minor physical anomalies in exceptional children: A review and critique of research. Journal of Abnormal Child P~ycltology,10,247-264. Kupyers, H.G.J.M. (1985). The anatomical and functional organization of the motor system. In Swash, M. & Kennard, C. (eds.), Scientific basis of clinical neurology (pp 3-18), Edinburgh: Churchill Livingstone. Le Row, A. (1979). Sex differences and the incidence of left-handedness. Journal of Psychology, 102, 261-262. Lesinski, J. (1975). High risk pregnancy: unresolved problems of screening, management and prognosis. Obstetrics and Gynecology, 46, 599-603. Leviton M. & Montagu, A. (1971). Textbook of Human Genetics. New York: Oxford University Press. Levy, J. (1976). A review of evidence for a genetic component in the determination of handedness. Behavior Genetics, 6, 429-453. Lombroso, C. (1903) Left-sidedness. North American Review, 170, 440-444. Matsunaga, E. (1973). Effect of changing parental age patterns on the chromosomal aberrations and mutations. Social Biology, 20, 82-88. Molfese, D.L. & Segalowitz, S.J. (eds.) (1988). Brain lateralization in children: Developniental implications. New York: Guilford Press. Montagu, A. (1962). Prenatal Influences. Springfield, Ill.: Charles C Thomas. Morgan, M.J., & Corballis, M.C. (1978) On the biological basis of human laterality, 11: The mechanisms of inheritance. The Behavioral and Brain Sciences, 2, 270-277. Oldfield, R.C. (1971). The assessment and analysis of handedness: the Edinburgh inventory. Neuropsychologia, 9, 97-113. Polednak, A.P. (1976). Paternal age in relation to selected birth defects. Human Biology, 48, 727-739. Porac, C., & Coren, S. (1981). Lateral preferences and human behavior. New York: Springer.

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Porac, C., Coren, S., & Searleman, A. (1986). Environmental factors in hand preference formation: Evidence from attempts to switch the preferred hand. Behavior Genetics, 16, 251-261. Redlich, E. (1908). Epilepsie and linkshandigkeit.Archives Psychiatria, 44, 59-83. Satz, P. (1973). Left-handedness and early brain insult: An explanation. Neuropsychologia, 11, 115-117. Satz, P. (1972). Pathological left-handedness: An explanatory model. Cortex, 8, 121-135. Satz, P., Orsini, D.L., Saslow, E., & Henry, R. (1985). The pathological lefthandedness syndrome. Brain and Cogriitiori, 4, 27-46. Searleman, A,, Porac, C., & Coren, S. (1989). The relationship between birth order, birth stress handedness and lateral preference: A critical review. Psychological Bulletin, 105(3), 397-408. Selvin, S. & Garfinkel, J. (1972). The relationship between paternal age and birth order with the percentage of low weight infants. Huniari Biology, 44, 501-510. Silva, DA., & Satz, P. (1979). Pathological left-handedness: Evaluation of a model. Brain arid Language, 7, 8-16. Wile, I.S. (1934). Haridedness: Right arid ref. Boston: Lathrop, Lee & Shepard. Woodruff, C.E. (1909). Expansion ofraces. New York: Rebman & Co.

LEIT-HANDEDNESS Behavioral Implications and Anomalies, S. Coren (Editor) 0 Elsevier Science Publishers B.V. (North-Holland), 1990

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Chapter 2

NonRight-Handedness and the Continuum of Reproductive Casualty Paul Bakan Simon Fraser University “the history of man for the nine months preceding his birth would probably be far more interesting and contain events of greater moment, than all the three score and ten years that follow it.” S. T. Coleridge

The Continuum of Reproductive Casualty In 1973 I reported (Bakan, Dibb and Reed, 1973) an association between pregnancy and birth complications (PBCs) and nonright-handedness (NRH). Left-handed and ambidextrous subjects were twice as likely as right-handers, to report PBCs associated with their birth. On the basis of the excess of PBCs among NRH subjects, we suggested that NRH is a result of prenatal or perinatal brain insult. In an earlier paper (Bakan, 1971) a relationship between NRH and PBCs was proposed to account for an observed excess of NRH among first born, and fourth or later born subjects, i.e. births to older mothers; these birth orders are associated with an excess of PBCs. On the basis of these results we concluded that NRH is one manifestation of a “continuum of reproductive casualty” (Pasamanick and Knobloch, 1966). The continuum of reproductive casualty is the result of untoward prenatal or perinatal events suffered by infants “whodo not die, but depending on the degree and location of trauma, go on to develop a series of disorders, extending from cerebral palsy, epilepsy, and mental deficiency, through all types of behavioural

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and learning disabilities, resulting from lesser degrees of damage sufficient to disorganize behavioral development." The events leading to reproductive casualty result from a variety of factors, including maternal-fetal blood type incompatibilities,maternal endocrine disorders,diabetes, radiation, maternal age, chronic stress, drugs, including nicotine and alcohol, infection, and hypoxia (Pasamanick and Knobloch, 1966). Though I was familiar with the concept of a "continuum of reproductive casualty," I was unaware of the interest of Pasamanick and Knobloch in the problem of NRH (Pasamanick and Knobloch, 1966). They concluded, after reviewing twelve manifestations of the continuum of reproductive casualty, that left-handedness "may turn out to be a thirteenth condition within the continuum." They said: It had been our clinical impression that we encountered significantly more left-handedness in preschool age children on whom a diagnosis of brain injury had been made. We felt that it was possible that if the injury was confined largely to the left motor cortex and its efferent system..., the child would... during the maturation of fine motor behavior tend to prefer the left hand ... In the sample of children...we examined the relationship of ambidexterity (non-established handedness) at three years to that of a diagnosis of brain injury made at 40 weeks. A statisticallysignificant association being found....we would like to confirm our clinical impression by examining the relationship of ambidexterity and left-handedness to diagnosis of brain injury in the large cohort of neurologic cases.. Secondly we intend to follow the pattern of investigation we have used before, i.e. to secure an experimental group of left-handed individuals from a school system with a control group of right-handed children from the same classrooms and compare perinatal events in both. (Pasamanick and Knobloch, 1966).

I have been unable to find a published report of the proposed studies. The design described for the retrospective comparison of right and left-handers with respect to PBCs, is essentially the one used in our study (Bakan, Dibb, and Reed, 1973), and the results are essentially those predicted by Pasamanick and Knobloch (1966).

Reproductive Casualty

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Implications of the Reproductive Casualty Context for NRH NRH takes on new meaning and significance, when considered in the context of reproductive casualty. This context provides new questions, hypotheses, and experimental approaches with which to advance the understanding of NRH. The context of reproductive casualty broadens the range of variables relevant to the etiology of NRH. Considering NRH in the context of reproductive casualty, is analogous to what happened in the history of the science of nutrition, when isolated syndromes such as pellagra, or scurvy, were understood to be manifestations of malnutrition or vitamin deficiency. Just as pellagra or scurvy are better understood as manifestations of malnutrition, so NRH may be better understood as a manifestation of reproductive casualty. Variables known to be involved in other forms of reproductive casualty can be examined in terms of NRH. Such variables include obstetric complications, hypoxia, birth weight, maternal smoking, use of alcohol and other drugs, and malnutrition. To the extent that some of these factors are associated with socio-economic variables, the context of reproductive casualty broadens still further the range of variables relevant to NRH. The context of reproductive casualty leads to investigation of relationships between NRH and other pathological conditions. It helps to account for numerous relationships between NRH and other manifestations of reproductive casualty, such as epilepsy, learning disorders, attention deficit disorders, mental retardation, and congenital defects. The context of reproductive casualty implies that NRH is not merely a static aspect of the distribution of handedness, but a behaviour subject to increase or decrease, by the action of variables that influence the rate of reproductive casualty.

Historical Approaches to Reproductive Casualty This section traces the history of interest in the relationship between prenatal/perinatal problems and subsequent morbidity. Some of the historical contributions have emphasized morbidity in general, and others have addressed particular outcomes, such as congenital malformations, epilepsy, mental retardation, cerebral palsy, and NRH.

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The Old Testament One of the earliest theories of NRH is found in the Old Testament. The Book of Judges, best known for the story of Samson and Delilah, is not generally noted for a "theory" of the etiology of NRH. But Judges 20:16 relates, that among the inhabitants of Gibeah, "there were seven hundred chosen men, ...left-handed; every one could sling stones at a hair breadth, and not miss." (Jewish Publication Society, 1955). This is one of only two uses in the Old Testament of a Hebrew phrase, ifteryud yemino, translated "left-handed." The other use of the phrase also appears in the Book of Judges (3:15), when "the Lord raised them up a saviour, Ehud, ...a man leff-handed." The left-handed Ehud girded a sword on his right thigh, so that his enemy, King Eglon of Moab, was caught off guard, and was killed by the sword in Ehud's left hand. Translators disagree about the translation of itteryadyemino as "left-handed." In the Septuagint and Vulgate translations, itter yud yemino is translated as "ambidextrous." The difference in translations reflects the fact that the phrase does not contain the Hebrew word for "left," shntol. The word yad means "hand," yemino means "right," and the phrase itter yad yeniino means "a right hand which is itter;" it says nothing at all about the left hand. The implied biblical theory of pathological left-handedness is based on the word itter (spelled afr in Hebrew). This word means impeded, shut-up, or maimed, and may have its origin in the Egyptian word am, meaning injury. The two passages in the Book of Judges refer to a pathological inadequacy of the right hand, and this has been translated either as "left-handed," or "ambidextrous." Where the Bible uses the word "left" to mean direction, as in left hand or left side, the word used is shniol. But in the two cases translated as "left-handed or "ambidextrous," the word itter is used to describe a pathologically inadequate right hand. Left-handedness or ambidexterity is deemed due to inadequacy of the right hand. The biblical theory of pathological left-handedness is further implied in Leviticus (21:17-21), where the rules for selecting priests to perform sacraments in the Holy Temple are described. The basic principle is that a priest with a blemish or physical defect may not be selected. The operational definition of blemish is then given as "a blind man, or a lame, or he that hath anything maimed, or anything too long, or a man that is broken-footed, or broken-handed, or crook-backed, or a dwarf, or that hath his eye overspread, or is scabbed, or scurvy" (Jewish Publication Society, 1955). The issue of the fitness of a priest to serve in the Temple is again discussed, with reference to handedness, in the Talmud, a set of rabbinical commentaries


37

on Biblical matters. In the Talmud the word itter is used as a noun, meaning "a left-handed person." This is based on what Preuss (1978, p. 309) considers the "incorrect translation" of itter yud yentino as "left-handed." According to the Talmud, a priest who is left-handed or left-footed, is not suited to serve in the Temple, because these conditions are deemed to be a blemish. The rabbis argue about the acceptability of an ambidextrous priest. One of the rabbis, considers an ambidextrous priest unfit, because he interprets ambidexterity as the result of an abnormally weak right hand. Other rabbis deemed equality of strength of the two hands to be the result of a strong left, rather than a weak right hand, and thus interpreted ambidexterity as non-pathological (Preuss, 1978, p. 309). But they all agree that if left-handedness or ambidexterity is due to a weakness or inadequacy of the right hand, the priest has a blemish, and thus is not fit to serve in the Temple. Ancient India: Caraka A collection of medical writings by the physician Caraka, who lived several centuries B.C., is central to the Ayurvedic medical tradition of Ancient India. Caraka emphasized the importance of prenatal factors in determining developmental outcome. He distinguished between genetic and congenital determination. Congenital abnormalities, he considered as either genetic, or the result of intrauterine factors. Caraka believed that conception involves the semen, the ovum and "the spirit which takes place in the womb." This "spirit" refers to the quality of the intrauterine environment. Caraka believed that congenital malformations, and sensory abnormalities result from poor intrauterine conditions due to "defects of the mother's diet and behavior during gestation." He urged physicians to understand the factors "which are helpful in the formation and development of the fetus, and those which are inhibitive of such formation and growth (Lele, 1986, pp. 165-167). Plato Plato believed there were two circuits or circles in the head, a circle of the Same, and a circle of the Different. This theory, appears to be a precursor to the doctrine of functional hemispheric asymmetry. Plato thought that rotational disturbances of the circles resulted in irrationality, the inability to make judgments about what is the same and what is different among things. Plato

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believed that the trauma of birth deranges the circles, and that the derangement can be alleviated or repaired by a proper education (Plato, 1971; Taylor, 1962). Another pathological result believed due to derangement of the circles in the head by birth trauma, was epilepsy. Interestingly, epilepsy is one of a number of pathological conditions associated with an excess of NRH. Plato himself did not suggest that NRH was related to the perturbations of the circles in the head. In fact he was an advocate of ambidexterity, and he attributed the weakness of the left hand to "the folly of nurses and mothers" in not encouraging the use of both hands equally (Lloyd, 1973, p.185). Sedgewick

James Sedgewick was an eighteenth century English apothecary who believed that many chronic diseases have origins in the prenatal period. According to Sedgewick, "half the ... chronical diseases with which we see children afflicted are only the secondary sighs and groanings, the evidential marks, and reproaches of parentive ill-spent life." He believed that "these consequences...will be brought on infants, by the debauchery of the mother ...so that ...the regulation of the mother, during her pregnancy, is an affair of the highest moment and consideration" (Plant, 1987).

Blondel James Blondel (1729), an eighteenth century obstetrician, also stressed the relationship between the prenatal environment and the welfare of the fetus. He suggested a continuum in fetal development, from loss of life, through feeble growth and weakness, to the healthy state. Among variables considered detrimental to the fetus he cited "distempers of the parents ..., great falls, bruises, and blows the mother receives,...the irregularity of her diet, ....immoderate dancing,...excess of laughing, frequent and violent sneezing, and all other agitations of the body..."And further: "The child may also suffer by the affections of the mother's mind. For the disappointment of what she desires is sufficient to make her uneasy...deprive her of sleep and quiet, and even of food, and...the child runs the risk for want of ...wholesome nourishment, to grow feeble and weak, and at last to lose its life."


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Little William John Little, in a series of lectures, and in a book entitled On the Nature and Treatment of the Deformities of the Human Frame (Accardo, 1989) considered the relationship between cerebral palsy, and perinatal events, in a series of 24 patients. He found spasticity associated with PBCs such as prematurity, difficult labour, instrument deliveries, asphyxia, and convulsions. Little delivered a paper to the Obstetrical Society of London (Little, 1861), in which he anticipated the idea of a continuum of reproductive casualty. He expressed surprise that previous medical authors seemed "quite unaware that abnormal parturition, besides ending in death or recovery, not unfrequently had ...a third termination in other diseases." He proposed a spectrum of long term deformity and disability, secondary to biochemical insult, acting most especially on the brains of "too early and unripe-born foetuses." Accardo (1989) reports that in the discussion following Little's paper there was a reaction of disbelief and defensiveness about this "utterly novel viewpoint that at a single stroke causally united both mental and motor disability in later childhood with the few minutes surrounding birth." And he quotes Cameron (1958) who reported that "Little's original communication unhappily failed to rouse the medical profession's interest in the question on any great scale." Little's emphasis on "the few minutes surrounding birth as the critical time in the etiology of cerebral palsy was criticized by Sigmund Freud (1968, p.257), who argued that difficulties in the birth process were themselves a manifestation of a fetus, compromised earlier, during intrauterine development. The issue of the relative importance, of earlier intrauterine problems, as opposed to problems during delivery, is still an important one. The balance of current evidence increasingly supports prenatal insult as relatively more important than perinatal insult as a determinant of morbidity (Nelson, 1989). The neurologist W.R.Gowers (1888,1893) strongly supported Little. Gowers accepted Little's theory of perinatal etiology, and proposed its extension to a broader spectrum of brain damage syndromes. After describing the symptoms of major brain damage, he suggested that "for every case in which severe effects result from serious injury, there are many cases in which a slighter lesion has more trifling consequences." This statement anticipates the modern idea of a continuum of reproductive casualty.

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Lombroso and Degeneracy Theory

Lombroso's contribution to the idea of reproductive casualty, was based on his observations of a relationship between criminality, and signs of congenital pathology, which he called "stigmata." Lombroso's concept of the "born criminal" implies that criminality, or the congenital conditions favouring it, is a manifestation of reproductive casualty. His work is still echoed in modern research on the relationship between crime or delinquency and conditions associated with PBCs, including NRH (Andrew, 1978, 1980; Gabrielli and Mednick, 1980). Lombroso studied thousands of criminals, alive, and post-mortem, and noted among them an excess of anatomical anomalies. In view of the congenital nature of these anomalies and their increased frequency among criminals, he suggested a congenital determination of criminal tendency, in a class of criminals he described as "born criminals." Lombroso was impressed by the high frequency of congenital defects among criminals. These defects included retreating forehead, exaggeration of the frontal sinus and the supercilliary arches, oxycephaly, open internasal suture, anomalous teeth, facial asymmetries, fusion of the atlas, and anomalies of the occipital opening (Lombroso, 1911). He considered such anomalies as the "result of error in the development of the foetal skull, or a product of diseases which have slowly evolved in the nervous centers." He also found anomalies in the convolutions of the brain, higher frequencies of abnormalities of the foot, precocious wrinkles, absence of baldness, low and narrow forehead, large jaws, peculiarities of hair, iris, ears, nose, teeth heart, genitalia, stomach, and frequent left-handedness or

.

ambidextenty

The handedness relationship was developed in a separate paper (Lombroso, 1903). Lombroso concluded that the excess of anomalies among criminals had a prenatal origin "by arrest of development or by disease acquired from different organs, above all, from the nervous centers.." Lombroso noted similarities between the epileptic and the "born criminal;" in fact he considered criminality as one of the manifestations of epilepsy. The various anomalies associated with criminality he considered as signs of degeneracy. Degeneracy was an important concept in late nineteenth century medicine. The term had negative emotional connotations. Lombroso, himself a Jew, had already defended Jews against their being labelled degenerate, during the first decade of the twentieth century, well before the rise of Hitler who used the term "degenerate" to label those he selected for elimination (Gilman, 1985, p. 156). The theory of degeneracy was formulated in 1857 by Benedict-Augustin Morel,


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one of the forefathers of modern psychiatry. Degeneracy, in its early usage, was associated with parental drunkenness, which according to Morel, produced congenital symptoms of depravity, alcoholic excess, and degradation in the first generation of offspring. This continues into the second and third generation, and by the fourth generation the line becomes extinct as a result of sterility (Plant, 1987). The concept of degeneracy came to be applied to a variety of conditions, including cretinism, masturbation, hysteria, madness, melancholia, epilepsy, and neurasthenia. Sigmund Freud, in his early writing, accepted the idea of degeneracy with respect to neurosis, which he felt had roots in prenatal life. By 1917, however, he was protesting the reliance of psychiatrists on concepts such as degeneracy, hereditary disposition, and constitutional inferiority (Gilman, 1985, pp. 205 ff.). In 1892 Mobius introduced the term "endogenous" to psychiatry. This emotionally neutral word began to replace the term degenerate, making it possible to refer to biologically determined congenital events without the negative connotation of terms like degenerate and degeneracy (Gilman, 1985, p. 277). Among the more recent additions to the continuum of reproductive casualty, is the fetal alcohol syndrome (Jones, Smith, Ulleland, and Streissguth, 1973), with symptoms resembling those noted by Lombroso in his "born criminals". The symptoms of fetal alcohol syndrome include prenatal growth retardation, facial anomalies, and central nervous system dysfunction. The syndrome is also associated with skeletal anomalies, cardiovascular defects, kidney anomalies, neural tube defects, and behavioural anomalies such as mental retardation, hyperactivity, sleep disorders and irritability (Abel, 1985). Though the relationship between fetal alcohol syndrome and handedness has not yet been studied, there is reason to predict an excess of NRH in victims of the syndrome (Zimmerberg and Riley, 1988). 1900-1910

During this decade, the problems of reproductive casualty, and the pathological aspects of NRH were of interest to others beside Lombroso. Charles Woodruff (1909) believed that ambidexterity and left-handedness resulted from problems in prenatal development. He suggested a relationship between sinistrality and nervous instability or neurosis. There was interest in the association between NRH and epilepsy (Redlich, 1908; Wallin, 1910). Ballantyne (1902) emphasized prenatal and perinatal factors in abnormal development. He

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believed that toxemia, bleeding during pregnancy, malnutrition, infection, fetal asphyxia, and trauma, were implicated in fetal disease, morbidity, and mortality. Wilhelm Fliess (1906), a physician, and friend of Sigmund Freud, postulated a relationship between handedness and sexual orientation. According to Fliess left-handed men display marked female secondary sexual characteristics, and left-handed women display marked male secondary characteristics. Effeminate men and masculine women, he believed, were more likely to be left-handed or ambidextrous. Fliess believed that left-handedness is symptomatic of incomplete sexual dominance, which might be expressed in homosexual behaviour (Harrington, 1988, p. 94). Fliess was influenced by the degeneracy theory, and considered the essence of degeneracy to consists in a displacement of the male and female qualities. He offered this as a reason why "so many left-handed people are involved in prostitution and criminal activities" (Fritsch, 1968, p. 133). Handedness was a topic in the correspondence between Fliess and Freud. In a letter to Fliess, Freud wrote "it seemed to me that you regarded me as somewhat left-handed, and if this were the case you would tell me, for such a revelation of myself would not hurt my feelings..Actually I am not aware of any preferences for the left, either now or in childhood. It would be more correct to say that there was a time when I had two left hands." In the same letter Freud also referred to himself as "right-left blind (Fritsch, 1978). The matter of a relationship between NRH and homosexuality has recently been resurrected by evidence of excess NRH among homosexuals (Lindesay, 1987). 1911-1950

During this period, an interest in the prenatal and perinatal determinants of schizophrenia was developing. Mackenzie (1912) considered the possible importance of "intrauterine disease" in the development of schizophrenia. He explored the possibility that some cases of schizophrenia were caused by prenatally induced brain deformity, whose effects did not appear until later in life. Turner (1912) believed that schizophreniawas due to developmental defects of the brain, interacting with the stresses of adult life to produce symptoms. Southard (1915) did post-mortem studies of the brains of schizophrenics, and reported morphological abnormalities in the frontal area. He concluded that schizophrenia results from embryonic maldevelopment of the frontal brain. Rosanoff (Rosanoff, Handy, Plesset and Brush, 1934) proposed interaction between genetic factors and early brain injury in the pathogenesis of


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schizophrenia. He likened schizophrenia to epilepsy, in so far as both might be late sequels of birth trauma. This organic view, which has gained support in recent years, was in the 1930's, at a relative disadvantage because of the popularity of psychodynamic or psychoanalytictheories of mental disease. Dalen (1988) in a paper emphasizing PBCs in psychopathology writes: "The idea that some cases of early brain damage only become manifest as psychological disorders in adult life is not new, but it has been kept out of the mainstream of psychiatric thought for a very long time." Quinan (1930) addressed the relationship between handedness and schizophrenia. Wile (1934) in a book on left-handedness, concluded that handedness may be affected by non-hereditary causes, such as factors in embryonic development, birth injuries to nerves, muscles, or brain, and neonatal difficulties. Wile also reviewed the relationship between NRH and cognitive problems such as writing defects, speech deficiencies, and reading disability. The relationship between atypical brain laterality and cognitive difficulties, especially dyslexia, was the focus of Samuel Orton during this period (Orton, 1937). At about the same time, Cyril Burt (1937, p.287) considered the relationship of left-handedness to learning disabilities. He considered left-handedness as "a mark of an ill-organized nervous system." Schwartz (1961) cites two German language papers bearing on the relationship between PBCs and handedness. In the first of these Brander (194O), argues that left-handedness is a persistent characteristic of prematurity, and in the second, Riemann (1949) considers left-handedness as a permanent "disability" following birth trauma. Gesell and Amatruda (1947) in a more general vein stated that perinatal cerebral injury might account for children with personality deviations, dullness, laterality problems, and various other forms of inadequacies and subclinical deficits. 1951-1970

It was during this period that Pasamanick and his associates developed the idea of a continuum of reproductive casualty. In a series of investigations, they found excessive physical and psychological morbidity in the offspring of compromised pregnancies. The continuum of reproductive casualty ranges from a lethal end, consisting of aborted fetuses, stillbirths, and neonatal death, to a variety of sublethal conditions of varying seriousness, including malformations, cerebral palsy, epilepsy, mental deficiency, autism, behavioural and neuropsychiatric disorders, learning disabilities, language problems, strabismus, accident proneness, increased variability, reduced threshold to stress, and as

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described earlier, NRH (Lilienfeld and Pasamanick, 1954; Pasamanick and Knobloch, 1960; Pasamanick and Knobloch, 1961; Pasamanick and Knobloch, 1966; Pasamanick and Lilienfeld, 1955). This wide range of problems, related to PBCs, was attributed largely to a vulnerability of the developing central nervous system to insults associated with pregnancy. Antecedent factors associated with morbidity include prematurity and low birth weight, maternal-fetal blood incompatibilities, maternal endocrine disorders, maternal age, hypoxia, radiation, infection, maternal smoking, alcohol intake, other drugs, and seasonal factors. These variables can effect pregnancy at any stage, in contrast to a prevailing belief that negative outcomes of pregnancy are due to the events around the delivery period. This issue had earlier been considered in a controversy between Little and Freud cited earlier. It was considered wrong, for example to equate breathing difficulty at birth with damage induced during delivery. Rather, prenatally determined pre-existing problems could interfere with adjustment to extra-uterine life and the initiation of respiration (Knobloch and Pasarnanick, 1962). Pregnancy complications believed to have the closest relationship to morbidity are the "prolonged and probably anoxia-producing" complications (Pasamanick and Knobloch, 196fj). This emphasis on atypical intrauterine factors, becoming manifest in perinatal complications, is supported in modern obstetrical thinking (Naeye and Peters, 1987; Nelson, 1989). Pasamanick and his associates drew, from their findings on reproductive casualty, important implications about prevention, socio-economic variables, and genetics. Manifestations of the continuum of reproductive casualty can, in principle, be prevented by any interventions which serve to reduce PBCs. It follows that prenatal medical care, optimal nutrition, and avoidance of harmful substances and harmful environments, can substantially reduce problems of prenatal development, and related reproductive casualty. In this sense the emphasis on reproductive casualty is basically optimistic, because it assumes that appropriate interventions, either medical or social, will reduce reproductive casualty, and the associated costs to society, families, and individuals. PBCs occur in a socio-economic context (Alvarez, 1982; Birch and GUSSOW, 1970; Oakley, Macfarlane, and Chalrners, 1982; Saugstad, 1989), as well as in a medical context. Many variables associated with less than optimal reproductive conditions, are also associated with poverty. Prevention of PBCs, and hence reproductive casualty, can be effected by interventions that minimize the negative effects of socio-economic disadvantage.


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This approach to reproductive casualty also leads to an emphasis on environmental rather than genetic determinants of prenatal maldevelopment, as reflected in the following passages (Pasamanick and Knobloch, 1966): little is known about the predisposing factors which might lead one mother to produce a damaged child while another exposed to the same complications, and even of the same severity, might have a normal offspring. There are some data to indicate that mothers who are themselves of lower- class origin and were exposed to lifelong deprivation from conception to adulthood, as indicated by their poorer physical growth, are the ones who are predisposed to produce children who will exhibit the ...disorders we are discussing. This predisposition is frequently on a post hoc basis, given a hereditary explanation by some writers. Epilepsy...what light do our results cast on the genetic hypothesis? ...It is reasonable to assume that if prenatal and perinatal factors play a significant role in the causation of some forms of epilepsy and genetic factors in others, our cases in which the pregnancy factors were absent should have had more epileptic parents than those cases in which these factors were present. This was not found to be true, and makes it necessary to re-examine the genetic hypothesis in epilepsy. May not the familial aggregation of epilepsy be a reflection of the occurrence of familial aggregation of the prenatal and perinatal factors under discussion...?

Recent Approaches to NRH and Pathology The relationship between NRH and other pathological conditions has been noted for a long time, especially for epilepsy and mental retardation (Pipe, 1988). Various theoretical positions have been taken in approaching this relationship (Porac and Coren, 1977). Since NRH often appears without other obvious pathology, a distinction between two kinds of NRH has been made, namely, pathological NRH and "normal" NRH. The issue is complicated by some evidence of familial factors in NRH, and this has encouraged genetic explanations. Often "normal" NRH is assumed to be genetic in origin. Genetic approaches construct models to account for the distribution of handedness. These models differ in assumptions about the kinds of genes involved. Thus, for example, a model may assume separate genes for right and left-handedness, or

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only a single right-handedness, or right shift gene, with different degrees of expression. Four theoretical positions which address the relationship between NRH and pathology are described, those of Satz, Bakan, Geschwind, and Annett. Satz: Two Kinds of NRH

Satz distinguishes between two kinds of NRH, pathological and normal (Satz, 1972; Satz, 1973). In the extreme, a person with left hemisphere damage, resulting in right hand or right arm paralysis, is forced to use the left hand for many functions. This is clearly a case of pathological left-handedness. More generally, early damage to one cerebral hemisphere results in impaired function of the contralateral hand which, if it is the right hand, results in pathological left-handedness or ambidexterity. This model also allows for pathological right-handedness, if right hemisphere damage results in left hand impairment (Satz, 1972). Satz and his associates have defined a clinical syndrome of pathological left-handedness which is defined by trophic changes in the extremities, reorganization of speech and visuospatial functions, early trauma and PBCs (Silva and Satz; 1979; Satz, Orsini, Saslow and Henry, 1985). This model considers the vast majority of left-handed people have normal or non-pathological handedness, where the left-handedness is due to genetic or cultural determinants. Pathological NRH, in this theory, requires evidence of actual or presumed pathology. When evidence of pathology is not apparent, NRH is considered "normal." A weakness of this model is the sharp distinction made between normal and pathological NRH. This dichotomy results from an overly restrictive definition of pathology. Pathological NRH, according to this model, has to be associated either with obvious pathology, such as paralysis of the right arm or hand (for pathological left-handedness), or other clear-cut evidence of brain dysfunction, such as epilepsy, mental retardation, or PBCs. There is a continuum of overt expression of pathology, where some pathological signs associated with NRH are obvious, such as right arm paralysis, and other signs, such as EEG or biochemical abnormalities are less obvious. In some cases pathology may be apparent, and in other cases pathology may be detectable only by EEG records (Shaw, Colter, and Resek, 1983) or biochemical assay. Pathology is no less pathological if it is less obvious. The criterion of clear evidence of pathology, when used to classify NRH as either normal or pathological, can be quite misleading. Furthermore, the pathologies associated with NRH, and possibly having a common or related etiology, may not be


47

obvious, even when NRH is obvious, because they do not become manifest until later. For example, there is evidence of a relationship between NRH and early onset Alzheimer’s disease (Seltzer, Burres, and Sherwin, 1984). Both NRH and early Alzheimer’s disease may have a common precursor in prenatal or perinatal insult to the brain. Should the NRH be considered normal in early life, and pathological some years later when the symptoms of Alzheimer’s disease become obvious? Another condition related to NRH is schizophrenia (Chapman and Chapman, 1987; Cur, 1977; Katsanis and Iacono, 1989; Manoach, Maher, and Manschreck, 1988). Schizophrenia does not usually become apparent until early adulthood. If both NRH and schizophrenia have their origin in prenatal insult to the left hemisphere, is it necessary to wait until schizophrenic symptoms occur before considering the NRH as pathological? There may be other cases where mild brain abnormalities, induced by prenatal or perinatal insults, result in NRH without entailing other obvious signs of neurological pathology, or where symptoms of neurological pathology are greatly delayed, or where pathology becomes manifest in non-neurologicalsymptoms. To consider such cases of NRH as “normal“ or as genetically determined, is to ignore the subtleties of pathological expression.

Bakan: NRH as Reproductive Casualty Bakan (Bakan, 1971; Bakan, 1975; Bakan, 1978; Bakan, Dibb and Reed, 1973) regards NRH, when occurring in the absence of other signs of pathology, as a relatively prevalent and benign manifestation of prenatal or perinatal stress. He suggests that NRH be added to the list of conditions which define a continuum of reproductive casualty. This view is based on relationships between NRH and other forms of pathology, and on the excess of NRH associated with PBCs, even when other signs of pathology are not apparent. This theory holds that it is possible for PBCs to so affect the central nervous system, as to result in a functional reorganization,that produces NRH, without producing other signs of obvious pathology. What might be interpreted as “normal,” or genetically determined NRH in Satz’s model, would be interpreted as not “normal,”and environmentally produced, by Bakan. Bakan suggests that hypoxic insult to the developing nervous system, is a likely mechanism leading to a reorganization, resulting in reduction of right hand use or efficiency (Bakan, 1978). Pyramidal motor neurons, involved in control of hand use, are especially vulnerable to hypoxic damage (Lassek, 1954).

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Damage to these cells need not be associated with gross evidence of pathology. Pyramidal lesions may initially produce transient contralateral motor weakness, power impairment, spasticity and paralysis, followed by rapid and remarkable recovery, and a high degree of compensation, so that functional defects are difficult to detect (Lassek, 1954). Decreased efficiency of the right hand, leading to a change of hand preference, may be the only apparent residual of prenatal or perinatal hypoxia. The major difference between the Satz and Bakan approaches to pathological NRH Lies in Satz's considering most NRH as normally or genetically determined, while Bakan maintains that the determination of NRH results from the consequences of PBCs. Though Bakan does not completely rule out genetic influences in the determination of NRH, he does reject the simple notion of a gene or genes for NRH. Genetic factors could possibly operate by influencing maternal anatomy, intrauterine variables, or perinatal variables that increase the probability of NRH. Essentially Bakan's position rejects two kinds of NRH, normal and pathological, and more parsimoniously assumes one kind of NRH, associated with a continuum from lesser to greater expression of pathology. The hypothesized relationship between PBCs and NRH has stimulated a considerable amount of research and controversy in the neuropsychological literature. Much of this research has been done with non-clinical groups such a$ "normal" university students, without evidence of paralysis, spasticity, or other pathology. Even within such groups there is evidence for a relationship between NRH and PBCs. The evidence for non-clinical populations has recently been reviewed and subjected to a meta-analysis (Searleman, Coren, and Porac, 1989). Taking the studies together they found statistical evidence in support of a relationship between NRH and PBCs in non-clinical samples. Even where individual studies fail to obtain positive results, they very often show directional effects favouring the hypothesized relationship between PBCs and NRH (McManus, 1981). A recent study (VanStrien, Bouma, and Bakker, 1987), not included in the meta-analysis, provides further support for the relationship between NRH and PBCs. In a large non-clinical sample of students, which included 243 who wrote left-handed, there was a significantly raised incidence of PBCs. Left-handed subjects reported two or more PBCs (out of 23 possible) twice as often as right-handers. In another recent study (Schwartz, 1988) left-handedness was associated with significantly lower Apgar scores at birth; low Apgar scores are associated with hypoxia and increased incidence of neurological abnormality (Nelson, 1989). In a recent follow-up study of prematurely born children (Ross,


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Lipper, and Auld, 1987) evaluated at age four, 36% were NRH as compared to 20% for members a control group born at term. The parents of both groups showed the same incidence of right-handedness. The authors of this study conclude that intrauterine events and perinatal illnesses associated with prematurity probably affect the brain in ways which lead to NRH. The model of NRH etiology proposed by Bakan assumes that NRH is a result of PBCs, which result in reduced effectiveness of the right hand, leading to decreased use of the right hand, or NRH. These PBCs may produce other forms of atypical laterality, such as left footedness, crossed dominance, or other manifestations of reproductive casualty. In a more specific form of the model, the noxious event leading to NRH is held to be a reduction in oxygen supply to the fetal brain, and especially to the motor area of the left hemisphere, which is more vulnerable to the effects of hypoxia (Braun and Myers, 1975; Brann, 1989). Direct examination of the noxious events in the prenatal or perinatal environment is not usually feasible. Support for the model has been sought through indirect indicators of prenatal or perinatal stress, i.e. PBCs. There are statistical relationships between these indicators and hypoxic stress, or other kinds of stress, leading to brain and behavioural reorganization associated with NRH. Among the indicators examined are birth order, birth weight, breech birth, multiple births, pre-delivery bleeding by the mother, prematurity etc. Sometimes combinations of indicators are used, such as number of PBCs, or a measure of neonate viability such as the Apgar score. This approach has significant problems, such as inaccuracy of reports of PBCs by the mother or child, inaccuracy and incompleteness of medical records, and relatively low degrees of relationship between PBCs and any single pathological outcome. The timing of the noxious events leading to NRH also poses a problem. Complications may have different effects, depending on whether they occur early or late in the pregnancy, or whether they occur prenatally or perinatally. In sum, there may be a low level of relationship between general indications of stress, and the occurrence of the specific stress or stresses which become manifest as NRH. In a recent study, Bakan (1987) has used reports of maternal cigarette smoking during pregnancy, as an indicator of prenatal chronic hypoxic stress. It is generally agreed that maternal smoking during pregnancy results in a hypoxic state for the fetus (Socol, Manning, Murata, and Druzin, 1982). Maternal smoking also produces low birth weight, higher infant mortality, decrease in fetal breathing movements (Manning and Feyerabend, 1976), and an increase in PBCs. It was predicted that offspring of smoking mothers would be more likely

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to develop NRH because of the chronic hypoxia related to maternal smoking. This hypothesis was supported by a significantly higher frequency of NRH among the offspring of smoking mothers, than among the offspring of non-smoking mothers.

Geschwind The Testosterone Connection Geschwind and his associates (Behan and Geschwind, 1985; Geschwind and Behan, 1982; Geschwind and Behan, 1984; Geschwind and Galaburda, 1985) proposed another theory of NRH, which emphasizes problems in prenatal development. This theory assumes that, in most humans, there is an innate bias to left hemisphere dominance for language and handedness. Certain influences during fetal life can diminish this bias, to produce NRH. The major factor responsible for the events leading to NRH is prenatal testosterone. As a result of either increased concentration of testosterone, or abnormal sensitivity to it, development of the left hemisphere is delayed. This delay leads to altered lateralization and a shift to the left in the distribution of handedness. The atypical development of the left hemisphere also results in cognitive problems such as dyslexia, attention deficit disorders, learning disabilities, and mental retardation, each of which is also characterized by an excess of NRH. Matters are further complicated because of the close relationship between prenatal sex hormones and the developing immunological system. Testosterone not only retards the growth of the left hemisphere, but it also retards the development of the thymus gland, an essential part of the immunological system. Individuals who suffer insult to the left hemisphere are likely to suffer insult to the thymus. Diseases related to immunological dysfunction, are likely to occur more often among those with NRH. The importance of testosterone, a male hormone, also leads to the expectation of sex differences in susceptibility to the effects of testosterone. Geschwind and his collaborators have reported evidence for relationships between gender, NRH, and a variety of medical and psychological problems associated either with malfunctioning of the left hemisphere, or the immunological system. The theory has stimulated research, especially on the medical correlates of NRH, such as immune diseases. The theory places NRH in a pathological context. The Geschwind model emphasizes the importance of testosterone on development of the brain and immunological system. If excess testosterone, or excessive sensitivity to testosterone, has a noxious effect on lateral neurodevelopment, does this imply that testosterone is the only stimulant to the


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neurodevelopmental processes, leading to NRH? Might there be other mechanisms leading to NRH, or immunological problems? Furthermore, what is it that leads to excess testosterone production, or increased sensitivity to testosterone? Prenatal stress may occur in a variety of ways, including malnutrition, psychological stress, maternal fever, infection, alcohol, cigarettes, bright lights, noise, polluted air, high altitude, and hypoxia. Different stresses, occurring at critical periods during gestation, may produce atypical development in physiological and anatomical systems, leading to NRH, atypical immunity, or other pathological conditions, by mechanisms unrelated to testosterone. Though testosterone status may be associated with some of the causes of prenatal stress, it may not be the most likely, or the only factor associated with NRH or immunological pathology. It has been shown, for example, that prenatal stress can produce dopamine asymmetries (Fride and Weinstock, 1989) associated with changes in the laterality of tail positioning in rats. The stress of prenatal hypoxia has been shown to produce increases in adrenalin, noradrenalin, ACTH, and vasopressin, as well as reduced EEG voltage and reduction of fetal breathing movements (Dawes, 1976). Perhaps testosterone abnormalities are secondary to other forms of prenatal stress. Testosterone levels in humans are known to fluctuate in response to stress (Rose, 1984), and stress-induced changes in maternal levels of testosterone may influence fetal levels of testosterone. Maternal stress from bright lights and loud noise can alter plasma testosterone in the rat fetus (Ward and Weisz, 1980, 1984), and demasculinize the behaviour of male offspring. Testosterone may have an effect on lateralization in utero, but it may not be the exclusive mediator of these effects. Annett: Genetics or Pathology? The genetic theory of NRH proposed by Annett (Annett, 1985) is not ostensibly a theory of pathological NRH. Unlike some other genetic theories, it does not postulate a gene for left-handedness and another for right-handedness. The model assumes only a right shift gene, leading to preferred use of the right hand, right foot, and so on. When this gene is denied expression, the result is development of random dominance, ambidexterity, or left-handedness, i.e. NRH. A weakness of the theory is its failure to specify conditions which prevent expression of the right-shift gene. The theory assumes that chance factors or "accidental biases to the left hand" are involved.

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If an additional assumption is added to the theory, then it becomes a pathological theory of NRH. The additional assumption is that some noxious prenatal or perinatal event, be it hypoxia, testosterone, or whatever, leads to developmental reorganization, such that the normal expression of the right shift gene is prevented. In a sense Annett (1988) already implies this in her discussion of the excess NRH reported among homosexuals (Lindesay, 1988). She argues that in homosexuals there may be a blocked expression of the right shift gene, but she attributes this to anomalous delay in cerebral maturation, occurring in the third trimester of pregnancy or shortly after birth. This delay is a likely result of a pathological pregnancy complication. If all goes well and normally, the right shift gene is expressed; if not, its expression is prevented and NRH is the result. With the addition of this assumption the theory becomes compatible with that of Bakan and also that of Geschwind.

The Comorbidity Factor Cooccurrence of NRH with other forms of pathology is the key factor in the diagnosis of pathological NRH. Thus, the joint occurrence of hemiplegia in the right arm or hand, and left-handedness, supports an inference of pathological lelt-handedness. NRH often occurs jointly with mental retardation (Pipe, 1988), often the result of PBCs (Gray, Dean, Strom, Wheeler, and Brockley, 1989; Hicks and Barton, 1975; Naeye, 1987). The joint occurrence of NRH and mental retardation suggests pathological NRH. A similar analysis could be made for epilepsy, often characterized by early brain insult, and also associated with excess NRH. Sometimes the classification of NRH is complicated by temporal factors. As mentioned earlier, diseases associated with NRH, may not become obvious until some years after NRH becomes apparent. Excess NRH is found with schizophrenia, and early onset dementia (Alzheimer’s disease). Victims of either of these diseases may manifest NRH years before the symptoms appear. NRH may have its origin in the same or related insult to the brain that leads to schizophrenia or dementia, but the pathological nature of the NRH would not be apparent until the later appearance of symptoms. If NRH is present, without indication of comorbidity, then a history of PBCs may support the inference of pathological NRH. Sometimes NRH appears jointly with other atypical behaviours, where the relationship to brain insult is possible, but not obvious. This might be the case with sleep disorders, developmental disorders, delinquency, learning disabilities, or accident proneness.


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As additional pathological correlates of NRH are discovered, an increased proportion of NRH, will be attributable to pathological origin. The hypothesis that all or most NRH is pathological has heuristic value, since it encourages the search for correlates of NRH. Theories which emphasize pathological NRH, encourage research on the joint occurrence of NRH with other pathological conditions. Investigators look for excessive NRH in groups with pathological conditions, or they compare the prevalence of pathological conditions in groups with and without NRH. This section summarizes conditions for which excess NRH has been found. Global Correlates

Excess left-handedness was found among men rejected for military service by the U.S. selective service system (Karpinos and Grossman, 1953). Rejection from military service is usually for medical or cognitive problems, and constitutes a global indicator of such problems. Another global indicator of medical pathology is life span. In a study of deceased baseball players, it was found that left-handed players had a shorter life span than right-handed players (Halpern and Coren, 1988). This could be due to early failure of physiological systems, higher accident rates, use of substances such as alcohol or tobacco, higher rate of suicide, or poor adjustment to products designed for a right-handed majority (Coren, 1989; London, 1989). It has also been suggested (Brackenridge, 1981; Neale, 1988) that the secular trend toward increased left-handedness during this century may be due, in part, to the reduction in infant mortality resulting from medical advances. Decreased infant mortality may differentially favor survival of medically compromised and more vulnerable left-handers, resulting in a relative increase of left-handers in the population. The Psychopathology Connection

Certain forms of psychopathology have prenatal or perinatal origins. This can be inferred from the greater frequency of PBCs, anatomical peculiarities of the brain, and neurological soft signs, associated with psychopathology. Since excess NRH is also associated with psychopathology, it appears that the joint occurrence of NRH and psychopathology, is evidence for the related origins of both. The relationship between handedness, psychopathology, and PBCs is especially marked among schizophrenics. Schizophrenics often have a history of

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PBCs (Goodman, 1988;Goodman, 1989; Lewis, 1989). Brain imaging techniques often show abnormalities in schizophrenics (Silverton, Mednick, Schulsinger, Parnas, and Harrington, 1988). Ventricular enlargement, an indicator of hypoxia, and reduced brain size,is a frequent finding ( Volpe, 1987; Weinberger, Torrey, Neophytides, Klein, Rosenblatt, and Wyatt, 1979). Ventricular enlargement is also found with other neurodevelopmental disorders (Bergstrom, Bilk, and Rasmussen, 1984). Abnormal thickening of the corpus callosum, callosal agenesis, ischemic encephalopathy, arteriovenous malformations, and unusual gyral patterns are also more frequent in the brains of schizophrenics (Bigelow, Nasrallah, and Rauscher, 1983; Lewis, 1989). Schizophrenics also have an excess of physical anomalies, and neurological soft signs (Green, Satz, Gaier, Ganzell and Kharabi, 1989). They have a reduced life expectancy (Allebeck, 1989), and are at special risk for suicide, cardiovascular disease, and breast cancer (Harris, 1988). Schizophrenia is associated with various forms of motor dysfunction, resulting from prenatal developmental defects (Crayton and Meltzer, 1976, 1979; Manschreck, 1983; Scheibel and Kovelman, 1981). In addition left hemisphere pathology is associated with schizophrenia (Gruzelier and Hammond, 1976; Gur, 1977), and this is consistent with the excess NRH among schizophrenics (Chapman and Chapman, 1987; Chaugule and Master, 1981; Green, Satz, Smith, and Nelson, 1989; Gur, 1977; Katsanis and Iacono, 1989; Manoach, Maher, and Manschreck, 1988; Nasrallah, Keelor, Schroeder and Whitters, 1981; Piran, Bigler and Cohen, 1982; Shaw, Colter and Resek, 1983). Left-handed schizophrenics have significantly greater ventricular enlargement, and poorer neuropsychological test performance, than right-handed schizophrenics, suggesting a greater degree of cerebral dysfunction (Katsanis and Iacono, 1989). Excess NRH is also a feature of infantile autism or childhood schizophrenia (Barry and James, 1978; Colby and Parkison, 1977; Tsai, 1983). Excess NRH is also observed in affective disorders. There is an old case (Bruce, 1895) of double personality, in a patient alternating between a manic and a depressed persona, while switching between English and Welsh speech, and between right and left-handedness. Left-handedness appeared when the patient was in the depressive state. Sackeim and Decina (1983) found excess NRH in cases of bipolar depression. In a recent study (Bruder, Quitkin, Stewart, Marin, Voglmaier, and Harrison, 1989) a high incidence of left-handedness was found in patients with "non-melancholic atypical depression," i s . a depression where pleasure capacity is preserved, while at the same time there are symptoms of


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depression such as sleepiness, extreme bodily inertia (leaden paralysis), and rejection sensitivity. There is evidence for an excess of both PBCs and NRH among suicides, who are often depressed. Adolescent suicides were found to have a higher than normal occurrence of respiratory distress at birth, absence of early prenatal care, and increased maternal disease during pregnancy (Salk, Lipsitt, Sturner, Reilly, and Levat, 1985). Other variables more often found in the suicide group, included a history of premature births to the mother, abnormal bleeding during pregnancy, infection, problems with labour, and placental disorders. The authors of this study believe that infants who survive adverse perinatal conditions, are more vulnerable to the stressful conditions eliciting suicide. A similar result was found in another group of suicides where PBCs occurred more often than in a control group (Jacobson, Eklund, Hamberger, Linnarsson, Sedvall, and Valverius, 1987). The authors suggest that the effects of hypoxia and obstetric injuries lead to brain damage, which increases the likelihood of self-destructive behaviour. From these results it appears that suicidal behaviour is part of a continuum of reproductive casualty. In yet another study, excess NRH has been found among the victims of suicide (Chyatte and Smith, 1981). Once again there is a pattern of excess NRH, related to a form of psychopathology, which is characterized by an excess PBCs. Excess NRH has been reported for a number of other problems which vary in severity, but have in common a psychological component. Alcoholism is an example. An excess of NRH in a group of hospitalized alcoholics was noted by Bakan (1973), and confirmed by others (Chyatte and Smith, 1981; Harburg, 1981; London, Kibbee, and Holt, 1985; Nasrallah, Keelor, and McCalley-Whitters, 1983). Left-handed alcoholics are more resistant to treatment than right-handed alcoholics (London, 1985; Smith and Chyatte, 1983). It has been found that prenatal exposure of rats to alcohol reduces lateral asymmetry (Zimmerberg and Riley, 1988). Prenatal alcohol also produces a hypoxic effect on the fetus (Abel, 1985), and prenatal hypoxia might account for the joint occurrence of alcoholism and NRH in affected individuals. Since there is a relationship between alcohol consumption and cigarette smoking (Harburg, 1981), it is interesting to note that left-handers are more likely than right-handers to smoke and to smoke more heavily (Harburg, Feldstein, and Papsdorf, 1978). Certain personality problems are also related to excess NRH. Studies have shown increased NRH related to anxiety (Hicks and Pellegrini, 1978), anti-social behaviour (Standage, 1983), field dependence (Silverman, Adevai, McGough, 1966), alexithymia (Rodenhauser, Khamis, and Faryna, 1986), and emotionality

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(Harburg, Roeper, Ozgoren and Feldstein, 1981). There are also relationships between NRH and sleep disorder (Coren and Searleman, 1987), hyperactivity (Bakan, 1988), delinquency (Gabrielli and Mednick, 1980; Grace, 1987), psychopathy (Cuff, 1930; Fedora and Fedora, 1983), accident proneness (Coren, 1989), and homosexuality (Lindesay, 1987). Left-handers are less likely to marry, and more likely to divorce than right-handers (Lansky, Feinstein, and Peterson, 1988), suggesting a possibility of personality problems in social or heterosexual relationships. The Immunological Connection

The Geschwind model of NRH has stimulated interest in the relationship between NRH and diseases implicating the immunological system. An excess of, or sensitivity to, prenatal testosterone, suggested as the cause of delayed left hemisphere development, also impairs development of the thymus gland, and the immunological system (Geschwind and Galaburda, 1985). Infants who suffer prenatal growth retardation are born with reduced peripheral T-lymphocytes, indicating dysfunction of the thymus gland (Ferguson, Lawlor, Neumann, Oh, and Stiehm, 1974). The immunological system is asymmetrically represented in the hemispheres. Left hemisphere brain lesions result in reduction of T-cell mediated activity, whereas similar lesions in the right hemisphere do not have this effect (Barneoud, Neveu, Vitiello, and Le Moal, 1987). Left-handers show less peripheral lymphocyte activity than right-handers (Yokoyama, Hara, and Shoitsuki, 1987). In their research and review of this area, Geschwind and his collaborators have implicated various immunological diseases, including allergies, thyroid disease, rheumatoid arthritis, migraine, myasthenia gravis, and gastrointestinal diseases, such as celiac disease, ulcerative colitis, and ileitis. They provide evidence of relationships between immunological diseases and both NRH and certain developmental disorders as dyslexia, stuttering, delayed speech, childhood autism, hyperactivity, and other learning disabilities (Geschwind and Behan, 1982; Geschwind and Galaburda, 1984). The predictions concerning these relationships have not always been confirmed, but there is a body of evidence showing relationships between developmental, immunological, and laterality variables. Smith (1987) found an excess of left-handers among patients attending an allergy clinic. This was particularly marked for patients with urticaria and eczema. In another study (Weinstein and Pieper, 1988) an excess of NRH was again found in a group of


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allergic patients. There is also convergent evidence of relationships between allergies, PBCs (Bakan, 1977; Salk, Grellong, Straus, and Dietrich, 1974) and EEG abnormalities, suggestive of atypical brain function (Czubakski, Massakowski, Zawisza, and Makowska, 1979). Among other diseases with an immunological component, there is also evidence of excess NRH. Searlman and Fugagli (1987) report excess NRH in patients with Crohn’s disease, ulcerative colitis, and insulin dependent type 1 diabetes. There are more immune thyroid disorders among left-handers (Schachter and Galaburda, 1986; London and Glick, 1988). NRH may be related to migraine disease (Guidetti, 1987), and there is an insignificant trend to more NRH in patients with systemic lupus erythmatosis (Salcedo, Spiegler, and Magilavy, 1985). Cancer is a disease characterized by immunological dysfunction. It was found that the onset of breast cancer occurs about three years earlier in left-handed than in right-handed women (Kramer, Albrecht and Miller, 1985). There is as yet no study implicating handedness in AIDS disease, but there is some indication of a laterality/AIDS relationship (Bear, Agostini, and Saporta, 1988). AIDS patients exhibit a significant reversal of the typically greater right frontal lobe width (CT scan measure), found in a control group. These authors also cite unpublished findings of increased prevalence of childhood learning disabilities in homosexual men undergoing evaluation for AIDS. Excess NRH has been found among homosexuals (Lindesay, 1987). Reversals of normal asymmetry have been reported for nonright-handed subjects (Bear, Schiff, Saver, Greenberg, and Freeman, 1986). Other Correlates of NRH

Other correlates of NRH which have been observed include medical conditions, anatomic, physiological, and behavioural anomalies. Some diseases characterized by chromosomal pathology show excess NRH. This has been found in Down’s syndrome (Giencke and Lewandowski, 1989; Pipe, 1987), Turner syndrome, and Klinefelter’s syndrome, or XXY disease (Netley and Rover, 1982). Various anatomical anomalies are associated with NRH. The coexistence of congenital anatomical anomalies and NRH is further evidence for the pathology/NRH association. Anomalies include increased thickness of corpus callosum (Witelson, 1985;Witelson, 1989), cerebral asymmetry differences (Bear, Schiff, Saver, Greenberg, and Freeman, 1986), dermatoglyphic anomalies (Cummins, 1940; Jantz, Fohl, and Zahler, 1979), arteriographic anomalies

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(Hochberg, and LeMay, 1975), hare lip and cleft palate (Geschwind and Galaburda, 1985; Rintala, 1985), adrenal hyperplasia (Nass, Baker, Speiser, Virdis, Balsamo, Cacciari, Loche, Dumic, and New, 1987), and fusion malformations (Boklage, 1987). Twinning is related to NRH. There is excess NRH among twins, which has aroused considerable interest among geneticists and developmental psychologists (Boklage, 1984; Neale, 1988). Excess NRH appears for both identical and fraternal twins (Springer and Searleman, 1980). Twinning is associated with PBCs and low birth weight, which may predispose toward NRH (Segal, 1989). The very occurrence of twinning may be a pregnancy complication (James, 1977; James, 1983), in that intrauterine hypoxia has been shown to be a determinant of twinning. A number of studies have found differences in physiological variables, between NRH and right-handedness. Left-handers have lower monoamine oxidase levels (MAO) than right-handers (Coursey, Buchsbaum and Murphy, 1979). In the same study it was found that low MA0 levels are also associated with more psychiatric problems, more psychiatric problems in relatives, more criminal convictions, more experimentation with illegal drugs, and elevated scores on the MMPI. Alcoholics, a group with excess NRH also tend to have low MA0 activity. There is evidence that left-handers are more reactive to drugs which influence the brain (Irwin, 1985). Differences between right and left-handers have also been found in EEG measures (Chyatte, Abern, Reddy and Botticelli, 1979), which tend to be more abnormal for left-handers. Left-handedness is also associated with delayed physical maturation (Coren, Searleman and Porac, 1986). Other correlates of NRH include essential tremor (Biary, 1985 ), strabismus and other visual problems (Lessel, 1986), de la Tourette syndrome (Shapiro, Shapiro, Brunn and Sweet, 1978), sleep disorder (Coren and Searleman, 1987), clumsiness (Bishop, 1980), vegetarianism (Chyatte, Chyatte and Althoff, 1979), and Rorschach figure-ground anomalies (Finn and Neuringer, 1968).

NRH and Beyond NRH is considered as one of many outcomes of a less than optimal prenatal or perinatal environment, or as a manifestation of reproductive casualty. The emphasis in the laterality literature, and in this paper, has been on NRH, but similar arguments apply as well to other anomalies of laterality such as pathological right-handedness and crossed dominance. In pathological


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right-handedness excessive reliance on the right hand results from effects of PBCs, leading to weakness or inefficiency of the left hand. Examples of crossed d o m i n a n c e i n c l u d e right-handedness/left-footedness, o r right-handedness/left-eyednesscombinations. Pathological right-handedness and crossed dominance are possible components of a continuum of reproductive casualty. There is very little research on pathological correlates of pathological right-handedness (Annett and Manning, 1989), but there is more for crossed dominance (Krinicki and Nahos, 1979, Piran, Bigler, and Cohen, 1982; Trembly, 1968; Trembly, 1976; Waddy and Kirkby, 1976). The prevalent view considers NRH as either normal or pathological. It is considered pathological, if associated with certain pathologies, (e.g. hemiplegia, seizures), especially those implicating the left hemisphere. However, the literature shows a much wider range of pathological correlates of NRH than has traditionally been considered in the determination of pathological NRH. At the least, this suggests that NRH is more often pathological than has heretofore been believed. NRH should be considered pathological, not only if associated with things like right hemiplegia, seizures, mental retardation (Pipe, 1988) etc., but with an extensive range of problems including various forms of psychopathology, personality disorders, behaviour problems, learning and cognitive disabilities, alcoholism, immunological disorders, sensory and motor disorders, and physiological and anatomical anomalies.

The Hypoxia Connection Hypoxia is a major factor in the production of a suboptimal fetal environment (Nelson, 1989). Impaired delivery of oxygen and other nutrients through the placental-umbilical circulatory system is a prime factor in developmental alterations leading to reproductive casualty (Towbin, 1978; Volpe, 1987). Hypoxia sufficient to alter brain development, may impair other physiological and anatomical systems (Perlman, 1989). Recent research is uncovering specific mechanisms by which hypoxic insult produces reorganization in the brain and other systems of the body (Goodman, 1989; Herschkowitz, 1988; Witelson, 1989). These mechanisms include selective neuronal pruning, synapse elimination, and neuronal misconnections. Such systemic effects may initiate vulnerability to diseases which develop later in life. Diseases, not usually associated with reproductive casualty, may have precursors in fetal development. The reproductive casualty model may include

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more pathological conditions than has been previously envisaged. The model may be relevant to an understanding of visual dysfunction (Groenendaal, Van Hof-van Duin, and Fetter, 1988), cardiovascular disease (Barker, Osmond, Golding, Kuh, and Wadsworth, 1989; Barker, Osmond, Winter, Margetts and Simmonds, 1989), kidney disease (Perlman, 1989), cancer (Kramer, Albrecht and Miller, 1985) and other diseases. The particular applicability of the model of reproductive casualty to NRH is likely due to the special vulnerability of the left hemisphere to hypoxic stress (Brann, 1989; Braun and Myers, 1975), and the fact that one of the most common effects of hypoxia is a decrease in manual dexterity and fine motor coordination. Manual dexterity and fine motor coordination are normally characteristics of the right hand. Hypoxic risk is present during the entire intrauterine period and continues into the perinatal period. There are physiological mechanisms to protect the healthy infant from normal birth-related hypoxia (Volpe, 1987). However, prenatal hypoxia or malnutrition can so compromise the fetus, as to increase complications at birth and thus potentiate the normal tendency to hypoxia, as the infant switches from an umbilical to an atmospheric supply of oxygen (Naeye, 1987). Problems classified as "birth injury" or "birth stress" may be the result of prenatal pathology already well advanced prior to labour. Congenital effects sometimes considered genetic in origin, may in fact be related to the combined effects of intrauterine insufficiency, perinatal hypoxia, and birth trauma. The inclusion of NRH in the context of a continuum of reproductive casualty, suggests an extended list of variables for study in connection with NRH. The enlarged context provides a working hypothesis, namely, that variables associated with reproductive casualty might sometimes be associated with NRH as well. Variables suggested by the context of reproductive casualty include low socio-economic status (Lansky, Feinstein, and Peterson, 1988; Saugstad, 1989), stress, maternal malnutrition, smoking, alcohol consumption, consumption of other drugs, maternal health problems, high altitude hypoxia, polluted air hypoxia, blood type incompatibilities (Kocel, 1977), infection, fever (Shiota and Kayamura, 1989), prenatal coitus (Grudzinskas, Watson and Chard, 1979; Naeye, 1982), male sex of fetus, temperature and seasonal factors (Naeye, 1982; Shiota and Kayamura, 1989), paternal factors (Little and Sing, 1986), and anaesthetics (Kolata, 1978).


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NRH and Reproductive Casualty: Small Effects and Negative Results In a recent review of the relationship between NRH and birth stress (Searleman, Porac, and Coren, 1989), the authors conclude that there is significant positive evidence for the relationship, but that the relationship is weak for "non-clinical"populations. A meta-analysis of relevant studies revealed that "birth stressors...considered collectively, are likely to be related to increases in nonright-sidedness" and "that all of the relationships... were very weak... and accounted for less than 1%of the variance." If NRH is added to the larger class of pathological outcomes which constitute a continuum of reproductive casualty, then small effects and negative results are to be expected. Consider a 2 x 2 table, where one dichotomy is Right-handed (RH) vs Nonright-handed (NRH), and the other dichotomy is PBCs vs. No PBCs. This table yields four cells, RH/PBCs, RH/No PBCs, NRH/PBCs, and NRH/No PBCs. A statistical excess of cases in the NRH/PBC and RH/No PBC cells would clearly support the hypothesized relationship between NRH and PBC. If NRH is a manifestation of reproductive casualty, the logic of this argument becomes diluted. The RH group includes those with PBCs resulting in pathological outcomes other than NRH. It would also include people with pathological right-handedness,where very strong right-handedness is actually a manifestation of PBCs. Or it may include cross-dominants, those who are right-handed and left-footed, or left-eyed. Since there is an association between crossed dominance and PBCs, right-handed cross-dominants would show up in the RH/PBC cell. The result is that the RH/PBC cell frequency will be inflated, not because of absence of relationship between NRH and PBC, but because PBCs can lead to forms of reproductive casualty which are not associated with NRH. The model maintains that where there is NRH, there are PBCs; but where there are PBCs, there may or may not be NRH. Analogously, if a person is a nurse it is very likely that the person is a woman; but if a person is a woman, she may or not be a nurse. The following are some implications of the reproductive casualty model: a)

PBCs can produce a wide variety of pathological results in physiological or anatomic systems, leading to

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Bakan syndromes, diseases, and congenital anomalies, which appear in the physical and/or psychological domain. b)

The particular result of PBCs is related to when, where, and how the embryo, fetus, or newborn is affected by the complications.

c)

If the PBCs affect areas unrelated to handedness, then any effect produced, though related to PBC, will not lead to NRH. (A similar statement would be applicable to footedness, eyedness, cross-dominance, pathological right-handedness etc.).

d)

If the PBC affects areas that influence the development of NRH, then NRH will result.

e)

The PBC may result in more than one pathological condition, and if the time, place, and degree of the PBC are appropriate, there will be correlations between the pathologies. An example would be joint occurrence of NRH and left-hemisphere oriented cognitivedifficulties, e.g. mental retardation.

f)

Among the various pathological results of PBC there will be varying degrees of correlation, or joint occurrence.

In sum, NRH is associated with PBC, but the measured relationship can be masked by the relationship between PBC and pathological conditions not associated with NRH. There will be varying degrees of relationship between NRH and other pathological manifestations of PBC. Consideration of NRH in the context of a continuum of reproductive casualty, seems to account for many of the facts about NRH, and offers leads for future research about NRH, and reproductive casualty in general. The model has implications that go beyond the considerations of other theoretical approaches to NRH. Because of the high frequency of occurrence of NRH, as compared to other pathologies associated with PBC, NRH frequency can be used as a comparative measure of adequacy of prenatal and perinatal


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conditions. If NRH has a pathological origin, then it follows that reduction of NRH is a worthwhile goal. As NRH is reduced, so other pathologies associated with PBC, are likely to be reduced, because PBC will be reduced. The model emphasizes variables that have not generally been of interest to students of laterality. These variables apply to maternal reproductive efficiency, and include things as maternal nutrition before and during pregnancy, maternal height and weight, maternal health, presence of toxic factors as alcohol, cigarettes, drugs, air pollution etc.,and psychological stress. The model also implicates the political and socio-economic factors which influence the availability of adequate nutrition, health care, and education. Such variables are influential in the reduction of PBCs, as well as many other pathological conditions on the continuum of reproductive casualty. Inclusion of NRH in the continuum of reproductive casualty suggests that a reduction of NRH would accompany a reduction of PBCs. Savings in costs of health care, education, and criminal justice, would more than compensate for the costs of preventing reproductive casualty.

Summary The occurrence of nonright-handedness(NRH) is considered in the context of reproductive casualty. NRH is viewed as one of the many possible results of pregnancy and birth complications (PBCs), which constitute the continuum of reproductive casualty. This continuum ranges from lethal outcomes, such as spontaneous abortion and stillborn births, to relatively minor outcomes. NRH, when unaccompanied by more serious problems, is a relatively benign outcome in a continuum of reproductive casualty. The role of prenatal and perinatal factors in the production of morbidity is a medical problem with a long history. This work is reviewed, especially as it relates to NRH. Four recent theories of pathological NRH are critically considered, those of Satz, Bakan, Geschwind, and Annett. The joint occurrence of NRH with other forms of morbidity is discussed as supporting the pathological origin of NRH. Hypoxia is considered an important factor in the development of NRH and other manifestations of the continuum of reproductive casualty. Research results on the relationship between NRH and PBCs, are discussed in the context of the continuum of reproductive casualty.

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LEFT-HANDEDNESS Behavioral Implications and Anomalies, S . Coren (Editor) 0 Elsevier Science Publishers B .V. (North-Holland), 1990

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Chapter 3

Left-Handedness and Prenatal Complications Murray Schwartz Victoria General Hospital, Halifax

“Left-handedness is one of the degeneracy signs of the born criminal.” This quote by the famous 18th century physician, criminologist and reformer C. Lombroso (1903) is intended as a warning to the reader since the author of this chapter is just such a left-hander. In addition to criminals, left-handers are found in disproportionate frequency in problem populations such as autistics, epileptics, dyslexics, learning disabled, stutterers, schizophrenics and mental retardates; individuals suffering from auto-immune disorders, childhood allergies and migraines; and, that most problematic group, graduate students (Geschwind and Galaburda, 1987; Harris, 1980; Habib & Galaburda, this volume; Halpern & Coren, this volume). It should also be pointed out that sinistrals are also found in disproportionate numbers in populations of architects, mathematically gifted and musicians (O’Boyle & Benbow, this volume; Geschwind and Galaburda, 1987). Many cultures have viewed right-handedness as proper, righteous and correct, and have considered left-handedness as evil, clumsy and cursed (Needham, 1973; Harris, 1980 and this volume). While mammals other than humans display lateral preferences, these are on an individual basis, i.e., any single animal is equally likely to prefer either hand (e.g., Corballis, 1983). Humans, on the other hand are much more likely to prefer the right hand (Hamilton, 1976; Webster, 1976, as cited in Hicks and Kinsbourne, 1976). Although always in the minority, left-handers have been present in the world since prehistoric times (Coren and Porac, 1977; Dennis, 1958; Harris, 1980; Hildreth, 1949; Spennman, 1984; Springer and Deutsch, 1981).

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Estimates of the frequency of occurrence of left-handers in the human population have remained surprisingly static from the beginning of recorded history. Although the estimated range of left-handedness in these retrospective "historical reviews" varies from 3% to 20%, the average is about 9%. The exact percentage of left-handedness in the population changes somewhat from study to study depending on the method used for assessing handedness and/or the means of categorizing left-handedness (e.g., Porac and Coren, 1981). Lefthandedness also appears to be relatively constant across racial and ethnic boundaries (Harris, 1980) although some recent variations are suggested by Porac, Rees and Buller (this volume). A number of more recent studies have suggested an increase in the number of left-handers within the past few generations (e.g., Spiegler and YeniKomshian, 1984). These findings, which appear to be independent of the method of classifying handedness, suggest a revision in the current estimate of lefthandedness from between 9-10% to between 13-14% (Annett, 1973; Ashton, 1982; Brackenridge, 1981; Carter-Saltzman, 1980; Spiegler and Yeni-Komshian, 1984). This increase in the incidence of left-handers, which occurs in the younger age groups, is often interpreted as reflecting a more tolerant attitude towards left-handers in recent decades and a coincident relaxation in cultural pressure to convert to dextrality. Prior to this increased acceptance of lateral preference, lefthacders were either subtly cajoled, or more overtly forced, into converting to right-handedness. The penalties for remaining true to one's natural sinistrality could range from enduring the wrath of a teacher or parent who ridiculed handwriting posture to getting hit across the knuckles to coerce a change in behaviour. Coren and Halpern interpret the decreasing number of left-handers with older generations as a reflection of the greater morbidity and mortality rate for left-handers (Coren, 1989; Halpern & Coren, 1988 and this volume). Numerous explanations have been proposed to account for the presence of left-handers (e.g., Hardwyck and Petrinovich, 1977; Harris, 1980; Hildreth, 1949). There does not appear to be a generally acceptable all-inclusive theory for the development of handedness. Current theories concerning the etiology of handedness can be grouped into three categories: genetic; environmental-cultural; and prenatal/environmental. The latter category includes hormonal influences and the pathological models of handedness. The three categories are not necessarily mutually exclusive, and possibly parts of all three may contribute to the determination of lateral preference.

Prenatal Complications

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Genetic Theories of Handedness Many explanations have been predicated on the presence of a relationship between genetics and handedness. Carter-Saltzman (1980) tested children adopted before they were one year old along with their adoptive and biological parents. He found a significant correlation between the biological parents and their offspring but not between the adoptive parents and their children. Although these findings lend themselves to a genetic explanation, there are problems with the study, not the least of which is the difficulty in obtaining reliable handedness measures prior to one year of age. Both single (Annett, 1964, 1972, 1975, 1978, 1985) and double allele (Levy, 1976, 1977; Levy and Nagylaki, 1972; Nagylaki and Levy, 1973) genetic models of handedness have been proposed and are supported, at least in part, by other researchers (e.g., Geschwind and Galaburda, 1987; Hardyck and Petrinovich, 1977; Hicks and Kinsbourne, 1976; Liederman and Kinsbourne, 1980). In many cases, the proponents of a genetic basis for handedness believe that environmental prenatal (Corballis, 1980a; Corballis and Beale, 1976 Geschwind and Galaburda, 1987; Rife, 1950) or environmental postnatal (Collins, 1970; 1975; 1977; Hecaen and Ajuriaguerra, 1964; Hecaen and Sauguet, 1971; Hudson, 1975; McManus, 1980; Porac and Coren, 1979) contributing factors are also present. The most detailed studies attempting to explain a genetic component for handedness have been done by Annett (e.g., 1985) who advanced the notion of random dominance. She suggests that the majority of persons in the population carry a "right-shift'' gene which increases the probability of left-hemisphere dominance for controlling function (and presumably preference). However, approximately 18% of the population have random dominance for handedness and accidental factors determine the lateralization of handedness for that segment of the population. Annett believes that half of the "random" 18% become right-handers and the remainder become left-handed. The accidental factors can be considered to include a wide variety of prenatal influences. Because the determination of handedness is subject to the whim of so many fetal environmental factors, no purely genetic theory can alone account for the determination of handedness. There are too many prenatal temperature and chemical variants that are known to have an influence on genetic unfolding for any theory to consider the genetic code in a vacuum.

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Environmental/Cultural Theories of Handedness Many theories have been based on cultural folklore (Needham, 1973) and few have survived advances in anatomical knowledge and closer experimental scrutiny. The premise of the cultural/learning position is that handedness is a learned phenomenon that is passed on through generations. Hildreth (1949) states that the proportion of children favouring their left hand decreases considerably between the first and fifth year of life. This can be interpreted as evidence favouring a learned component in handedness (Provins, 1967). Also, Collins (e.g., 1975) has convincinglydemonstrated that paw preference in rats can be altered significantly by environmental experiential factors. Hicks and Kinsbourne (1976) reviewed the human handedness literature and found little support for the hypothesis that handedness is learned. They present the view that any evidence that could be interpreted as favouring a learning/cultural theory of handedness is, at best, equivocal. Frustration over finding a parsimonious genetic explanation is not sufficient justification for defaulting to a learning determination of handedness. Weak and/or equivocal evidence similarly is not an acceptable basis for formulating a solid theoretical stand. Studies demonstrating a decrease in the frequency of occurrence of lefthandedness with increasing age (see Hildreth, 1949; Jones, 1937; Stellingwerf, 1975 as reported in Porac, Coren and Duncan, 1980) are interpreted as reflecting pressure to conform to an essentially right-handed environment, rather than the unfolding of a dextral, biological, maturational process. A few recent surveys report just the opposite trend, namely, a higher incidence of sinistrality with the older age groupings (Brackenridge, 1971; Fleminger, Dalton and Standage, 1977; Levy, 1974). These latter studies, in turn, are interpreted as demonstrating an increasing tolerance or acceptance of left-handedness and a consequent relaxation in cultural pressure to convert to dextrality. Halpern and Coren (this volume), counter this position with a literature survey. Based upon evidence from 34 studies since the turn of the century, they suggest that the percentage of adult left-handers has not changed over the past 80 years.


79

Prenatal Hormonal Theory Geschwind and Galaburda (1987) have expanded Annett's idea of random dominance by suggesting that a full one third of the population is subject to random determination of lateral dominance. This theoretical postulation dovetails well with Geschwind's finding that one-third of the population do not manifest a larger left-sided planum temporale. This subgroup of the population, according to Geschwind and Galaburda (1987), have anomalous lateral dominance, is., they are not clear right-handers and randomly develop patterns of hand preference that differ from the norm of strong dextrality. Both Annett (1985) and Geschwind and Galaburda (1987) argue that certain prenatal influences act to diminish the overall innate (genetic predisposition) towards right-handedness to create random dominance. Hormonal influence, particularly the concentration of testosterone, is the most salient hypothesized factor for Geschwind and Galaburda (1987). The higher the testosterone level during certain prenatal periods, the greater the likelihood of random determination of lateral dominance. It is important to note that the higher levels of testosterone along with the "random laterality which results in an increased number of left-handers are not considered pathological events, but aspects of normal prenatal development.

Prenatal Pathological Theory One group of researchers has advanced the position that right-handedness is the norm and that deviation from this manifestation, namely sinistrality, represents a pathological condition (Bakan, 1971, 1975, 1977; Bakan, Dibb and Reed, 1973; Gordon, 1920; Subirama, 1969). The leading proponent of this position, Bakan, claims that pregnancies involving a higher risk of cerebral insult (esp. hypoxia) to the fetus, produce a higher than normal frequency of sinistrality in the resulting children. He argues that prenatal stress causes left cerebral motor damage resulting in a "weakness" of the right hand, thus prompting a sinistral shift in handedness. While some studies support Bakan's position (e.g., Coren and Porac, 1980; Coren, Searleman and Porac, 1982; Hicks and Barton, 1975; Leviton and Kilty, 1976), there is a long list of studies which do not (Annett and Ockwell, 1980; Barnes, 1975; Hicks, Evans and Pellegrini, 1978; Hicks, Pellegrini, and Evans, 1978; Hicks, Pellegrini, Evans and Moore, 1979; Hubbard, 1971; McManus, 1981; Schwartz, 1977, 1988b; Sexton and Schwartz,

80

Schwartz

1987; Tan and Nettleton, 1980). With the assistance of an interesting and sophisticated meta-analysis statistical technique, Searleman, Porac and Coren (1989) reviewed and analyzed the findings of over 25 birth stress and laterality studies and found a significant relationship between the presence of birth stressors and a reduced frequency of right-handedness. The effect size, while statistically significant, was small. To further explore the premise that left-handedness may reflect cerebral deficiency, several researchers have compared left-handers and right-handers on a series of cognitive tasks. While some researchers suggest that left-handers show certain relative deficiencies in some cognitive skills (cf. McKeever, this volume; Porac & Coren, 1981), there are many others that find either no difference or a superiority for left-handers on some tasks (Ashton, 1982; Hardyck, Petrinovich and Goldman, 1976; Helm and Watts, 1976; Hicks and Beveridge, 1978; Newcombe, Ratcliff, Carrivick, Hiorns, Harrison and Gibson 1975; Wellman, 1985) while Lewis and Harris (this volume) argue that there may be important mediating factors that are often not considered. In any event, the general pattern of the data in the literature is consistent with Geschwind and Galaburda (1987) who argue that left-handers do not present as an overall disadvantaged group with reference to general disability or morbidity. Because the data has been so mixed in direction, the pathological model of left-handedness has generated much of the recent controversy surrounding the etiology of handedness. It is interesting that it was not until Bakan's (1971) publication of a one page article that the relationship between perinatal stress and left-handedness developed into a controversy (Searleman, Porac and Coren, 1989). The existence of some pathological left-handedness is not denied. On the contrary, the presence of a pathological condition in some left-handers would account for the high proportion of left-handers in problem populations where brain damage is suspected (Hecaen and Ajuriaguerra, 1964; Satz, 1972, 1973; Satz, Baymur and Vlugt, 1979). Brain (1945) introduced the notion of "shifted sinistral" or pathological left-handers, along with naturally occurring left-handers, several decades ago; and Satz and his co-workers have more recently reintroduced and popularized the terms "manifest"or "pathological" left-handers (Orsini and Satz, 1986; Satz, 1972, 1973; Satz, Orsini, Saslow and Henry, 1985). Satz's (1972,1973) succinct explanation is that the high percentage of sinistrals in "problem" populations is due to the expected number of so-called normal genetic left-handers augmented by the presence of pathological left-handers (see also Coren & Searleman, this volume). The pathological left-handers are persons who would have been right-handed were it not for some, presumably prenatal,


81

pathology to the left-hemisphere which forced them to use their undamaged, right cerebrally controlled, left hand. The parsimony of Satz's explanation makes it appealing. Annett (1981) and Geschwind and Galaburda (1987) worry that the normal vs. pathological distinction for left-handers has been too widely applied. They argue that the pathological classification should be restricted to those few individuals who have sustained serious prenatal or perinatal damage to the left hemisphere; i.e., those individuals who necessarily end up with a right hemispheric dominance for handedness. In the same vein, Geschwind and Galaburda (1987) do not agree with equating "normal" to "genetic,"or "acquired" to "pathologic," with reference to left-handedness. They strongly feel that the intrauterine influences that produce left-handedness are varied, numerous and only partially genetically determined. Since many normal left-handers became so for normally occurring, non-genetic reasons, they believe the terms "normal" and "genetic" should not be equated. Similarly, left-handers with physical abnormalities of the left hemisphere have had their brain organization altered by a mechanism that, in a less extreme case, likely produces the majority of normal left-handers. Touwen (1972) feels the statement that all left-handers are the products of brain injury is extending the argument beyond reasonable limits and is not logically sound. The salient point is that there is general disagreement with Bakan's view that all sinistrality is pathologic. The stronger prevailing view is that there is a continuum of left-handers with and without accompanying abnormalities. Even if one were more sympathetic to Bakan's views, there are severe methodological considerations which must be taken into account. The studies investigating handedness and birth complications are suspect because of indirect methods of determining perinatal risk or complications and inadequate methods of determining handedness. The presence or absence of birth stress factors usually has been determined by asking college students the nature of their mother's pregnancy (e.g., Bakan, Dibb and Reed, 1973; Schwartz, 1977). While such a procedure is convenient, its validity must be questioned. A few studies have used maternal reports for information about the nature of a pregnancy that occurred from 7 to 15 years earlier (Annett and Ockwell, 1980; Badian, 1983; Coren and Porac, 1980; Coren, Searleman and Porac, 1982; Dusek and Hicks, 1980; Searleman, Tsao and Balzer, 1980; Tan and Nettleton, 1980). Although maternal report is a move in the right direction, it is still dependent on recall of events several years in the past. Chamberlain and Johnstone (1975) questioned mothers hospitalized for the birth of a subsequent child, about their previous pregnancy. They found that 42% of the mothers either did not know the length

82

Schwartz

of their labour or were inaccurate by several hours. Schwartz (1988a) compared hospital pregnancy and birth records and maternal report two years postpartum and found significant discrepancies between the two data sources. In two-thirds of the cases where the mother reported pregnancy complications, there was no corroboration found in the hospital records. When the hospital records indicated the presence of serious stress factors (e.g., meconium staining) or complications (breech birth, toxemia) there was a lack of any similar indication in approximately half of the mothers’ reports. Clearly the findings in the Chamberlain and Johnstone (1975) and the Schwartz (1988a) studies cast doubt on the results of any investigations which rely on retrospective, second-hand source data collection. Consequently, the conclusions and theoretical formulations drawn from those results must be treated as no more than speculation at best. Another methodological problem in most of the birth stress studies is that handedness is determined in the most convenient, rather than the most accurate, manner. For example, Hubbard (1971) allowed for self-classification by his subjects, while Bakan (1971) and Bakan, Dibb and Reid (1973) both used writing hand as the criterion for determining handedness. Both procedures have been shown to be inadequate by themselves in the determination of handedness, particularly left-handedness (Annett, 1985; Benton, Meyers, and Polder, 1962; Bryden, 1977; Coren and Porac, 1978; Coren, Porac and Duncan, 1979; Crovitz and Zener, 1962; Knox and Boone, 1970; Oldfield, 1971; Raczkowski, Kalat and Nebes, 1974; Satz, Achenback and Fennell, 1%7; Steingrubber, 1975). Benton, Meyers and Polder (1962) have indicated that self-assessed left-handers are a highly variable group. Geschwind and Galaburda (1987) have succinctly stated that the high correlation between self-described handedness and test scores is of little use simply because there are many discrepancies in the group that matters most, namely, the subgroup which includes the left-handers. Geschwind and Galaburda (1987) similarly criticize the exclusive reliance on writing hand to categorize handedness. In light of the methodological limitations, it is not surprising that contradictory results abound (see Leiber and Axelrod, 1981). The magnitude of the methodological problem was illustrated by Schwartz (1977) who categorized left-handers according to three different criterion: selfclassification, writing hand or results of a 1Citem laterality questionnaire. He found all three methods yielded the same percentage of left-handers, but the composition in the sample, is., the persons who actually occupied those categories, were different. The personnel differences in the three left-handed categories ranged from 15% to 30%. Given the small percentage of left-handers


83

present in the population, the 30% discrepancy in categorization could readily account for many of the discrepancies in results from different studies. It is also important to appreciate that handedness is not a dichotomy but a continuum and that the decision of where on the continuum left, ambidextrous or righthandedness begins and ends is arbitrary and must be operationally defined. Hubbard (1971) and Schwartz (1977) were two of the first persons to report findings inconsistent with those of Bakan (1971). Bakan (1977) attempted to dismiss the negative findings by suggesting that their studies were suffering from sampling error. The argument became somewhat forced when Bakan proposed that the contrary results in the Schwartz (1977) study were due to the fact that subjects used in that study were from a geographic area with a high mortality rate and that the pathological left-handers were dead. Presumably the deceased left-handers, had they lived, would have altered the statistics in a manner more favourable to Bakan’s hypothesis. A decade after the Schwartz (1977) study, Sexton and Schwartz (1987) readministered a laterality questionnaire to over 650 university students. The questionnaire asked specific questions related to birth order, pregnancy complications, birth stress and early developmental problems. The design incorporated all of Bakan’s criticisms of the original Schwartz (1977) study (undifferentiated sample according to sex, lack of detailed questioning about possible pregnancy and birth complications). Nevertheless Sexton and Schwartz (1987) obtained results fully consistent with those of the original Schwartz (1977) study, is., there was no increase in the frequency of sinistrality as a result of high-risk pregnancies (as determined by birth order) or as a result of reported pregnancy or birth complications. The findings were consistent regardless of whether the handedness categorization process was based on self-assessment of handedness or by a 14-item questionnaire. The lack of any increase in sinistrality for high-risk birth orders or for reported complications was consistent whether left-handers were categorized on a strict criterion (performed all tasks always or usually with the left hand) or weakly (performed more tasks with the left hand) or when the sample was divided into right-handed vs. all others (i.e., left-handers t ambidextrous). Some additional measures of perinatal stress were also looked at, namely maternal age at birth, and early developmental problems. Those new measures also failed to provide any evidence favouring Bakan’s hypothesis. A summary of the results of the Sexton and Schwartz (1987) study are shown in Table 1.

84

Schwartz

Table 1: Stress factors and handedness (Sexton and Schwartz, 1987)

Stress Factor

I

I R

Males

Tota 1

Females L

R

L

R

L

Birth Order: 1st or > 3rd 2nd or 3rd

118 85

15 8

207 122

Birth Complications: Yes No Don ' t Know

41 139 26

8 14 1

86 206 36

4 15 2

127 345 62

12 29 3

128 188

7 14

204 312

12 32

Maternal Age: c19 or >30 19-30

Post Neonatal Difficulty: Yes No

NB None

29 15

1 43 291

8 36

of the results are significant.

The previously described study is yet another example of Searleman, Porac and Coren's (1989) complaint! They argue that the standard retrospective paradigm will not put to rest the controversy about whether a relationship exists between birth stress and laterality nor about the nature of the relationship, in non-clinical populations. They point to the methodological problem of surveying offspring or retrospective reports from mothers with no corroborating archival data backup, the lack of a longitudinal, prospective approach, and the use of dichotomous rather than continuous measures of lateral preference. They argue that a definitive statement is not possible until those characteristics are advanced in a more comprehensive investigation. Schwartz (1988a, 1988b) has presented preliminary reports on a longitudinal, prospective study investigating the relationship between perinatal stress and the development of lateral preference. Additional data will be presented here. Although the study does not pretend to be definitive, it is promising in so far as it complies with several prerequisites set forth by Searleman, Porac and Coren


85

(1989). Namely, the study uses archival as well as laterality questionnaire data, continuous as well as dichotomous values for handedness categorization;stresses longitudinal, prospective rather than retrospective data collection; and compares hospital records to maternally reported information. Over 400 children were tested on a variety of Iaterality measures which taken from included tests of lateral preference (ten-items "show me how you the Harris Tests of Lateral Dominance (Harris, 1947), with the important addition that the children were given concrete objects to manipulate rather than merely pantomiming the activity. The children were also given tests of manual dexterity such as the Purdue Pegboard, the Grooved Pegboard, a telegraph key tapping test and the tapping test from the Harris Tests. Two handedness scores were used as the dependent variables: a dichotomous score which classified the child as left- or right-handed depending on the hand with which the child performed better, or preferred, for the majority of tasks; and a continuous measure of handedness called the RH% score, obtained by taking the percentage of tasks preferred, or performed better with the right hand. The children were tested once yearly for four years, beginning at age 2. The mothers were extensivelyinterviewed when the two year olds were initially tested. The maternal interviews were aimed at obtaining pregnancy and delivery information including the presence or absence of specific stress factors; complications of pregnancy and delivery; post-partum and early developmental problem; developmental landmarks; and familial handedness history. The important third source of data gathered in the study was hospital pregnancy and birth records, The hospital records contained information about the pregnancy in general, including the presence of stress or complication factors and extensive information about the delivery stages and immediate post-partum status of the neonate. The Schwartz study looked at a wide range of stress/risk factors and complications including the following: Birth weight. Weight of neonate, according to the mother and, independently, according to hospital records. This was done since the Chamberlain and Johnstone (1975) study demonstrated that the maternal report of pregnancy birth history may not be accurate. Matenial smokirig. Maternal smoking may be considered a stress/risk factor as there is evidence suggesting that smoking adversely affects the health of the foetus, especially as manifested in lowered birth weight. Pregnancy order. The pregnancy (gravis) order is not necessarily the same as birth order since birth order may not take into account spontaneous abortions, stillbirths and neonatal deaths. ...'I)

86

Schwartz

Maternal age. The child bearing ages associated with the least risk are between 19 and 30 years of age. Apgar Score at 1 min. The Apgar rating (Apgar, 1953) is a neonatal rating out of 10, based on a maximum score of two points for each of the following: respiration, responsiveness, colour, tone and heart rate; and is a measure of the physiological status and well being of the neonate immediately after birth. Scores of 7-10 are considered normal or safe, scores from 4-7 are considered to be a sign of possible distress and should be monitored, and scores of 0-4 are considered to indicate serious distress and active intervention required. Meconium staining. Meconium is a dark secretion from the intestines of the fetus and, when present in different colourations before parturition, is considered a sign of fetal distress. Maternal report of complications. Mothers were interviewed two years postpartum and asked whether there were any complications with their pregnancy, delivery or immediate post-partum period. In addition to the general inquiry, specific stress/risk factors and complicationswere enumerated to the mother and she was asked if these situations were present (e.g., toxemia, blood pressure problems, water retention, circulation problems). Hospital report of complications. The hospital pregnancy/delivery record provided a type of multiple choice check list system for indicating the occurrence of any stress or complication factors at different stages of pregnancy, labour/delivery, and the immediate post-partum period. Not only was there a comprehensive list of possible stress and complication factors compared to previous studies, but two dependent measures of handedness were used: a dichotomous right-left measure (the hand preferred and/or used the majority of times when all the tests were compiled) and a more contiguous RH% measure (the number of times the right hand was used for all the tests, expressed as a percentage of the total number of tasks completed). A summary of the findings for each of the age groups, for all stress/complication measures for the right-left dichotomous measure and the RH% measure are found on Tables 2 and 3 respectively. T-test analyses were conducted for all the measures when the RH% score was the dependent variable with high and low risk defining the groups (Table 2). Chi square analyses were performed for each stress/risk or complication measure when the dependent variable was the dichotomized right-left handedness index (Table 3).


87

It is apparent from the tables that there are a plethora of negative findings between birth stress and handedness in the tables. Does this indicate that the relationship between birth stress and handedness must be abandoned? Well we certainly must call the issue moot. Several of the measures admittedly are what may be called weak stress indicators. These include birth order, age of mother, maternal smoking and birth weight. There are, however, several relatively strong measures of stress or complications (e.g., Apgar scores, meconium staining, maternal or hospital indication of complications). If any relationship between birth stress or complications existed, then it presumably would be manifested when using one or more of these measures. The so-called strong measures indicate the immediate post-partum physiological status of the neonate (Apgar), the amount of fetal distress experienced during birthing (meconium staining) and the complete objective hospital record of events (hospital report of complications). There were only five significant results out of 108 analyses run when the continuous dependent variable (RH%) was used in the analyses. Furthermore, only two of the five were in the direction predicted by the pathological theory of handedness (see Table 2). When the dichotomous (rightleft) dependent variable was used, 8 of 108 Chi square analyses were found to be significant (see Table 3). Certainly, these results cannot be construed as evidence favouring a birth stress and left-handedness relationship in the global sense. The one result from this study that seems consistent with the a relationship between birth stress and sinistrality, comes from the one minute Apgar scores. In the dichotomized data (Table 3) we find three comparisons that are statistically significant, and ten of the twelve comparisons are in the predicted direction, with higher proportions of sinistrality associated with lower Apgar scores. Low Apgar scores have been shown to be associated with hypoxia and increased incidence of neurological abnormality, hence this finding is suggestive. The problem of course is that one cannot prove the null hypothesis. In this study, for example, in Table 3, we are dealing with dichotomized data, with about 300 observations per comparison. There are many fewer stressed births than there are normal births (about 10% for an average comparison of about 270 vs 30 cases). This means that the incidence of left-handedness would have to rise from 10% in the normal group to 22% in the stressed group, to achieve a statistical significance of p700), or verbally precocious (SAT-Verbal > 630). The same classification procedure was applied to females, but because the number of mathematically talented females was quite small, they were merged with those designated as precocious in both verbal and mathematical ability. Members of each group were subsequently separated on the basis of hand preference using the Edinburgh Inventory: strongly left-handed (LQ < -a), mildly left- or mixed-handed ( -40 5 LQ 5 20), mildly right-handed (20 < LQ 70). The resultant 16 groups were then monitored for the presence or absence of FS, ID (for subjects and their parents), or some combination of these factors. This breakdown produced some cells with extremely small N’s. Thus, for each of the hypothesis tested, only trends in the appropriate or inappropriate direction can be suggested. With regard to strength of handedness, the literature reviewed in this chapter suggests that left hand dominance might relate more to enhanced verbal as compared to mathematical ability, especially in males. As can be seen in Table 1, the data are consistent with this hypothesis. In the Benbow (1986) sample, the frequency of the left- and mixed-handedness (LQ 20) is slightly higher among the verbally precocious (23,5% males, 15.8% females) as compared to the mathematically precocious ( 16.6% males, 9.5% females), particularly so for the strongly left-handed (LQ < -40) males (15.7%). As previously mentioned, two other studies have implied that left-handedness is especially detrimental to spatial ability in females (Klintenberg, Levander & Schalling 1987; Sanders, Wilson & Vandenberg, 1982). In the Benbow (1986) sample, only two mathematically talented females were left- or mixed-handed (9.5%). As a group, the mathematically gifted females were particularly right-handed (90.5%). Though difficult to draw firm conclusions from the literature on the relationship between FS and ability, indications were that FS was related to lower abilities with the possible exception that FS+ might serve to enhance spatial capacities in right-handed males (e.g. McKeever et al., 1983). As revealed in Table 1, in the Benbow (1986) sample, the incidence of FS was generally quite low among the intellectually precocious ( i s about 25% as compared to about 45% in the general population), a finding which is consistent with the idea that

362

O’Boyle and Benbow

Table 1: Reanalysis of frequencies of physiological correlates among various talent groups reported in Benbow (1986) - Percents by talent group Math Talented Males Laterality Quotient

Strong Left

Mild Left

Mild Right

Strong Right

Hand Preference

11

6

27

57

Fami 1 ial Sinistral ity

57

29

46

29

Immune Disorders

43

43

65

51

Parent has Immune Disorders

71

71

7a

67

Anomalous Lateral izat ion*

14

a6

60

53

Verbally Talented Males Lateral ity Quotient

Strong Left

Mild Left

Mild Right

Strong Right

Hand Preference

16

a

2a

49

Fami 1 ia 1 Sin i stra 1 i ty

33

25

13

30

Imnune 0isorders

a3

50

63

45

Parent has Immune Disorders

50

50

aa

55

Anomalous Lateral ization*

17

75

50

45

FS is related to a lower (at least lower than precocious) level of intellectual ability. Moreover as can be seen in Table 1, the incidence of FS t is relatively high in right-handed, mathematically talented males (57%) as compared to the other gifted groups (33%, 33%, 31%). Although less compelling, the data are at least congruent with the McKeever, et al. (1983) notion that in right-handed males, FS t and the spatial/mathematical faculties are positively related. According to Rich & McKeever (submitted a), the presence of both FS and ID or their combined absence are thought to relate to increased spatial

Ability and Talent

363

Table 1: Continued

Verbally Talented Females Laterality Quotient

Strong Left

Mild Left

Mild Right

Strong Right

9

7

28

56

33

33

17

31

Imnune Disorders

0

67

33

50

Parent has Imnune Disorders

0

100

50

65

33

33

67

65

Hand Preference Familial Sinistrality

Anomalous Latera 1 izat ion*

Both Mathematically & Verbally Talented Females Laterality Quotient

Strong Left

Mild Left

Mild Right

Strong Right

Hand Preference

9

0

5

86

Familial Sinistrality

0

0

0

24

Imnune Disorders

0

0

100

48

Parent has Imnune Disorders

0

0

100

73

100

0

0

53

Anomalous Latera 1 izat ion*

* Familial Sinistrality and has Imnune Disorders, or Familial Sinistrality and Does not have Imnune Disorders.

ability. The trends in our data are not entirely consistent with this view. Lefthanded females who were both verbally and mathematically precocious do show a tendency toward this pattern (100%). However, the actual number of subjects comprising this cell (N = 2) is too low to be seriously considered. Although ID of subject did not systematically relate to enhanced spatial ability, ID+ among their parents and siblings did. As can be seen in Table 1, 71% of strongly lefthanded, mathematically precocious males had parents or siblings who exhibited

364


some form of ID. With further investigation, parental ID t may yet prove to be related to mathematical precocity. Finally, Annett and colleagues, in light of her right-shift theory (Annett, 1085; Annett & Kilshaw, 1982) have postulated that a reduced preference for the right hand may be indicative of enhanced RH cognitive development. Such selective enhancement might then serve to promote the spatial/mathematical faculties. In the Benbow (1986) sample, some support for this hypothesis is found as three of the four groups (i.e. all but the mathematically talented females) exhibit evidence of reduced right hand preference.

Concluding Comment In this review we have attempted to pull together a selection of studies relating handedness to cognitive ability and talent. Unfortunately, the findings concerning this proposed connection have a distinctly piecemeal flavour to them and are often complicated and confusing. To us, it seemed that for each piece of data confirming a relationship between hand preference and a corresponding ability or talent, there appeared to be at least one other result that either a) failed to replicate the original finding, b) postulated some new second-order variable (e.g. sex, FS, ID, etc.) that served to moderate the connection or at least, confuse the issue, or c) flatly contradicted the notion that any such relationship existed. Needless to say, the variability of these findings speaks to the likelihood of a Type 1 error. We make no bones about the fact that our review does not paint a very unified explanatory picture of the proposed connection between handedness, ability and talent. We believe, however, that it accurately reflects the fragmented nature of our knowledge at this time. Presently, there are bits and pieces of evidence in the literature, with some pointing towards a connection, for example, the fairly consistent association between left-handedness and superior talents (e.g. athletics, architecture, mathematics and chess). Only after additional research, using a variety of experimental techniques to systematically converge on this issue, will we come to better understand the complex relationship between handedness, cognitive ability and talent.

Ability and Talent

365

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E

\

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Chapter 13

Familial Sinistrality and Cerebral Organization Walter F. McKeever Northern Arizona University

It is well-established that left-handers have a different cortical organization of some higher functions than do right-handers. Diverse data indicate, for example, that left-handers are less exclusively dependent on the left hemisphere for language functions. The incidence of persistent aphasia following brain lesions is lower in left-handers (Goodglass and Quadfasel, 1954; Segalowitz and Bryden, 1983), and they appear to recover speech functions more quickly than do right-handers following cerebral insult (Subirana, 1958; Luria, 1970). Wada Test data suggest that as many as %% of right-handers, but only 70% of lefthanders, are clearly left hemisphere dominant for speech (Rasmussen and Milner, 1977). Similarly, Borod, Carper, Naeser, and Goodglass (1985) found that only one percent of right-handers they studied were aphasic in response to right hemisphere lesions, but 24% of right-lesioned left-handers were aphasic. The possibility that language functions may also be less strictly left hemisphere-dependent in those with a history of left-handedness in their families is much less well-established. Various investigators have suggested, on the basis of limited case studies of aphasics, that positive familial sinistrality (FS + ) portends a favourable prognosis for more rapid and complete language recovery following aphasia onset (Subirana, 1958; Luria, 1970), and that right hemisphere language in dextrals is more likely to occur if the individual is FS t (Zangwill, 1960). Hardyck (1977) has proposed that lateralizations of language and visuospatial processing vary along a continuum as a function of handedness and FS

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characteristics. According to this model, the right-hander with no familial sinistrality (RHFS-) typifies the markedly left hemisphere language/right hemisphere spatial lateralization type, while the left-hander with familial sinistrality (LHFS t ) possesses a bilateralized type of language and spatial function organization. The right-handed person with familial sinistrality (RHFS t) is hypothesized to be less lateralized for both functions than are the RHFS-, but more lateralized than the LHFS t . According to Hardyck (1977), the left-hander without familial sinistrality (LHFS-) does not fit neatly into this handedness-FS model. Hardyck, citing the work of Hecaen and Sauguet (1971), suggests that the LHFS- person has a cerebral organization resembling that of the RHFS- person. Orsini, Satz, Soper, and Light (1985), on the other hand, have questioned the putative role of FS in cerebral organization. These investigators failed to find any relationship of the FS variable to language laterality as inferred from a dichotic verbal task and two concurrent activities (verbal output/manual tapping) tasks. The fact that the sample size was quite large and that significant effects of handedness (lesser language lateralization in left-handers) were obtained on all three tasks supplied credibility to the investigators’ negative conclusion regarding the importance of FS. Orsini et al. (1985) went on to suggest that FS may have been erroneously implicated in cerebral organization through two types of rystematic errors. According to the authors, the erroneous conclusion could reflect the fact that left-handedness is positively correlated with FS, so that effects due to left-handedness may have been wrongly attributed to FS. The second error could be publication bias in favour of positive effects of FS. It would seem that the first suggested source of error cannot account for positive FS effects where both handedness and FS have been carefully assessed. Indeed, assessment of FS without the accompanying assessment of handedness has seldom been conducted. The second suggested source of error is, of course, possible. Anyone familiar with the literature regarding the FS variable and cerebral organization can readily understand the frustration attending efforts to characterize the role of FS. The literature on the subject is diverse and resistant to nice generalization. In this paper I shall review data regarding the relationship of FS to a number of other variables. I shall not attempt to review every study which might be relevant, but shall review studies which seem to me to be the best in relation to a particular question, or which illustrate points or approaches which might ultimately prove fruitful. I can say at the outset that the final conclusion will riot be that FS influences are non-existent. I believe that FS

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is probably an important variable. The problems associated with isolating and documenting any effects of FS, however, are many, and I shall discuss some of these near the end of the paper, and suggest some strategies that might prove useful for research on the relation of FS to cerebral organization.

Clinical Studies I have already mentioned the case studies of Subirana (1958) and Luria (1970) which suggest a better prognosis for speech recovery in FS t individuals. These indicate that FS, regardless of the handedness of the patient, is associated with a more bilateral organization of language functions, the greater bilaterality resulting in less chronic disruption of language mechanisms by unilateral lesions. More formal and ambitious clinical studies have been conducted by Hecaen and Sauguet (1971), Newcombe and Ratcliff (1973), Warrington and Pratt (1973), and Hecaen, DeAgostini, and Monzon-Montes (1981). Because the Hecaen and Sauguet results were generally consistent with those of the more comprehensive Hecaen et al. study, I will review only the later study. Newcombe and Ratcliff (1973) reported a limited but interesting study of the effects of left and right lesions in 28 left-handed men who had suffered unilateral missile injuries more than 20 years earlier. A total of nine LHFS- men, three with left lesions and six with right lesions, and 19 LHFS t men, seven with left and 12 with right lesions, were examined. Assessments included performances on vocabulary, spelling, object naming, fluency, block designs, visual closure, and mazes. The data showed the left-lesioned LHFS t veterans to be more impaired on verbal tasks than were the left-lesioned LHFS- veterans, yet the LHFS t had higher scores on the spatial tasks, particularly mazes, showing that they were not more impaired generally. This suggests that the LHFS t were the more left hemisphere dominant for language, and this conclusion was reinforced by the observation that five of the 12 LHFS- men with right lesions had been dysphasic in the acute recovery period according to the medical records, while none of the six LHFS t men with right lesions had ever been dysphasic. These findings are not consistent with the Hardyck (1977) model. Results showing n o difference in inferred language laterality between LHFSand LHFSt individuals were presented by Warrington and Pratt (1973). Patients were 24 left-handers who received unilateral left and right hemisphere electro-convulsive therapy for depression. The authors noted that all patients were considered free of neurological disorder. Language laterality was inferred

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from dysphasic responses to four questions put to the patient immediately after the patient was able to respond to the question "What is your name?" Left dominance was inferred from greater dysphasia following left than right treatment, and right dominance was inferred from greater dysphasia following right treatment. This method, applied earlier to 55 right-handed patients (Pratt and Warrington, 1971), had indicated left dominance in 98% of the righthanders. Results showed that seven of the eight LHFSt patients were left hemisphere dominant; of the 16 LHFS- patients, 11 were judged to be left dominant, three right dominant, and two were indeterminant for language, is., their scores for dysphasia were equal after left and right treatments at several different doses of current. It is reasonable to regard these two patients as bilateral for language, and if one does, 87.5% of the LHFS t and 68.8% of the LHFS- were left hemisphere dominant. While this difference is not statistically significant, the direction of the difference suggests greater left dominance in the LHFS t . Again, this result is contrary to that hypothesized by Hardyck (1977). Finally, the most ambitious clinical study was conducted by Hecaen, DeAgostini, and Monzon-Montes (1981). Data were presented on 141 left and 130 right-handers with unilateral lesions. Six verbal functions were assessed: judged speech non-fluency; judged articulatory defect; confrontation naming; auditory comprehension shown in response to oral commands; visual comprehension shown in response to written commands; and writing, both to dictation and spontaneously. Four spatial functions were tested: spatial dysgraphia (repetitions in writing and margin size increase); unilateral spatial agnosia (neglect); constructional apraxia; and spatial agnosia (loss of topographic concepts and topographic memory). Results for the LHFS t showed only two verbal functions to be more strongly impaired by left than by right lesions. These were articulatory and naming performances. The LHFS-, however, were more impaired by left than right lesions on all six verbal functions. These results are consistent with the Hardyck model. On the spatial function measures, the LHFS t showed significantly greafer impairments on all four measures following right than left hemisphere lesions; the LHFS- showed no significant differences in response to left or right lesions. Indeed, LHFS- patients showed non-significantly higher incidences of impaired performance after left than right lesions, with the difference on constructional apraxia approaching significance (p< .07, computed by the writer). These spatial function results are not compatible with the Hardyck (1977) model, and suggest greater right hemisphere visuo-spatial function lateralization in the LHFS t than in the LHFS-.


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The RHFS- showed significantly greater impairment of all verbal functions, except articulatory disorder, following left than right lesions. The direction of the non-significant difference for articulatory disorder was consistent, however, i.e, a higher incidence of disorder following left than right lesions. The RHFS t , however, showed significantly greater impairments in response to left lesions on only two functions -- naming and auditory comprehension. The RHFS + showed greater frequencies of impairment of all four spatial functions in response to right as opposed to left lesions, but in no case was the difference significant. The RHFS-, however, showed significantly greater impairment following right lesions on three of the four spatial tasks, the only exception being constructional apraxia, where the difference was just short of significance (Fisher Exact Probability =.059, computed by the writer). The data for right-handers therefore were highly congruent with the Hardyck model (1977) expectations, showing greater bilaterality of both verbal and visuo-spatial functions in RHFS t as opposed to RHFS- persons. A final important aspect of the study concerned differences in response to anterior versus posterior lesions. Posterior lesions were defined as postRolandic, including the temporal lobes; anterior lesions were frontal and Rolandic. Only in RHFS-patients did the frequency and severity of deficits differ consistently between anterior and posterior lesion groups. Posterior lesions were significantly more disruptive than anterior lesions for three verbal functions and three visuo-spatial functions in the RHFS-. The RHFS t showed no significant differential effects of anterior versus posterior lesions on verbal functions, and only two significant differences on visuo-spatial functions. Again, posterior lesions were more disruptive when differences were found. Left-handers, regardless of FS status, showed little evidence of anterior-posterior differences, giving rise to the assertion of the authors that left-handers have a more diffuse intrahemispheric organization of functions. The same assertion would be appropriate for the RHFS t . In addition to analyses of specific language and spatial impairments, Hecaen et al. provided data on the incidence of aphasia and spatial disorders (any manifestation, severity ignored) following left and right hemisphere lesions. I have arranged these figures as shown in Table 1. The only statistical analysis conducted by Hecaen et al. on these frequencies tested for a sex difference within FS-handedness groups. The more interesting question is whether the various patient groups showed differential impairments in response to left versus right lesions. Fisher Exact Probability tests show that four of the eight handedness-FS groups did not show a significantly greater incidence of aphasia

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Table 1: Incidence of left and right brain-lesioned patients in each handednessFS-sex group who suffered ("YES")or did not suffer ("NO")aphasia or spatial disorder and significance of differences of incidences (Adapted from Hecaen et al., 1981)

Aphasia Data Left Les ioned Left -Handed FS- Male FS- Female FS+ Male

FS+ Female

All Patients

Significance Level

Right Les ioned

YES

NO

%YES

YES

NO

%YES

18 14 23 11 66

9 0 9 3 21

67 100 72 79 74

5 2 9 2 18

21 4 7 4 36

19 33 56 33 32

,006 .003 .919 .078 .001

18 6 5

11 11 9 3 34

62 35 36 70 51

0 3 1

18 13 11 13 55

0 19

.ooo

Right-Handed Male Female Male Female All Patients FSFSFS+ FS+

7 36

1 5

a

7 8

.251 .ii7 ,002 .001

Spatial Disorder Data Left Les ioned

Significance Level

Right Les ioned

Left-Handed

YES

NO

%YES

YES

NO

%YES

FS- Male FS- Female

10 7 12 5 34

17 7 20 9 53

37 50 38 36 39

11 2 11 4 28

15 4 4 2 25

42 33 73 67 53

,456 ,426 ,023 ,217

5 3 2 1 11

24 14 12 9 59

17 18 14 10 16

11 4 5 4 24

7 12 7 10 36

61 25 42 29 40

,003 .463 .130 .283 .002

FS+ Male FS+ Female All Patients

.115

R i ght -Handed FS- Male FS- Female FS+ Male

FS+ Female

All Patients


379

following left than following right lesions. These were the LHFS+ males and females, and the RHFS- females and RHFS t males. For spatial disorders, only two of the eight groups showed a significantly higher incidence of disorders following right than left lesions. These were the LHFS t and RHFS- males. Ignoring the FS and sex variables, the data ("all patients" rows) show that both left and right-handers suffered higher frequencies of aphasia following left than right lesions. The right-handers suffered a significantly higher incidence of spatial disorders following right lesions, but left-handers suffered spatial disorders with similar frequencies after left or right lesions. Finally, one can contrast the incidence of disorders in left and right-handers following left and right lesions. These contrasts reveal that aphasia was more common in left-handers than righthanders following left hemisphere lesions (X' = 10.2, df 1,p < .002) and following right lesions (X' = 10.1, df 1, p < .002). Spatial disorders were more common in left-handers than right-handers following left lesions (X' = 10.4, df 1, p < .002), but the frequency of spatial disorders following right hemisphere lesions did not differ between handedness groups (X' = 1.86, df 1, p c.175). Critique of the Clinical Studies

All of the studies have flaws. The small sample sizes of Newcombe and Ratcliff (1973) and Pratt and Warrington (1973) are obvious weaknesses. Another flaw, common to all, concerns the definition of handedness. In a footnote, Hecaen et al. (1981) mention that the hand used for writing was not considered in determining strength of hand preference since the investigators had never encountered a case of a left-handed writer in France who was over the age of 35. Most of the patients studied were over 35. Only 12 of the 24 patients of Warrington and Pratt (1973) wrote with the left hand. Social pressures to write with the right hand were probably less severe in the British samples, but again, most of the patients would have attended elementary school during the 1930's, when pressures presumably existed for right hand writing. It is certainly possible that the neurological organization of language functions could be influenced by the early adoption of right hand writing. The problem of defining handedness is magnified if one is asked to identify the handedness of relatives when hand used for writing cannot be employed as a criterion. Thus, especially in the Hecaen group studies, the validity of the FS- and FS+ designations is problematic. A related problem also concerns the definition of FS status. While FSt is typically based only on first degree relatives, because of the greater difficulty of securing information regarding the handedness of more distant

380

McKeever

relatives, the Hecaen group counted a diverse set of relatives in arriving at FS classifications. On the one hand, this approach can have its strengths, especially where the number of first degree relatives is very small. On the other hand, the Hecaen group included aunts, uncles, and cousins. Left-handedness in cousins has a 50% chance or arising from a family having no biological relationship to the patient, and the same is true of aunts and uncles unless the requirement that they be siblings of the patients’ parents is stipulated, and the Hecaen group did not indicate that this stipulation was made. Additional serious flaws of the Hecaen et al. (1981) study are (1) the abse,nce of data regarding the time of assessments in relation to the time post-onset of lesions; and (2) the absence of evidence that lesion sites were comparable in the various groups compared. It is well-known that left-handers show more transient disruptions of neuropsychological functions following brain lesions. The very high rate of symptoms, particularly verbal ones, in the left-handed as opposed to the right-handed patients suggests that the assessments characterize relatively early symptoms. Secondly, there is no assurance that lesion sites were comparable. Data on the anterior versus posterior lesion sites of part of the sample (surgically verified cases, Table 2 of the article) are reported and show that, at least for those patients, both left and right lesions were more frequently posterior lesions in the LHFS t than in the LHFS-. Among the right-handers, left lesions were more often posterior in the RHFS t than in the RHFS-, while right lesions were more often anterior in the R H F S t than in the RHFS-. Examination of the data shows that posterior lesions were generally more disruptive of both verbal and spatial functions. If these distributions characterized the whole sample, one might argue that left language function is overestimated in LHFS t and RHFS t patients in relation to LHFS- and RHFSpatients, while right hemisphere spatial function is overestimated in LHFS + relative to LHFS- patients and underestimated in RHFS t relative to RHFSpatients, Given the serious barriers to unequivocal interpretation of the data, the clinical studies can be regarded only as illustrating a (contradictory) range of possible influences of FS on cerebral organization for language and visuospatial functions. Because of the greater problems in defining handedness of relatives than of patients, the data would seem to provide better information regarding differences between handedness groups than between FS groups.


381

Experimental Studies of Normal Subjects Studies of possible differences in language laterality as a function of handedness and FS characteristics have often employed dichotic listening and lateralized tachistoscopic presentation methodologies. The rationales for these methods are detailed in Springer (1986) and McKeever (1986a). The studies to be reviewed all employed normal subjects (Ss), most of whom were college undergraduates. Other behavioural techniques, such as the concurrent activities paradigm (Kinsbourne and Hiscock, 1977) and tactile paradigm (e.g. Witelson, 1974), have been applied to the study of language laterality. It is my view that to date these techniques have less claim to credibility as measures of language laterality, and given page limitations, and the fact that they provide no substantial reinforcing or countervailing evidence to that supplied by dichotic and tachistoscopic studies, I shall forego a consideration of them. I have also omitted studies in which FS was thoroughly confounded with handedness, handwriting posture, or strength of hand preference, or which employed very small samples, or reported data on only a single subset of FS Ss, such as RHFS t males. Dichotic Listening Studies of Language Lateralization

The results of a number of studies are indicated in Table 2. The table indicates which handedness-FS or handedness-FS-sex group(s) failed to show the right ear advantages (REA) indicative of left hemispheric specialization or showed a reduced REA relative to the most strongly REA group (usually righthanded Ss). Zurif and Bryden (1969) found significant REAs in their right-handed Ss (all were FS-) and in their 10 LHFS- Ss, but the LHFS t tended to recall more digits from the left ear. Higenbottom (1973), employed a dichotic words task and found a significant REA for right-handers, but non-significant ear differences for left-handers, regardless of FS status. Hines and Satz (1974) found a significant REA across groups, with no differential asymmetry as a function of FS in righthanded Ss (FS was not assessed in left-handers). Briggs and Nebes (1976) classified Ss according to degree of hand preference (right, left, and mixed) as well as to FS. No differential aspmatries were found between any groups, including the handedness groups. Lake and Bryden (1976), found evidence of reduced REAs in FS t females, regardless of handedness, and in LHFS- males. It should be noted, however, that their dichotic task produced a low level of

382

McKeever

Table 2: Summary of dichotic listening studies involving assessment of FS effects, indicating groups showing weak or absent Right Ear Advantages (WAREA) ss

FS

Task

Z u r i f & Bryden (1969)

20 RH 20 LH

20 FS-/ 0 FS+ 10 FS-/lO FS+

Dichot i c Digits

LHFSt

Higenbottom (1973)

33 RH 56 LH

NA 27 FS-/29 FS+

D i c h o t ic Words

LH

Hines & Satz (1974)

60 RH 30 LH

30 FS-/30 FS+ NA

0 ichot ic

None

Briggs & Nebes (1976)

40 RH 40 MH 40 LH

20 FS-/20 FS+ 20 FS-/20 FS+ 20 FS-/20 FS+

D ichot i c Digits

None

Lake & Bryden (1976)

72 RH 72 LH

36 FS-/36 FS+ 36 FS-/36 FS+

D i c h o t ic Syll.

FS+ Fe LHFS- Ma

Lishman & McMeekan (1977)

22 RH 20 LH

26 FS-/16 FS+

D ichot ic Digits

FS+ SLH

McKeever & VanDeventer (1977a)

80 RH 71 LH

44 FS-/36 FS+ 34 FS-137 FS+

Dichot i c Digits

LHFS+

Geffen & Traub (1970)

39 LH

14 FS- males 25 FS+ males

Dichot i c Monitor.

LHFS- Ma

Piazza (1980)

32 LH 32 RH

16 FS-/16 FS+ 16 FS-/16 FS+

cv

Dichot i c Syll.

None

Sear leman (1980)

117 LH 256 RH

? FS-/ ? FS+ ? FS-/ ? FS+

cv

D i c hot ic Syll.

None

O r s i n i e t a1 (1985)

257 LH 215 RH

141 FS-/116 FS+ 145 FS-/ 70 FS+

Dichot i c Words

LH

60 LH 60 RH

30 FS-/ 30 FS+ 30 FS-/ 30 FS+

Dichot i c Syll.

LH

McKeever (1986b)

134 LH 225 RH

67 FS-/ 67 FS+ 127 FS-/ 98 FS+

D ichot i c

LH

Rich & McKeever (1989)

64 LH 64 RH

32 FS-/ 32 FS+ 32 FS-/ 32 FS+

Study

Bryden (1986)

WAREA

Digits

cv

cv

cv

Syll.

Oichot i c Syll.

cv

LH

Abbreviations: NA = not assessed; LH = left-handed; RH = right-handed; MH = mixed-handed; SLH = s t r o n g l y left-handed; Ma = males; Fe = females.


383

REA overall. Even among RHFS- females, only 67% of the Ss had REAS. Lishman and McMeekan (1977) found somewhat lower REAs in FS t than in FS- left-handed writers (not significant, however), but found significantly lower REAs in strongly left-handed F S t as opposed to strongly left-handed FShanders. Geffen and Traub (1980) employed the dichotic monitoring task in a study which found that 76% of LHFS t males, and only 35% of LHFS- males had REAs (Fisher Exact Probability = .0013). The number of Ss in other sexhandedness-FS groups were inadequate to permit meaningful analysis with respect to FS. McKeever and VanDeventer (1977a) found a non-significant REA in LHFS t females, but significant REAs in all other handedness-sex-FS groups. Piazza (1980) analyzed the data for male and female Ss separately. There was a significant REA across handedness-FS groups of males and no FS influences. Among females, there was no significant REA and no significant effects involving FS. Despite this, it is possible that an FS by ears interaction may have been found had male and female data been included in the same analysis. The FS t Ss had lower REAs than the FS- Ss in every handedness-sex group, although the REA of RHFS t males was nearly as large as that of RHFS- males. Rather than speculate about such possibilities, however, the best approach would be to accept the conclusions as presented. Searleman (1980), despite the fact that he employed very large samples of left and right-handers, failed to find effects of FS, or even of handedness. Degree of right hand preference, however, was found to relate positively to REAs. He concluded that REAs are pervasive. Four more recent studies, Orsini et al. (1985), Bryden (1986), McKeever (1986b), and Rich and McKeever (1989) all studied rather large samples and found highly significant REAs for right-handers and significantly smaller REAs for lefthanders. Despite these clear differentiations of right from left-handers, no effects of FS were seen. Conclusions from the Dichotic Verbal Studies. The best conclusion from these studies would seem to be that FS has shown no dependable influence on the language laterality processes involved in the mediation of dichotic listening tasks. The most recent, and in terms of methodology, the most sound studies, provide consistent negative data regarding an influence of FS. This conclusion is very strong with respect to right-handed persons. Two studies, those of Zurif and Bryden (1969) and McKeever and VanDeventer (1977a), employed dichotic digits and did find lesser left lateralization in LHFSt Ss. Piazza (1980) found no FS effects. The Lishman and McMeeken (1977) data showed LHFS t Ss to have significantly smaller asymmetry, but only if they were strongly left-handed

384

McKeever

according to a handedness inventory. Contrary to the outcomes reported by Zurif and Bryden (1%9) and McKeever and VanDeventer (1977a), Lake and Bryden (1976) and Geffen and Traub (1980) found lesser REAs in LHFS- males, consistent with the Newcombe and Ratcliff (1973) clinical data. Given that the two studies showing straightforward differences between LHFS- and LHFS + Ss employed dichotic digits tasks, one might speculate that a memory load is necessary to show the difference. Other dichotic digit studies, however (Hines and Satz, 1974; Brigs and Nebes, 1976), found no FS effects. Additionally, if one were to suggest that the digits tasks are more likely to find an FS effect because they involve a memory load, it must be noted that the Orsini et al. task also involves memory for words, the only difference being that the words are not digit names. In conclusion, the data show no hint of FS influences in righthanders, and only occasional findings of FS influence have obtained in lefthanded samples. It is possible that subtle differences in tasks exist, and that lesser lateralization for some aspect of language processing exists in the LHFS + , but the data merely suggest this possibility. Tachistoscopic Studies of Language Lateralization Table 3 presents the main features and findings of a number of tachistoscopic verbal studies in which possible FS influences were assessed. Three of the studies found no FS effects at all (Hines and Satz, 1974; Piazza, 1980; Seitz, 1986). The table also shows the word "none" after the Seitz and McKeever (1984) study, i.e., none of the groups had weak or absent right visual field advantages (RVFA). This experiment found a peculiar result, in which all handedness-FS groups had large and significant RVFAs, but FS + males had by far the largest, with the result that a significant handedness-sex-FS interaction was obtained. The RHFS + males, however, were the smallest group in the study (9 Ss) and an attempted replication (Seitz, 1986) with balanced and larger samples showed all groups having large RVFA of the same magnitude. Six studies found weak or absent RVFA in RHFS+ Ss generally. These included the Hines and Satz (1974) digit recognition accuracy study, the McKeever, VanDeventer, and Suberi (1973) and the McKeever and VanDeventer (1977a) studies of recognition of masked letters, the Hannay and Malone (1976) study of the recognition and recall of nonsense words, the McKeever and Jackson (1979) study of naming latencies for pure color patch stimuli, and the Sullivan and McKeever (1985) study of word naming latencies. Two other studies (McKeever and Hoff, 1982; and McKeever, Seitz, Hoff, Marino, and Died (1983)


385

found interactions of sex and FS status in right-handed Ss. Both studies found lesser RVFA in RHFS- females and RHFS t males in latencies for naming five recurring drawings of objects (the Object Naming Latency Task). While this interaction was initially unexpected, it is interesting that it parallels the sex-FS interaction in aphasia frequencies following left lesions in right-handers as seen in the Hecaen et al. (1981) data (see Table 1). In summary of the twelve tabled studies regarding FS and language laterality in right-handed Ss, then, four found no FS effects, six found that FS reduced left lateralization generally, and two others found that FS reduced left lateralization in RHFS t males but not females. Turning to the studies of left-handed Ss, two found lesser left language dominance in LHFSt Ss. One of these was the study of Zurif and Bryden (1969), which included only ten FS- and ten F S t males, and no female Ss; the other was that of Schmuller and Goodman (1979) which included both sexes, but only eight Ss of each FS designation. The latter study, using simple word recognition accuracy, found LHFS+ Ss to show a significant LVFA; LHFS- Ss showed no significant asymmetry. The outcome for LHFS t Ss is surprising given the very small sample sizes, since significant LVFAs have never been found in much larger samples. The procedure was somewhat unusual, in that Ss reported first the word that a furation point directional symbol indicated, and then reported the other word if they could. The LHFS- resembled, generally, the LHFS + Ss on first reports, but resembled the right-handers on second reports, is., right-handers and LHFS- Ss had more second report errors on LVF than RVF words. The basis for the significant LVFA across report order for LHFS t Ss was due to their having higher error rates on both first and second reports of RVF words. Two studies found no FS effects. One of these (McKeever et al., 1973) found a significantly smaller RVFA in left-handers, but no differential effect of FS within the left-handed group. It might be noted, however, that the sample was small. Seitz (1986), despite an adequate sample size, found no significant effects due to either handedness or FS. Six studies found lesser RVFAs in LHFS- Ss, and five of these (McKeever et al., 1973; Higenbottom, 1973; McKeever and VanDeventer, 1977a; Bradshaw and Taylor, 1979; McKeever, 1979) used letter or word stimuli. The sixth study (Experiment 1, of McKeever, 1979) employed the Color Naming Latency Task. It is perhaps worth noting that three of the studies finding lesser lateralization in LHFS- Ss also found extremely low levels of word recognition for this group, and that Bradshaw and Taylor (1979) explicitly raised the question as to a possible word naming deficit in LHFS- Ss. Piazza’s (1980) data, however, showed no such trend.

386

McKeever

Table 3: Summary of tachistoscopic language task studies involving assessment of FS effects, indicating groups showing weak or absent right visual field advantages (WARVFA)

Study

Subjects

FS

Task

WARVFS

Z u r i f & Bryden (1969)

20 RH 20 FS-/ 0 FS+ Ma. 20 LH 10 FS-/lO FS+ Ma.

L e t t e r Recognition Accuracy

LHFS+

Hines & Satz (1971)

84 RH 66 FS-/18 FS+

D i g i t Recognition Accuracy

RHFS+

McKeever e t a l . (1973)

48 RH 24 FS-/24 FS+ 23 LH 14 FS-/ 9 FS+

Masked L e t t e r Recognition

RHFS+ LH

Uni- & B i l a t e r a Word Recognition

LHFS-

Higenbottom (1973)

33 RH NA 56 LH 29 FS-/27 FS+

L e t t e r Recognition Accuracy

LHFS-

Hines & Satz (1974)

60 RH 30 FS-/30 FS+ NA 30 LH

D i g i t Recognition Accuracy

None

Andrews (1977)

48 ?

Trigram Recognition

FSt

McKecver & VanDeventer (1977a)

80 RH 44 FS-/36 FS+ 71 LH 34 FS-/37 FS+

Masked L e t t e r Recognition

RHFS+ LHFS-

15 FS-/33 FS+

Hannay & Malone 30 RH (1979)

15 FS-/15 FS+

Nonsense Word Recognition

RHFS+

McKeever & Jackson (1979)

24 RH

12 FS-/12 FS+

Colour Naming Latency Task

RHFS+

Piazza (1979)

32 LH 32 RH

16 FS-/16 FS+ 16 FS-/16 FS+

B i l a t e r a l Word Recognition Accuracy

None

Bradshaw & Taylor (1979)

36 LH 36 RH

18 FS-/18 FS+ 36 FS-

U n i l a t e r a l Word Naming Speed

LHFS-

McKeever & Hoff (1979)

64 RH 32 FS-/32 FS+

Object Naming Latency Task

McKeever (1979)

51 LH

Colour Naming Latency Task

15 FS-/36 FS+

RHFS- Fe RHFS+ Ma LHFS-

387

Cerebral Organization Table 3: Continued

Study

Subjects

FS

Schmuller & Goodman

16 LH 8 RH

8 FS-/ 8 FS+ 8 FS-/ 0 FS+

McKeever (1979)

25 LH

1C FS-/15 FS+

McKeever e t a1

50 RH 27 FS-/23 FS+

(1983)

Task

WARVFS

B i l a t e r a l Word Recognition

LHFS+

Uni & B i l a t e r a l Word Recognition

LHFS-

Object Naming

RHFS- F .

Latency Task

RHFS+ M .

Sullivan & McKeever (1985)

40 RH 21 FS-/19 FS+

Word Naming Latency Task

RHFS+

Seitz & McKeever (1984)

50 RH

29 FS-/21 FS+

B i l a t e r a l Object Naming Latency

None

Seitz (1986)

48 RH 48 L H

24 FS-/24 FS+ 24 FS-/24 FS+

B i l a t e r a l Object Naming Latency

None

A b b r e v i a t i o n s : NA = n o t assessed; LH = Left-handed; males; Fe = females

RH = right-handed;

Ma =

Conclusions from the Tachistoscopic Language Laterality Studies. The majority of the evidence suggests that FS acts to reduce left hemisphere language lateralization in right-handers, particularly males. In left-handers, the balance of the evidence suggests that LHFS- Ss are the group who are most apt to be less left hemisphere dominant for language. Exceptions to this finding come from the very small sample studies of Zurif and Bryden (1969) and Schmuller and Goodman (1979). The Schmuller and Goodman study was the only one assessing FS in left-handed Ss and requiring the memory storage of the second to-be-reported word, and it indicated the LHFS t Ss had a Bradshaw significant LVFA. A replication of their finding would be important. Again, however, the sample was small and significant LVFAs for bilateral word stimuli is an unusual finding. The lessened left hemisphere specialization in LHFS- suggested by the majority of the studies may be particularly for letter stimuli and brief presentations, although naming latencies for colour stimuli, a non-demanding task in perceptual terms, have also shown lesser left language specialization.

388

McKeever

Thus, unlike the situation in regard to dichotic listening studies, FS effects for the processing and reporting of visual language stimuli have been obtained with some regularity in the tachistoscopic studies. The direction of the effect most often obtained in right-handers is consistent with the view that FS acts in the direction of bilateralization in right-handers (Hardyck, 1977). The results for left-handers, however, are not consistent with the Hardyck model. The tachistoscopic studies agree more with the Newcombe and Ratcliff (1973) conclusion that LHFS- Ss are less left dominant for language function than are the LHFS t . Studies of FS and Lateral Dissociations of Language Processing. The Hecaen group studies suggest that one effect of FS on language might be to laterally "dissociate" different language processes. Whereas LHFS- and RHFSpatients were found to have virtually all tested language functions more impaired by left than by right lesions, the LHFS t and RHFS t had only two of the six functions more impaired by left than by right lesions. This suggests that the FS- persons are left hemisphere dominant for the various verbal functions, while the F S t are left hemisphere dominant for some but not other verbal functions. Information regarding the lateral coherence of language functions can be gained from the degree of correlation between multiple language laterality tasks administered to the same Ss. A few such studies have been reported, though the motivation has not been to study the lateral coherence of language organization, but rather to address the "problem" of apparent low correlation between dichotic and tachistoscopic verbal task results. The problem has been seen to exist on the logic that if a person is "diagnosed" as left hemisphere language dominant on a dichotic task, a tachistoscopic task purporting to measure "language lateralization" should provide the same diagnosis. Bryden (1965) failed to find any correlation of asymmetries from a dichotic digits task and a task involving unilateral tachistoscopically presented letters. He speculated that the result could be due to differences in the two tasks or to a dissociation of laterality effects for the two modalities. In an effort to make the tasks more similar, Zurif and Bryden (1969) devised a letter recognition task which presented four letters bilaterally on each trial. The dichotic digits task presented four digits per stimulus item to each ear. Ss were 20 RHFS-, 10 LHFS-, and 10 LHFS t male undergraduates. No significant cross-modal correlations were found. Indeed, the largest cross-modal correlation (between the bilateral ordered administrations) was only t .18, well short of significance.


389

Zurif and Bryden (1969) did not examine the cross-modal correlation in the different handedness or FS groups. Hines and Satz (1974) addressed the question of cross-modal correlation by testing a larger sample than tested by Zurif and Bryden (1969), and assessing the reliability of the two tasks. Both tasks presented series of digits on each trial. The cross modal correlation was significant for RHFS- Ss (r = +.39). The authors stated that the correlation for RHFS + Ss (r = + .34) was also significant at the .05 level, but actually a correlation of .36 would be required for significance with the 28 df available. The correlation for left-handers was clearly non-significant (r = t .02). They concluded that auditory and visual language processing were "dissociated" in left-handers. Since the correlation for RHFS + Ss was actually non-significant, the same conclusion would be justified in relation to RHFS- SS. Fennell, Bowers, and Satz (1977a; 1977b) did not directly correlate ear difference scores with visual field difference scores, but correlated left ear scores with left field scores, and right ear scores with right field scores. Such correlations would not necessarily be informative regarding the communality of language laterality in the two modalities, but, in any event, the correlations were non- significant. Smith and Moscovitch (1979) correlated half field recognition accuracy score differences with ear difference scores of 15 non-inverted handwriting posture (NHP) left-handers, 15 inverted handwriting posture (IHP) left-handers, and 15 right-handers. The visual task presented vertically-spelled CVC trigrams, unilaterally, and the auditory task was a standard dichotic consonant vowel discrimination task (DCVT). Correlations were negative and non-significant for all three groups. Dagenbach (1986) administered a tachistoscopic task similar to that employed by Smith and Moscovitch (1979), and a dichotic "fused word" task to 230 Ss. He computed cross-modal correlations for right-handed, ambidextrous, and lefthanded groups. Contrary to the thrust of the findings of Hines and Satz (1974), Dagenbach found no correlation for right-handers (r = -.08), but low positive correlations for ambidextrous and left-handed groups (r = + .20 and r = + .26, respectively). An important requirement for assessing the degree of lateral coherence from correlations between tasks is that the measurements be reliable. The studies reviewed above provided no assurance that this requirement was met. Indeed, those investigators who did assess the reliability of their measurements of asymmetry found them to be rather poor. Hines and Satz (1974) obtained split-

390

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half reliability data for their dichotic and tachistoscopic tasks. They found the split-half reliability of the dichotic task to be good (rtt = t .%), but the reliability of the tachistoscopic task was poor (r,, = t.46). Dagenbach (1986) also calculated split-half reliabilities for his tasks, but did not report them. Since he presented both raw correlations and correlations corrected for attenuation for his major groups, however, one can calculate that the mean reliability of his tasks was approximately .65. If tasks possess adequate reliability, lack of correlation between dichotic and tachistoscopic task asymmetries can be interpreted as implying that different neural networks are involved in the processing of the two tasks. We have been concerned with the need to develop reliable measures of functional asymmetries for dichotic and tachistoscopic tasks. We found that requiring Ss to identify only the syllable they were "most certain of hearing" on the DCVT yielded much higher reliability than had been reported for the task when Ss had been encouraged to report both syllables presented on a trial (e.g., Teng, 1981), a procedure that results in a great deal of guessing. Further, we have the S indicate her/his response by bracketing, with both forefingers, the printed syllable from the list of syllables displayed on the table at which he/she is seated. The split-half reliability for the DCVT, thus administered, was found to be .88 (McKeever, Nolan, Diehl, and Seitz, 1984). Two additional tasks with excellent reliability, developed in our laboratory, are the Bilateral Object Naming Latency Task (BONLT) and the Dichotic Object Naming Latency Task (DONLT). The BONLT (Seitz and McKeever, 1984) is a bilateral version of the Object Naming Latency Task (ONLT) originated by McKeever and Jackson (1979). The BONLT was developed in hopes of providing a visual task which might show a larger asymmetry than the ONLT. Seitz and McKeever (1984) found that the BONLT yielded much larger asymmetries than did the ONLT, and in addition, unpublished data show the split-half reliability of the BONLT, calculated from the performances of 146 Ss, to be .87, much better than that of the ONLT (.42 to .55 in various studies). Finally, Krutsch and McKeever (1987) developed the DONLT in order to have an auditory task highly similar to the BONLT which could be used along with the BONLT to assess the question of cross-modal correlation of language laterality. The DONLT delivers the names of two of the five objects from the BONLT (apple, clock, lamp, moose, shoe) on each of 180 trials, with precisely the same stimulus orders as on the BONLT. Krutsch and McKeever (1987) found that the DONLT yielded a split-half reliability of .90 in a sample of 40 Ss.


391

In addition to reliability, verbal laterality tasks should provide robust rightside superiorities in right-handers. These tasks are rather exemplary in this regard. All three tasks show highly significant right-side advantages in righthanded samples, and the percentages of right-handers showing these advantages for the DCVT, BONLT, and DONLT are 83.1% (McKeever, 1986b), 95.9% (composite data, 98 Ss), and 92.5% (Krutsch and McKeever, 1987), respectively. The percentages of right-sided advantages in left-handers for the three tasks have been found to be 73.9% (McKeever, 1986b), 83.0% (Seitz, 1986), and 54.2% (Krutsch, 1989), respectively. Two studies in our laboratory have administered the BONLT and one of the auditory tasks just described to the same Ss. Krutsch (1989) administered the BONLT and the DONLT to 27 right-handers and 24 left-handers. The correlation between the asymmetries across all Ss revealed a small but significant correlation (r = t.28, 49 df, p < .025). The correlations for right and lefthanded Ss were highly similar ( t .27 and t .%, respectively). Thus, the data suggest that language processings of these tasks are equally "dissociated in right and left-handers. Because of the data of the Hecaen group indicating that FS t persons may have less focal, or more laterally dissociated, language functions, correlations between asymmetry measures were computed for FS t and FS- Ss across and within handedness groups. The correlation for FS t Ss was -.02, nonsignificant; that for FS- Ss was t.54, df 25, p < .004). For LHFS- Ss the correlation was t .52 (11 df, p < .07), and for RHFS- the correlation was t .66 (12 df, p < .Ol). For the LHFS t and RHFS+ Ss, the comparable correlations were -.08 and -.07, respectively. These data suggest that FS t Ss, regardless of handedness, had quite different asymmetries for the processing of the DONLT and BONLT. The FS-, however, regardless of handedness, have substantially similar degrees of asymmetry for processing these tasks. The strongest correlation was obtained for FS- males ( t .82, df 11, p < .OOl). A second study (VanEys and McKeever, 1988) had administered the DCVT and the BONLT to 64 right-handed Ss, all of whom had been classified for FS. Although the study had manipulated several variables, essentially no effects of these manipulations on asymmetries had been observed. Having found the crossmodal correlation results just cited, we were interested in whether cross-modal correlations might be found in the VanEys and McKeever data. The results showed no relationship across the 64 right-handed Ss (r = t.13, p < .307). Thus, the data suggest that the BONLT and DCVT are processed less similarly than are the BONLT and DONLT. When the cross-modal correlations were computed for F S t and FS- Ss separately, the correlation was again non-

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significant for the RHFSt (r = t.01, df= 30,p

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