Language Communication and the Brain: A Neuropsychological Study 9783110819410, 9789027930675

Table of contents :
CONTENTS
FOREWORD
CHAPTER I. LANGUAGE COMMUNICATION AND THE BRAIN: THE BROADER CONTEXT
CHAPTER II. HISTORY OF RESEARCH ON THE RELATION BETWEEN SPEECH AND THE BRAIN. MAJOR CONTEMPORARY THEORIES
CHAPTER III. RESEARCH METHODS FOR THE STUDY OF THE SPEECH-BRAIN RELATION
CHAPTER IV. SPEECH AND THE ANATOMICAL AND PHYSIOLOGICAL PROPERTIES OF THE HUMAN BRAIN
CHAPTER V. CEREBRAL MECHANISMS OF SPEECH PRODUCTION
CHAPTER VI. CEREBRAL MECHANISMS OF SPEECH RECEPTION
CHAPTER VII. SPEECH AND COGNITIVE PROCESSES IN THE LIGHT OF APHASIA RESEARCH
CHAPTER VIII. SPEECH AND GOAL-DIRECTED ACTIVITY IN THE LIGHT OF NEUROPSYCHOLOGICAL RESEARCH
FINAL CONCLUSIONS
REFERENCES
AUTHOR INDEX
SUBJECT INDEX
SOURCES OF FIGURES

Citation preview

JANUA LINGUARUM STUDIA

MEMORIAE

N I C O L A I VAN WIJK DEDICATA edenda curai C. H. VAN SCHOONEVELD Indiana University

Series

Maior,

80

LANGUAGE COMMUNICATION AND THE BRAIN A NEUROPSYCHOLOGICAL STUDY

by

MARIUSZ MARUSZEWSKI

1975

MOUTON THE HAGUE • PARIS

P W N - P O L I S H SCIENTIFIC PUBLISHERS WARSZAWA

Copyright © by PWN —Polish Scientific Publishers — Warszawa 1975

No part of this book may be translated or reproduced in any form, by print, photoprint, microfilm or any other means, without written permission from the publishers

This translation has been made from Mowa a mdzg Zagadnienia neuropsychologiczne published in 1970 by Paristwowe Wydawnictwo Naukowe Warszawa

Translated by Grace Wales Shugar

Graphic design: Zygmunt

Ziemka

Printed in Poland (D.R.P.)

CONTENTS

Foreword

ix

Chapter I. Language communication and the brain: The broader context . .

1

§ 1. Introductory remarks § 2. Some theoretical premises Chapter II. History of research on the relation between speech and the brain. Major contemporary theories

1 7 18

§ 1. Early observations on speech disorders following cerebral damage . . § 2. First discoveries of speech "centres". The narrow localization theory § 3. Crisis of the localization theory. One-factor theories § 4. Jackson's views on aphasia. Their significance for understanding of cerebral speech mechanisms § 5. Current localizationist theories § 6. Current antilocalizationist theories and one-factor conceptions of speech § 7. Linguistic views on aphasia. Lenneberg's biological theory of language § 8. The theory of dynamic localization of function. Luria's conception of the functional system § 9. Concluding comments

42 45

Chapter III. Research methods for the study of the speech-brain relation . .

47

§ 1. General description of methods for the study of the relation between behaviour and brain § 2. The clinical method: Causes and properties of brain damage and ways of localizing it § 3. The clinical method: Research on speech disorders caused by brain damage. Shortcomings and difficulties § 4. Other methods for study of the speech-brain relation Chapter IV. Speech and the anatomical and physiological properties of the human brain § 1. Cerebral hemispheric dominance for speech A. Lateralization of body functions B. Effects of damage to left and right hemispheres in adults

19 21 26 29 31 35 38

47 49 54 63 67 68 70 71

VI

C. Effects of brain damage in children. Ontogenetic formation of dominance D. Experimental methods for ascertaining dominance and results obtained by these methods E. Dominance and anatomical differences between the hemispheres . . F. Speech and the nondominant (subordinate) hemisphere G. Conclusions § 2. The speech area and its inner differentiation § 3. Speech and the general regularities of brain functions Chapter V. Cerebral mechanisms of speech production § 1. Introductory remarks § 2. General characterization of the processes involved in speech production § 3. Selected questions pertaining to the anatomical and physiological bases of speech production § 4. Cerebral mechanisms of speech production in the light of its disorders due to dominant hemisphere damage: Locus in anterior divisions . . A. Dysarthria and aphasia B. Afferent motor aphasia: Disintegration of somesthetic speech sound patterns C. Efferent motor aphasia: Disorders of speech sound linkage in word formation D. Efferent motor aphasia: Disorders of sentence construction . . . . E. Dynamic aphasia: Disorders of discourse construction F. Other disorders of speech production due to frontal lobe damage: "Subcortical motor aphasia"; disorders due to lesions in the supplementary motor speech area § 5. Cerebral mechanisms of speech production in the light of its disorders due to dominant hemisphere damage: Locus in posterior divisions . . § 6. Conclusions Chapter VI. Cerebral mechanisms of speech reception § 1. Introductory remarks § 2. General characterization of speech reception. Associated physiological and psychological problems A. Speech sound perception. The motor theory of speech reception . . B. Temporal and sequential factors in speech reception. Verbal memory C. Speech reception. The decoding of meanings § 3. Cerebral mechanisms of speech reception in the light of its disorders due to dominant hemisphere damage: Locus in the temporal lobe . . A. Pure word deafness

74 76 78 79 83 83 88 92 92 93 94 101 101 102 105 107 Ill

115 117 121 124 124 126 127 130 132 134 135

vii

B. Phonemic hearing disorders. Acoustic aphasia C. Sensory aphasias unrelated to phonemic hearing disorders. Transcortical sensory aphasia and conduction aphasia as contrasted with Luria's acoustic-mnestic aphasia D. Verbal memory disorders associated with left temporal lobe damage § 4. Cerebral mechanisms of speech reception in the light of its disorders due to dominant hemisphere damage: Extra-temporal locus . . . . A. Speech reception disorders due to lesions in the parieto-occipital region. Semantic aphasia B. Speech reception disorders due to damage in the anterior divisions of the speech area § 5. Conclusions

136

139 141 144 145 146 148

Chapter VII. Speech and cognitive processes in the light of aphasia research

151

§ 1. Introductory remarks § 2. Naming disorders in aphasia. Controversy about amnestic aphasia . . § 3. Major interpretations of aphasic naming disorders A. Naming disorders as indicative of intellectual deficit B. Naming disorders as indicative of deficient perceptual functions . . C. Naming disorders as indicative of disturbed cross-modal association processes D. Naming disorders as indicative/of impaired simultaneous synthesis . E. Confrontation of the various interpretations of aphasis naming disorders. Conclusions § 4. Disorders of intellectual processes in various forms of aphasia . . . .

151 153 157 158 163

Chapter VIII. Speech and goal-directed activity in the light of neuropsychological research § 1. The role of speech in the regulation of goal-directed activity . . . . § 2. Behavioural disorders and disturbances of the regulatory function of speech accompanying frontal lobe damage Final conclusions References Author index Subject index Sources of

figures

168 171 173 174 177 177 183 193 196 207 211 216

FOREWORD

The purpose of this monograph is to survey those findings of neuropsychological research that can help us in answering the question: What structural and functional properties of our brain have equipped us, unique among living beings, with the capacity for language communication? In order to enable the reader to form his own opinion on the soundness of our interpretations, we shall try to illustrate the complex nature of the problem and the difficulties inherent in methods of its study; we shall also examine the divergent views that have been advanced on both the broader and the more particular questions. To avoid excessive detail and technicality, we shall have to pass over a number of the more poorly studied and more specialized aspects of the problem. It would appear that our present knowledge of the cerebral mechanisms of speech has advanced far enough to permit the reader to gain at least a general picture of their spatial arrangements. In the light of available evidence on the role of cerebral structures in the regulation and programming of the organism's activity, we may conceive of the brain as an organ differentiated both in structure and in function; with greater or lesser exactitude, we may formulate statements as to the role served by its separate parts and try to establish the responsible structures for the regulation of the various activities, including those involved in speech. Some of these formulations are grounded on solid experimental evidence, others leave numerous aspects open and vague; in the latter case, alternative hypotheses may be advanced which only future research will corroborate or reject. Our aim is to inform the reader as fully as possible about the issues under current discussion and about the gaps in our knowledge. But these will not alter the fact that what is known today about the cerebral mechanisms of speech constitutes, in broad outline, an impressive body of knowledge based on sound scientific data which hundreds of investigators have amassed in research centres throughout the world. Due to this fact we are able to elucidate the human capacity to communicate through language as a natural phenomenon without recourse to nonscientific speculation. This body of data will comprise the principal subject matter of this book. It is not our purpose to set up one more theory or hypothetical construction as an explanation of the cerebral mechanisms of speech; we wish only to report on what is in fact known, although we may not yet be fully able to interpret this knowledge.

X

FOREWORD

The author wishes to express his gratitude to Andrzej Maksymczuk M. A., Dr. Halina Mierzejewska, Professor Halina Spionek and Associate Professor Jan Strelau, who read the typescript and offered invaluable critical comments which have contributed greatly to the final version of this book.

CHAPTER 1

LANGUAGE COMMUNICATION AND THE BRAIN: THE BROADER CONTEXT

§1. INTRODUCTORY REMARKS

One of man's most distinctive features, specific to his species, is the capacity to communicate through language. Talking and listening, reading and writing, constitute the daily universal forms of a normal human being's activity from infancy till death. Moreover, with the progress of civilization, these peculiarly human forms of activity continue to gain in importance, as exemplified in the mounting number of those whose activity—as viewed from the exterior—is almost wholly reducible to acts of speech production and reception. It seems beyond doubt that a constantly increasing part of human wakeful time is devoted to activities associated with verbal communication. Simultaneously we witness efforts to increase maximally the number of "collocutors", people whom we speak to and write for and, ultimately, all those we listen to and whose writings we read. Technical progress in communication and mass media has led to ongoing verbal intercourse among human beings and groups great distances apart on the earth's surface. These circumstances appear to be of crucial import in the shaping of contemporary life; their significance however is not always fully credited. The process we are considering consists primarily of transmitting diverse kinds of suggestions, recommendations, commands, prohibitions, and instructions; of exchanging information about events past, present, and anticipated in the future, which affect the lives and environments of those in communicative contact; of passing forward the products of man's cognition of reality. These kinds of information are required for the smooth flow of the individual person's activity, which has with time grown increasingly complex and at the same time dependent on the intake of various types of information inaccessible to a single individual through his own resources. Moreover, these kinds of information are indispensable for the proper functioning of social organizations, which embrace increasingly wider groups of individuals. This is the principal reason behind the trend to broaden the scope of verbal communication, the characteristic feature of man's social way of life.

2

I. LANGUAGE COMMUNICATION AND THE BRAIN

The ability to communicate by means of language is, as stated at the outset, an exclusively human property. Although we observe various forms of interindividual communication, including vocal1, in the lower species, there is an essential difference between these forms and the human form of communication. Let us try to characterize this difference more closely, since it constitutes a major premise for what is to follow. The question we are discussing has long been the subject of speculation and debate among philosophers, linguists, biologists and psychologists. Various formulations on the differences in question have been advanced, often divergent on fundamental points. We shall not probe into this discussion, as it is irrelevant to our task, but shall limit ourselves to one point on which all writers dealing with this problem show agreement, namely, that the difference between animal communication and human verbal communication is not one of quantity alone but of quality as well. Relatively speaking, the most precise treatment of this difference may be found in the work of the American linguist, Charles F. Hockett (1958). In his view, the human communicative system can be characterized by seven salient features. Some of these features recur in nonhuman communicative systems, but in none can the whole set of seven be found. A brief presentation of these features follows: 1. Duality. Every human language makes use of two sets of component elements. One is the set of phonemes (sounds) of that language from which any utterance can be arranged. These elements—such as /p/, /z/, /t/, /a/, /I/, etc.—are in themselves devoid of meaning, but when contrasted one with another determine differences in the meaning of words. For instance, if we exchange the p-sound for the t-sound in the word "pen", we obtain a change of meaning not only of the word but of the utterance containing that particular set of sounds. At the same time, any utterance consists of another set of components, i.e., it is an arrangement of meaningful elements or morphemes. Morphemes are the smallest individually meaningful elements of the language, each of which is represented by an arrangement of phonemes. By virtue of the feature of duality, the human communicative system can be extraordinarily productive, since it permits a great amount of information to be transmitted by means of a very limited number of basic elements. This feature does not occur in any of the nonhuman animal communicative systems so far investigated. 2. Productivity. This feature implies that a speaker of any language may say something that no one has ever said nor heard before and yet is understood by his audience. This feature recurs in certain animal communicative systems; for example, the honey bee can report on entirely new sources of nectar. 3. Arbitrariness. This feature refers to the fact that between the linguistic sign and its designate—with some exceptions—there is no similarity. For instance, the word "cat" or "dog" has no likeness in any respect to the animal in question, and in addi1

A fairly full account of forms of animal communication can be found in Hubert and Mable Frings (1964).

1. I N T R O D U C T O R Y R E M A R K S

3

tion the difference between the words "cat" and "dog" bears no analogy to the difference existing between the two animals. 4. Interchangeability. Any speaker in any language is, in principle, a hearer as well; theoretically he can say anything he is able to understand when someone else says it. This feature is involved in some animal systems as well. 5. Specialization. Any communicative activity tends to evoke some behaviour in another individual. To some degree any behaviour can produce this effect; for example, seeing someone setting the table at the right time of day tells us that dinner is about to be served. But the communicative aspect of the action of table-setting is in this case marginal, the main purpose being to bring about direct physical changes in the surroundings. On the other hand, an action composed of linguistic elements has only minor direct physical consequences, for it is specialized as a communicative function. We find specialization in animals as well, but human language has developed this feature to an incomparably greater extent. 6. Displacement. This feature proper to the human communicative system implies that it is possible to communicate on topics concerning phenomena not only directly perceptible but also remote in time and place. This feature is manifested in some animal communicative systems in embryonic form. 7. Cultural transmission. Man does not inherit genetically the activity involved in language communication; it can be acquired solely in conditions of exposure to language users. Elementary manifestations of this feature as well recur in nonhuman communicative systems, but in man language acquisition dependency upon contact with language users has attained a particularly high degree. The essential difference, in Hockett's view, between human language as communicative system and all nonhuman forms of communication resides in the fact that all seven of the aforementioned features occur together in the former. One might consider whether this set of features is exhaustive or whether some additions are necessary for a complete characterization of this difference. In another work (Hockett, 1960), the same author listed up to 13 characteristic features of language as communicative system. Other authors have also advanced certain proposals. But it would seem that the list presented here is sufficiently illustrative of the unique position of human language capacity in the world of living beings. Once the above fact has been established, the question arises of its consequences for human psychology and for our knowledge of the specifically human mechanisms that govern behaviour. The significance of this problem, which exceeds the scope of the present considerations, will be simply pointed out against the background of an experiment conducted some years ago in Pavlov's laboratory by Vatsuro (1955). This was an experiment with Rafael, one of a pair of chimpanzees on whom Pavlov and his collaborators conducted research. During the investigations prior to the experiment we are about to describe, Rafael learned to perform a few simple actions, such as extinguishing fire with water drawn from a faucet into a mug, and constructing a bridge made of a bamboo pole to cross from one raft to another over water.

I. L A N G U A G E C O M M U N I C A T I O N A N D T H E BRAIN

4

The experiment in question was held on a hot summer's day. Two rafts were situated on a lake a short distance apart, with Rafael on one of them. Overheated, he kept reaching for water from the lake and pouring it over himself, using either his hand or a glass jar. Meanwhile, the experimenter rowed over to Rafael's raft and deposited some equipment containing fire (an apparatus with a reward placed behind a burning wick in such a way that it was accessible to reach only when the fire was extinguished). Alongside was placed the bamboo pole which Rafael ordinarily used for making 'bridges'. Then on the other raft the experimenter placed a cask of water fitted with a faucet. For a few moments Rafael eyed the fruit in view on the far side of the flame; then he rose and, holding the glass jar in his hands, went to the edge of the raft. After a few extra manipulations, he heaved the bamboo pole across to the other raft and crossed over to the water cask. He filled his jar with water from the cask, and then crossed back to the former raft. Since one jarful did not suffice to extinguish the flame that barred the way to the reward, Rafael crossed over again and refilled his jar. This time he put out the flame and retrieved the fruit. The above experiment is a sort of model illustration of the fundamental difference between the behaviour of animal and man. What is striking about Rafael's behaviour is that he did not utilize the water at hand which he had just been using to cool himself off. Although he was perfectly able to obtain water from the lake, he did not apply this knowledge to extinguish the fire. Instead of this simpler course of action, he executed a far more complicated series of acts resulting in getting water from the cask. Presumably any normal human being would have acted otherwise, that is, would have taken water from the lake. To what can this difference be ascribed? It would seem that the answer is to be sought in the fact that the chimpanzee, like all other animals, does not have at his disposal a general concept of water, of which an essential element is knowledge that any water anywhere can put out any fire2. At his own level Rafael acted very intelligently. He associated two separate actions which he had previously learned: to draw water from the faucet of a cask and to make a bridge with a bamboo pole. Yet he was limited in his resolution of the problem to conjoining the products of his previous experiences touching upon portions of reality that were part of the situation comprising the immediate problem. In contrast, any human in this situation would surely use lake water, for the reason that he has at his disposal general concepts gained not only from his own direct experience but also from the experience of other like individuals, accumulated over the ages and transmitted from generation to generation through forms of instruction. Thus Vatsuro's experiment signals a very important feature of human action, namely, that this action is controlled not only by the products of a single individual's 2

This is an oversimplification for our purposes, which undoubtedly would raise objections from, for example, fire-fighting specialists.

1. I N T R O D U C T O R Y R E M A R K S

5

experience but also by the products of other individuals' experience, that is, social experience. This question has been raised in a broader theoretical context by Leont'ev (1959). He draws attention to the fact that animal behaviour is determined by two kinds of mechanisms. One kind is the inherited and innate behavioural mechanisms which include the unconditioned reflexes, instinctual patterns, and so on. Each member of a species is equipped with a certain number of genetically conditioned forms of acting, either ready-made at birth or maturing with development; these forms are the manifestations of species experience, the inborn mechanisms. The second kind of mechanism, which also conditions his behaviour in situations of life, is that which permits each member of an animal species to acquire individual experience during ontogenesis, in contact with the environment. The range and shape of this type of experience depends on the scope of innate behavioural forms, and comprises a kind of superstructure upon this base. Thus individual animal behaviour depends on two kinds of experience: that of the species, transmitted genetically, and that of the individual, shaped in ontogenesis. Undoubtedly both kinds of experience play a role in human behaviour. Man as well is born with a certain repertoire of innate, species-specific behavioural forms and, throughout his life span, accumulates individual experience. But, in contrast to the lower species, we find that man has yet another kind of experience, namely, social-historical experience. This is also species experience in the sense that it has taken shape in the course of man's phylogenetic development and is the product of experience accumulated by prior generations and transferred onward to each succeeding one. This type of experience is distinctive by the basically different way it is transmitted: not by inheritance through genetic mechanisms, but by re-acquisition, generation by generation, through a more or less organized social process of rearing and teaching. Thus it is in one sense an individual experience as well, for it is an ontogenetic process of acquisition. We shall leave aside the aspect of the consequences of the above fact for the regulation of human behaviour; interested readers are referred to the cited work of Leont'ev. There can be no question, however, that the consequences are vast and far-reaching. It is highly relevant to our discussion that one of the basic factors underlying this distinctively human mode of transmitting species experience is the ability to communicate through language. The products of human activities and cognition have been perpetuated as linguistic texts, transferred from one to another in spoken or written forms. Whereas the experience gained by an individual member of a lower species is purely his own, and disappears with him, individual human experience can be transferred to others immediately in spoken form or, as frequently is the case, is perpetuated in written forms as sources of knowledge that will exist as long

6

I . L A N G U A G E C O M M U N I C A T I O N A N D T H E BRAIN

as do the texts themselves. Herein lies the explanation (in simple and broad terms) why each one of us, if confronted with a situation similar to that of Rafael, would use lake water for the task at hand, despite the fact that very few of us have ever had to put out a fire on a raft in the centre of a lake. Our behaviour is marked not only by what our own experience has taught us concerning the real world about us but also by what we have learned from others' experience through spoken and written texts. And knowledge thus won also includes information about water and fire. The case of Rafael illuminates one more very important difference between human and lower species which is closely connected with language capacity. Rafael's associations had a particularized and concrete quality; for instance, that this particular fire could be extinguished with the help of this particular water located in this particular cask. On the contrary, our knowledge of the real world gained from social-historical experience is of a general nature: any water (barring certain exceptions) will do for extinguishing any fire (barring certain exceptions). Empirical data is not lacking to support the belief that, in order for such formulations and general concepts to emerge, an important condition is for our experience to be couched in verbal form (cf. Chapter VII). We have examined the conclusions from Vatsuro's experiment in some detail in order to show language's fundamental significance for the specifically human behavioural mechanisms, hence for the general psychology of man. People have long been aware that speech, language, or verbal communication, are of immeasurable importance in man's individual and social existence. Speculation on language and human ways of communicating reach back to antiquity; these questions continue today to preoccupy the minds of philosophers, anthropologists, ethnologists, logicians, physicians, and biologists. A separate scientific discipline has emerged, namely, linguistics, which is addressed exclusively to the description and analysis of the various systems of linguistic communication. Paradoxically, psychology stands out as the exception—or at least has done until fairly recently—to this common interest in the role of language communication in human life. For there is an astounding discrepancy between the role of language and speech in human life and the extent to which this question has preoccupied human thought throughout history, on the one hand, and, on the other, the extent to which the psychological aspects of verbal communication and their consequences for human psychology have been elaborated. We could easily name a number of important and relatively recent psychology textbooks which either ignore the problem of speech and language, or else treat it marginally and as related to other presumably more weighty subjects. Nor do we always find mention within prominent psychological theories of human development and functioning of the seemingly obvious fact that man is the unique living creature capable of communicating through language with his kind and for his own behavioural regulation.

2. SOME THEORETICAL PREMISES

7

More recently, however, a noticeable change has occurred in this state of affairs in psychology. Firstly, we note that other disciplines, such as linguistics, philosophy, medicine, anthropology and ethnology, cybernetics and information theory, are inquiring into a number of purely psychological questions related to language communication and have been attempting to draw psychologists into their discussions and research. This has placed some pressure upon psychologists to devote attention to language and speech. Secondly, partly due to the influences mentioned, psychologists have started to probe into the psychological aspects of the human language capacity, as evidenced by the establishment of special research centres, the appearance of publications, and the treatment of general psychological problems within the context of language and speech. Among the many particular problems relating to the human capacity for language there is one of special interest which has been relatively well studied through an interdisciplinary approach. This aspect is the organic bases of language capacity, or the anatomical and physiological properties of the human organism which underlie the ability to acquire and use language. The aim of this book is to present one of the most fertile research approaches to this question, consisting in the neuropsychological analysis of speech disorders connected with brain damage. In the chapters to follow, we discuss the findings of neuropsychological investigations in terms of their contribution to an elucidation of localization and function of cerebral structures which underlie the human capacity to communicate through language.

§ 2. SOME THEORETICAL PREMISES

Before proceeding further, we are in need of more detailed definitions of the terms "language" and "speech", if only because of the chaos prevailing in the literature around the applications of these two terms, a chaos responsible for much confusion in the treatment of both theoretical and particular questions3. Partly these are divergencies arising from interlingual differences and lack of equivalence in the usages of terms; partly, however, they are confusions arising from differences of theory and interpretation. Without delving into this discussion we present the differentiation that is accepted in the present writing. However arbitrary, this distinction has been drawn in line with the purposes of this study. Language is understood as a socially formed system of signs having set meanings, which are utilized in the communicative process according to the existent rules for construction of utterances (i.e., existent independently of the individual). Otherwise stated, language is an objective system comprising a store of socially created means 3

Interesting information on the various usages of these terms and the difficulties stemming therefrom in speech pathology research can be found in Critchley's paper addressed to a conference on aphasia research in Italy, 1966 (Critchley, 1967).

8

1. L A N G U A G E C O M M U N I C A T I O N A N D T H E BRAIN

to designate elements of reality (in a general sense of the term) as perceived by the speaker, and to express relations between these elements. The system is objective in the sense of comprising a social norm, i.e., a set of rules for verbal communication used by a given speech community and which must be acquired by each new member of that community in order to participate in communication (cf. Doroszewski, 1965). Speech is understood as a set of active processes, or activities, which make up verbal communication. Proficiency in these activities is acquired by the individual through contact with other speaking individuals. Consequently, speech is constituted by processes which actualize the rules of language for communicative purposes. Two basis groups of speech activities can be distinguished, those of production and those of reception; these may take the spoken or the written form. The term speech, or speech activities4 (active processes involved in speech), will be used throughout in this sense. In the broadest sense, therefore, the subject of this book concerns the organic bases of the human capacity to perform the activities that constitute speech. Unquestionably, this ability rests upon certain specific features of the human anatomy and physiology given that, as stated earlier, only members of the species Homo sapiens are capable of acquiring language when in contact with speaking persons. No lower species displays this ability 5 . These specific features of human anatomy and physiology will be the subject of discussions to follow. Before entering into this discussion, however, it seems necessary to touch upon a few other general questions which are relevant to our subject. The first question we encounter is the following: Are the conditions underlying the human ability to communicate through language social or biological in nature? This problem is sometimes phrased more drastically as follows: Is the language capacity acquired or innate? The latter formulation of the question may arouse strenuous opposition in many readers. According to Lenneberg (1967), whose views we shall have more than one occasion to comment upon, the notion of innateness in relation to human behaviour was on the index of forbidden concepts for a certain period, and explanations based on mechanisms of this nature were regarded as unscientific. This state of affairs was the outcome of a long and devious course of scientific development during which battles were waged both for recognition of individual experience as a determinant of development of mind and against any idealistic conception seeking sources of the psyche outside the sphere of natural phenomena as also against the fatalistic assumption of a priori directions and limitations upon mental development. This * Translator's note: Sometimes this concept (czynnoSc in Polish) is rendered in English as function (cf. for example Luria, 1966) 5 The oft cited ability to utter words and expressions found in some birds, for example in parrots, is solely the ability to imitate with a high degree of precision certain audially perceived sequences of sound, which is not however an ability serving communicative purposes.

2. SOME THEORETICAL PREMISES

9

historical process has led to the point where it has become habitual to put the stress on learning and on ontogenetic acquisition of behavioural mechanisms, this approach being treated as a measuring rod of the scientific value of any psychological conception. In the case of language development, still another fact has spoken against the above placement of the question. This is the fact that language acquisition is very obviously dependent upon the social contacts of the individual and upon phenomena which, by their very nature, seem to be something other than biologically inherited. Let us look at this question a little more closely. As already stated, the primary argument in favour of the position of social determination of speech is the fact that no human being is born with the ready-made skill to perform this activity and in addition that the precondition for its formation is exposure to actual speech. In the absence of such contact, the possibility of acquiring language and speech is excluded. Further, the matter of which language will be spoken by a given individual depends totally upon the language spoken in his environment: the ancestral language is an irrelevant matter. In other words, we do not inherit the language of our forebears but we take over the language of our surroundings regardless of differences between the two. We can go further: we are potentially capable of mastering any language existing in the world provided exposure to it occurs at the proper time. All these circumstances would appear to supply conclusive evidence for the thesis that language acquisition is entirely independent of species experience and is grounded exclusively upon processes of ontogenetic learning within the social environment. This would bring us inevitably to the conclusion that speech is not an innate function, or biologically conditioned, but is an acquired and learned function of purely social determination. The above line of argument omits the fact, earlier raised, that only members of Homo sapiens as a species possess the power to acquire speech. This statement can be subdivided into two more particular propositions, as follows: 1. Only members of the species Homo sapiens possess the ability in question, by virtue of which fact they differ is some purely biological aspect from non-members of this species. If it were otherwise, the repeated efforts to teach language to other species members would not invariably end in failure. Experiments have demonstrated that even the most far-reaching attempts to ensure young animals conditions identical to those in which human children are reared have failed to produce even the beginnings of verbal communicative actions of any significant value. 2. Each and every normal member of the species Homo sapiens is equipped with the ability in question. Speech, or use of some language, is a universal function proper to all human beings raised in appropriate conditions, and an integral part of man's "typical equipment". To use Lenneberg's (1967) phrase, it is a species-specific form of behaviour; further, as shown by developmental studies, it displays an extraordinarily regular onset and developmental history, which occurs in approximately

10

I. L A N G U A G E C O M M U N I C A T I O N A N D T H E BRAIN

the same period of life in all human children regardless of the particular language acquired. Thus, on the one hand, human speech is a unique function in the world of living creatures and, on the other, a Universal one shared by'all human species members. By establishing this fact, we eliminate the possibility of dismissing as invalid the notion of inherited or innate mechanisms conditioning language acquisition. In addition, numerous data bear witness to direct genetic determination of the capacity for language communication. For example, a distributive analysis of. various types of language developmental disorders has brought to light familybound factors affecting congenital language disability or delay, stuttering, word deafness, and so on (Mitrynowicz-Modrzejewska, 1963; Lenneberg, 1967). Likewise, greater similarity in language developmental history has been found in identical than in fraternal twins. (See Fig. 1.) Identical twins normal onset

Onset of speech

Fraternal twins delayed identically (

y delayed identically

Speech development

I

normal onset

35%

>

% \ y

only one twin lelayed (or more delay ed)

90%

same histo y

I

40%

different his tory

Fig. 1. The onset of speech and subsequent development in identical and fraternal twins (Lenneberg, 1967).

All together, the above findings point unequivocally to a genetic determination of the human ability to acquire speech; they indicate a dependency of this ability upon innate properties of the human organism. If we accept the existence of organic determinants of human speech, we come up against the question of where to look for the specific properties of man's anatomy and physiology upon which language and speech depends. Broadly speaking, the answer would seem to lie in those organs directly connected with and participant in the activities of speech. These would include the peripheral organs necessary

2. SOME THEORETICAL PREMISES

11

for productive and receptive speech and the central nervous system governing their functioning. The question can thus be reformulated as follows: What are the specific properties of the peripheral organs and of the central nervous system, as well as their structural features and neurophysiological mechanisms, on which the human capacity for language communication depends? As regards the peripheral organs, the best known differences, relatively speaking, are those to be found by contrasting the human organs of speech production and homologous organs in the lower species. An examination of these differences shows that to some extent these organs precondition both the ability to emit speech sounds and certain properties of those sounds. From this angle, very interesting distinctions between man and chimpanzee have been noted as, for example, in the facial muscles (Fig. 2), the structure of the oral cavity and larynx, and so on (cf. Lenne-

Fig. 2. Facial muscles of chimpanzee (a, b) and man (c, d). a —inner layer; b—outer layer; c-router layer; d—inner layer. (After Lenneberg, 1967.)

berg, 1967). Various facts, however, may be adduced to show that these properties do not play a fundamental role in the preconditioning of speech activity. Severe retardation in articulation during the early developmental phase, for example, does not exclude acquisition of the language communicative ability in the child, i.e., comprehension of spoken and written language as well as writing (Lenneberg, 1962, 1967; author's observations). Also, as concerns the adult, even far-reaching

12

I. L A N G U A G E C O M M U N I C A T I O N A N D T H E BRAIN

pathological changes in the articulatory organs do not lead to significant disorders in speech activities which are not connected with this apparatus (e.g., speech reception), and, furthermore, does not exclude the possibility of regaining oral speech based on other organs than those normally in use. The most obvious example of this is voice and oral speech recovery in patients after larynx ablation (cf. Mitrynowicz-Modrzejewska, 1963). The foregoing facts suggest that, whereas anatomical and physiological properties of the peripheral organs have a certain formative role in the human capacity for language, they do not constitute a sufficient condition. In view of this, organic determination of the language capacity must be sought primarily in the anatomical and physiological properties of the human brain. This statement provides the topic of the considerations to follow. Concluding the above argument, two groups of facts seem to invite two divergent and mutually exclusive interpretations. On the one hand, various data provide apparently unequivocal evidence for speech as a set of active processes acquired in conditions of social contact, but on the other hand different facts point to speech as a set of innate functions, genetically transmitted by mechanisms for the transfer of species experience, or a product of specific properties of the human brain. Still another view, however, seems permissible, namely, that the contradiction we are confronted with is superficial and that we are not forced to assume the truth of one interpretation to the exclusion of the other. The fact of language as a unique phenomenon in the animal world speaks only for man's exclusive possession of a special equipment necessary for acquisition of language; in this sense, these functions are dependent upon innate mechanisms and are biologically determined. As already established, this specific "equipment" is to be sought primarily in the brain's anatomical and physiological properties. At the same time, the dependency on social conditions of language acquisition and on opportunities of contact with other speakers shows that this biologically and organically determined language equipment cannot be activated autonomously but must perforce be "programmed". The condition for "programming" is contact between the individual and the objective language system (as earlier defined). This contact allows for the rules of the language to be "coded" into given neuronal structures, that is, speech performance rules which must be adhered to for effective communication with the environment. Thus, acquisition of speech is neither a purely biological process nor a purely social one; both biological and social factors interact during the formative process. Accordingly, we may now reformulate the subject of further considerations as follows: We shall seek those specific properties of the human brain which are responsible for the acquisition of the programmes of speech activities constituting the language as a system. #

#

#

2. SOME THEORETICAL PREMISES

13

The next general problem which calls for inspection before we enter upon the more particular aspects is language communication as an activity of man and its functions in human life. Our basic assumption underlying all further discussion on the subject of language communication and its organic determination is the following: Both the production and the reception of speech constitute actions. The notion of the action is one of the basic ideas in contemporary psychology (Tomaszewski, 1963); to accept this concept as the starting point for language research opens various interesting vistas, both methodological and theoretical, and, at the same time, places this research within a broader framework of psychological inquiry. As Tomaszewski postulates, an action has two primary characteristic features, i.e., directedness, and organization. Directedness is understood in the sense that any action tends towards some given end state (a result), and terminates when that state is reached. If any perturbation arises in the course of that action, or any deviation that thwarts or jeopardizes the attainment of the result, there will occur compensatory changes which enable the course of the action to be maintained in terms of its result. Organization as a characteristic feature of action is manifested in that any action possesses a certain structure or, in other words, constitutes an entity which is separable from other processes occurring in the environment and is also divisible into interrelated parts. Now there can be no doubt that the foregoing characterization of the action as a general concept applies fully to speech activities. In fact, it would appear that these forms of activity offer particularly good examples of the directed and organized nature of actions. Any speech act aims at a strictly specialized kind of result, i.e., communication with others. Clearly, the particular results aimed at by speech acts are highly diversified: they range from evocation of immediate behaviour in the addressee, participation in some practical task by stimulating his verbal responses—to attainment of social recognition in the remote future. Goals striven for by communicating with others are highly differentiated and are determined by the broader situations within which communication occurs. Failing to attain the result (broadly, communication), speech activity can be continued; if circumstances arise of a nature to impede that activity and jeopardize its outcome, various compensatory changes can occur, from increasing the volume of voice to complete reformulation of the utterance. Equally apparent is the organized character of speech activity. Utterances are produced in strict accordance with the rules of the language, which must be adhered to for effective communication. In any final analysis, the best known of all human actions, in terms of their organization or structure, are the acts of speech. Data pertaining to this question comprise the subject matter of a rich linguistic literature. The foregoing statements are obvious in respect to speech production; some doubt may arise, however, as to the fitness of this characterization for speech recep-

14

J. LANGUAGE COMMUNICATION AND THE BRAIN

tion. As with all perceptual activity, these acts are often experienced introspectively as passive processes. This conclusion, however, is erroneous, as best demonstrated by evidence concerning the general perceptual processes: perception displays various properties of active processes, inaccessible to introspection but ascertainable by objective means. That this applies equally to speech reception has been established in pathology research (see Chapter VI). There is good reason to believe that receptive acts of speech are no less active as processes than are productive acts; it is simply far more difficult to observe them objectively. Finally, we come to the important problem of the functional significance of language communication, its role within the sum total of human activity. Tradition holds that the answer to language's basic place in man's life rests on its communicative function, or the transmission of information as products of cognition. However, as research stands today, we can afford to attempt a broader answer and at the same time a more elaborated one. Let us begin by stating that the classic view of the communicative function of language has tended toward "intellectualization" ; it has been almost entirely reduced to the use of language for exchange of cognitive products. Yet it is undeniable that the scope of the communicative function of language is vaster than this and primarily operates in the context of practical collaboration between communicating persons. Probably the original function of speech was to regulate the behaviour of others in the course of collective action through communication of suggestions, prohibitions, orders, wants and needs as also information deemed important by the speaker in relation to the common task at hand. Accordingly, speech subserves functions, as Marx and Engels (1955) earlier pointed out, which are mainly connected with the process of practical human collaboration 6 . Only after the establishment of this groundwork could the transmission of cognitive content develop, starting from content of importance for the practical collaborative process. Presumably, as a later development, a certain autonomy developed in the communication of cognitive products, relatively independent of the immediate tasks confronting the communicating individuals. Once we recognize the significance of speech in cooperative activity of a practical kind, in terms of effects upon others' behaviour, we are led to appreciate a certain very crucial aspect of speech, i.e., its regulatory function in respect to the speaker's 6

A very interesting theory of language origin viewed from this angle has been offered by Diamond (cf. Brain, 1965). This author, convinced that the origin of language can be revealed by establishing the kinds of words most frequently used in the earliest language systems, pursued various comparative studies on ancient languages. His conclusion was that the first words used were imperative forms of verbs in the second person, such as cut, break, hit, etc. Basing himself on this finding, the author advanced the hypothesis that these words arise from vocal sounds involuntarily ejaculated at moments of intense physical effort. Built on associations such as these, the sounds become signals by which primitive man began to externalize his need for aid from others. The original function of language would thus be the call for aid during work.

2. SOME THEORETICAL PREMISES

15

own conduct. In the course of ontogenesis (first noted in the 1930's by Yygotsky, 1956), and presumably of phylogenesis, a differentiation emerged. Arising from the communicative utterance addressed to another person for the evocation of behaviour desirable from the standpoint of the speaker's own needs, some utterances were directed to the speaker himself as self-instructions, having the role of regulating or guiding his own conduct. These self-governing utterances, as the work by Vygotsky and others has shown (see Chapter VIII), are transformed into inner speech, which plays an extremely important role in man's control over his own behaviour and is behind the changes in the structure of his psychological processes. Thus, in addition to the communicative function of speech for interindividual collaboration, we must distinguish the intraindividual function of behavioural regulation. Both theory and empirical facts (particularly in the domain of developmental psychology) have pointed to one more very important aspect of language and speech function, albeit still a highly controversial one. We refer to its role in processes of reality cognition, in perception, memory, concept formation, mental operations, and so on. The widely debated problem of whether language and speech affect these processes in man and, if so, in what way, still awaits fuller elucidation. Data in existence, however, fully substantiate the view that the fact of language acquisition in man has an essential influence upon what he perceives in the world around him, on how he solves his problems, in short, on the course of his cognitive activity. Admittedly, this introductory discussion of the nature and function of language communication is a very sketchy one, but it provides a framework for pursuing the main topic of this book. As it happens, the empirical material available from a variety of sources (see Chapter III) as to the cerebral determination of language permits a treatment of the activities involved in speech both from the viewpoint of the mechanisms responsible for their directed character and structure, and from the viewpoint of the functions they serve in human life. Thus in the discussions to follow, we shall attempt to present the actual state of knowledge on the brain's specific properties as determinants of language and speech processes, on their directed and organized character and on the functions they subserve as understood above. It would seem that for this purpose, as already mentioned, the findings of neuropsychological research will be particularly useful, since this research is addressed to the role of particular cerebral structures in various active processes of the organism, including acts of speech. Since in this latter respect (for reasons given in Chapter III) the main source of evidence lies in observation of cases of brain damage causing speech disorders (aphasia), we shall employ mainly this material to consolidate conclusions about the cerebral mechanisms of normal language communication. But it should be constantly borne in mind that certain of the questions dealt with here remain unresolved. Part of our task will be to point to these open and controversial problems and to present arguments for alternative hypotheses concerning them.

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Since we shall be concentrating on questions falling within the scope of this book (as given in the title), we are obliged to bypass, or treat cursorily, many important problems theoretically or specifically related to the problems under discussion.7 At the same time, since this book is also addressed to the human scientists—psychologists, linguists and philosophers—we shall leave aside more specialized questions of brain anatomy and physiology which would only impede an orientation on the subject-matter. Before concluding this introduction, it is pertinent to mention the general significance of research on the neuroanatomical and neurophysiological determinants of language communication. This significance is twofold. First and foremost, this research has major theoretical implications. Clearly, to establish the cerebral determination of language and speech is fundamental to all research on language communication. Secondly, as mentioned earlier, speech as a human activity can in some sense serve as a relatively well examined model of human action in general (though not yet well studied from the psychological point of view). Research on the cerebral mechanisms underlying speech will yield valuable data from a broader point of view, that of a general theory of the role of the brain in human behaviour, for it supplies evidence on how the nervous system regulates the activity of the human organism. At the same time, such research plays an essential part in any attempt to clarify the functional organization of the brain. It is not accidental, as Chapter II will show, that the findings of investigations into the cerebral mechanisms behind language communication have always contributed the major arguments at the core of the historical controversies over theoretical explanations of the functioning of brain and nervous system and the relations between cerebral structures and the organism's activity. Finally, this research area has obvious practical implications. If we can ascertain the role of particular cerebral structures in the active processes of speech, we lay the groundwork for diagnosis of the locus of brain damage in cases of speech disorder. By an examination of the type of disorder, the locus of lesion can, with greater or lesser accuiacy, be diagnosed, which is the first requirement for treatment of the patient. Neurologists and neurosurgeons have therefore a vital interest in research into speech pathology. On the other hand, elucidation of the cerebral mechanisms of language communication should lead to a better grasp of the mechanisms of speech pathology incurred through brain damage. This, in turn, is the necessary condition for establishing a scientific approach to the reeducation of 7 For instance, we shall omit the question of language development in the child. Research in this area has supplied considerable information relative to the subject, but the scope of this book does not permit of detailed treatment of this aspect. Barring a few exceptions necessary to clarify certain aspects, we shall use developmental data only to supplement our discussion. The same applies to data on the mechanisms underlying reading and writing. Despite their direct connection with our topic, these questions have various additional aspects of a specific nature whose full discussion would exceed the scope of this book.

2. SOME THEORETICAL PREMISES

17

patients suffering from speech disorders of central origin. Since the number of brain damage survivors is apparently increasing as a result of technical and medical progress as also of other factors, the problem of their rehabilitation is making itself felt as a major social problem (Maruszewski, 1966, 1968). In like proportion, there is an increase in the practical importance of research on the cerebral conditioning of speech.

CHAPTER H

HISTORY OF RESEARCH ON THE RELATION BETWEEN SPEECH AND THE BRAIN. MAJOR CONTEMPORARY THEORIES

There is a long history behind the problem presented as title to this chapter, and one that abounds in controversy over both the broad theoretical issues and the more specific ones. Our brief review in this chapter will have to omit mention of many who have contributed to what we know in this domain; we shall also pass over many questions of scholarly dispute (cf. Maruszewski, 1966). Our purpose is to delve more deeply into the aspect of cerebral localization of the psychological functions, a central problem throughout the history of speculation and research on the speech-brain relation, as it still remains today. In a sense, it is the main thread running through all the major debates. This problem extends, of course, far beyond the subject matter of this book, which is restricted to only part of the question of the brain's functional organization and regulatory role in all the functions of the organism, including speech. But the way we resolve this problem bears essentially on how we treat the narrower question to which this book is addressed: the localization and interaction of neural structures controlling the active processes involved in speech. The various theories about functional localization in the brain have been described in more detail elsewhere (Maruszewski, 1967); we shall deal here only with the major propositions that have emerged during the last two centuries, in other words, since the moment when speculation on cerebral localization began to stem from scientific premises. Although with some simplification, the localization issue can be reduced to two opposing theories, one postulating localization and the other denying this idea. The former conception posits a brain that is functionally differentiated, or composed of structures that serve different roles in controlling the activities of the organism. In the original narrow version (the psychomorphological conception), it was contended that, for every function of the organism, there is a corresponding distinctive "centre", or organ, in the brain. Present-day proponents of the localization theory reject the existence of such "centres"; their more moderate views stress only that particular brain structures perform separate and distinct physiological functions necessary for the normal course of the organism's many different activities. Functionally differentiated, these structures interact dynamically to ensure each such activity. In its contemporary version this conception is labelled the dynamic theory of functional localization.

1. EARLY OBSERVATIONS OF SPEECH DISORDERS FOLLOWING CEREBRAL DAMAGE

19

The opposing theory of anti-localization, in its most extreme version, denies any localization whatsoever as to the higher functions of the organism. The cerebrum is viewed as an undifferentiated and equipotential structure in respect to function. Higher functioning is the outcome of the activity of the entire brain tissue. It then follows that the search for "centres", or structures with more or less fixed functions, is foredoomed to failure. It is clear that acceptance of one or the other of these positions has crucial significance for the problem we are tackling; each entails radically different consequences in any undertaking to elucidate the cerebral mechanisms of speech. Let us repeat that this controversy has had a determining effect upon both the historical growth of knowledge and the present state of thinking in this domain.

§ 1. EARLY OBSERVATIONS OF SPEECH DISORDERS FOLLOWING CEREBRAL DAMAGE

Mention was made in our first chapter that one of the principal methods for obtaining data on the speech-brain relation is the clinical method. This method involves the examination of speech disorders and the correlation of findings with particular lesions in the brain causing these disorders. The study of speech derangements consequent to cerebral damage of diverse origin makes up an integral part of the history of research into the speech-brain relation. For many years it had been thought that the scholarly investigation of aphasia dated back only to the nineteenth century, that is, to Broca's discovery (see § 2 of this chapter). More recently, however, a number of publications have appeared which contradict this belief; a substantial body of observations on aphasia, of interest even today, were recorded at a much earlier period 1 . In ancient Greece, derangements of speech related to head injuries were noted by Hippocrates, Valerius Maximus, Pliny, and others. The two latter writers described an educated Athenian who lost his "memory for letters" following a head injury; this, probably, is the first reference in existence to reading disorder, known as alexia. Again, the first mention of the term aphasia was made in ancient times, by Sextus Empiricus, used not in the sense of language disturbance but of a given philosophical position, namely, scepticism, which is neither affirming nor negating. Much later, in 1864, Trousseau suggested this term in reference to speech disorder connected with cerebral injury. These early writings tell us that the ancients were well aware that speech disorder was often the result of cerebral damage. In a later period the distinction was drawn between speech impairments caused by paralysis of the articulatory apparatus and speech disorders caused otherwise. 1

Abundant documentation and summaries of early aphasic studies are available in Benton's work (Benton, 1964, 1965; Benton and Joynt, I960), on which the present section has been based.

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II. HISTORY OF RESEARCH ON THE RELATION BETWEEN SPEECH AND BRAIN

During the Renaissance period more data were collected on the relationship between speech disorders and brain damage. A German medical scholar, Johann Schenck von Grafenberg, made some interesting observations in the 16th century, to the effect that speech disorders can occur even when the tongue is not paralyzed, the faculty of memory being obliterated. As we know today, this was a recognition of the fact that speech disorder can result from impairment of the higher brain functions. In the 17th and 18th centuries numerous writers dealt with aphasic disorders. The work of three investigators stands out in particular. In 1667 Johann Schmidt described alexia without agraphia; he was probably the first to distinguish between motor aphasia and paraphasia (substituting one word for another in speaking). In 1683 Peter Rommel labelled a case as "rare aphonia", a severe motor aphasia including total inability to repeat but with speech production and comprehension intact. In 1770 there appeared the major contribution of Johann A. P. Gesner on "speech amnesia" as part of a larger medical work. This author described various forms of aphasia and attributed them, not to a general intellectual decline or memory loss, but to a specific impairment of verbal memory, namely, the inability to associate images or abstract ideas with their linguistic signs. The causes of this defect, he thought, lay in disturbance to cerebral functioning. It is interesting to note that in this same period of history there appeared three descriptions of enduring interest dealing with short aphasic episodes experienced by the respective writers (Jean Paul Grandjean de Fouchy, 1787; Johann Joachim Spalding, 1783; Samuel Johnson, 1783). Goethe's story about his grandfather, written in 1795, has often been cited as a description of motor aphasia. The state of knowledge about aphasia before the year 1800 led Benton and Joynt (1960) to the following conclusions: first of all, nearly all the clinical forms of aphasia had already been described with the exception of sensory aphasia; secondly, the relation between aphasia and cerebral damage had also been ascertained, although without precision as to the relevant portions of the brain; and lastly, the hypothesis had already emerged, under study still today, that the pathopsychology of these disorders is based on a rupture in the connections between images or ideas and their corresponding linguistic signs. The 19th century marked a turning point in the research on aphasia and on the localization of cerebral structures related to speech processes. At the start of the century Gall advanced his phrenological theory. Relying on what then seemed sound premises, but today untenable (see Chapter III, § 1), Gall suggested that the seat of language was in the frontal lobes of the brain. This idea inspired the French physician Bouillard to publish a paper in 1825 supporting Gall's hypothesis on the evidence of his own observations (cf. Benton, 1964). Several other papers appeared as well describing various forms of aphasia, such as jargon aphasia with comprehension preserved, differential language impairment in polyglot patients, varieties of abnormal writing, and others. Certain attempts were made to verify the hypothesis of locali-

2. FIRST DISCOVERIES O F SPEECH "CENTRES'

21

zation of structures responsible for these speech disorders. A very remarkable discovery was made in 1836 by the French physician Marc Dax. This author prepared a paper on the association between aphasic disorders and left hemisphere lesions accompanied by right hemiplegia. This paper, prepared for a local medical congress, appeared only in 1865, when it was finally submitted by the author's son, Gustav Dax. It initiated a hot debate between the Parisian surgeon, Paul Broca, and Gustav Dax, who defended his father's claim to priority for this discovery, one of the most significant in the domain of aphasia research (cf. Benton, 1964; Critchley, 1964; Joynt and Benton, 1964). Essentially, this hypothesis is that aphasia occurs most frequently with accompanying hemiplegia or hemiparesis of the right limbs, and is principally connected with cerebral injury in the left hemisphere. Thus research began into the question of hemispheric dominance for speech (see Chapter IV, § 1).

§2. FIRST DISCOVERIES OF SPEECH "CENTRES". THE NARROW LOCALIZATION THEORY

As we have seen, clinical evidence had gradually been accumulating for many centuries about the various forms of speech disorder and the first hypothesis had been formulated as to the cerebral localization of speech structures. Then, in 1861, certain events occurred which sparked off a period of extremely lively discussion and investigation into aphasia and speech localization. On April 4, 1861, at a meeting of the Paris Anthropological Society, Auburtin, who was the son-in-law of the phrenologist Bouillard, presented a paper on the cerebral localization of language, in which he sought to show that the speech centre lies in the frontal lobes. Present at this meeting was the surgeon Paul Broca, secretary of the Society. Only a few days later, a patient suffering from a leg abscess was admitted to his ward in the Bicetre hospital; this patient had right hemiparesis and a long history of speech disorder. Broca invited Auburtin to examine the patient. On April 17, the patient died; a postmortem examination revealed a lesion in the posterior division of the second and third frontal convolution of the left hemisphere. The day following his decease, the patient's brain was exhibited at a meeting of the Society; little interest, however, was evoked. Shortly afterward, Broca demonstrated a second case with the same syndrome: speech disorder with a lesion in the left frontal lobe. Now a fiery controversy arose. Broca's own conclusion, based on his two cases, was that speech is localized in the left hemisphere in the posterior divisions of the second and third frontal convolutions; Bouillard and other supporters of Gall's theory maintained that Broca's cases comprised evidence for the phrenological theory of localization (cf. Brain, 1965; Critchley, 1964; Head, 1920). Thus began the key discussion in the history of research into the relation of speech and brain. The issue was whether there are any special centres correlated with the

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II. HISTORY OF RESEARCH ON THE RELATION BETWEEN SPEECH AND BRAIN

human capacity to use language, or whether this capacity is a function of the brain as a whole. In the period we are now describing, this debate had a highly passionate flavour. As Head (1920) writes, speech localization became a political issue. Representatives of the older conservative school defended the theory of integral brain function, while the young liberals and republicans took sides with Broca's contention and the localization theory. This polemic raged for a number of years throughout the scientific world of Paris. The significance of Broca's discovery was that, for the first time, it was strictly established (according to contemporary scientific canons) that a lesion in a given part of the brain produced a given type of speech disorder. This finding inspired many investigators to attempt new descriptions of speech disturbances and to search for the destroyed cerebral areas responsible for them. We shall mention the most noteworthy of these studies.2 In 1867, Ogle described the different forms of writing disorder and introduced the term "agraphia" to cover them. In 1869, Bastian described "word-deafness" and "word-blindness". The "word-deaf" patient cannot recognize words as such although his hearing is retained; the "word-blind" patient cannot recognize words in the visual field but his vision is intact. A remarkable observation was made in 1874 by Wernicke3, who described a case of abnormal speech in which the patient displayed a profound deficit in comprehension of oral speech but could himself speak. Postmortem examination led Wernicke to surmise that the root of this failure lay in a lesion in the posterior division of the superior temporal convolution of the left hemisphere. In 1881 Dejerine made the claim that word-blindness was produced by a lesion in the angular gyrus in the left hemisphere. That same year, Exner postulated the writing centre to be located in the posterior part of the second frontal convolution. Meanwhile, investigations into localization of various "centres" were being conducted on animals. In 1870, Fritsch and Hitzig discovered the motor centre in the dog's cerebral cortex; in 1873, Ferrier localized the auditory centre in the temporal lobe, while Munk in 1877 ascertained that the visual centre in animals is located in the occipital lobe. Taken together, the facts presented above spoke unequivocally for a localistic position; that is, they comprised evidence for the claim that the brain is composed of a determinable number of "centres" in control of specific functions of the organism, speech included. Now there arose the question as to how these various "centres" work together. We shall not dwell on the history of the search for an answer to this problem and the debates that arose among the adherents of this line of reasoning; we shall 2 Sources for the above information include Brain (1965), Freud (1953), Head (1920), Penfield and Roberts (1959). 3 Geschwind (1966, 1967) Ms made a detailed analysis of Wernicke's findings and their significance for research into the cerebral mechanisms of language.

2. FIRST DISCOVERIES OF SPEECH "CENTRES'

23

simply outline the emergent theories. Freud (1953) offered an interesting analysis of the various concepts in a little-known work on aphasia, first published in 1891. The founder of psychoanalysis proposed that current aphasia theories rested on two assumptions, which included premises for a theory of how the brain controlled normal speech. The first tenet was that aphasia could be produced by damage to centres and to their connecting pathways; the second entailed certain more particular propositions on the topography of these pathways. The discoveries reported above disposed investigators to the view that several basic speech sites existed in the brain, whose function was based on the storage of memory traces, or word images. For example, the function of Broca's area was to store the representations of the articulatory movements required to produce words, while the function of Wernicke's area was to store the auditory representations, or images, required to recognize words as they are heard. Other centres were repositories for the visual representations of words, motor representations for writing, and so on. In addition, there were centres serving intellectual functions that collaborated with the speech centres. While there was disagreement over the number of such centres, all were in principle of one mind as to their existence. Thus a point of view had taken hold about the basic elements of the system in control of the processes involved in speech. However, for speech to occur, these centres had to interact in some way. This was the role of the connecting pathways. A purely theoretical analysis of language activity started off attempts to schematize the connections involved. In 1869, Bastian published the first schematic diagram; this was succeeded by other versions, all attempting to trace the connections between the main speech centres (Fig. 3). In 1874, Wernicke presented a particularly useful diagram, later modified by Lichtheim in 1885 (Fig. 4). In Lichtheim's diagram, "M" stands for Broca's motor speech centre, "A" for Wernicke's verbal auditory centre, "B" for other cortical centres which may activate the speech centres. Various pathways connect these three points in the diagram, as well as inputs and outputs to the system (to use modern terminology). Damage to given parts of the system produces different symptoms; for example, damage to the centres M and A (1 and 2 in the figure) produces "aphasia of the centres", motor aphasia or sensory aphasia. Damage to the pathways 3,4 and 6 in the figure produces "central conduction aphasia", while injury to the input-output pathways of the system (5 and 7) leads to "peripheral conduction aphasia". Wernicke later modified the terminology. Thus arose the famous Wernicke-Lichtheim classification of the aphasias, which still has present-day adherents (cf. for example Tkachev, 1961). It should be emphasized that this classification comprises a clearcut theory of localization and of the interaction of cerebral structures regulating speech. Later in the chapter we will find that this line of reasoning and theorizing about the relation between speech and the brain remains a popular one today. For this reason alone

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Fig. 3. Charcot's diagram to illustrate the anatomical basis of speech, reading and writing. IC— ideational centre; CAM—auditory centre for words; CLA—articulatory language centre; CVC— common visual centre; CVM—visual centre for words; CLE—centre for written language; CAC— common auditory centre (After Brain, 1965).

it seems worthwhile to examine in more detail one of the earliest proposals of this type. The Wernicke-Lichtheim classification assumes the existence of seven forms of aphasia: 1. Cortical motor aphasia (1 in Fig. 4) results from destruction of Broca's area, where motor images of words are stored. Speech comprehension should be preserved, but the ability for both spontaneous and repetitive speech is impaired. 2. Subcortical motor aphasia (5 in Fig. 4) is due to an interruption of the conduction pathway between Broca's area and the articulatory apparatus. This form differs from the foregoing only in that the patient can write. The difference between the abilities to speak and to write is that the intact motor images of words in Broca's area can be transmitted to the writing centre but not to the articulators, since the latter pathways are ruptured. 3. Transcortical motor aphasia (4 in Fig. 4) results from the dissociation of Broca's area and the other "intellectual" cortical areas. The patient can repeat speech that

2. FIRST DISCOVERIES OF SPEECH "CENTRES"

25

he hears (auditory and motor images of words are preserved), but cannot speak spontaneously, since Broca's area receives no impulses to speak—as if there was nothing to talk about. Comprehension is, of course, preserved. 4. Cortical sensory aphasia (2 in Fig. 4) results from lesions in Wernicke's area where auditory word images are stored. The patient can neither understand nor repeat the utterances he hears but he is able to speak spontaneously. At the same s

Fig. 4. Lichtheim's diagram (after Freud, 1953). Description in the text.

time his own speech is deformed, because he does not have the auditory images necessary to control what he utters. For the same reason, writing and reading are also deranged. 5. Subcortical sensory aphasia (7 on the diagram) is produced by interruptions between the projective auditory region and Wernicke's area. The patient does not grasp what he hears, nor can he repeat or write from dictation, since the auditory impulses do not reach Wernicke's area. Spontaneous speech, reading and writing are retained, however, since the required auditory word images remain intact. 6. Transcortical sensory aphasia (6 on the diagram) is due to disrupted conduction pathways between Wernicke's area and other "intellectual" cortical regions. The patient can repeat what he hears but does not understand. This results from the fact that, although the auditory impulses reach the intact Wernicke's area, they are transmitted only to Broca's area, thus making repetition possible, and do not reach those areas where meaning is decoded (to use a term in current use), that is, where words are assigned senses and concepts. 7. Conduction aphasia (3 on the diagram) comes from the dissociation of Broca's area and Wernicke's area, and has the typical symptom of disturbed repetition with intact comprehension and spontaneous speech. The latter ability also undergoes some distortion, for the same reasons as in cortical sensory aphasia. We have just outlined the emergence of one of the earliest prominent theories on the localization and interaction of cerebral structures underlying speech, and the classification of disorders that may be expected to result from the various focal lesions. Given the possibility to demonstrate two facts, this theory would be validated. The

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first is that all these forms of aphasia, and only these, occur; the second is that the occurrence of each form is accompanied by damage to the site marked on the diagram. Evidence for these two conditions, however, has turned out to be remarkably elusive. As mentioned earlier, the diagram we have been discussing was only one of a number of proposals published in that period; and others gave different models of the entire mechanism. This one was the most popular because it allowed for the best prediction, relatively speaking, of the various syndromes of speech disorder (and by this token fulfilled the first condition for confirmation of the theory). Yet the stubborn fact remained that other forms of aphasia occurred which did not fit into the scheme. This in itself warranted some modification, at least, in the design. Moreover, validation of Lichtheim's scheme (and all other similar ones) turned out to be highly problematic, mainly from the viewpoint of localizing the damage causing various aphasic syndromes. Certain data indicated that other regions than those marked on the diagram were responsible for some speech disorders; different data concerned lesions in the centres marked on the diagram which produced unanticipated abnormalities. Finally, doubts were expressed as to the basic theoretical assumptions for this type of diagram, as, for example, the premise that certain centres constitute a kind of repository for images of different sorts, or that the functioning of the brain is based on the association of such images. Broadly speaking, in the course of subsequent research, doubts arose about the narrow brain-localistic position, which assumed that complex functions could be ascribed to specific brain structures. Quite different propositions were then advanced to describe and interpret aphasic disorders, leading to a completely new theory of brain functioning and cerebral speech mechanisms.

§ 3. CRISIS OF THE LOCALIZATION THEORY. ONE-FACTOR THEORIES

Despite its initial successes, the localistic view of cerebral mechanisms of speech began to founder under mounting difficulties. No doubt a major contributing factor was the emergence of new trends at the turn of the century in various scientific disciplines, including psychology, neurology and physiology of the nervous system, away from the static analytic approaches and toward dynamic and holistic interpretations of phenomena. At the beginning of the 20th century, the localization theory faced a frontal attack from investigators among whom figure Pierre Marie, Henry Head and Kurt Goldstein. An essential element was the revival of earlier authors' work which cast various doubts upon the universally lauded localization theory and contained suggestions for other approaches. Soon the second basic theoretical approach to cerebral language mechanisms took the limelight—the antilocalistic position, which assumed the existence of a fundamental language factor without locus in any one cerebral structure but dependent upon total brain functioning.

3. CRISIS OF THE LOCALIZATION THEORY

27

As we have had occasion to mention earlier, this theory is of a vintage as old as the localistic conception. In 1870 Finkelnburg expressed the view that speech disorders were part of a much broader disturbance which he called loss of "the symbolic function". This "asymboly" is essentially the inability to express concepts by means of acquired signs and to understand the meanings of these signs, affecting other sign categories as well as linguistic. Kussmaul (1879) elaborated this point of view still further. Since the symbolic function is highly complex, it is precluded that a separate centre could exist for it. Asymboly, or better, "asemia" (pathology of the use of signs), embraces diverse clinical "deformations" in the production and comprehension of signs. Numerous articles appeared in this period by Hughlings Jackson (1958)4 polemizing with the reigning conception of aphasia. But the state of euphoria accompanying the discoveries of "centres" prevented the arousal of much interest in these articles, which remained forgotten until early in the 20th century. In 1906, the medical world was shaken by the appearance of three articles on aphasia written by the French neurologist, Pierre Marie (cf., for example, Cole, 1968). The first article bore the provocative title: "The third frontal convolution plays no special role in language function". Marie's challenge was that the anatomical material on which Broca's conclusions had been based did not afford sufficient evidence for his interpretations. Marie had reexamined the brains of Broca's first two patients (the brains having been conserved as museum exhibits) and had found that the lesions extended far beyond Broca's area alone. This fact constituted his argument for insufficient substantiation of the thesis that the speech motor centre was located in the third frontal convolution. Marie also attacked the distinction drawn between motor and sensory aphasia; he claimed that every aphasic patient displays some defect of comprehension and, furthermore, a reduction of intellectual capacity. His view was that there is only one true form of aphasia, what Wernicke had described as sensory aphasia; it was attributed not to the loss of auditory word images but to a general deficit of intelligence and disorders of inner speech. Lesions in Broca's area do not produce aphasia (that is, impairment of the intellectual base of language) but only anarthria, or derangement of speech as a motor function. The disorders described by Broca, apparently associated with lesions in Broca's area, were in fact produced by much more extensive destruction and were, in Marie's view, a combination of Wernicke's aphasia with anarthria. Accordingly, aphasia was seen as a homogeneous disorder determined invariably by the same mechanism; no special language centres existed in the brain; aphasic disorders were associated with lesions in the posterior divisions of the brain serving the intellectual functions. These tenets naturally evoked sharp opposition from the proponents of localization, and again for a number of years Paris was the scene of violent dispute, this time between the adherents and opponents of Marie's conception. * Jackson's work will be treated in a separate section in view of its significance, and to account as well for its distinctness from the two conceptions under present discussion.

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The next weighty assailant of localistic views was Henry Head (1920a, 1920b, 1926). To start with, Head, who had begun his study of aphasia with a reading of the literature, came across Jackson's papers, and published them in 1915 in the British neurological journal "Brain". Jackson's views, as mentioned earlier, were diametrically opposed to the narrow orthodox localistic theory, which was the reason why so little curiosity had been aroused by his work at the time. Only subsequently, at a propitious moment, did the revival of his outlook fall upon fertile ground. Now his writings contributed to the rising opposition against the localistic theory. At the same time, Head adopted a highly critical attitude to the classic conceptions. Describing the actual state of "localistic" knowledge about aphasia and the cerebral speech mechanisms, Head used the term "chaos", a term which was frequently to appear from then on. He sharply attacked the producers of schematic outlines, and used the scornful epithet "diagram-makers". Though Head related his own position to Jackson's work, his conception is in fact a variant of the one-factor theory of aphasia. Head contended that language should be examined as part of the indivisible mind. Speech is, essentially, the use of symbols; it is the performance of symbolic acts. Disorders incurred through cerebral damage lead to the disturbance of symbolic thought, formulation and expression. If the lesion is extensive, the loss can be total; if more restricted, the disorder may manifest itself more selectively in various aspects of symbolic thought. In the latter event, four groups of aphasia can be distinguished as characteristic of selective disorders of symbolic formulation and expression. These were named verbal, syntactical, nominative and semantic aphasia. Finally, a leading role was played by Kurt Goldstein in the formulation of antilocalistic ideas and in the bolstering of positions in support of the one-factor theory (Goldstein and Scheerer, 1941; Goldstein, 1948, 1959, 1960; cf. also Maruszewski, 1958; Geschwind, 1964b; Luria, 1966a). Goldstein's views had an enormous influence upon research into cerebral speech mechanisms and aphasia. Several circumstances, noted by Geschwind (1964b), help to clarify this fact. Goldstein outlived other advocates of the antilocalistic view, remaining very active throughout his long lifetime. His first work on aphasia appeared at the turn of the 20th century, his final one in thel960's. His ideas coincided with the growing interest in holistic approaches; his descriptions of speech disorders, which were extremely vivid and fascinating, aroused interest not only among specialists but also among humanists who, being little oriented in the problem, were poorly prepared to examine them critically. Finally, Goldstein achieved an eminent position as a neurologist of broad horizons, with interests extending far beyond purely neurological matters. One of the theoretical currents that affected his thinking was Gestalt psychology, with which he remained in close contact for many years. In short, Goldstein's views made a powerful impact upon the further course of thought on cerebral speech localization. His views took shape in collaborative research with the psychologist Gelb, studying naming disorders in head-injured

4. JACKSON'S VIEWS ON APHASIA

29

invalids of the First World War. Their investigations led Goldstein and Gelb to conclude that inability to name was a manifestation of a wider disorder involving the whole personality, which was the loss of the power to extract the general and essential attributes of objects and phenomena and therefore to deal with objects as members of a category, or conceptual class (see Chapter YII § 3A). Continuing his investigations along these lines, Goldstein came to the belief that the normal human being could adopt two different attitudes toward the world. One is the concrete attitude, which is manifested in behaviour marked by the unique and concrete features of the situation; the other is the categorial attitude, as shown in behaviour governed by rules and abstract concepts. Fully effective use of language demands the categorial attitude. When the brain is damaged, the functioning of the organism as a whole is disordered, but primarily the categorial attitude; speech disturbances of the aphasic type are secondary effects. In such an event, words lose their function to organize the world in a specific abstract, or categorial, fashion; they remain merely sound sequences correlated with concrete objects. In the various stages of his long and productive career, Goldstein expressed different views on cerebral sites connected with the categorial attitude. One hypothesis was that the frontal lobes have a special role. On the whole, however, Goldstein's successors adopted a straightforward non-localistic position; only in recent years has attention been drawn to the fact that, in Goldstein's resolution of many clinical problems, his position was not dissimilar to that of the classical localistic conception in neurology (Geschwind, 1964b). Thus, it was mainly Marie, Head and Goldstein (as well as certain others) who led the revolt against narrow localizationism in the search for the relation between the psychological functions and the brain in general, and the speech-brain relation in particular. In this early period of research, a third theoretical current is distinguishable, that related to the work of Jackson. The antilocalizationists have made an apparently unfounded claim that Jackson's work supports their side; his work, however, ought not to be treated in a purely antilocalistic light, despite his criticisms of the diagram-makers. A brief discussion of his viewpoint follows.

§ 4. JACKSON'S VIEWS ON APHASIA. THEIR SIGNIFICANCE FOR UNDERSTANDING OF CEREBRAL SPEECH MECHANISMS

J. Hughlings Jackson's first article on aphasia appeared in 1864 (Jackson, 1958), only three years after Broca's discovery. During the next 30 years this author published a number of highly illuminating studies on different facets of aphasia, which knit together his conception. But, as stated earlier, these works remained obscure until the second decade of our century. The immense interest they have since aroused

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dates from the time when the idea of localization5, in the narrow sense, first came into question. Jackson began by differentiating two kinds of language use: the emotional (expressive of emotional states) and the intellectual (expressive of thought). Broadly speaking, this introduced a separation of the capacity to perform acts of speech into involuntary and voluntary, or intentional. In Jackson's idea, these represent two levels of speech organization, in analogy with levels characteristic of any other motor activity of the organism. Now, cerebral injury produces the typical symptom of disturbing first and foremost the higher, intentional level of action. For example, a brain-damaged patient may be able to carry out various activities in natural situations but is incapable of so doing when requested by the examiner. He cannot protrude his tongue at the doctor's order although he utilizes it freely while eating, whistling, and so on. Similarly, an aphasic patient may often be unable to utter a simple word when asked to do so, but will sometimes use lengthy forms (as in swearing) when wrought up and under emotional tension. Damage in a circumscribed area does not, therefore, lead to the complete loss of any one function. The capacity to speak remains intact, but is more than normally dependent on emotional conditions. What is impaired is the intellectual level of speech, the formulation of propositions or sentences. The essential thing about language is not merely the use of words while speaking, but that these words are linked in grammatically ruled ways, thus modifying the sense of the individual words composing the whole. It is this capacity to combine words and to form propositions (cf. Riese, 1965, for a closer examination of Jackson's use of this term), expressing thoughts, which is impaired when certain regions of the brain are injured. Not only does this affect external speech; the aphasic patient fails as well to combine words in inner speech, that is, in the intellectual use of words to express thought not only externally to others, but internally as well. Jackson's contention was based on the belief that all speech functions are ordered under a general capacity to form sentence-propositions. This does not imply that the patient is deprived of the general thinking capacity; defective thinking occurs only in especially novel situations. As to other highly interesting reflections of Jackson on aphasia, we refer the reader to the original works. The above cited arguments seem to adequately clarify the characteristic feature of Jackson's theory, which is his emphasis on a functional s It is difficult to refrain from the comment that a similar fate, in some sense, was met by Jackson's assailants. At the turn of the century, when the works of Marie, Head and others had apparently dealt a shattering blow to the narrow localizationist theory, there arose a sort of stereotyped historical outline covering the period between Broca's discovery and Marie's appearance on the scene. The gist of it was that this period was one of cerebral mythology, speculative schematization, and the like, unworthy of closer attention. Only in the recent decade has a new interest arisen in the earlier investigators, associated with the crisis over the antilocalizationist and one-factor theories (see succeeding sections § 5 and § 6).

5. CURRENT LOCALIZATIONIST THEORIES

31

analysis of disorders in terms of normal language activity and the regularities manifested in the deviations of aphasic speech from normal speech. Jackson's views on the cerebral localization of speech functions were less well developed, but they were not in line with the antilocalizationist theory. He saw a dependency of various aspects of speech on both hemispheres; one of his hypotheses was that the left side plays an important role in intentional speech, while the right plays a similar role in emotional and automatic speech. He considered that the left frontal lobe had main significance for speaking, while the posterior lobes of both hemispheres, but mainly the right, were of consequence for speech perception. The main stress in Jackson's writings is placed, not on connections between various kinds of disorders and the sites of damaged structures, but on a functional analysis of the disorder itself. This tended to draw him toward the antilocalistic conception, which also accentuated the functional approach to disorders; yet he remained relatively free of the rigid attitude of proving or disproving a strict correlation between brain and language, an attitude which weighed heavily upon the whole history of this problem. Apparently this aspect of Jackson's work has often been overlooked 6 .

§ 5. CURRENT LOCALIZATIONIST THEORIES

With necessary brevity we have outlined the early history of research on the cerebral speech mechanisms by use of the clinical method, and summarized the main interpretations. There is little doubt that the sources of many of the divergencies which emerged during this period reside in the particular difficulties attendant upon use of this method in aphasic research (see Chapter III). Since we are still a long way from overcoming the shortcomings of this method, it is not surprising that the theoretical tendencies that took shape in this earlier period continue to thrive today. In contemporary efforts to resolve the problem, we still encounter conceptions both for and against localization. In the present section we shall survey those localizationist conceptions of the cerebral speech mechanisms that play a role in current discussions7. 6 A similar tendency can be found in Sigmund Freud (1953) in his work on aphasia published in 1891, to a large extent under the influence of Jackson's writings. Freud assumed the existence of structures specifically related to speech functions (what would now be labelled speech areas), but he denied the existence of separate centres as repositories for word images in the various sense modalities (auditory, visual, etc.). To Freud, aphasia was essentially a differential degree of impairment in the functioning of the area in question. The investigator's task was to effect a functional description of the various forms of disorders connected with lesions in the speech area. 7 Note that the procedure chosen to report on the history of the various theories is not congruent with the distinguishable historical periods. Theoretical controversy continued through the interwar years; mention has been omitted of a number of partisans of either side in contexts of

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Generally speaking, the localizationist conception has developed in three directions: the search for new "centres", the search for connective pathways and their role in the speech processes, and synthetic approaches to account both for criticisms of the narrow localistic view and for the empirical data flowing from the two former directions of research. Of the first of these three trends, the classic representatives include Nielsen (1946, 1947) and Kleist (1962). Both these authors take the narrow orthodox view, currently unpopular, on the localization question. At root, this approach is based on the belief that narrow facets of speech activities have equally narrow structural counterparts in the brain. For example,. Kleist (whose first publications appeared after the First World War and fuller elaborations in 1934), in a recent work (1962) distinguished the following selective disturbances of comprehension, each linked with damage in a strictly demarcated area of the left temporal lobe. These are phonemic deafness, word deafness, name deafness, and sentence deafness. In other words, Kleist's contention is that the brain has one centre for a function such as name comprehension and elsewhere another centre for sentence comprehension. Destruction of one of these centres leads to selective impairment of the corresponding function. It has just been mentioned that this way of looking at the question (that is, in terms of centres) has few adherents today. Much broader backing can be found for the "connexionist" approach; this trend emphasizes the role played in speech by the connective pathways between different parts of the brain, in particular, the cortico-cortical pathways. Geschwind has fully expounded this viewpoint in numerous publications (1962, 1964a, 1965, 1967a; Geschwind and Fusillo, 1964; Geschwind and Kaplan, 1962). Reporting on the early localizationist theories about the cerebral mechanisms of the higher functions, particularly the work of Wernicke, Dejerine and Liepmann (see § 2 above), Geschwind analyzed in detail the clinical and anatomical material relevant to the various kinds of speech deficits produced by cerebral lesions. He started from the hypothesis that many disorders of the higher nervous functions described as aphasia, apraxia (behavioural disorders or impairment of goal-directed activity) and agnosia (perceptual disorders) can be explained most fully when they are seen as the result of "disconnexion" or interruptions of pathways connecting the motor and sensory projection areas in the cortex. Geschwind has presented considerable data of interest on the diverse aphasic syndromes and, with varying degrees of exactitude, has shown how they can be explained as symptoms of disrupted connections between particular cortical zones (hence, transcortical connections) and, consequently, as disturbances of the associaboth earlier and more recent research. At the same time certain authors, such as Goldstein or Kleist, do not fit easily into either historical period, if only because of their longevity and active participation in discussions of both earlier and later date. Our presentation therefore sidesteps to some extent the historical divisions.

5. C U R R E N T LOCALIZATIONIST THEORIES

33

tive function between the various sense modalities. At the same time his analyses of anatomical studies have demonstrated that given kinds of connective tracts are absent in animal brains and present in the human brain; these differences furnished him with indications as to where to look for the anatomical bases of language. We shall be referring to these data in later parts of this book when treating certain questions. However, it should be emphasized that Geschwind's theory, although presented in a suggestive way, has met with serious opposition, and a number of doubts, both of a general and particular nature, have been cast upon his views. We shall deal only with two of the more general objections raised. First, it has been pointed out that there is no substantiation for treating as congruent the concept "association", which is a psychological concept, and the concepts "connection", "nerve tract", etc., which are anatomical concepts (Lenneberg, 1967). It has still not been shown that this type of nervous tract serves to associate stimuli or that they are the neuroanatomical correlates of associations. It is just as probable to suggest that they form the anatomical base for relaying fully elaborated "instructions" or "programmes" from one area to another. Credence has also been questioned of the view that all behaviour, including speech, can be explained exclusively via the collaborative activity of cortical loci through transcortical pathways (Lenneberg, 1967; Myers, 1967). This doubt arose from the more general trends in current neurophysiology now focussing on the role qf cortico-subcortical connections in brain function, in contradistinction to the traditional horizontal model of cortical organization of the brain as the organ of the higher functions, i.e., a vertical organization model in which a very important place is ascribed to the subcortical structures in the regulation of the organism's higher functions (McCleary and Moore, 1965). At this point note should be taken of Penfield and Roberts's (1959) conception which ascribes the principal role in speech regulation to cortico-subcortical connections, mainly cortico-thalamic. These authors advanced anatomical, neurophysiological and clinical data as evidence that the functions of three cortical loci for speech, distinguished by them, are integrated by the thalamus through participation of cortico-thalamic and thalamocortical projection fibres (Fig. 5). Thus we see that, in addition to the theory of isolated centres, another approach to a localizationist interpretation of speech mechanisms is emphasis on the role of connective pathways between speech functions, that is, the "connexionist" theory. In one of his recent publications, Konorski has offered an interesting proposal for synthesizing the two theoretical approaches. In his previous writings, Konorski (1961) took a "connexionist" view of the base of language activity as connections between excitatory patterns of the auditory analyzer and those of other analyzers, the latter patterns representing objects and phenomena of the external world (as a condition for speech comprehension) and also connections between these and other excitatory patterns in the cortical region which commands the articulatory muscles (as the base of nominative-descriptive speech). These connections arise

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PEDUNCULUS THALAMI POSTERIOR

Fig. 5. One of the fibre tracts connecting the thalamus with the speech areas (Penfield and Roberts, 1959).

on the basis of already existing tracts in the human brain associating the particular cortical analyzers. In his more recent publications, Konorski (1967, 1968) considerably modified his conception by bringing in the role of individual centres, or the cortical projection areas of the analyzers, into speech activity. These cortical representatives of the analyzers serve as gnostic loci responsible for perception of particular categories of linguistic stimulus patterns: spoken words (acoustic gnosis), written forms (visual sign gnosis), postures of the oral cavity (gnosis responsible for correct postures of the articulators during oral speech), and kinesthetic oral movements of speech (gnosis responsible for the motor sequence of speech sounds). Damage to the gnostic areas leads to corresponding agnosia of speech functions, that is, impairs the perception of given stimulus patterns (words). The above description does not exhaust the cerebral mechanism of speech, according to Konorski. Gnostic loci partake in speech processes through constant collaboration, the basis of which lies in the ontogenetically formed associations between the particular analyzers. These latter are formed by means of special pathways connecting the analyzers. Damage to these tracts also causes speech disorders, but of a different nature. Gnostic functions are spared while those functions requiring collaboration between analyzers are disordered. Thus, for instance, a patient with intact comprehension of oral speech will not be able to repeat what he has heard because, while auditory perception is preserved, transmission is disrupted between the perceptual and the motor speech centres. The source of trouble is the break occurring in the appropriate associative pathways.

6. CURRENT ANTILOCALIZATIONIST THEORIES

35

Thus Konorski's theory is an attempt to link the theory of centres with the "connexionist" theory, which is indubitably a step forward towards overcoming the excessive onesidedness of both these approaches on the question of brain structures related to speech. As we shall see, similar tendencies are to be found amongst other authors who, however, proceed from very different premises.

§ 6. CURRENT ANTILOCALIZATIONIST THEORIES AND ONE-FACTOR CONCEPTIONS OF SPEECH

Antilocalizationist theories on the cerebral mechanisms of speech are abundantly represented in the current scientific literature. We report the views of several authors in order to illustrate this clearly defined current of thought. One of the best-known proponents of the one-factor theory is J. M. Wepman (Wepman, 1951; Wepman et al., 1956; Wepman et al., 1960; Jones and Wepman, 1961; Wepman and Jones, 1964). In his earliest work, a monograph dealing with aphasic rehabilitation, this author associated his views directly with Goldstein's theory (see § 3 above). According to Wepman, the brain acts as a functional whole; any damage it suffers will impair to some degree all the higher functions of the organism, best manifested in personality disintegration. Speech disorder is only one of the symptoms of this disintegration; it signalizes the impairment of the ability to form integral wholes on an abstract level as also losses of the symbolization function 8 . Already in Wepman's first publication, however, there were evidences of theoretical nonsequiturs, which have since come into full light in his latter work. Guided by certain broad theoretical assumptions, Wepman and his collaborators (Wepman et al.s 1956, 1960) examined an appreciable group of patients by means of a special battery of tests and made a factor analysis of the results. They were led to the conclusion that there are certain "dimensions of language modalities" in view of which aphasic deficits cannot be treated as the symptom of a homogeneous and general disorder (Jones and Wepman, 1961). This interpretation evoked discussion between Wepman's group and Schuell and Jenkins (Schuell, 1960; Schuell et al., 1959, 1961 a,b; Schuell et al., 1962). The latter authors defended the position that aphasia was a unidimensional trait, independent of modality. Since then, Wepman has advanced the "regression hypothesis" to explain various forms of aphasia (Wepman and Jones, 1964). Cerebral damage reduces cortical function, and leads to a regression of the speech function to earlier infantile stages, but, as progress is made in compensatory processes, the patient moves progressively through the stages of language acquisition similar to those occurring in the child. Various 8

The consequences of this position for speech reeducation of aphasic patients have been discussed elsewhere (Maruszewski, 1965, 1966).

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forms of aphasia simply mirror the various stages of language development in childhood 9 . Kogan (1962) takes a similar position. His view is that aphasia is always a violation of the connection between word and object, and inevitably disorders the internal system of verbal generalizations. The various forms of aphasia refer only to various degrees of disruption of these connections or various phases of clearing of aphasia. The advocates of the one-factor theory cited above developed their hypotheses mainly from observations of patients during rehabilitation. Bay (1962, 1964) has presented a very interesting and relatively well documented one-factor conception of aphasia based on selected clinical materials. His proposal is that speech depends upon a large number of extralinguistic factors which are disordered when the brain is damaged. These may be "nonlinguistic" speech disturbances not affecting the essential function of language, viz., transmission of information. When this function is disordered, true aphasia results. In accordance with Marie, Bay claims there to be only one form of aphasia, related to a reduction of the intellect; he also shares Schuell and Jenkins' view that aphasic disorders are evoked by a general linguistic deficit. Information transmission by means of speech is related to the actualization of concepts; when this latter process is deranged a general linguistic deficit results, laying the basis for aphasic disorders. This does not mean that the aphasic patient is incapable of using concepts; the main point is that his concepts are pathologically distorted. Evidence is adduced from drawings and clay modellings of aphasic patients, a collection of which was made by Bay from tests and which displayed distortions of the contours of the object represented. The same deficit, according to Bay, is manifested in aphasic speech. The concepts actualized are blurred, deformed and poorly differentiated. Thus aphasia is understood as a disorder of operating with concepts and of conceptual thinking. The essential point in the theories outlined above is the link made between aphasia and disorder of some "fundamental" factor in speech, tantamount to the assumption, more or less tacit, of a specific "linguistic" factor. Note that in this report of the current thinking along these lines little mention has been made of opinions on the localization of cerebral structures related to this general factor. This is no accident; one-factor theorists today find this a very unwieldy question. It is no longer easy to reject the idea of the functional differentiation of the brain, a fact detrimental to the one-factor position. There are some striking inconsistencies to be found in the argumentation of some authors: they make the qualification that there are "extralinguistic" factors in speech, that there are speech disorders not produced by a disorder of the general factor and so are not "true aphasia", and so on. These are the evident symptoms of a crisis in the antilocalization position, 9 The regression hypothesis as an explanation of aphasia has been advanced by many authors; in any final analysis, it can only be a variant of the one-factor theory, the premise being that some general factor is reduced.

6. C U R R E N T ANTILOCALIZATIONIST THEORIES

37

breaking down under the pressure of the growing body of fact in support of an interpretation of the brain not as a functionally homogeneous organ but as composed of structural parts with distinctive roles in controlling the general activity of the organism, including speech. In this context it is of interest to consider a model presented by Brown (1968) at a meeting of the American Academy of Aphasia in Rochester, 1968. His basic assumption is that there is a "central language process" (CLP); and that damage to this central process results in abnormal behaviour known as aphasia. At first glance this may appear to be another hypothesis about some general language factor. But the author proceeds to state that this CLP possesses numerous "satellites" or "peripheral language processors" (PLP) related to speech that serve as input or output channels for the central language process. Brown suggests that the "central language process" is tantamount to what has been known in the past as inner speech, the inner form of language, symbolic formulation, or the like. Its function is to transform internal meaning into language and language into internal meaning. "Peripheral language processors", on the other hand, are the analyzers or abstracting devices in respect to sensory input and on the side of exteriorization are concerned with motor programming. "Central language process" as a conceptual notion needs clarification. Since its function is to transform internal meanings into linguistic utterances, which are combinations of words in accordance with rules of grammar, CLP must include both words and syntax. Another component is the ability to retain for a certain time span the ongoing speech and meanings. The fourth function of CLP is the ability to make a rapid and appropriate selection from one of the input or output channels and from the vocabulary. In addition CLP receives inputs from all other parts of the brain supplying information that can be expressed verbally and from the source of energy, the activation system. In the,above conception we have a theoretical model of the cerebral mechanism controlling the processes involved in speech (Fig. 6). Apart from the question of its completeness or adequacy, we have reported in detail on this model in order to illustrate the point made earlier about the crisis in the antilocalizationist and onefactor theory. Although Brown accepts similar premises, his model is in fact a multifactor one since it assumes that speech regulation involves the interaction of many different neural mechanisms. No suggestion is offered as to where the specific mechanisms are located, but clearly the assumption is that they have different loci. We have here an expression of the most modern lines of thought on the cerebral mechanisms of speech. Thus all discussion is spurious as to whether speech is a function of the entire brain or of certain cerebral structures only; it is the function of the whole insofar as all structures play some role, and is the function of certain structures in the sense that the latter serve specific functions in speech regulation. Obviously this does not mean an end has been reached to the controversy for and against the localization of speech mechanisms. Quite the contrary, one still

II. HISTORY OF RESEARCH ON THE RELATION BETWEEN SPEECH AND BRAIN

38

emotions desires

feelings beliefs

memories thoughts

ideas concepts

abstractions perceptions

power input (activation)

Fig. 6. Theoretical model of the cerebral mechanisms of speech according to Brown (1968). Description in the text. (By author's permission.) Specifications of aphasic symptoms providing evidence of disorders in the functioning of the different links of the mechanism in the original version have been omitted.

encounters "orthodox" views against the localizationist theory. But in current directions of research the most typical attitude appears to be a rejection of the antilocalizationist position and a turn toward search for the functional distinctions of speech structures in the brain.

§7. LINGUISTIC VIEWS ON APHASIA. LENNEBERG'S BIOLOGICAL THEORY OF LANGUAGE

Speech disorder connected with cerebral damage has also evoked interest among linguists, who have regarded this phenomenon as one which opens a way for verifying some of their general contentions about language. Studies of this type are unfortunately very rare, and the majority of them are rather theoretical, in the sense that they discuss various linguistic hypotheses in the light of evidence collected in the main by nonljnguistic studies. Linguistic approaches to aphasia are, necessarily, seldom of direct relevance to the problem of present concern, i.e. the cerebral mechanisms of speech10. However, there are some linguistic descriptions of speech disorders which facilitate a more precise analysis of aphasia. In such an approach, the emphasis is usually laid upon 10

This trend in Polish linguistic literature is best represented by W. Doroszewski (1963, 1966).

39

7. LINGUISTIC VIEWS ON APHASIA

a functional analysis of the disorder itself—an approach which we have come to realize is a very important aspect of aphasia research. Linguistic descriptive methods, applied systematically in aphasia research, could assist greatly to resolve many of the disputed problems and could thus contribute to a better understanding of the brain's role in normal speech. More recently, linguists have been displaying a noticeable growth of interest in the problems of aphasia. Some authors have even suggested the term "neurolinguistics" to cover this province of study. Among the best known linguistic works on aphasia are the writings of Roman Jakobson (1956, 1964). In his earlier work, he advanced the general theory that language use involves two kinds of operations: selection of linguistic units and their combination into superior linguistic units of more complexity. Correspondingly, there are two main forms of aphasia: one, similarity disorders, as displayed in the impairment of selection operations and in substitutions by phonetically or semantically similar units, with intact ability to form the verbal context; the other, contiguity disorders, in the case where selection operations are preserved but combination is impaired, as in agrammatism. After contact with Luria's work, (see further § 8) Jakobson revised his theory considerably i 11111111 II 1 ; DECODING .'minim siftserwr tic 1

'-/, dynamic ' ' / / , fron tal

DISINTEGRATION

tMMmm * fl 11

iantero-temporali'^yi?]} SEQUENCE

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LIMITATION

I

amnestic central-temp oral

N\\\K \\\Js s\\\k s\\sK \\\K \\sjs \\\S svsK wsK

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ooste ensor ipo ra ro-ten SCONCURRENCE\

., ...>.,

Fig. 7. Dichotomies underlying various aphasie disorders (Jakobson, 1964b).

(Jakobson, 1964). He interpreted aphasic disorders in terms of three basic dichotomies: (1) encoding versus decoding operations, (2) limitation versus disintegration, (3) sequence (successivity) versus concurrence (simultaneity). These threefold divisions of aphasia are not mutually exclusive and may assume various complicated forms of reciprocal overlapping. For example, acoustic-gnostic aphasia in Luria's terminology is, according to Jakobson, a combined disorder of decoding operations, concurrence, and disintegration (Fig. 7). A particular place in future research on cerebral language mechanisms may be envisaged for Chomsky's psycholinguistic conceptions (1967a, b), which have met with broad resonance not only among linguists but in related disciplines concerned

40

II- HISTORY O F R E S E A R C H ON T H E RELATION BETWEEN SPEECH A N D BRAIN

with language communication. On the basis of a formal analysis of the structures of sentences in relation to their semantic interpretations, Chomsky arrived at conclusions bearing directly upon the cerebral regulation of language use. In his view, the language user (speaker-hearer) possesses, as cerebral equipment, a highly abstract system of grammatical rules which enable him to generate and decode utterances ("linguistic competence"). Analysis to these rules brought Chomsky to the belief that such a system could not be the product of learning but constitutes the prerequisite for all language learning. The "deep structure" of language is an a priori structure in the human brain, a determinant of language acquisition, in contradistinction to being the product of that process. These theoretical views prompted Lenneberg (1967) to write a monograph on the biological foundations of language summarizing the present state of knowledge on the specific properties of human anatomy and physiology in respect to language, taking as premise Chomsky's explanatory principle. Lenneberg proceeded from the tenet that language, like other types of behaviour, is determined by innate, species-specific biological equipment. He proposed five general premises as the bases for a biological theory of language, as follows: (i) Every species has its own specific cognitive processes; each species, metaphorically speaking, possesses its own world image, (ii) The species-specific properties of cognitive processes are replicated in every member of the species, in the same way as are structural properties; in other words, every individual is a replica of his species in both cognitive structure and function, (iii) Cognitive processes mature ontogenetically by a process of progressive differentiation, which is practically independent of environment; in some cases, environment acts only to initiate them; it "triggers a cocked mechanism", but does not shape the function itself, (iv) Relative to other species, man is immature at birth; certain aspects of behaviour and cognitive function emerge only gradually during infancy, (v) Certain social phenomena of interaction emerge through the spontaneous adaptation of the growing individual's behaviour to that of the surrounding individuals. On the foregoing premises rest the following statements which serve as the foundation for a biological theory of the human capacity for language. 1. Language is the manifestation of species-specific cognitive propensities. It is the consequence of the biological properties of the species. 2. The cognitive function underlying language consists of an adaptation of a ubiquitous (among vertebrates) process of categorization and extraction of similarities. 3. Certain human specializations in peripheral anatomy and physiology account for some of the universal features of natural languages, but the description of these human peculiarities does not constitute an explanation for the phylogenetic development of language. Species-specific cerebral function is the determining factor for language behaviour. 4. The biological properties of the human form of cognition set strict limits to

7. LINGUISTIC VIEWS O N APHASIA

41

the range of variations in natural languages. Within the limits set, however, there are infinitely many variations possible. 5. The human capacity for language communication develops ontogenetically in the course of physical maturation; however, certain environmental conditions must be present as well to make it possible for language to unfold. Maturation brings cognitive processes to a state of "language-readiness". Suitable material must be supplied from the outside for this latent structure to become actualized. This "raw material" is the language spoken by the adults surrounding the child. 6. The actualization process of biological propensities takes place always when contact between child and speaking environment occurs, even in cases when peripheral blockage prevents the child himself from speaking. But in cases where peripheral damage (e.g., deafness) prevents the intake of others' speech, the latent structure fails to become actualized either temporarily or permanently. 7. The maturation of cognitive processes comes about through progressive differentiation, or through rearrangements' to overcome states of disequilibrium. "Language readiness" may be regarded as a disequilibrium state which begins around two and declines in the early teens with the termination of cerebral maturation. 8. Language capacity is replicated in every normal human being because it is a consequence both of the human mode of cognition and of the human course of maturation. Universal grammar is of a unique type, common to all men, and is the product of a peculiar mode of cognition based upon the biological constitution of the individual. 9. All natural languages have an inner (deep) form of an identical type. Therefore every child may learn any language with equal ease. The child realizes his own inner structure upon the model of the outer form of the language that surrounds him. All languages are so constructed as to conform to the requirements imposed upon them by cerebral language-data processing mechanisms. 10. External social influences upon the child are not the causative agents that determine his language development. These influences act only as a "trigger" that sets off the process of actualization on internal mechanisms. In the critical state of maturation, exposure to adult language behaviour leads to actualization of the innate mechanism. Starting with general assertions derived from theorizing on the formal properties of language, we have thus arrived at very radical and particularized statements on the cerebral regulatory mechanisms of speech. Lenneberg made considerable efforts to document his statements; evidence was adduced from observations and research into normal and abnormal speech behaviour and the ontogenetic development of language 11 . Space precludes a closer examination of the arguments and findings 11

It is not implied that onesidedness has been avoided in the presentation of empiric fact on which the author has based his statements. While attending to that evidence which confirms the

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II. HISTORY O F RESEARCH ON T H E RELATION BETWEEN SPEECH A N D BRAIN

reported; they leave no doubt that Lenneberg's work raises very important issues which demand full consideration in any theory about cerebral language mechanisms. We shall be returning to them in the context of more specific questions. It should be emphasized, however, that many questions he raises are far from settled, and call for further and deeper study. Nevertheless, his conception is bound to spark off valuable discussion around the central topic of this book, i.e., the language mechanisms of the brain.

§ 8. THE THEORY OF DYNAMIC LOCALIZATION OF FUNCTION. LURIA'S CONCEPTION OF THE FUNCTIONAL SYSTEM

The foregoing survey of theoretical approaches to localization of cerebral speech mechanisms has brought us to the conclusion that, at the present juncture, the antilocalizationist view is receding and research is concentrating around inquiry into the functionally distinctive cerebral structures underlying speech. This trend is most fully expressed in Luria's conception of the functional system of speech, a particular application of the theory of dynamic localization of function. The theory so named originates with Pavlov and his collaborators. In 1916 Pavlov made the point that, in order to understand the mechanisms of complex behaviour, explanations about elementary nervous centres will not suffice. It must be accepted that functional linkages between various parts of the nervous system may be created by a special kind of trail-blazing, which permit the emergence of given reflexive acts (Pavlov, 1952). The behaviour of the organism does not result from the functioning of isolated and fixed brain structures, but shapes during the ontogenetic development of dynamic and changeful systems made up of interconnected structures located at various points in the nervous system. This dynamic approach to the analysis of function localization was developed further by Vygotsky, whose ideas were first published in a little known collection in 1934 and appeared in English only in 1965 (Vygotsky, 1965; Luria, 1965). Vygotsky emphasized the point that, before asking where a given function is localized, it should first be asked what is to be localized. In other words, we should first analyze the structure of the function for which we are seeking the cerebral regulating mechanisms. Moreover, in conformity with his broader conception of psychological development, Vygotsky (1956) gave central place to the fact of the complex history of ontogenetic formation behind the specifically human higher functions. In the successive develgenetic determination of language, Lenneberg displays a clear inclination to pass over other observations which point to the substantial influence of environmental factors on language development in the child and on speech recovery following cerebral damage. He has thus been led to pessimistic conclusions as to, for example, the utility of reeducational work in cases of aphasia; such a view is untenable in the light of experience gained in rehabilitation centres for aphasic patients (Maruszewski, 1966, 1969b).

8. THE THEORY OF DYNAMIC LOCALIZATION OF FUNCTION

43

opmental stages of formation, various parts of the brain can be presumed to have different roles. The determinant for finding the localization of the cerebral mechanism for a given function is, basically, the functional analysis of that activity, with due regard to the peculiar ontogenetic process of formation. A similar line of reasoning was pursued by Anokhin, one of Pavlov's close collaborators. In 1935, Anokhin (1962, cf. also Luria, 1962) separated two applications of the term "function", one referring to the activity of a given organ or tissue, and the other to the complex adaptive activity of the organism as an integral whole, aimed at the accomplishment of a specific task. The latter activity may be performed in various ways and may require the interaction of several different organs; while the structure of this activity may be altered, the result remains the same, i.e., the fulfilment of the given task. It is evident that the connection between a function, thus understood, and the structures of the organism takes shape differently than in the case of simple functions. This point had escaped the narrow localizationists. Function, in this second sense, is actualized through a dynamic constellation of many different morphological links controlled by nervous structures localized in different parts of the nervous system. Adopting the above views, Luria proceeded to develop his theory of the functional system (Luria, 1947, 1948, 1960, 1962, 1963, 1967). This is a theory which resolves the problem of the localization of neural mechanisms regulating the higher functions of man. A higher function is a complex adaptive act by the whole organism, which may be performed in various ways utilizing different organs. In composition it is an integrated set of more particular interrelated functions, whose collaboration ensures the attainment of a given result. By the same token, a higher function cannot be attributed to any strictly circumscribed "centre"; it is realized through the interaction of numerous neural structures situated at different points in the nervous system and together composing the functional system for a given activity. This does not mean that the constituents of a functional system are equally important or "equipotential"; neuropsychological analysis of disorders caused by damage to specific parts of the brain testifies to the different ways in which each element subserves a functional system in its own manner, ensuring the smooth operation of the whole. At the same time, any structure, because of its specific functional properties, can be a component of many different functional systems, all of which constitute the anatomicphysiological base of man's diversified higher activities. The views reported in the foregoing paragraphs define a certain approach to cerebral functional organization; they comprise an interpretation as to how the nervous system regulates the higher functions. The brain is composed of many functionally differentiated fields, each having its own role to play in the analysis and synthesis of external stimuli arriving through the sensory modalities, and in controlling the work of the various organs. Each complex higher function "makes use", shall we say, of the potentialities contained in various anatomical elements. To acquire a higher function means to form a functional system, or to set up dynamic and inter-

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changeable connections between the required constituents. The term interchangeable applies here because, as a function undergoes formation, its inner structure changes progressively and thus the degree of engagement of the various constituents is altered in the regulation of a given activity. At the same time, any element can be utilized in forming other functional systems, thus assisting in the operations of more than one higher function. In this light, we look in vain for "centres" of any complex process; our task is to reveal the functional meaning or role of the particular brain structures. We should establish their roles in the regulation of behaviour in its diverse manifestations. This is a kind of factor analysis of brain function, which can be effected by use of special methods of neuropsychological investigation. Luria applied the theoretical assumptions reported above to aphasia research. Over long years of practice, Luria had collected a wealth of clinical material, which was used in making his own classification of aphasia, understood as a disorder resulting from damage to one or another link in the functional system of speech. His opinion was that, underlying normal speech, there are six main "factors" connected with different left hemisphere regions. They are as follows: 1. Phonemic hearing, or the specifically human capacity to analyze and synthesize speech sounds, as the indispensable condition for speech; related to Wernicke's area in the left temporal lobe. Damage to this area disturbs phonemic hearing and leads to acoustic-gnostic aphasia. 2. Verbal auditory memory, or the capacity to remember auditory word-patterns necessary for encoding and decoding, also for writing, particularly lengthy texts; related to the cortical area beneath Wernicke's area in the left temporal lobe (posterior parts of the second and third temporal convolution). Damage to this area disturbs auditory memory of words and leads to acoustic-mnestic aphasia. 3. Analysis-synthesis of kinesthetic sensations from the oral cavity and its organs (articulatory apparatus), required for correct posturing of the tongue during speaking; related to the inferior postcentral region of the left hemisphere (operculum parietale). Damage to this area disturbs analysis and synthesis of afferentation from the articulators and leads to afferent motor aphasia. 4. Sequential (temporal) organization of articulatory movements necessary for the smooth continuous flow of strings of words, related to Broca's area in the inferior premotor left region. Damage to this area disturbs the sequential organization of articulatory movements and leads to efferent {kinetic) motor aphasia. 5. Simultaneous synthesis, the condition for grasping the logical-grammatical relations between word combinations; related to the left parieto-occipital region. Damage to this area leads to semantic aphasia, or the inability to comprehend and produce word groups requiring complex simultaneous organization. 6. Inner speech, the condition for constructing complex utterances (discourse). It is not yet clear what more fundamental factors make up this highly complicated phenomenon; however, it is already known that disorders of the capacity for discourse

9. CONCLUDING COMMENTS

45

are connected with damage to the left frofttal lobe, situated anteriorly to Broca's area; such damage causes dynamic aphasia. In Luria's opinion, not all the above factors have been sufficiently well studied, particularly the latter two. However, one can be fully assured that all these factors, hence the related cerebral areas, play an essential role in normal speech. Thus Luria's theory does not envisage "centres" for particular speech functions and their collaboration. Instead, it postulates cerebral areas fulfilling specific functions which happen to be important for speech activities as well as for other activities. Their collaboration in the framework of one functional system comprises the cerebral mechanism of language. The line of reasoning reported above calls for a fundamental change in the kind of questions that the student of cerebral speech mechanisms ought to pose. It is not merely a matter of establishing whether an area or connective pathway has significance for speech, but of ascertaining what this role is, or what this area contributes to the normal flow of speech. This appears to be the most fruitful procedure to follow. In our further discussions, therefore, we shall attempt to arrange our material in such a way as to furnish a more precise, albeit sketchy, answer to this question; or, alternately, to present the emergent hypotheses, not excluding those awaiting fuller verification.

§9. CONCLUDING COMMENTS

In this chapter we have presented a cursory survey of the history of inquiry into the cerebral mechanisms concerning speech, up to and including the present situation. The fact that important theoretical divergencies exist can be attributed, as this review shows, to the complexity of the problem and to the methodological difficulties associated with its investigation (see Chapter III). These difficulties are fundamentally bound up with a much broader problem, that of the cerebral localization of general psychological functions and of the functional organization of the brain as the organ directing all activities of the human being. Even today this question is being attacked in various ways, ranging from the narrow localizationist conception of isolated "centres" for particular functions, through the conceptions on the role of neural pathways and collaboration of centres, to a view of the brain as an equipotential organ with no functional differentiation. We have tried to show that this third line of reasoning has reached a state of crisis and its proponents are forced today to retreat from it; the amassed data on the diverse functional roles of cerebral centres vitiate for all practical purposes any attempt to present the brain as an organ operating on the principle of equipotentiality. The emergent model of the brain is that of an organ composed of functionally differentiated structures, each fulfilling its specific role in the government of behaviour and, in its own fashion, ensuring the normal course of many different activities. When

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a number of such structures collaborate in one functional system, only then is the anatomic-physiological base, or "brain organ", constituted for the regulation of that activity. In subsequent presentation of our material we shall adhere to the principle laid down above. As we proceed we shall come upon many unresolved problems, suggestive of mutually exclusive interpretations. Far from concealing these divergencies from the reader, we shall accentuate them, in this way avoiding premature closure of problems or poorly substantiated hypotheses. In following this course of action, we risk leaving the reader dissatisfied; he may be left in doubt as to the full reliability or adequacy of the knowledge we hold today. But such a conclusion would be ill-considered; for, despite the theoretical divergencies and the methodological hurdles still to be overcome (to be discussed in the next chapter), the long years of investigation have borne fruit in a wealth of factual knowledge regarding the role of particular cerebral structures governing speech. The fact that many questions remain open makes the problem all the more intriguing; what is more, the fact that this problem bears upon that which distinguishes us from all other living organisms is cogent enough reason for its cognitive significance. We hope to give the fullest possible account of those neuropsychological findings that have been of relevance to a clarification of the cerebral properties by virtue of which man is the exclusive possessor of language communication. Against the background of contemporary controversies, we proceed now to deal primarily with concrete facts. Our first step will be to provide the reader with an account of the methods by which these facts have been ascertained. This furnishes the subject matter of the next chapter.

CHAPTER III

RESEARCH METHODS FOR THE STUDY OF THE SPEECH-BRAIN RELATION

§ 1. GENERAL DESCRIPTION OF METHODS FOR THE STUDY OF THE RELATION BETWEEN BEHAVIOUR AND BRAIN

In the present chapter we report on the sources from which our knowledge has been drawn on the subject-matter of this book, the methods which have produced this knowledge, and the difficulties inherent in this type of research. This survey is important to make, since it covers a domain of research which is constantly under discussion and where opinions and interpretations are in perpetual collision, despite the large amount of evidence at hand. This state of affairs is in large part due to the difficulties besetting research into the speech-brain relation, and also to the specific nature of its methods, an aspect not always fully appreciated (Maruszewski, 1966).

The problem of the speech-brain relation belongs within a broader context, namely, the relation between all the higher functions and the brain. It may rightly be treated as a particular case of a more general question: the cerebral regulation of the functioning organism. Research into this broader province—that of neuroanatomists, neurophysiologists, clinicians and psychologists—has more recently been marked out as a borderline discipline called neuropsychology, and assigned the task to ascertain the relation between the features of cerebral structure and function, and the higher activities of the organism. Among the methods applied in this newer discipline, an important place is ascribed to experimental work with animals. The basic research design might be outlined as follows: A given behaviour of the animal is described in detail (or, alternately, the animal is trained in some form of behaviour by special procedure), the corresponding brain structures are then stimulated or destroyed, and the ensuing behavioural changes are analyzed. There are many variants to this basic procedure, but the essential point in all of them is that a strictly defined change is introduced into the animal's brain by the investigator, in maximally controlled conditions, for the purpose of studying the changes in behaviour that follow, and, on this basis, a conclusion is drawn as to the significance of the given structure for the animal's behaviour. Highly reliable results may be obtained in this way, provided that the essential requirements in studying the behaviour, and in performing the surgical or other measures, are satisfied (the latter usually verified by detailed postmortem examination). For obvious reasons this method is not applicable to human subjects. Therefore

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HI. RESEARCH METHODS FOR THE STUDY OF THE SPEECH-BRAIN RELATION

in many questions relating to cerebral regulation of man's higher activities, we must rely largely on evidence derived from animal experiments. Thus the significance of particular brain structures in man is often deduced from findings based on animal studies. Naturally, hypotheses so derived are subject to confirmation through anatomical research on the human brain and clinical observation of persons who have suffered cerebral damage. As to such issues as the motor and sensory functions and their relation to cerebral structures, as also brain mechanisms of memory and emotions, there are grounds to believe that between man and other animal species (particularly the higher species) there is a fair degree of similarity in functional organization of the brain, or that known differences occur; consequently, evidence obtained from animal investigations is extremely useful for constructing hypotheses about man. To be sure, extreme caution is called for in interpreting such data; but the fact remains that in the history of neuropsychology we find many examples illustrating how animal experimentation has contributed to building up an understanding of the cerebral organization of human behaviour. But the above procedure and reasoning fails totally when we examine the relation between speech and the brain. As stated before, language communication has no real duplicate in the world of living organisms, man alone possessing this capability. No animal research such as that described above will provide us, then, with even indirect evidence on the cerebral mechanisms of speech. Only studies in comparative anatomy, contrasting the structural features of the human brain with animal brains, may possibly yield some information of value. Certain authors draw radical conclusions about the brain mechanisms of language from the uniqueness of certain structures in the human brain. But, as we shall soon see, this is a risky way of reasoning; difficulties are bound to arise since we know even less about the properties of the cerebral structures of various animal species—including the nonhuman primates— than we do about those of man. In the light of the above considerations, it seems apparent that, in studying the speech-brain relation, we must lean almost entirely upon research on the human brain and efforts to correlate its features with speech. Before we start on our review of the basic sources of neuropsychological evidence on this question, let us recall a certain pre-scientific effort to establish the relations in question. This was called phrenology, founded by the eminent Viennese anatomist Francis Joseph Gall (17581828) on what seemed to be plausible premises in those days. Gall believed that every psychical ability and every human action depended necessarily upon the function of some specific group of nerve cells composing the "brain organ" of that function. If such a function is more developed in one individual than in another, then presumably the corresponding brain organ would be proportionately larger. Gall, who judged that the organs of intellectual functions, "moral functions" and psychical features of man are lodged within the cortex, accepted the following basic tenet: If the organ of a given function, action or feature is enlarged, in order for it to be lodged within the cranial cavity, the latter should display a convexity in that

2. THE CLINICAL METHOD

49

place. In line with this assumption, Gall studied the bulges and bumps in the skulls of distinguished persons—mathematicians, artists, poets, military leaders, and so on. On the basis of the data he collected, Gall outlined precise maps of the protuberances of the human skull which, in his opinion, corresponded to the sites of brain organs for the various psychical abilities. One of Gall's guesses was that the speech centres were located in the frontal lobes of the brain, for he had observed that persons with protruding eyes had greater language abilities than average. He interpreted this to mean that language abilities depended on the size of the frontal lobes : when the latter are enlarged, the eye-balls are pushed outward. This fantasy of Gall's played a certain role in the investigation into cerebral localization of language and contributed—quite by accident—to the discovery of the first important cerebral speech area (see Chapter II, §2). Gall's efforts to localize the psychological functions in the brain were, as already noted, unscientific since his premises were unsound. (Take for example, the belief that individual differences in psychological function correspond to variations in brain size great enough to produce different skull formations.) True scientific research on localization started with the examination of individuals suffering from brain injury. Research into brain pathology, or the symptoms of disease leading to destruction of cerebral structures, is the principal source of knowledge on thé speech-brain relation. The basic line of reasoning in this method is similar to that discussed earlier in animal experimentation. A pathological process leads to certain brain damage; from observations of behavioural change, conclusions are drawn as to the functional role of the destroyed structures. But here an essential difference occurs : in contradistinction to animal experimentation, the investigator does not himself provoke the brain damage, but must wait upon natural processes (nature's own experiment), and can utilize only the results of processes occurring independently of his will. As we shall see shortly, this is a fundamental difference which has grave consequences for the accuracy of the information yielded. The basic method for the study of the speech-brain relation is therefore the clinical method, which is the description of speech disorders in individuals afflicted with cerebral lesions resulting from pathological processes. The research procedure has a twofold aspect; we may speak of it as having two components. One is to ascertain the locus of the lesion and to demarcate the affected cerebral areas; the other is to describe in detail the speech behavioural changes, to establish the deviations in the speech of the patient with a defined structural brain lesion from normal speech of persons with undamaged brain. We shall now discuss in greater detail the relevant circumstances for conducting both aspects of research by the clinical method. §2. THE CLINICAL METHOD: CAUSES AND PROPERTIES OF BRAIN DAMAGE AND WAYS OF LOCALIZING IT

Our first concern is to determine the possible causes of the brain lesion and to characterize it. Broadly speaking, the primary causes of brain lesions that lead

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III. RESEARCH METHODS FOR THE STUDY OF THE SPEECH-BRAIN RELATION

to speech disorder (aphasia) and thus furnish information on the locus and functional role of particular brain structures involved in speech are as follows: cranial trauma, both closed and open; cerebro-vascular accident (mainly cerebral strokes); intracranial tumours; deliberate or accidental effects of surgical excision in the brain; infected states and toxic damage to the brain. We shall briefly discuss the properties of brain damage in relation to their causes. Cranial trauma is a frequent cause of brain tissue damage. These may be gunshot wounds in the head, traffic accidents, and the like. Many authors treat this group of patients as a particularly good material for research on our problem, since this type of cerebral damage—more precisely, traumatic types such as gunshot wounds on the battlefront—happens most often to young persons in good health up to the moment of the injury, and usually are relatively selective in nature, that is, limited to a circumscribed cerebral region, leaving the rest of the brain intact. This latter factor is particularly important in the study of the functional role of cerebral structures and for this reason many studies on aphasia are based on findings with this group of patients. But it should also be borne in mind that this material is only relatively "pure" since cranial trauma can lead not only to focal brain damage but also to changes diffused through the brain of varying intensity according to the extent of the injury and its mechanical properties. In these cases as well, it is not always possible to localize the damaged site reliably, and interpretations based solely on external localization of the skull wound can be very misleading. Cerebro-vascular disease, particularly cerebral strokes, is another very common cause of brain tissue déstruction. In such accidents, the arterial vessel is occluded (embolism and thrombosis), so that the blood supply to a greater or lesser cerebral field is blocked and necrosis of nerve tissue ensues or, as in cerebral hemorrhage, the vascular walls are ruptured, leading to extensive destruction of nervous tissue through blood penetration into cerebral matter. A large proportion of aphasia research is based on data from studies of this group of patients. Unfortunately, from the standpoint of localization of cerebral structures involved in speech, this source shows up some essential shortcomings. First is the fact that this type of disease occurs mainly amongst elderly persons whose brains are affected by other types of diffused change. Postmortem examination of cerebral stroke cases very often shows multi-focal damage embracing areas quite remote from each other and of heterogeneous function (Fig. 8). Another serious weakness is that the extent and locus of the lesion depend on a great many as yet unaccountable factors. In particular, there is the question of the site at which the blood supply was interrupted. If one of the larger vessels is involved, then the mortified area is very extensive, incomparably greater than when the blockage occurs in one of the arterial end-branchings. It is also important to take into consideration the anatomy of the cerebrovascular system and the frequency with which pathological processes occur in particular cerebral arteries (Fig. 9). For these reasons strict localization of the damage without postmortem examination is exceptionally difficult, and therefore

2. THE CLINICAL METHOD

51

f. Rotandi

f. Sylvii

Fig. 8. Results of cerebral postmortem examination schematically presented, of a brain stroke patient: left hemisphere lesion (Tonkonogi, 1968).

Fig. 9. Left hemisphere fields supplied with different branchings of the middle cerebral artery (from Ajuriaguerra and Hecaen; after Lenneberg, 1967).

the material obtained is of limited value for interpretations of the functional significance of given structures! Intracranial tumours and cerebral lesions resulting from their surgical excision also cause damage to structures involved in speech and as such yield information bearing on our research problem. One undoubted advantage of this material is that the report of surgical intervention contains extensive information both on the nature and site of the tumour and on the state of adjacent cerebral territory, data facilitating localization of the damage. On the other hand, some features of this material detract from its usefulness for localization purposes. We know, for example, that

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HI- RESEARCH M E T H O D S FOR T H E STUDY O F T H E SPEECH-BRAIN RELATION

because of differences in such properties as histological structure, type and growth rate of the tumour, presence of cysts, possible pressure on adjacent blood vessels, accompanying dislocation of nerve tissue, etc., two identically located tumours may produce quite different disturbances and dysfunctions (¿arski, 1964). Cerebral ablation in treatment of epilepsy, aneurisms and certain psychiatric disorders1 invariably causes a lesion in the nervous tissue. Since speech disorder is an immeasurably profound disablement, it is only in very exceptional cases that a neurosurgeon will deliberately traumatize the areas important for language use. In the majority of post-operative cases of this type, speech dysfunctions are the effects of unforeseen complications (e.g., hematoma, post-operative infection). It is exceedingly difficult to localize with precision those changes that are attributable to surgery; a sharp demarcation of destroyed regions is out of the question. The usefulness for research of findings based on these cases is further diminished by the fact that this sort of intervention is usually practised upon individuals who have already manifested clearcut pathological changes in cerebral function prior to operation, sometimes even of an organic nature, and so their brains are different from normal brains. The final group of causes underlying brain lesions where speech impairment is involved is infected states and intoxication. These necessarily lead to extensive changes beyond any one cerebral focus, so that a strict description of destruction without postmortem examination is, to all practical purposes, impossible. The above review points up certain basic features which differentiate the clinical method for studying the speech-brain relation from the animal experimental method for studying the functional role of diverse cerebral structures. These differences ensue from the nature of the cerebral damage. In animal experiments, the investigator introduces into the normal animal a strictly defined damage in that structure whose functional significance he wishes to ascertain, while clinical studies are based solely on material derived from pathological processes and, in addition, from lesions which are rarely limited in scope to the structures of interest; to complicate matters further, localization of these lesions requires application of special research methods. Another obstructive factor is that lesions arising under such conditions as just described differ not only in extent and localization, but also in degree of impairment 1

One of the more common neurosurgical measures applied in treatment of epilepsy is the removal of epileptogenic foci. Depending on the extent of the ablated area, this operation is called topectomy (field removal) or lobectomy (lobe removal). In the case of very extensive damage in one hemisphere, a hemispherectomy is sometimes performed, that is, the entire cerebral hemisphere is removed. In some cases an operation is performed consisting in the dissection of the great commissure, which comprises the nerve tracts connecting the hemispheres. In treating aneurisms, the neurosurgeon has to remove those cerebral fields which block access to the aneurism. In psychosurgery (surgical treatment of psychiatric illnesses), lobotomy (or leukotomy) is well known; this is the cutting-oflf of nerve tracts which connect the frontal lobes with the other parts of the brain. More recently stereotactic interventions have been introduced by which various deep cerebral structures are destroyed for therapeutic purposes with the aid of a specific device.

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to particular structures. A given area may be totally destroyed, partially damaged, or may only display a dysfunction connected with a lesion in an adjacent area, not embracing the structure in question but affecting its state. There is every reason to believe that disorders symptomatic of varying degrees of damage to the same cerebral area differ considerably among themselves, which is still another source of confusion in the interpretation of the interrelation between a circumscribed area and a given function. The implication of the foregoing is that a central difficulty with the clinical method is the degree of rigour with which cerebral changes underlying speech impairment can be localized. Unless we can delimit with precision the areas destroyed, it is a foregone conclusion that any inferences as to the links between cerebral damage, structure, and functional role are groundless. From the standpoint of research goals, the best method for localizing a lesion is, of course, the postmortem examination, that is to say, a refined anatomical and histological examination of cerebral damage. This can only occasionally be practised, obviously; it is in fact rarely performed, since it is a costly procedure in time and means, requiring highly specialized personnel. Therefore there is relatively little information of this type in the literature, though some highly significant data have been obtained in this way. For the above reasons other methods applied in clinical research play the basic role in localizing lesions. These are mainly neurological examination procedures which take advantage of certain well-known localizing symptoms. They include examination of changes in motor and sensory function in brain-damaged cases which, once established, allow for a fairly accurate demarcation of the damaged area. For instance, if the limbs on one side of the body are paralyzed, it may be inferred that the lesion can be found in the cerebral hemisphere on the opposite side; if certain additional hemiphlegic features are identified, inferences can be made as to the extent of the lesion, its cortical or subcortical focus, and so on. Sensory impairment, restriction of the visual field, and many other neurological symptoms, serve similar purposes. Yet this type of symptomatology usually bears an undefined degree of uncertainty and does not always lead to a precise topical diagnosis. Therefore, various auxiliary techniques are used for localization diagnosis. These include radiological examination, as for example X-ray of the skull, arteriographic examinations (introduction into the cerebro-vascular system of a special substance producing photographic contrasts which serve to establish changes in the state and distribution of the main cerebral blood vessels), radiological examination of the cerebral ventricles, and so on. Such observations yield information permitting the specialist to delimit, sometimes with fair accuracy, the focus of one or another pathological process. Another important method is electroencephalographic investigation, i.e. the examination of brain electrical activity. Electrical phenomena occurring in damaged cerebral tissue are clearly distinguishable from electrical activity in the normal brain. When appropriate registration is conducted, this method, too, can yield extremely valuable topical

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information. More recently other methods have been developed, such as use of radioactive isotopes; this method is based on the fact that destroyed cerebral tissue has heightened absorptiveness in relation to certain substances. Still another method involves the application of ultrasound. Data amassed by the above methods and techniques enable us with fair accuracy to define the focus and size of a lesion. Clearly, the possibility of error cannot be excluded, but such error is relatively minimal. Bearing in mind the reservations mentioned earlier in this section, it may be taken that contemporary methods of localizing brain damage are sufficiently well developed—though not without their limitations—to permit the pursuit of research into the relation of speech and brain.

§ 3. THE CLINICAL METHOD: RESEARCH ON SPEECH DISORDERS CAUSED BY BRAIN DAMAGE. SHORTCOMINGS AND DIFFICULTIES

The second component of the clinical method is, as earlier stated, the description of speech changes. To be in a position to draw conclusions about the functional role of a destroyed structure, we must first be precise about the kind of deviation from normal behaviour caused by that damage. In this second facet of research, as in the first, the clinical method is beset with difficulties, greater by far than its analogue in the animal experimental method. For it involves, on the one hand, the incomparably greater complexity of human behaviour, which includes speech activity, and on the other hand, the nature of the damage in question which is, as earlier pointed out, both nondeliberate and uncontrollable in the strict sense. Studies of speech disorders have posed a number of methodological problems not yet fully resolved (Maruszewski, 1966). Generally speaking, these studies concern detailed qualitative descriptions and classifications of the symptoms in various aspects of speech activity, experimental studies of speech function, and the correlation of symptoms typical of given focal damage leading to description of their syndromes (Maruszewski, 1969a). The description and classification of symptoms is based on an analysis of records of diverse forms of speech activity, with attention to the patient's particularities. For the crux of the matter is that variously located brain lesions can cause qualitatively differing deviations from normal performance. For example, take a very simple situation: the patient is asked to name an object shown him; in this situation he may commit fundamentally different errors. Sometimes there is no reaction of any kind; sometimes the reaction is a helpless gesticulation indicating inability to produce the name; sometimes the patient tries to describe the object in detail without naming it (e.g., electric bulb: You screw it in and get light... for electric light... you buy it, and screw it in... and so on); sometimes, instead of producing the right name, he gives a semantically or phonetically similar one [instead of "narty" (skiis)—

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55

"lyzwy" (skates); instead of "grzyb" (mushroom)—"grob" (tomb)]; finally, he may distort the name some way [instead of "filizanka" (cup)—"*hibliianka"; instead of "szyszka" (pine cone)—"*keszka", etc.]. On this level of analysis certain guesses can be made about the functional role of the damaged cerebral structures. Such guesses become the hypotheses for verification in experimental studies on the patient's speech functioning. As in any other experiment, a given activity (here, some form of speech) is elicited in conditions as strictly controlled as possible and, by manipulation of these conditions, their effect upon performance is ascertained. For example, one can discover whether the patient has the same degree of difficulty when repeating a name by ear as when naming an object seen visually or when verbally described to him. Many types of experiments have been designed in aphasia research, and their findings will be dealt with in ensuing chapters. Finally, a very important element in research on speech disorders is a special kind of "correlation" of symptoms which establishes the syndrome, or set of symptoms typicalfor damage in a given cerebral area. For practical reasons of clinical treatment, which depends on a strict localization of damage, this type of procedure is the most common in aphasia research. The aim here is to determine the symptoms characteristic of lesions in a specific area in terms of the various speech functions. For example, a typical syndrome for lesions in the left anterior parts of the brain (especially Broca's area) is thought to be impaired speech production with relatively intact speech reception. Speech production disorders include difficulties in uttering and writing words, impaired fluency and prosody, "telegraphic" style (use of nouns mainly), and difficulties in discursive speech. Many different syndromes have been described as being connected, apparently, with lesions in circumscribed cerebral areas. But there still remain serious differences of opinion among students of aphasia as to the number of such syndromes and their typical locations. This testifies to the necessity for further verification of findings obtained to date. The foregoing comment reflects the difficulties inherent in the second component of the clinical method for the study of the speech-brain relation; these difficulties are numerous. It should be emphasized that, in view of the complexity of speech activities, both normal and impaired, they may be described in many divergent terms and on different premises, theoretical as well as methodological, that vary from author to author. Depending on what theory of cerebral functional organization an author subscribes to, on whether he is a humanist, psychologist, neurophysiologist or neuroanatomist, he will perceive in the totality of disorders studied only that aspect which concerns him and will pass over the others, although they are no less important for an integrated interpretation of the phenomena. This leads to profound discrepancies in both description and interpretation—a fact which seriously obstructs the descriptive synthesis of the present state of substantive fact in this domain. * Here and henceforth: form devoid of sense.

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Our difficulties are further magnified by the complex nature of the disorders caused by cerebral damage. Since we are most often dealing with nondeliberate cerebral damage resulting from pathological processes, this damage is usually not restricted to functionally homogeneous structures but simultaneously produces various degrees and types of changes. As a result the pertinent disorders have a multifactorial character; some of them are the result of total destruction of a certain area, others of only partial damage or of dysfunction in adjacent cerebral tissue. To this we must add other circumstances further complicating an analysis of the symptoms. An important phenomenon to mention here is what is called diaschisis, i.e., the symptoms of systemic shock including derangement in the normal activity of areas relatively remote from the site of the lesion. These areas are normally connected functionally with the damaged territory and, now deprived of collaboration with an incapacitated "partner", function abnormally. This means that, in addition to symptoms directly connected with a lesion, there are additional symptoms of dysfunction in remote intact areas. The next major factor to complicate the profile of a patient's disorder is the differentiation to be made between pathophysiological and pathopsychological mechanisms. Broadly speaking, the mechanisms making up the clinical picture are the following: conditions originating from permanent damage: effects of inhibited function in some adjacent structures; effects of irritant action on some other structure, and the effects of subjective adjustments to resultant disorders. To illustrate, take the last factor mentioned. Now, it goes without saying that a person who has always communicated normally with his environment up to the moment of accident will try, in one way or another, to adjust to the new situation. Sometimes the trouble is so profound that these attempts are ineffectual, in which case a number of secondary changes are observable in the patient; he may, for example, completely withdraw from any effort to communicate, characteristic of "total aphasia" (cf. Maruszewski, 1966). These are psychogenic changes, connected with the extremely difficult life situation the patient finds himself in; they can occur in practically any aphasic case and, when they do, serve as a very effective mask of the disorders resulting directly from the lesion. On the other hand, in the patient's trials to adjust to his new situation, he may learn various ways—not always normal nor optimal—to circumvent his difficulties, such as compensatory behaviour aimed at improving communication with his surroundings. Since such compensatory behaviour very often diverges from normal speech, it can also be regarded as a direct result of the damage, that is, as a symptom, which it is not. This holds true particularly for speech disorders investigated at later rather than earlier stages after the onset. The next factor acting against accuracy in the description of a disorder is the considerable variability of that disorder. The same activity may be variously performed by the same patient after extremely short intervals of time (Fig. 10). What was impossible a moment earlier is now easily performed; and conversely, an activity performed earlier becomes very difficult a moment later. We do not know all the

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6

8 10 12

32

28 24

20 16 12

patient 6

8

4 2

4 6 8 10 12

Successive

trials

2 4 6 8 10 12 14 Successive

trials

2 4 6 8 10 12 Successive

trials

Fig. 10. Variability of reaction in 6 aphasic patients in a naming task. On 12 successive trials the patient was asked to name the same set of 50 pictured objects, order unchanged. The vertical axis shows the number of errors, and the horizontal axis the successive trials. All patients, regardless of degree of their disorder, display variability in the numbers of errors (Gamska, 1970).

factors underlying this variability, but they undoubtedly include such circumstances as the patient's emotional attitude to a task or situation, his general physical and psychological state, and so on. It has long been known, for example, that in some forms of aphasia the patient cannot utter a word at the doctor's request but can produce complex expressions, as in swearing, when emotionally aroused. Observations have also shown wide differences between a patient's ability to perform during medical or psychological examinations and his ability to communicate in real life situations in hospital or home. Some patients manage better in normal communicative contexts while others display greater possibilities in contacts with doctors or psychologists. Such differences create great difficulties in arriving at an evaluation of the factual state of the disorder in any one patient. A final, and cardinal, consideration in diagnosing a disorder is the selection of methods and techniques to be applied. Ultimately, most of the factors mentioned above can be eliminated, provided we select the proper tests and comparative analyses. This involves, however, an exceedingly time-consuming procedure and developed skills in the use of methods for studying speech. Unfortunately, it frequently happens that the methods employed by different investigators only minimally satisfy the requirements of methodological precision.

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The circumstances we have mentioned combine to produce wide discrepancies in the description, interpretation and classification of speech disturbances connected with cerebral damage (see Chapter II); this fact seriously undermines the use value of the accumulated material for drawing conclusions about the speech-brain relation. Two more weighty considerations, which often pass unnoticed, place additional hindrances in our path. The first was laconically formulated by the eminent British neurologist, J. H. Jackson, referred to earlier; he stated that localization of damage causing speech disorder, and localization of speech itself, are two separate and distinct things (Jackson, 1958). This means that to ascertain the fact of destruction of a circumscribed area does not legitimize the inference that this site is the "centre" of some activity; the same activity may be impaired when different cerebral areas are damaged. For instance, it is known that writing is disturbed when left hemisphere destruction occurs in any one of the frontal, parietal, temporal or occipital lobes. In each case the same writing disorder is found, although, on analyzing qualitatively the types of disorders, we find differences that depend on the site of the lesion. The current state of knowledge on the cerebral localization of psychological functions forces us to reject a conception of the brain as an ensemble of "centres" for particular activities and favours the conception of dynamic localization. According to this latter approach, any normal activity results from the collaborative interaction of many differently located cerebral structures, each subserving that activity differently (cf. Luria, 1962; see also Chapter II). Thus, damage always deranges the activity of an entire system, and not any single function. Therefore, if we wish to know what was "localized" in the destroyed area and how it subserved a given activity, we must look for something more than simply the fact of damage impairing the performance of that activity. We must uncover the pathophysiological mechanisms underlying disorders due to the damage in that area, and only then will we be in a position to begin to appreciate the functional significance of that area (cf. Luria, 1962, for a specific factor analysis of disorders in cerebral lesion cases). We turn now to another grave risk involved when insufficiently critical judgements are made about localization of cerebral speech mechanisms on the basis of clinical findings. This risk lies in the often tacit acceptance of an absolutist principle (no exception to a given rule). When we consider the functions of any organism and their connection with particular organs, we usually assume that, for all members of that species, a given function is always performed the same way by the same organ. This belief is well-founded for many aspects of anatomy and physiology, but we often go beyond that substantiation to imply that, if a given state of affairs is found for a normal member of a species, then this allows the inference that the same state of affairs holds—by and large—for all others of that species. Now, there are grounds to suppose that, in dealing with the higher functions and their connections with cerebral structures, we need to be much more cautious about applying this rule; it may very likely no longer hold for certain problems under study. Specifically, relations between the higher functions and the brain may, especially in the

THE CLINICAL METHOD

59

human species, undergo different formative processes in the individual; we may discover a certain dispersion, or an interindividual variability, which is far greater for higher than for simpler functions. Evidence from a number of sources points to such an eventuality. Primarily, certain anatomical data show that human brains differ very considerably not only in overall2 and relative hemisphere size but also in number of cerebral fissures and convolutions, and even in certain microstructural features. For example, it has been established that particular cortical fields differ among individuals in surface area, magnitude and density of "neuronal cells as well as position in relation to the main fissures and convolutions (Fig. 11). We are not yet in a position to evaluate

20/38

20b

Fig. 11. Individual differences in the cortical cytoarchitectonic structure of the external hemisphere surface in man. A schematic presentation of findings for two brains (Preobrazhenskaya, 1960). 2

According to Roginsky and Levin (1955), average human brain weight varies from 1100 to 1700 grams. Overstepping these bounds should not, however, be viewed as a pathological phenomenon, since cases are known of eminent persons whose brain weights were outside those ranges. For example, Turgenev's brain weighed 2012 grams, Byron's 1807 grams and Anatole France's 1017 grams. Cobb (1965) cites Clark's data which place the normal range of human cerebral mass at 850-2100 grams.

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HI. RESEARCH M E T H O D S F O R T H E STUDY O F THE SPEECH-BRAIN RELATION

unequivocally the functional significance of these differences, but the fact deserves attention that this interindividual variability is particularly in evidence in the phylogenetically younger territories (Preobrazhenskaya, 1960), and therefore is connected with the higher functions. Since the absolutist principle does not apply to the structure of these regions, it seems highly probable that it does not apply to their functions either. We also come across a broad diversity of language systems employed by Homo sapiens. There are more than 2500 natural languages, which are known to differ in many respects. It is quite feasible to suppose that such interlingual differences can produce—within limits—variations in the formation of the speech mechanisms in speakers of different languages. For example, European speakers may have differently localized speech mechanisms than Chinese speakers. There is instructive information on this subject in aphasic descriptions of polyglots, or persons possessing more than one language. One well-known description concerns a patient who had in childhood mastered both Chinese and English, spoken and written. After the left parieto-occipital region had been destroyed by a malignant process, his reading was severely disordered but to a different extent for the two languages. The patient had relatively little trouble reading in English but found it practically impossible to read in Chinese. This difference emerges from the fact that Chinese writing is wholly based on ideographic signs that refer to concepts and are not linked to the sound elements of speech, as in the case of English. Since the destroyed area in this case is related to analytic and synthetic processes dealing with visual data, identification of Chinese written signs was totally lost, while reading in English was to a certain extent retained; the relation of sound to letter enabled the patient to read English texts fairly correctly. Another doubtlessly relevant fact was that Chinese graphic signs are much more numerous and complex than English ones. A similar divergency has been observed in Japanese aphasics with left temporal lobe lesions. Written Japanese employs both graphic (corresponding to phonetic units) and ideographic signs derived from Chinese. Damage to the temporal lobe in Japanese patients causes loss of reading and writing the "phonetic" signs but leaves intact the ability to use ideographic signs (Charlton, 1964; cf. also Wald, 1961). In this case, temporal lobe damage, which impairs auditory analysis and synthesis, precludes reading "phonetic" signs while the intact parieto-occipital region ensures normal reading of ideographic signs. So it seems that such functions as reading and writing are in fact localized differently in the brain and depend on the normal functioning of different cerebral structures; which structure shares in government of reading and writing depends on the properties of the given language. Other data as well support the hypothesis that the absolutist principle does not necessarily hold for the speech-brain relation. These include such facts as interindividual variability in body lateralization and hemisphere dominance for language (see Chapter IV), the diversity of teaching methods as, for example, for reading and writing, and the high frequency of fragmentary developmental deficits in speech

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61

function connected with decreased functional efficiency of the different sensory modalities (Spionek, 1965) which are presumably compensated for by some speech regulation deviating from the normal. The inference that can be drawn from the foregoing data is that the speech-brain relation is probably characterized by interindividual variability to a far greater extent than for the elementary functions of the organism. We can therefore expect that this relation has a different formative history in individuals, at least to some extent. If we accept the above line of reasoning, the interpretations as to the speechbrain relation must be based on a sufficiently extensive material to allow for some estimate of the range of variability. Conclusions must also be of a statistical kind that show the typical state of affairs while not excluding possible exceptions. It often happens that some interesting fact from a particular standpoint is derived from a relatively small sample (see Chapter IV for information derived from dissection of the corpus callosum in the human brain). In weighing the consequence of such facts we are always faced with the vexed question whether these are exceptional or typical cases. The following illustration is a case in point. There is a very interesting syndrome described in the neurological literature called pure alexia without agraphia. The patient is unable to read but he can write. His reading loss is so profound that he cannot even read what he has written a moment earlier. The first postmortem verification of such a case was described in 1892 by the French neurologist Dejerine (cf. Geschwind 1962, 1965). Today about 20 such descriptions can be found in the literature, including anatomopathological documentation (Geschwind, personal communication). At postmortem, analysis of the 20 cases of alexia without agraphia revealed lesions that always involved the left occipital pole and the splenium (posterior part of the corpus callosum). The syndrome was interpreted as follows: If only the left occipital pole is destroyed, the patient receives visual stimuli exclusively through the right occipital lobe. As we know, the centres important for speech (i.e., for the majority, see Chapter IV) lie in the left hemisphere; therefore a patient with a damaged left occipital pole can read only if visual information is transmitted from the right to the left hemisphere. Anatomical data show that this transfer takes place along pathways lying in the posterior part of the corpus callosum. Since this part of the corpus callosum is destroyed in patients with alexia without agraphia, the visual stimulation in the right occipital pole resulting from perception of the text cannot reach the speech areas of the left hemisphere, leaving the patient powerless to read. On the other hand, writing is based on collaboration with other areas that remain intact in this case and function normally. Thus, reading involves collaboration between the occipital lobes and the speech centres of the left hemisphere, the decisive role being played by the cortico-cortical pathway running through the posterior part of the corpus callosum.

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i n . R E S E A R C H M E T H O D S FOR T H E STUDY O F T H E SPEECH-BRAIN R E L A T I O N

The interested reader will find more detail in the references cited. We shall limit our discussion to a logical analysis of the argument leading to the conclusion about the localization of structures involved in reading. This argument can be reduced to the following elements : 1. There is a given specific syndrome: alexia without agraphia (AWA). 2. All postmortem examinations of AWA cases have established the same type of lesion : destruction of the left occipital lobe and the splenium (LOS). 3. Therefore destruction of these structures leads to the syndrome in question, 4. The three foregoing statements imply specific conclusions about the localization and interaction of cerebral structures involved in reading. In the above argument there is the implicit assumption that the coincidence of AWA and LOS in 20 cases provides sufficient grounds to make general statements about the functioning of the cerebral mechanism for reading in all human beings. Let us take a closer look at this assumption by applying a purely formal analysis. Let us grant that in the historical period in question there were 10,000 cases3 of brain damage. Of the 20 which manifested the syndrome AWA, the damage LOS was found. The question now arises as to the nature of the disorder and the locus of damage in the other 9980 cases. In order to satisfy statements 3 and 4 above, we should have to assume that in all the other cases where AWA did not occur, neither did LOS occur. That is to say, the following situation should hold :

LOS no LOS

AWA

no AWA

20+x4

0

0

9980—x

Our data, however, deal only with the left upper box. Since not all AWA cases were verified by postmortem examination, we cannot even be sure about the contents of the right upper box. As for brain damage cases where AWA did not occur, we have no postmortem data for the overwhelming majority and therefore we cannot know if the two right boxes even approximate the true state of affairs. Let us consider two other feasible distributions of the results, theoretically and practically possible if all the brains of the 10,000 patients had undergone postmortem examination: I

LOS no LOS 3

II AWA

no AWA

20

20

0

9960

AWA LOS no LOS

no AWA

20

480

0

9500

In fact, there existed many more, but this figure simplifies our argument. "x" represents the number of cases nonverified by postmortem examination in which AWA and LOS coincided. 4

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63

According to Situation I, coincidence of AWA and LOS in 20 cases, and lack of coincidence in 20 more cases, would compel us to conclude that only for half the cases can the reading mechanism be envisaged in a way that conforms to this distribution. On the other hand, according to Situation II, coincidence of AWA and LOS is apparently the exception rather than the rule, and therefore the typical reading mechanisms are formed otherwise than a sporadic coincidence suggests. The above is a purely formal argument but it demonstrates unequivocally the difficulty we are confronted with in drawing conclusions on the basis of co-occurrence of certain symptoms and of certain cerebral structure damage. These difficulties could be resolvedif a massive programme of clinical research were to be supplemented by a massive programme of anatomo-pathological examination of damaged brains; only then would we be in a position to approach a strict correlation. Since such research has not yet been undertaken, we remain with interpretations that are saddled with a large margin of error, the extent of which we cannot even guess. With this we conclude a broad characterization of the clinical method, which at the present time yields the most extensive data for interpreting the speech-brain relation. When we analyze the particular features of this method, we find that it entails intractable problems and risks: to discount or belittle this fact leads only to poorly substantiated or erroneous conclusions. There is little room for doubt that these difficulties are the source of the divergencies in the present state of substantive knowledge and theory on the cerebral speech mechanisms. However, this is not tantamount to a denial of the value of the material derived by this method; on the contrary, a large body of information compiled in this way has contributed to formulations of certain well-founded hypotheses on the problem at hand. But an awareness of the risks involved is indispensable for further verification of these hypotheses.

§ 4. OTHER METHODS FOR STUDY OF THE SPEECH-BRAIN RELATION

A review of research methods for study of the relation of speech and brain, and associated problems, should not omit mention of certain other sources of information utilized for this purpose. These pertain mainly to information supplied by means of cerebral stimulation during surgery. The method of electrical stimulation of the brain surface was initiated by Fritsch and Hitzig in 1870, in animal studies. They discovered the functional significance of the precentral gyrus as the motor region for the opposite side of the body. This method has since been employed by many outstanding neurophysiologists. First to apply this method to human beings was the American neurosurgeon Harvey Cushing, in 1909. Taking advantage of the fact that cerebral neurosurgery is generally performed under local anesthesia, Cushing demonstrated that the conscious patient ex-

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III. RESEARCH METHODS FOR THE STUDY OF THE SPEECH-BRAIN RELATION

periences various sensations in the contralateral extremities when the postcentral gyrus is electrically stimulated. Since then, other neurosurgeons have collected data to show that electrical stimulation in diverse cortical regions elicits subjective experiences in the corresponding sensory modalities. When the visual cortex is stimulated, the patient reports that he is seeing something; when the auditory cortex is stimulated, he reports hearing something, and so on (cf. Penfield and Roberts, 1959). Penfield has fairly recently established that electrical stimulation of the cortical surface during surgery can elicit not only motor and sensory responses of various sorts, but also definite psychical phenomena, such as the "flash-back" recall of past events with the illusion of re-living them. Penfield went further to apply electrical stimulation to the cortex of the operated patient for the purpose of mapping speech-related fields. The routine procedure is as follows: While the patient lies conscious on the operating table, an observer sitting beside him engaging him in conversation. The patient is asked to perform simple verbal tests such as naming objects on pictures, repeating words or figures, reciting verses, counting, reading, etc. Meanwhile the surgeon places an electrode at a given spot on the cortex and applies electrical stimulation. The observer's task is to register every speech change evoked by electrical stimulation 5 . Broadly speaking, two groups of verbal phenomena are evoked by stimulation of the human cortex in such conditions. One group is "positive", i.e. during stimulation vocalization of speech sounds occurs either in continuous or broken fashion; the other group is "negative", that is, speech is arrested or disrupted in some way. By means of this method Penfield and Roberts (1959) assembled evidence from a large number of patients which led them to certain interpretations about both localization of the speech fields and the functional role of particular sub-fields. These conclusions will be treated more fully in Chapter IV. Despite the fact that the results obtainable by this method are of great cognitive value, it must be noted that they suffer from certain flaws; information thus obtained cannot be regarded as a totally solid base for explaining the speech-brain relation. In the first place, as already mentioned, the results are obtainable on the occasions offered by surgery in connection with specific pathological brain conditions (Penfield and Roberts' cases were largely surgical treatment of epilepsy in persons with previous brain damage), therefore there is no certainty that the same results would be forthcoming if completely healthy brains were stimulated. On the other hand, as Lenneberg has aptly pointed out (1967), the action of the electrical current upon a given cortical field cannot be regarded as physiologically equivalent to normal 5 The procedure described is painless and presents no risk whatsoever to the patient's well-being: in fact, it contributes to successful surgery by enabling the surgeon to delimit sharply the functional role of the regions where excision is to be performed, thus minimizing the losses involved. Therefore the results of this form of investigation can also be evaluated from the patient's point of view.

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65

nervous activity in that field. This kind of stimulation has very different properties from those of nervous impulses received by a given area in normal physiological conditions. It is more than likely that electrical stimulation deforms the activity of the stimulated area rather than activating it in the normal way. Consequently, extreme care should be exercised in handling the results of the stimulation method. Other methods which lend themselves to the study of our problem include the already mentioned methods of comparative anatomy. They involve a comparison of the morphological features of brains in animal species and in man. An example of how such findings have been applied to hypothesizing on the cerebral mechanisms of speech can be found in Geschwind's (1964) attempt to explain the origin of language by the fact that the human brain possesses an exceptionally well developed —as compared to animal brain—gyrus angularis, lying in the inferior posterior parietal part. Geschwind believes that this structure is responsible for intersensory associations which bypass the limbic system and make possible a cross-modality transfer. In Geschwind's view, the naming ability in humans, lacking in animals, is determined by this factor (see Chapter VII). A number of very interesting hypotheses have been advanced on the grounds of this type of data. Yet, here again, difficulties obstruct our way. As already stated, substantive knowledge about the structure of the animal brain (of greatest interest, the anthropoidal) is still too poor to admit of well-grounded hypotheses. Also, even if we could state with certainty that a given structure is characteristic and species-specific to the human brain, this is not enough to imply that this feature is responsible for the emergence of the human capacity to use language. After all, it is well known that the same functions can be carried out by various structures and organs working in collaboration; otherwise said, the fact that a species is capable of a given behaviour is an outcome not only of its structural properties, or how that species is constructed as a whole, but also the ways his organs interact as elements of this structure. In addition, we face the fact that there is no way of comparing the human brain with that of our nearest predecessor; we have only access to data on living species, which are not the ancestors of Homo sapiens but rather his contemporary "kin", each of whom shares common forebears but possesses its own evolutionary history. In this event, any interpretation grounded on structural differences runs the risk of cardinal error. #

*

*

We have passed in review the most important methods in neuropsychology by which evidence has been obtained on how the human brain determined man's ability to use language in communicating with his fellows. We have presented these methods in such a way as to expose their flaws and the risks of inferential error attendant upon their use. Far from wishing to discourage the reader from continuing into the subject, it is rather our desire to ensure a full awareness of the fact

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that, due to the specificities of the methods in use, the present knowledge of our subject does not repose upon the firm foundation of unambiguous fact: many hypotheses forwarded are either totally unfounded or awaiting verification. This, however, does not shake the author's conviction that the question of cerebral features that allow men to speak and understand each other is one of the most striking problems of the human sciences. It is worth succumbing to the temptation to learn more about the attempts, however imperfect, to answer this question in accord with the present state of knowledge.

CHAPTER IV

SPEECH AND THE ANATOMICAL AND PHYSIOLOGICAL PROPERTIES OF THE HUMAN BRAIN Among the most striking anatomical differences between man and any other species, including the nonhuman primates, are differences in brain size and structure. Some of the distinguishing features of human brain structure can be listed as follows : the greater proportion of hemisphere mass relative to total brain mass ; the deeper and more extensive fissuration, yielding increased cortical surface; and the more highly developed histological differentiation of the cortex, particularly in the larger nonprojective fields (not directly connected with the peripheral organs). The size of the human brain also suggests that this organ in man is much more developed than in other species, although no conclusive evidence to this effect has been forthcoming by hitherto available indices. Brain weight in man and other primates, both absolute and relative to whole body weight, may be compared in the data presented in Table I. TABLE I Absolute and relative brain weight in man and ape (after Roginsky and Levin, 1955). Index of brain size Species Man Chimpanzee Gorilla Orangutan Gibbon

Absolute brain weight (in grams)

Relative weight (brain: body)

1360 354 420 400 130

1:45 1:61

1:220 1:183 1:73

As Table I informs us, the human brain takes precedence over the other primate brains in terms of magnitude. But this fact does not legitimize any generalization as to man's place in the animal world, since certain other species show even more advantageous indices in this respect. In terms of absolute brain weight, bigger animals have bigger brains, as may be expected; for example, the whale has a brain

68

IV. SPEECH AND THE ANATOMICAL AND PHYSIOLOGICAL PROPERTIES OF HUMAN BRAIN

weighing 7 kilograms, the elephant's brain weighs 5 kg and the dolphin's brain about 1.7 kg. Nor can this matter be resolved by establishing a superior ratio of brain weight to body weight, since some species can also boast a better index than can the human species [e.g., the marmoset (monkey) Leontocebus geoffroy 1:19, the Japanese mouse 1:22, the house mouse 1:40 (cf. Cobb, 1965)]. Thus purely quantitative indices do not provide sufficient grounds to arrive at any conclusions about the specific properties of man 1 . Hence language capacity cannot be directly linked with human brain size. Another interesting argument against treating brain mass, either absolute or relative, as a decisive factor for language in man, has been advanced by Lenneberg (1967), who pointed out that very severe reduction of brain mass in some pathological conditions does not prevent the individual from acquiring the capacity to use language. The most typical illustrations of this are early childhood cases of radical brain surgery (hemispherectomy), where up to one-third of the brain mass is removed, yet the child still can acquire language (see below, § 1 C). Consider as well the clinical condition first described by Virchow (after Lenneberg, 1967) called "birdheaded dwarfism" (nanocephalic dwarfism). Individuals with this type of developmental deficiency attain a maximum height of one meter and their brain weight is comparable to that of a three-year-old chimpanzee; yet these persons can acquire language. Even such a drastic reduction of brain mass does not invalidate man's capacity for language. It would seem to follow that the decisive factor for the language capacity lies in the morphological features and functional organization of the human brain. We shall commence our review with a discussion of a phenomenon which appears to be, by common agreement, exclusively specific to man and also directly connected with speech mechanisms. We refer to the functional differentiation of the cerebral hemispheres and the dominance of one of them in respect to speech.

§1. CEREBRAL HEMISPHERIC DOMINANCE FOR SPEECH

We have already had occasion (in Chapter II) to refer to Marc Dax's observation of 1836 in which he noted, probably for the first time in history, that speech disorders are usually connected with damage to the left cerebral hemisphere. This observation has since been confirmed by many other observers, although, as we shall soon see, a fair number of exceptions to this rule have come into evidence. A highly important inference to be drawn from this state of affairs is the following: The two 1 Roginsky and Levin (1955) have suggested a special index devised by them called "cerebralization" by which the effect of body mass on brain size is excluded. According to this index man has a decided advantage over other animal species.

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69

hemispheres do not share equally in the cerebral regulation of language; one of them has a determinative role, whereas the other does not apparently share in the process, as witnessed by the fact that, when the latter is damaged, speech is on the whole left intact. In other words, man displays a functional differentiation in the cerebral hemispheres in respect to speech regulation; only one hemisphere is, in principle, needed for normal speech activity. This fact is referred to as the phenomenon of dominance. Later studies have shown that this kind of functional differentiation between the cerebral hemispheres concerns not only speech, but also other higher functions in man (such as mathematical operations, spatial orientation, memory, etc); for some of these functions the dominant hemisphere is the same as for speech, while for others the contralateral hemisphere is the dominant one. We are thus dealing with a functional asymmetry of the brain. The most obvious example of asymmetry in body function is what is known as handedness. The vast majority of people show a decided lateral dominance in respect to the hand; generally they are righthanded 2 . Morphological and functional asymmetry of the body is not a specifically human phenomenon. Subirana (1964) reviewed the empirical data on asymmetrical relations of body halves in animals and showed that this phenomenon exists in a large number of species ranging from the simplest to those closest of kin to man. For instance, in some varieties of snail, interindividual differences have been found in the direction of the shell spiral; snails can be divided accordingly into "sinistrals" and "dextrals". It has also been reported that 80% of rats prefer one paw to the other in extracting food hidden by an experimenter. Similar phenomena have been described in monkeys. A fuller analysis adduces the evidence that functional asymmetry has reached an incomparably higher degree in man than in the lower species. Furthermore—a salient point—asymmetry is typical of the human species. We do not find this phenomenon in animals; the likelihood of encountering right or left preference is about equal in the lower species. Right preference in man is therefore a species-specific feature 3 . The picture changes, however, when we consider the question of functional differentiation of cerebral hemispheres. Empirical data from animal research seem fully compatible with the view that such differentiation exists only in man; that is to say, functional differentiation constitutes a specifically human feature. Discovery of this fact has naturally aroused deep interest. Earlier research had 2

The percentage of lefthanded persons in the normal population has been estimated variously (cf. Brain, 1965; Spionek, 1965); most authors tend to accept 5 to 10 percent as a likely approximation. 3 Various attempts have been made to explain this fact. One theory, now regarded as a curiosity, claimed that primitive man used his right hand to fight with because he used the left to hold the shield that protected the vital organ of the heart. Subirana (1964) comments ironically that in those days injury to the liver, which is located in the right side, would have been equally fatal. Another "theory" linked righthandedness with manual demonstration of the sun's movements.

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IV- SPEECH A N D T H E ANATOMICAL A N D PHYSIOLOGICAL PROPERTIES O F H U M A N BRAIN

worked on the hypothesis, based on poorly analyzed data, that there was a strict relation between lateralization preference for the upper extremities and hemisphere dominance for speech. It had been noted that righthanded aphasic patients had left hemisphere lesions while lefthanded patients had lesions in the right hemisphere. It seemed evident that the dominant hemisphere for speech was the left one for righthanded persons and vice versa for lefthanded persons. Consequently rightand lefthandedness was treated as a strict and unequivocal indicator of cerebral hemisphere dominance for speech. More recently the validity of this rule has been questioned on the basis of a number of findings. First, it has been noted that lateralization is in itself a complex phenomenon, since it is not restricted to various degrees of preference in respect to the upper limbs but concerns other paired organs like legs, eyes, etc.; often partial lateralization or crossed lateralization is found, as When righthandedness co-occurs with leftleggedness or lefteyedness (cf. Luria, 1947; Benton et al., 1962; Spionek, 1961, 1965; Satz et al., 1967; Subirana, 1961). Thus the question arose as to whether laterality for the upper extremities could be treated as the sole and sufficient criterion of hemisphere dominance for speech, or whether to establish dominance it would not be necessary to take into account all available indices of lateral preference. In this context a fact of salient importance was noticed, viz., that, when the clinical picture was closely analyzed, no clearcut correlation could be found between the handedness of the patient and the damaged half of the brain that led to speech disorder. It turned out that left hemisphere lesions in lefthanded patients and right hemisphere lesions in righthanded patients could all produce speech disorder. Various authors began to present arrays of facts on larger groups of aphasic cases to show that no categorical dependence could be found between handedness and dominance as formulated in earlier studies. This matter became the subject of lively debate in which contradictory views were expressed. Certain voices tended to disregard handedness as a significant criterion of dominance, concluding that, handedness apart, the dominant hemisphere for speech is always the left one (cf. Wepman, 1951; Penfield and Roberts, 1959). Others took a more moderate position, focussing on facts which suggested the existence of a sort of continuum for all laterality phenomena, hence hemisphere dominance for speech as well. This latter position now seems to be fully vindicated in the light of the latest published findings. We shall turn now to a discussion of the most recent developments on this question.

A. LATERALIZATION OF BODY FUNCTION

We have just referred to the fact that the concept of handedness, earlier employed by investigators of dominance, has been replaced by the concept of laterality of body function. The reason for this is that functional differentiation is found not

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71

only for the upper limbs but also for the lower limbs, the eyes and other paired organs. To define the degree of lateralization, the concept of "lateralization profile" has been introduced; this is derived on the basis of a battery of tests on function of hands, arms, legs, eyes, etc. (Spionek, 1961, 1965). The findings obtained from these methods suggest that between the extreme groups with total right or left laterality of body function, there is a fair-sized proportion of individuals with partial laterality, either right or left, as well as a group which lacks clearcut laterality (i.e., a bilateral group). It has thus become apparent that in respect to lateralization of body functions, human beings form a kind of continuum of degree, embracing full laterality—dextral or sinistral—as well as partial laterality and bilaterality. Handedness, or lateral preference in the function of the upper limbs, is only one component of overall body function laterality and is not always strictly correlated with lateral preference for other paired body organs. Interpretations have been advanced as to the factors determining laterality and its dependence upon environmental and inherited conditions. Apparently both social and innate factors play essential roles. In the light of our present discussion there is one noteworthy fact, viz., the tendency for lefthandedness to occur in families (Luria, 1947). This may perhaps serve to clarify certain phenomena relevant to dominance which we shall shortly deal with.

B. EFFECTS OF DAMAGE TO

LEFT AND RIGHT HEMISPHERES IN ADULTS

As pointed out above, in the majority of cases lesions in circumscribed areas of the left hemisphere result in speech disorder, whereas lesions in the same contralateral areas as a rule do not lead to such disturbances. But there are some exceptions to this rule. 1. Occasionally we come across cases of aphasia caused by lesions in the right hemisphere. Luria (1947) mentions 12 such cases where gunshot wounds in the right hemisphere led to aphasia. Roberts (1955) found 117 aphasic cases in the literature where only the right hemisphere was involved. Russell and Espire (1961) report their own observations on 7 aphasics with wounds in the right hemisphere. Similar information is forthcoming from other studies. All the above reports, however, agree on one point, viz., that the number of aphasic cases with right hemisphere lesions is small. In other words, although right hemisphere damage may on occasion lead to aphasia, it is much more rarely encountered than in cases of left hemisphere lesions. Another comment made by all the above-mentioned authors is that aphasia due to right hemisphere damage is usually less severe than that due to left hemisphere damage and, in the majority of cases, tends to clear rapidly.

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IV. SPEECH A N D THE ANATOMICAL A N D PHYSIOLOGICAL PROPERTIES O F H U M A N B R A I N

Aphasia linked with right hemisphere damage has also been studied in terms of laterality of body function. While the authors do not all agree on the proportions found, they make the same fundamental observation that either sinistral or dextral laterality is involved in such cases. For instance, in Roberts' (1955) study of 117 aphasia cases with right hemisphere lesions, 40 were righthanded, 37 lefthanded, 22 partially lefthanded, while for the remaining 18 unilaterality was not established. Luria (1947) found no latent lefthandedness in 4 of his 12 cases of right hemisphere damage, though sinistrality in the patients' families existed. Similar data have been reported by Zangwill (1960). 2. Other exceptions to the rule linking aphasia with left hemisphere damage are those cases where left hemisphere lesions have either not affected speech—even when the focus and extent of the lesion would have rendered this most likely—or else have produced a transient speech disorder clearing more rapidly than usual when such areas are involved. This point is illustrated in an array of data published by Luria (1947) on speech disorders in 160 cases of gunshot wounds in the left hemisphere area important for speech, classified according to different periods after onset, with data included on handedness (Table II). We find that, among the 160 cases with lesions in speech areas located in the left hemisphere, even in the initial period after the trauma 21 cases (13.1% of the total) did not incur aphasia. In the later periods, aphasia was absent in 63 cases (39.3%). Thus for an additional 42 cases aphasia receded. Note that for the 21 cases where aphasia did not occur, despite lesions in left hemisphere speech areas, there was not a single clearcut case of righthandedness; and, of the 63 cases without aphasia in the later period, only 2 cases of total righthandedness were found, while the other 61 cases displayed either latent lefthandedness or familial sinistrality, or else were completely lefthanded or ambidextrous. It is also interesting, that for all 73 cases with symptoms of latent lefthandedness or with familial sinistrality, aphasia occurred in 56 cases at the initial period (44 severe and 12 light cases), but later severe aphasia persisted in only 5 cases. Similar evidence is forthcoming from other authors, but less well analyzed. Zangwill (1960, 1968) in a summary of extensive literature concluded that, for righthanded persons, left hemisphere damage leads to aphasia in approximately 60%, while right hemisphere damage entails aphasia in only about 1.5%. However, in lefthanded persons, left hemisphere lesions evoke aphasia in approximately 54% of the cases and right hemisphere lesions in only about 20%. In other words, while the dominant hemisphere for speech is the left one for most persons, including the lefthanded, we still find among lefthanded persons, much more so than among righthanded, cases with right hemisphere participation and even dominance in speech regulation. At the same time we find a group embracing both rightand lefthandedness in which both hemispheres are presumably engaged in speech regulation. Moreover, we find interindividual differences in the degree to which

12 (63%) 4 (21%) 8

S 44 (36.6%)

8

Total in percentages

15 (12.6%)

46 (73%) 15 (23.8%) 22 (52.6%) 6 (14.1%) 5 (9%) 2 (3.7%)

17 (80.9%) 4 "(19.1%)

o\

B. Righthanded with latent lefthandedness or familial sinistrality (73) C. Lefthanded or ambidextrous (23)

2 (3.2%)

14 (33.3%)

48 (87.3%)

no aphasia

mild aphasia

0

severe aphasia

8

3 (16%)

no aphasia M

61 (50.8%)

mild aphasia

Later period

TT

A. Totally righthanded (64)

severe aphasia

Initial period (3-4 weeks)

m \o

Total number of patients

Type of handedness

Aphasia degree

1. CEREBRAL HEMISPHERIC DOMINANCE FOR SPEECH

8vH

8

8^

73

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IV. SPEECH A N D T H E ANATOMICAL A N D PHYSIOLOGICAL PROPERTIES O F H U M A N BRAIN

one hemisphere dominates for speech: presumably dominance is stronger in individuals with complete right laterality than in those with partial or left laterality. Brain (1965) also arrived at similar conclusions in his summary of the relevant literature.

C. EFFECTS OF BRAIN DAMAGE IN CHILDREN. ONTOGENETIC FORMATION OF DOMINANCE

So far we have considered dominance in adults. But, as wejcnow, neither laterality of body function nor hemisphere dominance for speech emerges readymade at birth; rather, it takes shape in the course of individual development. Laterality is the better studied aspect, for obvious reasons, but here as Ayell a fair amount of difference can be found in opinions as to the age when lateral preference appears (cf. Spionek, 1961, 1965). Ontogenetic formation of hemisphere dominance for speech is much less well known; the bulk of our information in this field comes from brain damage cases which are relatively rare in comparison to adult cases. Generally speaking, it is thought that under age five—therefore after onset of speech—brain damage to one hemisphere will not provoke aphasia at all, while between ages five and ten brain damage most otten entails transient and rapidly clearing aphasia-type disorders (Mecham et al., 1960; Alajouanine and Lhermitte, 1965). The above data suggest that at birth both cerebral hemispheres are—in terms of speech—functionally equipotential and only later does hemisphere localization of speech mechanisms emerge, leading to the phenomenon of dominance. Basser (1962) has made an interesting analysis of data on two groups of children. One was a group of 72 with early hemiplegia who had incurred brain damage in the first year of life, 34 in the left and 38 in the right hemisphere; in only 5 cases was speech development permanently arrested and of the remaining 67 only about half were delayed (Table III). TABLE III Speech development in children with early cerebral lesions (during the first year of life) (After Basser, 1962). Speech development

Left hemisphere lesion Right hemisphere lesion

normal

delayed

totally arrested

18 19

15 15

1 4

The second group studied by Basser consisted of 30 children who incurred cerebral lesions between the ages of two and ten. The results, as shown in Table IV, look somewhat different from those in Table III.

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75

TABLE IV Speech disorder in children suffering brain damage between 2 and 10 years of age (After Basser, 1962). Speech following lesion normal

disturbed

2 8

13 7

Left hemisphere lesion Right hemisphere lesion

A comparison of the data in the two foregoing tables suggests clearly that after onset of speech the first signs of hemisphere dominance begin to manifest themselves, while prior to onset of speech, lesions in neither hemisphere alter speech development, though they may slow it down. Thus we have evidence pointing to the nonexistence of dominance in earliest infancy. Lenneberg (1967) has summarized the data on the effect of hemispherectomy4 upon speech. His findings appear in Table V. It would appear from Table V that, if a cerebral hemisphere lesion is incurred before age ten, speech functions are completely taken over by the other hemisphere, be it right or left. For in none of these cases did the hemisphere removal lead to aphasia except for those with aphasia prior to the operation. When the dominant hemisphere is removed in adults, however, such a takeover of function is not likely TABLE V Effect of removal of an entire hemisphere on speech functions and age at which the original damage was incurred (After Lenneberg, 1967).Speech not affected or improved postoperatively

Age when original lesion was acquired

Hemisphere removed

Before ten

Left Right

49 38

Adult

Left

None

Right

25

Permanent aphasia 3 5 (all 8 cases had aphasia before operation) 6 (1 had aphasia before operation) None

* Hemispherectomy is the surgical removal of a cerebral hemisphere, usually in treatment of uncontrollable epileptic seizure (failing other therapeutic means), in cases of patients with epileptogenic foci caused by prior brain lesions. At times this operation is. performed in order to excise large infiltrating tumours.

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IV. SPEECH A N D T H E ANATOMICAL A N D PHYSIOLOGICAL PROPERTIES O F H U M A N BRAIN

to occur, and for this reason left hemispherectomy is very rarely practised on adult persons; as Table V shows, the number of operated cases after puberty was low. These data lead to the conclusion that dominance of one hemisphere for language is an ontogenetic process occurring probably between the ages of 10 and 13. This constitutes one of the premises for the hypothesis about a critical age for speech acquisition (cf. Lenneberg, 1967). It has also been speculated that not only early damage in the left hemisphere, but also early injury or loss of the right arm, can alter dominance. Subirana (1964) describes a case where the right arm was lost in early infancy and in adulthood a lesion was sustained in the right hemisphere. Speech disorder ensued despite absence of data suggesting that latent lefthandedness existed prior to loss of the limb. To summarize the above findings, it may be stated that during infancy both cerebral hemispheres are of equal importance for speech development and only subsequently, through the influence of multiple factors, is dominance of one hemisphere acquired. D. EXPERIMENTAL METHODS FOR ASCERTAINING DOMINANCE AND RESULTS OBTAINED BY THESE METHODS

So far our discussion on the subject of dominance has been supported by findings derived from the observation of brain damage cases. In recent years methods have been devised to establish dominance by other means, some of which are applicable to normal persons. We shall now discuss what findings have been obtained by these methods. A very important method, practically as well as theoretically, is the amytal test. This technique has been developed by neurosurgeons in order to ascertain whether the dominant or nondominant hemisphere is being involved in surgery. This is important information in view of the degree of caution necessary in removing brain tissue that could lead to profound disability. This test was first proposed by the Japanese investigator Wada (after Branch et al., 1964; Milner et al., 1964), and later verified and employed regularly at the Montreal Neurological Institute as well as at other centres. The drug sodium amytal is injected into the circulatory system of a single hemisphere (by intracarotid injection), which leads to brief dysfunction of that hemisphere, displayed in hemiplegia of the contralateral limbs and other neurological abnormalities in the opposite side of the body. If this is the dominant hemisphere for speech, there is also a transient speech disorder reminiscent of aphasia; this is the important symptom. In this manner, information is forthcoming whether or not this hemisphere is the one connected with speech in the case of this particular patient. Since the procedure for this test is fairly complicated, it is used only for patients undergoing preparation for neurosurgery for reason of brain lesions (often dating back to childhood). The

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77

results obtained concern this group alone, a fact which restricts the validity of these findings in respect to the normal population. As an illustration, we cite some findings of this test gathered at Montreal (after Branch et al., 1964) on dominance in a group of 119 patients undergoing preparation for surgery for relief of focal cerebral seizures (Table VI). TABLE VI Handedness and hemisphere dominance shown by the sodium amytal test (after Branch et al., 1964). Handedness

Right Left or ambidextrous

No. of patients 48 (100%) 71 (100%)

Speech lateralization left

right

none (bilateral)

43 (90%) 34 (48%)

5 (10%) 27 (38%)

0 10 (14%)

Table VI gives a similar picture to what we already know. As for speech disorder frequency in right and left cerebral lesion cases, so we find, by the amytal test, that righthandedness much more often accompanies dominance of the left hemisphere, while lefthandedness is a relatively frequent accompaniment of right hemisphere dominance or lack of clearcut dominance. True, the proportions found in this table are slightly at variance with those established by analysis of lesion effects, but this is undoubtedly linked to the fact that the group under study was a special one as to type and etiology of brain damage. In another publication (Milner et al., 1966) the same research group summarized the findings of the amytal test for a group of 212 patients in which special attention was devoted to the fact that bilateral localization of speech mechanisms was found for about 15% of lefthanded or ambidextrous cases. This was established from the fact that speech 'disorder occurred when the drug was injected into either left or right hemisphere. The same phenomenon was observed in only one righthanded patient of a grpup of 95. However, it should be noted that other investigators employing the same test have arrived at different results. For instance, Rossi and Rosadini (1967) found 5 cases of right hemisphere dominance in a total of 84 patients, and 2 cases of bilaterality, results which did not give any clear correlation with handedness in this group of patients. Other methods of establishing hemisphere dominance for speech have lately aroused wide interest. These include tests for auditory and visual perception of verbal and nonverbal material displayed in special conditions. Some very interesting findings have been obtained by the technique of simultaneous auditory presentation, by a special apparatus, of two different series of digits, each to a different ear (the dichotic listening task)-, after presentation the subject is asked to report the digits he has heard. Generally speaking, the results show that in the described con-

78

IV. SPEECH A N D T H E ANATOMICAL A N D PHYSIOLOGICAL PROPERTIES O F H U M A N B R A I N

ditions the subjects with left hemisphere dominance (verified by the sodium amytal test) reproduce better a series of digits arriving at the right ear, while subjects with right hemisphere dominance report more accurately those digits that arrive at the left ear (Kimura, 1961, 1967). Children have also been tested; it was found that for children typical dominance of the right ear in perception of a series of digits emerges at about 4 years, with boys lagging somewhat behind girls (Kimura, 1963, 1967). The above cited data on the connection between the functional preference of one ear in perceiving verbal material and hemisphere dominance for speech can be interpreted as a new indication of speech dominance emerging in the ontogenetic history of the individual (see Section C). There have been some attempts to examine the possible correlation between this phenomenon and handedness (Curry, 1967; and Rutherford, 1967). These authors ascertained that in lefthanders right ear preference is less marked than in righthanders; in their opinion this supports the view that lefthanders possess a more evenly balanced functional relationship between the hemispheres in respect to speech. Similar research has been conducted on perception of verbal material in the right and left visual fields (Goodglass and Barton, 1963; Hines et al., 1969; McKinney, 1967; Orbach, 1967). However, these findings are less clearcut, which is probably due to the fact that visual perception of verbal material depends on many different factors only one of which is dominance. Some interest has recently been shown in certain asymmetries found in EEG (electroencephalogram) of the right and left hemispheres (Giannitrapani, 1967). As yet their connection with cerebral functional asymmetry is unclear and requires further study.

E. DOMINANCE AND ANATOMICAL DIFFERENCES BETWEEN THE HEMISPHERES

Once the functional asymmetry of the cerebral hemispheres was established, the question naturally arose as to whether this reflected some anatomical differences. This question is a longstanding one (cf. von Bonin, 1962). Certain anatomical disparity between the two hemispheres has been indicated by various measures, but the differences found were very slight when contrasted to the obvious functional differences. For this reason most investigators have regarded them as of small consequence, particularly since paired organs as a rule display some anatomical asymmetry which has often no connection with their functional differentiation. However a more recent study by Geschwind and Levitsky (1968) has thrown new light on this question. These authors conducted a detailed analysis of 100 normal adult brains at postmortem, free from pathology of the nervous system. They paid special attention to the upper surface of the temporal lobes (the supratemporal planes), particularly to those regions which are known to share in speech

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79

regulation. It was shown that the planum temporale, the area behind Heschl's gyrus, was significantly larger on the left side in 57 cases and on the right side in 18 cases, while in 25 cases no differences were found between left and right side. A specimen which demonstrates typical left-right asymmetries, to the advantage of the left, is shown in Fig. 12. In the authors' opinion; this area (left planum temporale), known to lodge the auditory association cortex, corresponds to Wernicke's area where a left lesion in most cases (see above) leads to aphasic disorders. The fact that this area is significantly larger on the left side in 57% of the cases enhances the

Fig. 12. Structural differences in left and right human temporal lobes. The scheme shows the upper surfaces of the temporal lobes. The posterior margin (PM) of the cortex behind the sulcus of Heschl (planum temporale—PT) slopes backward more sharply on the left than on the right, so that end y of the left Sylvian fissure lies posterior to the corresponding point on the right. The anterior margin of the planum (PT) formed by the sulcus of Heschl (SH) slopes forward more sharply on the left than on the right. In this brain there is a single transverse gyrus of Heschl (TG) on the left, but two on the right (TG t , TG2). TP—temporal pole, OP—occipital pole, SI—sulcus intermedius of Beck (from Geschwjnd and Levitsky, 1968).

likelihood that it is related to hemisphere dominance for speech. This is, of course, a hypothesis to be further substantiated, but it would seem that there is a striking consonance between the data on dominance cited earlier established by other methods and the data from Geschwind and Levitsky. Apparently these authors have succeeded in devising a method for discovering the anatomical differences between the hemispheres which constitute correlates of functional differences.

F. SPEECH AND THE NONDO.VIINANT (SUBORDINATE) HEMISPHERE

We have been discussing empirical findings testifying to the existence of functional differences between the cerebral hemispheres, including speech regulation. For the great majority of persons, one hemisphere, usually the left, plays the dominant

80

IV. SPEECH AND THE ANATOMICAL AND PHYSIOLOGICAL PROPERTIES OF HUMAN BRAIN

role in speech activity. There now arises the question about the other hemisphere, which is nondominant. Is it completely excluded from this function? The fact that ! this hemisphere, when damaged, does not disorder speech seems to favour an affirmative answer. But various reservations may be voiced. First of all, research on the ontogenetic formation of dominance (see Section C) permits the inference that in the early stage of development, but after speech onset, functional differences between the hemispheres have not yet developed, or the process has not yet terminated. One would then expect that initially both hemispheres share in regulating speech activities and that subsequently something in the nature of a "concentration" of speech mechanisms occurs in one of the hemispheres. We have also found that the emergence of dominance does not occur in each and every case; there is a fair percentage of adults for whom both hemispheres share in speech regulation. Some speculations have been advanced, in line with Jackson's (1958) suggestions, that even in individuals with total left hemisphere dominance, the right hemisphere is not completely left out of speech regulation (Critchley, 1962). Eisenson (1962) used a series of verbal tests to compare righthanded nonaphasic patients without latent sinistrality, suffering from right hemisphere lesions, with a matched nondamaged control group. He was led to conclude that lesions in the right nondominant hemisphere, while not leading to aphasia, impair "high-level language functioning", as exemplified in the sentence completion test, especially involving use of abstract words. Eisenson's conclusion has been questioned, however, on the grounds that the differences he found are not connected with lesion effects upon the nondominant hemisphere but with a nonspecific effect of brain damage. Boiler (1968) compared several verbal test performances for groups with left and right lesions without aphasia, and demonstrated that, even when left destruction did not lead to clinically observable speech impairment, it is possible to establish certain losses in speech function when appropriately sensitive tests are used. Boiler's findings show that this loss is even greater in persons with left destruction than in cases of right damage. In his view every brain injury, even not involving the speech area, regardless of hemisphere, produces a nonspecific deficit in speech function. Similar interpretations were drawn by Archibald and Wepman (1968) from observations of 8 patients with right hemisphere lesions who displayed subtle speech impairment, leading to the generalization that these disturbances are manifestations of a general deterioration, mainly involving attention. Some highly interesting observations on the role of the right hemisphere for speech have been reported from examinations of postoperative patients who had undergone callosal section (interruption of the commissural connections linking the two cerebral hemispheres) (Gazzaniga et al., 1962, 1965; Sperry and Gazzaniga, 1967). This operation, which is a treatment for epilepsy, destroys the neural fibres connecting the cortical areas of the hemispheres. For many years it had been thought from the earlier observations of authors who had performed this operation that the

I. CEREBRAL HEMISPHERIC DOMINANCE FOR SPEECH

81

post-operative functioning of the individual was not affected in any significant way, since the tracts running through the deeper cerebral structures connecting the two hemispheres remained intact. More recent observations have, however, shown that in special conditions very clearcut impairments are revealed, which, in general, bear witness to the fact that the hemispheres function to some degree independently one of the other. This may be demonstrated in the following way: Some well-known object, such as a key, is placed in the left hand (controlled by the right hemisphere) of a blindfolded patient. The patient is able to show that he recognizes the object by making the appropriate movements with it, thus distinguishing this object from others presented for tactile recognition—but only by the left hand. At the same time the patient is unable to name the object, since this involves the left hemisphere, which "knows nothing" about what the right hemisphere "is doing". Also, such a patient cannot find with his right hand (controlled by the left hemisphere) an object held in his left hand. Similar events were observed when a patient was shown certain objects in the right or left visual half-field (by means of appropriate devices) (Fig. 13). Since here

Fig. 13. Apparatus employed in examining patients after surgical disconnection of the right and left cerebral hemispheres. Subject (S) seated before shield which hides test items and hands, and examiner (E). (From Sperry and Gazzaniga, 1967.)

as well the principle holds that all stimuli presented in the left half-field go to the right hemisphere and vice versa, the patient could not name objects displayed in the left half-field, but could readily name them when they were displayed in the right half-field since the information arrived at the left dominant hemisphere. Similarly the patient was incapable of reading even simple printed words exposed in the left visual field. There are additional facts which lead to the inference that the cerebral hemispheres,

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in conditions created by surgical separation, function as if each were a separate and independent "brain". In the context of our discussion, we are mostly interested in those observations which relate to the participation of the nondominant hemisphere in speech activities. Basing themselves on the fact that the hemispheres function separately, by and large, Sperry and Gazzaniga (1967) set up conditions in which the right hemisphere had to resolve various kinds of verbal tasks. In most of the cases studied, inability was noted to perform tasks requiring use of words, comprehension of verbal utterances, etc., the right hemisphere being the minor one in respect to speech activities. But it appeared that certain specific verbal tasks could be performed, at least to some degree, by the right hemisphere. For instance, when the patient heard the names of various objects, he could distinguish these objects by palpation of right or left hand. He could also carry out simple verbal instructions using the left hand. When cards with printed words were presented in the left visual half-field, the patient could indicate the correct objects, but only with the left hand; but he was unable to read the word aloud, or name the object he had just picked out with the left hand. The patient could also point out from among several word cards the name of the object shown him in the left visual half-field or just held in the left hand. Sperry and Gazzaniga (1967) drew from these facts the conclusion that at least some right nondominant hemispheres possess a certain capacity to comprehend speech, both spoken and written, even when this hemisphere is totally bereft of "help" from the left dominant hemisphere. To conclude this discussion on the share of the nondominant and subordinate hemisphere in speech activities, it is appropriate to mention some highly interesting observations on nonaphasic disorders in the speech of patients with right hemisphere damage reported by Weinstein et al. (1963, cf. also Weinstein, 1964), who examined 40 righthanded patients of whom 20 had left, and 20 right, hemisphere lesions. The task was to name 40 selected objects. In the left lesion group, errors were made on 56% of the items presented, the errors being mainly confusions with either phonetically or semantically similar names, a phenomenon typical of aphasia (see Chapter VII). The right lesion group gave only 9% erroneous answers; their misnamings were of a different nature from those of the other group, involving items connected with hospitalization, illness and medical procedures. For example, a patient called a thermometer a "temperature gauge", a wheelchair an "armchair", and so on. At the same time, all cases displayed a given type of disorder, viz., spatialtemporal disorientation; in some cases symptoms were found of "anosognosia", that is, denial or unawareness of the disorder. The authors' opinion was that the speech disorders in question are linked to the fact that cerebral damage causes a change in the patient's attitude to his environment, and disturbs his situational orientation as manifested in his speech; it would then seem that speech disorder due to lesions in the subordinate hemisphere are symptomatic of other pathological mechanisms than those of aphasia resulting from dominant hemisphere lesions.

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G. CONCLUSIONS

To summarize the above discussion of research findings pertaining to dominance, our conclusions may be synthesized into the following statements: 1. The phenomenon of dominance of one hemisphere for speech is an integral part of the cerebral functional asymmetry typical of man, manifested not only in speech regulation but also in relation to the other higher functions. There is good reason to suppose that cerebral functional asymmetry corresponds to certain anatomical differences in hemisphere structure. 2. Functional asymmetry of the human brain is formed in ontogenesis, both inherited and environmental factors being apparently involved in this process. The two hemispheres are initially equipotential in respect to speech; only later do thè speech mechanisms "concentrate" in one of them. 3. For the majority of the population, left hemisphere dominance for speech is typical; however in a normal population a certain proportion of persons will be found who display right hemisphere dominance or who lack clearcut dominance of one hemisphere for speech. At present it is difficult to evaluate the exact proportions of the three groups distinguished here; we can only say that the first group is clearly superior in numbers (the left dominance group). At the same time many facts suggest that when the right hemisphere is dominant, the degree of dominance is less accentuated than when the left dominates. 4. Dominance of one hemisphere for speech is intricately related to the phenomenon of hemisphere dominance for other higher functions as well as to diverse manifestations of lateral preference in body function. No unambiguously correlated index of speech dominance has yet been discovered in respect to laterality of body functions, though in the case of handedness this correlation seems higher than for other lateralized functions. 5. The combined evidence is that, in respect both to laterality of body functions and hemisphere dominance for speech, there exists a continuum of degree of lateral dominance, beginning from total dominance of one hemisphere, through partial dominance, to bilaterality or no clearcut dominance. 6. The available evidence suggests that, even with clearcut hemisphere dominance for speech, the possibility cannot be excluded that the nondominant, subordinate hemisphere participates, at least to some extent, in the regulation of speech.

§ 2. THE SPEECH AREA AND ITS INNER DIFFERENTIATION

From our previous discussion we find that for most people only one cerebral hemisphere partakes in speech regulation. This does not imply, however, that the entire hemisphere is involved or all structures contained within it. There is considerable evidence, both from clinical findings and from other research, that the dominant

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hemisphere contains structures which are not involved in speech regulation, since lesions in these structures do not entail aphasia. Once this fact was established, researchers were led to introduce the concept of "speech area" to designate those regions in the dominant hemisphere directly connected with speech. A particularly good method to map out the speech area and fix its boundaries is that of stimulating the cortical surface, employed by Penfield and Roberts (1959) during curative neurosurgery on patients with epileptic seizures (this method has been described earlier in Chapter III). After analyzing the various kinds of reactions noted during electrical stimulation in diverse parts of the cortical surface, these authors distinguished the following three regions as parts of the speech area: Broca's area, lying in front of the lower precentral gyrus of the left frontal lobe; what has become known as the supplementary motor area on the medial surface of the hemisphere, extending up on the superior surface, just in front of the precentral leg area; and the posterior temporo-parietal area (Fig. 14). When the electric current is

Fig. 14. Speech area in the dominant cerebral hemisphere (usually the left) from studies by the method of electrical stimulation (from Penfield and Roberts, 1959).

applied to these areas, the following kinds of interferential alterations occur: speech arrest, hesitation and slurring, impairment of repetition, naming, reading and writing, i.e., symptoms typical of aphasic disorders. On the other hand, stimulation in other regions of the left hemisphere will either not affect speech at all or will evoke speech arrest or involuntary vocalization. This latter result was noted during stimulation of the motor area for the articulatory organs directly in front of the Rolandic fissure on both the right and left side; what followed was simply an interference in the motor control of the articulatory organs, viz. disturbances of phonation unlike true speech disorders.

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The foregoing observations largely coincide with our knowledge about localization of speech areas gained from research on speech disorders following cerebral injury. Luria's (1947) analysis of 394 patients with gunshot wounds in the left hemisphere led to identification of the following principal speech areas: fronto-parietotemporal, temporo-parietal, and postero-temporal. Other authors have reached similar conclusions. In other words, the region involved in the regulation of speech lies, roughly speaking, in the middle part of the left hemisphere. This does not mean, however, that only damage in this area will disturb speech. Speech disorders have also been noted when other regions are damaged, though these are much rarer and less marked. There may be certain individual differences; dysfunctions in the speech area may likewise be attributed to various consequences of damage in neighbouring areas (see Chapter III). Interesting information bearing on the localization and function of the speech area is included in the report of a very rare case of widespread cerebral damage sparing the speech area itself. This syndrome, called isolated speech area, was described by Geschwind et al. (1968). A 22-year old woman, following carbonmonoxide poisoning, survived after rapid medical intervention; her brain was extensively destroyed, causing permanent and profound motor disability and disorders of a number of higher functions so that she remained hospitalized until her death ten years later. During this period the case was studied in detail from the point of view of speech; at postmortem a refined cerebral analysis was performed. Now, the most striking clinical feature found in the speech of this patient was that, while comprehension was totally lacking and spontaneous speech almost wholly absent, the patient could with excellent articulation repeat single words, phrases and sentences. She also showed a tendency to complete stereotyped phrases or rhymes she knew. For instance, when asked: "Is this a rose?" she would reply with the rhyme: "Roses are red, violets are blue, sugar is sweet and so are you". Postmortem analysis of this case showed that, despite extensive destruction of cerebral tissue, the left hemisphere speech area (posterior temporal area, temporoparietal area and posterior frontal area) was only lightly affected, while adjacent areas were almost totally destroyed (Fig. 15). As a result, the speech area was isolated from the other portions of the brain which normally interact with it. This was the authors' explanation for absence of speech comprehension and spontaneous speech. Since the areas for both speech reception and production and their interconnections had remained relatively untouched, the patient could repeat what she heard (without understanding) and could produce previously established verbal stereotypes. If we compare the intact speech areas shown in Fig. 15 with the speech area mapped out by the electrical stimulation method (Fig. 14), or with the area for speech established by clinical analysis of aphasic cases, we can immediately see a considerable correspondence as to localization. So we have here the reverse of the previously analyzed situations: instead of a damaged speech area, we have an intact speech area surrounded by damaged tissue. Analysis of the symptoms manifested

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Fig. 15. Isolated speech area in a patient described by Geschwind in a schematic diagram based on postmortem analysis. Density of dots represents degree of cortical destruction; oblique lines represent subcortical white matter destroyed (Geschwind et al., 1968).

by this configuration of damage confirms other observations as to the peculiar significance of this portion of the brain for speech5. To close our discussion on localization of the speech area in the dominant hemisphere, it is of interest to note a fact mentioned by the anthropologists Roginsky and Levin (1955). In certain forms of human fossils, namely, Pithecanthropus and Sinanthropus Pekinensis, a distinct concavity can be found on the inner surface of the skull at a location which corresponds to the posterior portion of the temporal lobe and the parieto-temporo-occipital junction, i.e., those areas which make up the posterior part of the speech area in modern man. It is tempting to postulate that this fact marks the beginnings of the formative process of the area connected with emergent speech in the human species. Of course this interesting hypothesis has little basis so far. Other attempts to explain the fact of the emergence of this concavity have also been made. Now that the speech area in the dominant hemisphere has been localized, there arises the next question as to whether this area is functionally homogeneous or whether there is some inner differentiation. Do the separate parts of this area subserve the same functions, or do they have different functions in speech regulation? In our second chapter, we outlined the history and present state of opinion on the subject of functional localization in the brain. We pointed out that the view which negates the functional differentiation of cerebral structures is today in severe 5

The case described offers tempting interpretations as to the collaboration of the speech area with other cerebral regions. For instance, it is clearly indicated that for normal comprehension of speech, as well as for normal construction of discourse, the speech area must collaborate with other portions of the brain. We shall return to these matters later on.

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crisis because of the many facts testifying to the existence of differentiation; this statement concerns the structures of the speech area as well. Although Penfield and Roberts (1959) mention no differences in the effects of stimulating various parts of the cortex, all clinical experience with aphasic patients points unequivocally to the conclusion that the speech area embraces structures of differing significance as to speech function. Bearing this in mind, let us look at the very instructive findings obtained by Howes (1964; cf. Howes and Geschwind, 1964), who applied statistical methods to analysis of patients' utterances in cases where brain damage was diversely located. Howes talked with patients under maximally natural conditions, registering their speech for as long as necessary to obtain a sample of 5000 words, and then analyzed the frequency with which particular words were produced as well as the rate at which they were uttered. These findings were correlated with the results of clinical observations on the condition of the patients' speech, including comprehension. On these grounds Howes distinguished two groups of aphasics according to rate of speech and certain features of word distribution in utterances. One group comprised patients with impaired verbal fluency; typical features were slow tempo of word production, a higher number of immediate word repetitions (e.g., boy—boy) and impoverished vocabulary reduced to words of highest frequency in normal speech. Impaired verbal fluency was accompanied by very light clinical symptoms of speech reception deficit. The other group of patients displayed a normal or even accelerated speaking rate, normal immediate repetitiveness, a lesser deviation from the norm in word frequency, accompanied by a considerable impairment of speech reception. By using the clinical data on locus of damage for each case, the author was able to ascertain that the first group, or the nonfluent patients, had lesions in the anterior portion of the speech area, whereas the second group, or the fluent cases, had lesions in the posterior portion. Accordingly, we find that damage to the posterior or anterior portions of the speech area will lead to qualitatively different speech dysfunction. Broadly stated, anterior lesions cause deficits mainly in the productive aspect of speech while posterior lesions affect primarily the perceptual aspect (speech reception). As we shall soon see, this division is neither strict nor exhaustive enough to account for the complexities of speech disorders incurred through brain damage; nonetheless it reflects a certain overall regularity in the inner differentiation of the speech area. In our treatment of the question of participation of cerebral structures in speech regulation, we have so far limited our discussion to the cortical portions of the cerebral hemispheres; the speech area we have been discussing refers to a part of the cortex. This has been dictated by the still prevailing belief that speech regulation is mainly connected with the cortex. Rather recently a number of reports have appeared dealing with the participation of deeper-lying cerebral structures in the regulation of speech. As pointed out in Chapter II, certain anatomical data suggest that subcor-

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tical structures have a share in normal speech processes (cf. Penfield and Roberts, 1959); more recent observations tend to confirm this view. The latter evidence has been obtained mainly from the stereotactic procedure, •a. curative measure for parkinsonism. This operation consists roughly in an extremely selective interference, by means of a special apparatus, in structures located in the depths of the brain without incurring damage to surface structures. The stereotactic procedure affects a strictly defined and extremely minute site. In the course of this operation, electrical stimulation is also applied to the operated areas. Since local analgesia is used, contact with the patient is maintained throughout, thus enabling information to be collected as to the state of speech processes during stimulation. Guiot et al. (1961) report that in the above described conditions, electrical stimulation of one nucleus of the thalamus (ventro-lateral nucleus) will evoke either arrest or acceleration of speech, when the patient is asked to count slowly. Ojemann et al. (1968), who systematically investigated a large group of patients, found that stimulation of the pulvinar thalami on the left side will evoke disturbance in naming familiar objects, in other words, an impairment reminiscent of aphasic naming disorder. Lenneberg (1967) cites a number of similar observations and concludes that not only surface cortical structures partake in speech regulation but also subcortical portions and midbrain structures. The data we have just reviewed cannot be taken as resting on completely firm foundations, for much awaits clarification as to the physiological mechanism at the basis of the observed alterations in speech processes under the effect of stimulation. Lenneberg has noted that stimulation is a very artificial way of influencing the functions of a given structure, which in normal conditions is not at all bound to perform the same functions that are disturbed during stimulation. Nonetheless, the facts described unquestionably suggest that speech regulation involves the participation not only of the cortical structures in the dominant hemisphere, but probably the deeper subcortical structures of that hemisphere as well. In other words, instead of a surface cortical speech area we may probably have to accept the notion of a "three-dimensional" cortico-subcortical space. Of course the boundaries of this "third" dimension are as yet less well known than are the boundaries of the cortical surface area.

§ 3. SPEECH AND THE GENERAL REGULARITIES OF BRAIN FUNCTIONS

We have previously established two facts, one that inequality of the two cerebral hemispheres in regulation of speech activities is a typical feature of the human brain, and, the other, that a specific area can be distinguished in the dominant hemisphere which contains those structures that regulate speech. In other words, we have so far focussed our attention on the question of where the structures responsible for the human capacity to use language lie within the brain. Let us bear in mind that this

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approach predominates, in some sense, both in past and current neuropsychological research on the speech-brain relation. It would seem, however, that this concentration on localization of human cerebral structures linked with speech has to a certain extent impoverished the domain of inquiry. It does not hold forth promise of a full answer to the question why man stands alone in his capacity to acquire speech. There is another aspect to this entire question, roughly stated as the relation of speech to human brain functioning or to the properties of cerebral physiology. This aspect has received far less attention in neuropsychology in view of the preoccupation with the structural aspect, although the available evidence suggests that the former aspect is of no small import 6 . In the present section we shall try to discuss—as an illustration of the issue—some findings on speech disorders following brain damage which point to the possibility of reaching a more profound understanding of speech mechanisms in the context of broader neurophysiological regularities. These are studies aimed at discovering the degree of dependency between disorders of word use due to brain damage and various kinds of word properties. For instance, it has been shown that a high correlation exists between the degree to which word use is impaired and the age at which that word was acquired. Benton (1967) compared the number of errors committed by aphasic patients in naming a set of objects against data about the age when these names first appear in child vocabulary. A strict correlation was found between the number of naming errors—hence, use of the appropriate words—and the age at which they appear in the child's lexicon. Thus brain damage causing naming disorders disturbed to a greater degree the use of name acquired later than of those acquired earlier in development. Gamska (1970) used a set of objects which the patient named twelve times at 6 successive sessions. These items were so selected that the names of 20 belonged to the vocabulary of the two-year-old and 20 to the later vocabulary. This study confirmed the finding that the degree of impairment of word use, measured by errors in naming the corresponding object in successive trials, was strictly related to the age of its active acquisition. Another parameter correlated with degree of impairment in word use in aphasia is its frequency of occurrence in normal speech. Bricker et al. (1964) used a word frequency list for American English (Lorge Magazine Count, cf. Thorndike and Lorge, 1944) to test spelling errors in aphasic patients for 100 words of varying frequency from a total sample of 4.5 million words. They found that the number of spelling errors increased in inverse proportion to the frequency of word usage. The 6

This question has long been of concern to neurophysiologists who are continuators of research initiated by Pavlov's conception of the two signal systems, and who study the specific properties of the physiology of man's higher nervous activities. Specifically, this research deals with the formation and functioning of what is termed the second signal system, and covers a wide scientific literature. But, since its methodology is fundamentally different from that of neuropsychological research, any attempt to synthesize the findings of the two research trends does not at the moment appear feasible.

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rarer the word, the more errors in spelling performance in conditions of brain damage. Similar findings were reported by Siegel (1959), Howes (1964) and others. Another finding reported by Bricker et al. (1964) was a correlation between word letter length and the number of spelling errors. The longer the word, the more difficulty it posed to the patient in spelling it. This result has been confirmed by Gamska (1970) who found that the number of naming errors using longer words was greater than when using shorter ones. Lansdell et al. (1963) studied the relation between degree of difficulty in naming common objects during the amytal test (see § 1, D in this chapter) and the frequency of English phonemes occurring in the initial and final positions in the word. They found that, in the condition studied, it is easier to use words beginning with low-frequency phonemes but ending with high-frequency phonemes. When the first phoneme is highly familiar, and the last phoneme less common, the number of naming errors is greater. The above cited research leaves much unexplained on the more particular aspects of the question, but points very clearly to the fact that word properties such as time of acquisition in ontogenesis, frequency of normal use, as well as structural properties such as word length and phonemic composition, determine the extent to which speech processes employing these words are disordered as a result of brain damage. We are led to assume that these properties are also of significance in the formation of the cerebral speech mechanisms, and that this is most likely governed by the general physiological properties of cerebral functioning. For instance, the fact that early acquired and more frequent words are less vulnerable to brain damage seems to testify to a dependency known generally to hold in other physiological research, viz. that the more often an activity is repeated, the more firmly it is rooted, and inversely, the less frequently an activity is performed, the less solidly it is acquired. As we have just stated, this line of inquiry does not currently constitute the mainstream of neuropsychological research on the cerebral mechanisms of speech; rather the central line of research is addressed to analysis of the structural properties of the human brain relevant to speech. Yet we cannot but agree with Lenneberg's (1967) view that elucidation of many problems relevant to the regulation of speech processes lies hidden in the organization of physiological processes of the human brain and that we may expect an intensified research programme in this domain to disclose the answers to many questions which could never be clarified by a purely structural approach to the problem. We shall have further occasion to return to this matter as we take up the more particular aspects. #

#

#

The present chapter has surveyed the major findings of neuropsychological investigations on the structural and physiological properties of the human brain which determine the human capacity to use language. This review has led to the conclusion that there exists—laterally located in the majority of cases—a group of neural struc-

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tures which play an essential role in regulating speech activities. The structures composing this group—the speech area—are functionally differentiated, that is to say, they have different roles in the regulation of speech activities. In the chapters to follow we shall go into greater detail in discussing the role of the various elements composing this area. However, bearing in mind that functional differentiation within the speech area is manifested in the varying degrees to which the diverse speech activities are disordered under conditions of brain damage (and considering certain didactic advantages of such an approach), we shall pursue the following line of treatment of t»ur subject: In presenting further material on the regulatory mechanisms of speech, we shall be guided, not by anatomical differences within the speech area, but by groupings of problems discernible in speech processes as such. In the next chapter we shall consider the cerebral mechanisms that regulate the processes involved in speech production.

CHAPTER V

CEREBRAL MECHANISMS OF SPEECH PRODUCTION

§ 1. INTRODUCTORY REMARKS

In this chapter we shall attempt to report on the present state of knowledge about the cerebral regulation of speech production. The first point to be made is the relativeness of the distinction made here as to the activities involved in speech production. Purely from the outside this seems a fairly obvious distinction to make. Two people are talking, of whom one at a given moment makes certain movements with tongue, lips and other less visible organs, thereby emitting a sequence of sounds that make up an utterance; meanwhile the other interlocutor hears what is said., Thus two interlocutors perform two distinct activities, one producing and the other receiving speech. Superficially viewed, the speaker's behaviour might appear merely motor in kind, reducible to certain movements of the articulatory organs. This belief underlay the early observations and classifications of speech disturbances arising from cerebral lesions. In Chapter II it was mentioned that at first two main forms of aphasia were distinguished: motor aphasia, or disorder of speech production, and sensory aphasia, or disorder of speech reception. It was also assumed that two separate centres existed in the brain, one regulating speech production (Broca's area) and the other regulating speech reception (Wernicke's area). But it soon became apparent that the distinction loses its sharpness the more deeply we penetrate into the mechanisms responsible for the disorders of these two great processes and try to associate them with cerebral areas. The boundaries between disorders of speech production and of speech reception become blurred in respect both to type of symptoms manifested and to locus of brain lesions causing the symptoms. This state of affairs has led certain authors lately to deny the validity of this differentiation and to advance the thesis that the sensorimotor dichotomy has no basis in fact, nor do grounds exist for differentiating cerebral mechanisms in line with that dichotomy (cf. for example Schuell and Jenkins, 1959, 1961; Osgood and Miron, 1963). The main argument which has been used against distinguishing between the motor and sensory aspects of cerebral speech regulation is the established fact that practically never do "pure" disorders of either production or reception occur. In other words, whenever we have a disorder of speech production, we can always discern

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some disorder of speech reception as well (see Chapter VI, § 4 B), and conversely, when the latter is disturbed, some disorganization of speech production can also be found (see § 5). The above fact will become clearer once we have reviewed the relevant data on the cerebral regulation of speech. In view of the goals of the present chapter, it is important to stress at the beginning that every motor activity, hence speech production also, has its sensory side; no motor activity can occur without a corresponding sensory control, that is, without information as to the conditions of performance and the course of the activity. Bearing this in mind, we see that the disengagement of the two processes involved in speech is a kind of abstraction; in terms of its regulatory mechanisms, speech is one sensorimotor activity embracing processes both of production and reception. However, for purposes of convenience, we shall hold to this abstraction in reporting empirical data. Having alerted the reader to the oversimplified nature of this treatment, we now proceed to discuss the regulatory mechanisms of speech production.

§2. GENERAL CHARACTERIZATION OF THE PROCESSES INVOLVED IN SPEECH PRODUCTION

Speaking is a highly complex activity with numerous levels of organization. As we analyze the product of speaking, or the text, we readily note that it is made up of units which vary in degree of complexity. The most elementary unit of a spoken text is the speech sound, or phoneme. Every language has a fixed number of such units (ranging from 13 to 75, depending on the particular language) out of which all the utterances in that language are constructed at a circumscribed period of its history. Speaking could ultimately be reduced to the emission of a sequence of sounds, each of which is produced by means of a slightly different set of articulatory movements. The different speech sounds are employed with varying frequency, some occurring in utterances with a high frequency and others very rarely. For example, of the 40 English phonemes, 9 make up more than half the utterances in that language; the most common is /i/ (as in bit) which is used more than 100 times as often as /z/ (as in azure), the least used sound (cf. Miller, 1951a). The characteristic function of the phoneme is to differentiate word meanings while bearing no meaning itself. The minimal meaningful element of any text is the morpheme, which is a composition of speech sounds in sequence. Apart from the complex relation between morpheme and word, note the fact that the morpheme and the word cannot be equated; a word may contain one or more meaningful elements. For example the word "bridges" is made up of two morphemes, the lexical morpheme "bridge" signalling a certain class of referents, and the grammatical morpheme "s", signalling plurality. As this example shows, a text is a lawful ar-

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rangement (in terms of the rules of the language) of speech sounds combined into morphemes, and of morphemes combined into more complex units such as words, sentences and still larger segments of text. The number of meaningful units in a language is very great. An English dictionary, for instance, contains about half a million lexical items. Here again we find that such units are employed in utterances with varying frequency; some of them are very frequent in use, while others are extremely rare. Speaking as an activity, therefore, involves producing a text composed of units differing in complexity and related hierarchically (i.e., more complex units are formed out of simpler units). The rules for constructing utterances are contained in the language system. Linguists employ a variety of terms to define these rules, depending on their theoretical approach. An illustration is the description of the language system presented by Hockett (1958). In his theory the language system is composed of five basic subsystems. These are (1) the grammatical system, which is the stock of morphemes and the arrangements in which they occur; (2) the phonological system, which is the stock of phonemes and the arrangements in which they occur; (3) the morphophonemic system or code which ties together the grammatical and phonological system; (4) the semantic system which associates the morphemes, the morpheme combinations and arrangements in which morphemes can be put with things and situations, or kinds of things and situations; (5) the phonetic system, or the ways in which sequences of phonemes are converted into sound waves by the articulation of a speaker, and are decoded from the speech signal by a hearer. The above citation is a good illustration of how complex and multifaceted is the process of speaking, or constructing utterances. Very broadly, this process is reducible (Jakobson, 1964a) to two fundamental operations: the selection of linguistic units and the combination of these units into units of higher degrees of complexity. In speaking, we select phonemes, words, and sentences to correspond to the information we are trying to transmit, and we combine them into larger texts. In the normal person this process flows along with extraordinary efficiency and productivity; it can even last for many hours at a time. We shall now turn to a discussion of the anatomical and physiological bases of speaking.

§ 3. SELECTED QUESTIONS PERTAINING TO THE ANATOMICAL AND PHYSIOLOGICAL BASES OF SPEECH PRODUCTION

Speaking is based on formation of appropriate sound waves by means -of audible sound, or voice; this is accomplished by the interplay of several anatomical systems, the major ones being respiration, phonation and articulation (Fig. 16). Through this interaction air penetrates into the lung vesicles during the phase of inhalation and is forced into the windpipe, larynx, throat and oral cavities during the phase of

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Fig. 16. Diagram of the structure of the human system of phonation and articulation. I—upper throat, II—mid-throat, III—lower throat; a—first articulatory zone, b—second articulatory zone, c—third articulatory zone; A—exit of the Eustachian tube, B—sphenoid sinus, C—frontal sinus, D—tip of tongue, E—shaft of tongue, F—base of tongue, G—epiglottis, H—spurious cord, I— vocal cords, J—trachea or windpipe (after Mitrynowicz-Modrzejewska, 1963).

exhalation when speaking occurs. Voicing (phonation) occurs in the larynx as the air expelled from the lungs presses against the tensed glottal cords. The latter are opened and closed, lengthened and shortened, by muscular adjustments which produce pitch differences according to the vibrational frequency of the vocal cords. Vocalization from the larynx is transformed into speech sounds by the interplay between the articulatory apparatus and vocal cord vibrations. The breath stream arrives from the larynx into the throat cavity. Respiration through the nose is temporarily halted during speech; the passage between the throat and nasal cavities is closed to permit the air to be expired through the oral cavity. Sometimes the closure is only partial and sounds acquire a nasal resonance. As the articulatory apparatus goes into action, movement occurs of the posterior and lateral walls of the throat,

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the velum (soft palate), lips, tongue and glottis. As each speech sound is produced, the articulators assume a particular position, or posture, together with the organs of phonation. When articulators and vocal cords are both involved, voiced vowels and consonants are produced; when the vocal cords do not participate, consonants are unvoiced. The work of the articulators during speech emission has been described in great detail with the aid of appropriate techniques of registration. For vowels the main role is played by the tongue, lips and velum. For example, the Polish vowels /a/, Jo/ and /u/ are produced by the flattened tongue and the lips in various open positions, while /a/, /e/ and /if are produced by the oral and throat cavities being widened and shortened. The processes involved for producing (Polish) consonants are very intricate ; according to Mitrynowicz-Modrzejewska (1963) their components are as follows: 1. State of the vocal cords during production of a given consonant. 2. Points of articulation. 3. Degree of muscular contraction of the articulators. 4. Duration of contact between the articulators. 5. Balance of resonance of the oral and nasal cavities. Polish consonants have been classified according to the component processes involved in their production (see Table VII). As we see from examining the positions for each consonant as presented in Table VII, each one involves a particular configuration of factors, or criteria, differentiating the articulation of one from another speech sound. Each configuration must be accurately produced if the utterance is to be heard as the speaker intends it to be heard. If some deviation occurs beyond the limits permissible in the language, there are acoustic changes in the quality of the speech sound, with the effect of deforming the utterance and disrupting the communicative process. In this light it becomes evident how extraordinarily subtle and precise the work of the articulators must be for an utterance to be produced according to the rules of the language and to meet the specifications of verbal communication. Further testimony to the intricacy of speech regulatory mechanisms can be found in other data on speech production. Measurements made of English utterances show that, for those of a given length (100 syllables or over), the rate of speech production per minute is about 210 to 220 syllables, including hesitation pauses, while for shorter utterances, the rate may be as high as 500 syllables per minute (Miller, 1951a, b; Lenneberg, 1967). An English speaker can thus produce up to 8 syllables per second. Lenneberg (1967) has presented the following argument: he calculated that, at a mean speaking rate of 6 syllables per second, and an average English syllable length of approx. 2.4 phonemes, an English speaker produces about 14 phonemes per second. During speaking, about 100 different muscles belonging to the phonative-articulatory systems must be coordinated. Since transition from one phoneme to the next is determined by differences in muscular adjustments, fourteen such changes must occur involving some at least of these muscles, and perhaps all; each muscle must

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receive the order either to maintain its tonus, contract or relax. It is not yet possible to make more precise calculations, but the above suffices to demonstrate that during the act of speaking several hundreds of separate muscular adjustments must occur each second with very precise order and timing. TABLE VII Classification of Polish consonants (After Mitrynowicz-Modrzejewska, 1963). Classification of consonants according to: Duration

Type of contraction of articulators

short

long

Vocal cord voiced

unvoiced

Participation of resonance cavities nasal

oral

First articulatory zone (lips and front teeth) Stops, or plosives (p, b, m) Fricatives, or spirants (w, f)

p, b, m —

—

w,f

b, m w

m

P f

—

Second articulatory zone (tip of tongue and hard palate) n,ú — d, n, n t d, t, n, n

Stops, or plosives (d, t, n, 6) Fricatives, or spirants (s, s, sz, z, i, z)

Plosive-fricative (c, c, cz, dz, dz, dz) Vibrationals (laterals) (r, I) Vocalic (1, j)

—

s, á, sz, z, z, z

c, c, cz, dz, dz, dz — —

r,l U

z, i, z

s, s, sz

dz, dz, dz

c, c, cz

r, 1 U

—

.—.

—

—

—

—

Third articulatory zone (tongue base, velum and posterior throat wall) — k — Stops, or plosives (k, g, h) k, g,h g,h ch ch Fricatives, or spirants (ch) — — —

P,b w,f d,t s, s, sz c, c, cz, dz, dz, dz r,l

k, g,h ch

Speaking is controlled, therefore, by the regulation of approximately 100 muscles at a rate of about 14 muscular changes per second in strict sequential order. Another complicating factor is that these muscles are located at differing distances from the central nervous system so that the nervous impulses initiated in the brain have various distances to travel (Fig. 17). The speed at which neuronal impulses travel depends both on the length of the nerve and on the diameter of the nerve fibre. An analysis of these and other data has shown that the difference in the time it takes to innervate the different muscles involved in articulation may be 30 msec. It becomes reasonable to assume that the firing order of the central neuronal impulses initiated in cerebral structures may differ in its timing from the order of innervations of the peripheral organs (Lenneberg, 1967). Such considerations point to the extreme complexity of the physiological processes occurring in the central nervous system during speech production. The question

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Fig. 17. Efferent nerves supplying selected muscles essential for articulation (Lenneberg, 1967).

arises as to the basic mechanisms that ensure the regularity and orderliness of these phenomena. One of the most popular theories about the mechanisms responsible for the motor behaviour of the organism as a whole is the conception of reflex chains, which has also been applied to explain the regulatory mechanisms of speech. According to this theory, each successive motor event, or component element of a more complex motor action, is evoked on the reflex principle by a kinesthetic impulse initiated in the peripheral motor organ during the preceding movement, which in turn supplies the stimulus for the next successive movement. Thus a motor action is a succession of motor reactions, each of which is evoked on the basis of existent associations and in turn serves as a signal for the next reaction. In other words, a complex motor action is an associative chain of particular components which are simple motor reactions. This theory, applied to speaking, led to the peripheral motor theory of thinking, according to which thinking consists of a chain of minimal muscular changes in the articulators (cf. Humphrey, 1951). Lashley (1960) criticized the above theory in a penetrating analysis. He Started from the fact that the elements pronounced in speaking a word may be the same elements pronounced in speaking other words but in a different order; for example, in the words "tire" and "write", the same motor elements occur but in reverse order. Therefore order must be imposed upon the motor elements by something other than direct associative connections between them. The same applies to the ordering of words in sentences; elements ordered on this level of organization cannot be explained by previously formed associations between words.

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The high motor rapidity of speech production (see above) forms another essential argument against the associative chain theory. On occasion the speed is such that it would be impossible for impulses from the proprioceptive muscles to travel to the central nervous system and back again to the muscles, as assumed in the chain reflex theory. The time intervals between the component elements of such a chain of movements are too short to allow for such an afferent-efferent circuit. Hence the efferent impulses from the central nervous system to the executory muscles must be initiated, at least to some extent, independently of the stimulation aroused during a motor action. These and other arguments led Lashley to postulate the presence of central mechanisms that integrate motor activity and are independent of sensory feedback afferentation. In his view this central nervous mechanism is thé spontaneous rhythmic activity of the brain connected with metabolic processes. This central "cerebral pulse" imposes spreading waves of nervous excitation which are modulated by the actual state of the cerebral structures stimulated by these waves. Lashley's hypothesis was further analyzed by Lenneberg (1967), who drew on research work on various aspects of normal and abnormal speech production. Lenneberg concluded that an innate rhythmic nervous activity lies at the base of speech which has a periodicity of about 6 cycles per second. This constitutes the organizing principle and the pacemaker for articulation; the basic time unit is onesixth of a second for the programming of motor speech patterns. These suggestions for the elucidation of the regulatory mechanisms of speech production—leaving aside their speculative nature—are obviously not exhaustive. Even if we accept that the rhythmic activity of the brain—this central pulse, or beat— is the pacing mechanism in terms of which the timing of motor phenomena is worked out, the question remains how it is that rhythmic impulses activate some muscles and not others at any moment, and at the next the timetable changes according to the specifications of a particular language; in other words, what brings about such modulations? This question in itself poses the need for one more very important elucidatory hypothesis, namely, the existence of speech patterns. Brain (1961,1965) was greatly preoccupied with precisely this problem. He pointed to the fact that the manner of producing the sounds of speech varies widely, depending on many factors such as individual differences in speakers, the word context in which the phoneme occurs, and so on. Despite this fact, if the phonetic variants do not exceed acceptable limits, the speech sound maintains its identity and is distinguished by the hearer from all others and therefore plays its role in communication. The same holds for the word ; any word is produced in a great variety of ways, and with different intonations, yet it maintains its uniqueness and can be recognized. This implies, according to Brain, that all the variants of a speech sound or of a word must possess something in common which enables reference to be made to the same basic value. He surmised that this act of reference must be determined by a specific physiological phenomenon which he calls a "schema", understood as a physiological

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standard of comparison against which stimuli received can be matched and which elicits motor responses. Such schemas, or patterns, exist presumably for both phonemes and words, and subserve both speech reception and production by fixing the selection and order of activation of neural cells and muscular correlates in the articulators. Other authors lend support as well to the hypothesis of hierarchically organized auditory-motor patterns which determine the course of speech production. They use a variety of terms such as stereotype, complex, system, configuration, plan, programme. But in all cases the fact is signalized that somewhere in the nervous system there must exist something that determines the normal orderly flow of speech production; some process 09curs in the organism that governs the order in which action sequences are to be performed (Miller et al., 1960). For reasons elaborated elsewhere, we have suggested that the most fitting term seems to be "speech programming mechanisms" coded into the appropriate cerebral structures (cf. Maruszewski, 1966). As for their hierarchical organization, evidence for this lies in the above-mentioned fact that any text, or product of speech processes, is composed of units varying in degree of complexity, the more complex being composed of the simpler ones. This implies that the complex unit becomes the context for the simpler unit and determines their selection. For example the word-pattern for "pen" determines the selection of phonemes /p/, /e/ and /n/ in a set order. In this sense the auditory-motor pattern of a word constitutes the programme for the selection and arrangement of speech sounds required to actualize that pattern in speech. By the same token, the sentence: "Your pen is on the desk", constitutes a programme for selecting and combining the words required to formulate that sentence. The above exemplifies the complexity and importance of context as determinant of the selection of linguistic units of a text. Just as the word is the context for the speech sound, so the sentence is the context for the word, at the same time comprising a unit within a larger text on a higher level of complexity. The linguistic literature contains many divergencies in the characterization of this level of text organization; we shall turn to Brain's (1965) description of the sentence, which is relatively the most apt from the point of view of our present discussion. According to Brain, the sentence has the following properties: (1) A sentence usually consists of more than one word. (2) Its purpose is to communicate something from one person to another. What it communicates may be called its meaning, if that term is understood to include feelings, commands and ideas. (3) Words are related to each other in certain ways, which often involves a modification in their form. (4) Within the range of a word's possible meanings, the meaning it assumes in the context of the sentence often depends largely upon its relation to other words in the sentence. (5) The words in a sentence are arranged in order, and the sentence is therefore a structure persisting in time and as a whole which cannot be fully apprehended until it is complete and unless its beginning and middle are retained in consciousness to be brought into relationship with its end. (6) The meaning of a whole

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sentence is modified by intonation and voice inflection. (7) Its meaning often depends upon its nonverbal context, i.e., in the broadest sense, the circumstances in which it is uttered. Thus the sentence comprises the third organizational level of the text. By this is meant that, in addition to sound- and word-patterns, there are also patterns, or schemas, of sentences, which programme the selection of words needed to produce a sentence. These patterns have the specific property—as underscored by psycholinguists of the Chomskyan school—of generating not only sentences with the same meaning, though made up of diiferent words, but an infinite number of sentences, i.e., sentences never yet produced by anyone before. We still have inadequate knowledge of the properties of such schemas, or grammatical structures, but there can be no doubt as to their existence (cf. Chapter VI, § 2). On this point we terminate this review of the major statements about speech production, both as process and as product, drawn from an analysis of linguistic texts and from data pertaining to the anatomy and physiology of the speech organs. The following sections of this chapter will be devoted to a discussion of the findings from observations of patients who, due to cerebral damage, have incurred disorders of speech production.

§4. CEREBRAL MECHANISMS OF SPEECH PRODUCTION IN THE LIGHT OF ITS DISORDERS DUE TO DOMINANT HEMISPHERE DAMAGE: LOCUS IN ANTERIOR DIVISIONS

A. DYSARTHRIA A N D APHASIA

Broadly speaking, lesions in the central nervous system can lead to speech disorders of two kinds: dysarthria and aphasia. Dysarthria is a speech disorder resulting from disturbances of the activity of the executory apparatus of speech. The damage may affect the nerves supplying the articulatory muscles or neural nuclei in the brain stem; or the damage may be bilateral lesions of the nerve fibres connecting the cortical centres with the neural nuclei in the brain stem which innervate the articulatory muscles; or the cerebellum may be damaged. These types of damage all lead to paresis, loss of control or poor muscular coordination of the articulators, hampering in various ways the work of the oral cavity parts. Chewing and swallowing may be impaired; and obstructed articulation is displayed by a slow monotonous manner of speaking, defects of pronunciation, stammering, and even totally unintelligible speech. These articulatory disorders are purely executory in nature (Dowienko and Jakimowicz, 1959); they affect the manner of production. On the other hand, aphasic disorders of speech are caused by lesions in the speech

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area of the dominant hemisphere (see Chapter IV). Analysis of aphasic disorders has demonstrated that the programming mechanisms of speech are apparently disordered, while the executory apparatus of speech remains intact (Maruszewski, 1966). "Programming mechanism" is understood as the programmes for speech processes fixed within the structures of the speech area. These programmes are constituted according to the rules of the language system, objectively existing and socially derived; these are the rules for speech performance—production and reception— which must be adhered to as the condition for communication. Aphasia is, then, a speech disorder qualitatively different from dysarthria; it is a particularly interesting type of disorder within the context of our problem, since it concerns the cerebral mechanisms specifically related to processes involved in speech. For this reason we shall give priority in subsequent discussions to findings based on observations of aphasic patients 1 . Aphasic disorders of speech production are often very severe; at times there may be a total loss of ability to utter words, or verbalization may be reduced to a few residual expressions, pathologically perpetuated, such as "tiu bu bu", "ki ki ki", and the like. Ordinarily, however, speaking ability is not completely lost, as many observations show, for even if a patient is quite incapable of saying a word at the examiner's request, he can under certain circumstances, such as emotional tension, produce curses which are fairly complex articulatory products. This type of severe aphasic disorder is not easily amenable to analysis useful from the point of view of interpretations about the underlying speech mechanisms that are disordered. Since very extensive cerebral destruction is usually involved, such disorders are symptomatic of damage to numerous interconnected pathophysiological mechanisms. Less extensive impairment lends itself better to analysis. By registering the kinds of speech errors involved, differentiations can be made as to the diverse types of deviation from normal speech. This sort of clinical material has enabled researchers to distinguish a number of speech production disorders. An important step in this direction was made by Luria (1947, 1962) who analyzed motor speech impairment in cases of gunshot head wounds, where relatively limited and selective cerebral destruction was involved. Luria concluded that motor aphasia includes two basically different syndromes associated with different locus of lesion. We shall now discuss these two syndromes in detail.

B. AFFERENT MOTOR APHASIA: DISINTEGRATION OF SOMESTHETIC SPEECH SOUND PATTERNS

As our earlier discussion of normal speech production showed, the basic condition for normal speaking is the appropriate choice of the most elementary units of speech, The above distinction between dysarthria and aphasia is not universally accepted. A more detailed discussion of the various views on this subject may be found elsewhere (Maruszewski, 1966). 1

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viz., speech sounds. Each speech sound is a special configuration of muscular activities performed by the articulatory apparatus. The ability to produce speech sound» is impaired by lesions situated in the inferior portion of the postcentral region sloping back from the Rolandic fissure (the "parietal lid"). The postcentral region contains the cortical representation of the sensory modalities for touch and body posture. When this region is damaged, either these kinds of sensation are lost or—if the direct projection areas are unaffected and only adjacent areas involved—analysis and synthesis of somesthetic2 stimulation is impaired, resulting in what is known as postural apraxia; this refers to difficulties in finding positions of body parts needed to perform certain movements. The superior and middle divisions of this region ensure the posture of the limbs, while the inferior division is connected with the facial surface, tongue and other parts of the oral cavity. When lesions are incurred in the latter part, oral apraxia, or the difficulty in finding the positions of the oral organs, results. Thus the patient cannot whistle, protrude tongue between lips and teeth, and so on. His speech production is profoundly disordered; in severe cases or in the initial phase after onset of damage, the patient is totally unable to speak or deforms the sounds so that they cannot be identified. But in the later phase after onset, or in milder cases, the main symptoms are abnormalities in production of speech sounds, i.e. the articulatory patterns produced deviate from those required by the phonetic pattern of the whole word; these deviations may sometimes be relatively minor. In addition the patient makes a major effort to pronounce the sounds; he visibly gropes for the correct positions of the articulators. Certain regularities may be noted in the deformations caused by this type of aphasic disorder. A speech sound proper to the phonetic context of a given word is substituted by another sound which is close in manner of articulation, but which distorts the pattern of the whole word; this symptom is called literal paraphasia. Analysis of literal paraphasias in the speech of such aphasic patients has revealed that such substitutions arise from inaccurate execution of the set of articulatory movements needed for a specific speech sound; they are "derailments" of the typical motor configuration for a given phoneme. For instance, the patient may say "vale" instead of "fail", "cikar" instead of "cigar", or "auno" instead of "auto", and so on. This is a grave handicap in communication; at times the sound sequence of a word is so distorted as to be unintelligible. Similar disorders are found in the patient's written texts, for articulation plays an essential role in writing. Letters are substituted one for another (letter paragraphia). The patient who makes errors in articulating the sounds of a word will also misrepresent a word graphically. This is exemplified in the following text by a patient with afferent motor aphasia (author's own observations). "Jest ju£ zima. Na dlore [dworze] jest broz [mr6z], Dzieci idq na lod. Mam j u i 2

Luria uses the term "kinesthetic". Konorski (1967, 1968) proposes the term "somesthetic", reserving the term "kinesthetic" for sensation of movement.

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fy&y [ty£wy] i sanki. Ojcies [ojciec] kupil na giazdk? [gwiazdk?] narky [narty]. (Roughly translated: "It is winter. Outside it is frosty. Children are sliding on the ice. I have skates and a sled. Father bought me skiis for Christmas." The correct versions are given in brackets). The fact of writing impairment as accompaniment to defective phonemic articulation has been utilized in a study of types of articulatory errors made by a patient (Maruszewski and Mierzejewska, 1963). Table VIII shows the results of an analysis of letter paragraphia in the written texts of a patient with afferent motor aphasia during a lengthy reeducation programme. TABLE VIII Letter paragraphia in texts written by patient J. L. (engineer, 25 years, left side lesion) (after Maruszewski and Mierzejewska, 1963). Type of error Total 3 Unvoicing Voicing Nasalization Loss of nasality Change in place of articulation

Number 810 155 135 43 34

Type of error

Hardening Change in degree of openness Sound omissions Substitution u-1 Substitution i-j

Number

30 151 100 55 87

20

A close look at Table VIII shows one feature typical of all the errors occurring in the writing of this patient, viz., they all result from confusions either in pronunciation or graphic representation of speech sounds which differ only in certain distinctive elements of the articulatory configuration involved. For example, voicing of speech sounds ("blease" instead of "please") or unvoicing ("towntown" instead of "downtown") is related to a defective movement of the vocal cords in the particular instance: when the vocal cords are spread, the sound is voiced, and when they are closed, it is unvoiced. Nasalizing oral sounds ("ban" instead of "bad") or denasalizing nasal sounds ("rudway" instead of "runway") is due to a defective position of the velum. When the point of articulation is altered, the quality of the sound changes ("capegory" instead of "category"). All the other errors can be interpreted in like manner. Thus we find that cerebral damage has deranged or disintegrated a whole articulatory complex necessary for the production of a speech sound 4 . Sometimes an 3

This table excludes the following types of error: graphic derangement, errors based on regional dialect pronunciation, errors related to perseveration or anticipation; these imply other pathophysiological mechanisms than those now under discussion. 4 More detailed discussion of this conclusion based on the analysis of sounds produced by aphasic patients is contained in an unpublished study by Mierzejewska (1969).

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element is omitted, sometimes one is added. From this we may infer that such distortions are symptomatic pf a disorder of differentiation between similar articulation patterns, probably connected with impairment of analysis and synthesis of somesthetic impulses arriving from the articulators. The patient mixes up similar sound patterns and is unable to select the correct one instantly and automatically, as in normal speaking. At the same time, as Luria points out, this type of patient has maximum difficulties when called on to articulate separate sounds, and much less trouble when producing them within the context of the whole word. This finding may be a very useful starting point for reeducation (cf. Maruszewski, 1965). Furthermore, it supplies evidence that the process of linking articulatory patterns together, transitions from one speech sound to another to form larger sequential units, remains intact in the event of damage to the postcentral region.

C. EFFERENT MOTOR APHASIA! DISORDERS OF SPEECH SOUND LINKAGE IN WORD FORMATION

We stated earlier that in afferent motor aphasia the main disturbance lies in the production of speech sounds; that is, the basic units of text are disordered but normal proficiency in linking them together into larger wholes remains. We shall now deal with the reverse situation, i.e., aphasic disorders in which individual speech sounds are easily produced but combining processes to form words are disrupted. In other words; the serial organization of speech production is impaired at the level of the word. This type is called efferent motor aphasia in Luria's terminology. According to Luria, this type of speech disorder arises from lesions on the inferior portions of the premotor region (Broca's area). Patients with lesions in this area do not display disorders of oral praxis. They have no difficulty in correctly posturing the articulators, and so they can pronounce the individual speech sounds. Their disorder involves the transition from one articulated unit to the next so that the speech flow is hampered. In very severe cases, the patient cannot even utter one word; producing the sequences of sounds that make up a word presents an insurmountable hurdle. Responsible for this condition is the loss of rapid inhibition of the articulatory motor pattern once it is actualized, without which the next unit cannot be executed. The automatic flow of any phonetic word pattern, typical of normal speech, is lost, and as a result each successive sound or syllable requires an individual effort. Scanning, i.e. reciting separate syllables in strings, then results. Perseveration is another symptom; this is the multiple repetition of sounds or syllables just produced. For instance, when the patient tries to say the word "ruler", he repeats the first syllable "ru" over and over as he tries to go on to the next syllable but cannot surmount the perseverating first syllable; what he produces will tend to be "re", which is a fusion of the two syllables. Instead of saying "ruler" he will say: "ru...ru...ru...re".

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We find a similar phenomenon in the patient's writing. He may easily write each letter separately, but he has great trouble in writing a whole word: he switches the order of letters, he ponders before starting to write the next letter, and letters and syllables perseverate. As mentioned earlier, the speech disorder we are now describing is a consequence of selective lesions in Broca's area, which is a part of the premotor region. According to Luria this region has the function of ensuring the temporal flow of motor organization, which gives a smooth automatic character to movement of any kind. Broca's area has this function in terms of the flow of speech. Thus lesions in this area are responsible for disorders in the serial organization of speech sounds in word formation. But Konorski (1967,1968) considers this area (Broca's) to be that part of the kinesthetic analyzer connected with speech. It is necessary for the retrieval of the motor patterns of the articulators, in contradistinction to retrieval of postural patterns which depends on the postcentral region. The two forms of motor aphasia just discussed, afferent and efferent in Luria's terminology, constitute disorders of the most elementary operations, as it were, in speech production. The former involves the production of phonemes or speech sounds, and the latter their combination into more complex units. Before we proceed to discuss aphasic disorders pertaining to other organizational levels of speech production, it would be well to consider for a moment the localization of the neural structures whose pathology is responsible for these disorders. The fact is that, despite rather fixed views to the contrary, there is good reason to doubt the association of these disorders with firmly demarcated regions. This is particularly true of efferent motor aphasia, or Broca's aphasia. Since the time when Broca described his cases (see Chapte^ II § 2), the opinion has taken root that the posterior third portion of the left third frontal convolution, called Broca's area, constitutes the motor centre of speech where damage causes motor aphasia. Subsequent research, as earlier mentioned, has differentiated between at least two syndromes of motor aphasia. Thus the accepted view has been questioned on grounds of symptomatology. In addition, certain data in the literature alert us to caution in interpreting the specific role of Broca's area for speech; while not adequately grounded to quash the accepted view, current findings and discussions merit careful note. As we recall, Pierre Marie tried to disprove the thesis that Broca's area constituted the motor centre for speech, using postmortem cerebral analyses of Broca's cases. This question is today still a subject for debate. First of all, patients have been described who, despite left lesions in Broca's area and absence of lefthandedness, did not incur aphasia. Tonkonogi's (1968) review of the literature yielded descriptions of 16 patients with postmortem verification of the destruction of the left Broca's area who were nonaphasic during their lifetime (11 cases) or incurred only slight transient aphasia (5 cases). The author himself

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observed one patient with a lesion in Broca's area which produced only temporary speech disorder of brief duration. Tonkonogi makes the point in his review that the descriptions of patients with apparently persistent aphasia after selective lesions in Broca's area are less than convincing for two reasons. Either the lesions were widespread, embracing other left hemisphere structures, or the disorder was too brief in duration. In such a state of affairs, certain rare cases of bilateral selective lesions of Broca's area take on high significance; three such descriptions are cited by Tonkonogi from the literature and one more from his own observation. These cases show that, even in this pathological condition, speech can be recovered. Thus it seems that absence of speech disorder in the event of unilateral damage to Broca's area does not necessarily entail, as often claimed, the takeover of the function of the injured area by the normal homologous area of the contralateral hemisphere; neither must it be assumed that destruction of Broca's area necessarily entails chronic aphasia. A similar view has been expressed by Penfield and Roberts (1959); from their own experience and that of other neurosurgeons, they concluded that the entire left third frontal convolution may be ablated even in adults producing only a transient aphasia, provided that the rest of the brain is normal. Lenneberg (1967) notes in this respect the findings on the cytoarchitecture of Broca's area. It has been shown that, although the architectonic map of this area does in fact differ from that of the adjacent cortical regions, yet very wide individual variations can be found in this structure: also the cytoarchitecture of Broca's area has some similarities to homologous cortical areas in the monkey brain. The question therefore arises as to whether this is, in fact, an area specific to humans and related to specifically human functions; it is also questionable whether this area has a homogeneous function. The arguments we have just raised do not settle one way or another the functional role of Broca's area; the question remains whether this area is specifically connected with a certain aspect of cerebral speech regulation or whether other parts of the dominant frontal lobe are involved. Further investigations are clearly needed on this disputed point. However it is firmly established that the posterior portions of the frontal lobe and the anterior portions of the parietal lobe in the dominant hemisphere—hence the anterior part of the speech area—play an essential role in speech production. We shall now turn to those forms of aphasia where the more complex organizational levels of speech production are affected.

D. EFFERENT MOTOR APHASIA: DISORDERS OF SENTENCE CONSTRUCTION

The disorders of word formation described in the foregoing section occur in severe cases of efferent motor aphasia when the premotor region is extensively damaged

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or during the initial phase after the injury. In milder, cases of this form of aphasia, disturbances affect mainly sentence construction. Such patients have little difficulty in forming single words, although some distortions occur, but are clearly deficient in the construction of simple sentences. Goodglass, Quadfasel and Timberlake (1964) analyzed the speech of aphasic patients in conditions of free and structured conversation, isolating groupings of words uttered without pauses or hesitations and comparing them according to the number of words in each grouping. The ratio: the number of 5-or-more word groups divided by the number of both 1-word and 2-word groups, was determined for each sample, yielding an index called the "phrase length ratio". When several samples of conversational speech from the same individual were compared, considerable stability of phrase length ratio was found. Comparison of three groups of subjects—motor aphasic patients, other types of aphasic patients and normal speakers—showed clear differences in terms of this index. The two latter groups were "long-phrase dominant"," i.e., they showed a high ratio, whereas the motor aphasia cases were "short-phrase dominant", with a ratio lower than 0.15. These patients spoke only one or two words without pauses (out of 100 1- and 2-word groups, there were about 15 groups of 5 or more words, as compared to the other subjects who had ratios between 0.31 and 1.5). We have in this report a precise characterization of a feature long recognized as typical of motor aphasic speech. Most frequently, the verbalizations of these patients consist of single words, usually nouns, without normal syntactic or morphological relations. This clinical symptom has been called "telegraphic style". Luria (1962) illustrates this type of speech in the following observation: "Vot front ... i vot... nastplenie ... vot ... vzryv ... i vot nichego ... vot... operacja ... oskolok ... rech, rech ... rech." (Translated: Here front ... and then ... attack ... then ...explosion ... and then ... nothing ... then ... operation ... splinter ... speech, speech, ... speech.) Telegraphic style in motor aphasia speech has become a point of controversy. Luria (1947, 1962) links it to a disorder of the predicative function and to disintegration of sentence schemas. In his view, a sentence contains essentially a predication about a subject; a comment is made about something. The motor aphasic patient is incapable of the use of words to propositionize and so restricts himself to the subject of the sentence as if shifting the predicate to nonverbal forms of expression, such as gesture or physical action. In such utterances the noun in the nominative case5 predominates. Pick (cit. in Goodglass, 1962) holds the view that telegraphic style is a consequence of the patient's altered attitude toward speaking; his difficulties in expressing himself force him to focus on the most meaningful words, as the best vehicles of information, and omit words with merely grammatical function. Goldstein (1948) associated 5

In inflected languages (such as Polish and Russian) the form of the word changes according to the case in which it is used in the sentence.

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telegraphic style with the difficulty typical of aphasic patients to employ the "little words" signalizing syntactic relations within the sentence. Bein (1964) suggested an interesting explanation of this phenomenon. In her opinion telegraphic style is not necessarily a constant element in the clinical syndrome of motor aphasia; it may result from the patient's own efforts to regain speech by focussing first on names of concrete objects. It may also be the consequence of incorrect therapy: the therapist, by stressing nouns on the assumption that they are the most useful in communication, trains the patient to use nouns in the nominative case or, in other words, to acquire the telegraphic style of speech. If from the start therapy is correctly oriented so that not only nouns, but all parts of speech, are practiced in forming simple sentences, then the telegraphic style can be avoided. The author supports her conclusions with evidence from observations. Telegraphic style is—in this view—the outcome of faulty compensations during recovery. Telegraphic style in motor aphasic patients is part of a broader phenomenon described as agrammatism, involving difficulties not only of combining words into sentences but also of constructing well-formed sentences. The patient confuses case, mood, tense, etc. This type of disorder occurs in various forms of aphasia—not only motor but sensory as well, where speech reception is mainly affected and speech production symptoms are secondary (see below, § 5). The term "motor agrammatism" has been introduced to cover those deviations of sentence construction found in motor aphasic speech. Research into this symptom has been conducted by Goodglass (Goodglass and Berko, 1960; Goodglass, 1962; Goodglass et al., 1964). We have already quoted findings from this source on utterance length in motor aphasic speech; we now report data found by thase workers on other features of motor aphasia. Goodglass and his group experimented on the differences in degree of difficulty which use of English inflections presents to the aphasic patient. Their subjects were a group of patients who could complete sentences on request. The sentence completion task involved using words in their various grammatical forms. Distinct differences were found in the difficulty of inflectional endings according to grammatical function. This was particularly marked when the patient had to use the same sounding word (homonym) in different sentence contexts where it served varying grammatical functions. In English the ending "s" has several functions; depending on context, it can mark plurality, possession, or third-person singular present tense of the verb. [For example: I have two brothers ("s" marks plurality); I shall take my brother's car (possession); He works (3rd person verbal form).] It was found in this study that there was a constant degree of difficulty for aphasics using various inflectional endings, linked not with phonetic quality but with grammatical function. In the above example the ending "s" to mark possession was most difficult. Patients made 5 times as many errors in completing sentences where this function of "s" was called for than when plurality was required.

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Another kind of symptom associated with agrammatism in motor aphasia is disorder of prosody, i.e. of stress, beat and intonation. These melodic features of speech play a large role in communication; simply compare the intonations of interrogative and declarative sentences. These features can be very severely disordered in motor aphasia. The patient's speech becomes monotonous, devoid of stresses and other prosodie features; there may also be deviations from the normal distribution of prosodie features in the utterance. Since these features have a semantic function, i.e., as vehicles of meaning, prosody disorders produce a deficit in the communication process. A special technique of speech registration has been designed called the dynamogram, by means of which one can diagram the distribution of stresses in sentences. Winarska and Ruda (cit. after Luria, 1962) asked patients to repeat the sentence: "I am going to the movies", stressing first "I" and then "movies" (Fig. 18). A com-

]_am going to the movies"

"J_ am going to the movies"

"J_am going to the movies'

'I am going to the movies'

"I am going to the movies"

"I am going to the movies"

Normal case

Patient with damage of the left parieto-occipital region

Patient with damage of the left premotor region

Fig. 18. Dynamogram of the sentence "I am going to the movies" expressed by (1) a normal person, (2) a patient with damage in the posterior portion of the left hemisphere, and (3) a patient with damage in the left premotor division. The stressed word is underlined. (After Vinarska and Ruda, cit. after Luria, 1962.)

parison of normal sentence repetitions and versions by patients with afferent and efferent aphasia showed that the latter displayed disorders of the prosodic organization of the utterance. Not only was the ability lost to switch the stress, but stress as a feature was entirely absent. It is worth noting that disorder of prosody is a somewhat separate symptom from motor aphasia whose pathology lies in the premotor region. This fact comes to light in two conditions. In the first, we have cases of very severe disorders of speech production where prosody is intact; in fact, the use of prosodic features, especially

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intonation, is the patient's only basis for communicating with the environment. This applies to cases where speech is reduced to residual stereotypes such as "ki ki ki", "tiu bu bu", etc. By endowing such verbal residues with a rich intonation, the patient can convey a great deal of information such as surprise, doubt, request (to repeat the question), and so on. Intonation can thus substitute for the lost ability to transmit meaning through articulated words (Kogan, 1962). The second condition in which prosodic disorders stand apart from motor aphasia is found in those patients with lesions in the premotor region whose dominant aphasic symptom is prosody disorder. The first description of this kind was reported by the Norwegian neurologist Monrad-Krohn (after Tonkonogi, 1968), who observed a patient born, bred and dwelling only in Norway, who after brain injury began to speak Norwegian with a German accent, having very minor symptoms of motor aphasia. At present a number of descriptions are available where the main symptom of disorder is alteration of prosodic features, conferring upoii the patient's speech properties of other languages than his own. But there is not precise enough data to permit a deeper examination of locus of cerebral damage causing these disturbances, or of their mechanisms.

E. DYNAMIC APHASIA: DISORDERS OF DISCOURSE CONSTRUCTION

We have been discussing those disorders of speech production which invariably involve some derangement of speech sounds and words, although not always as the dominant symptom. We have also discussed those speech production disorders where the prevalent symptom is disturbed sentence construction. These disorders are revealed in circumstances where the patient initiates speech or repeats what the examiner has said. In other words, we have been dealing with disorders of articulatory processes in situations of both spontaneous and reproductive speech, where afferent motor aphasia and both variants of efferent motor aphasia are concerned. There is another highly specific form of aphasia which differs fundamentally from the forms discussed so far. It is distinguishable by the fact that only spontaneous speech is affected. Such patients have no trouble in saying single words or simple sentences in answer to questions, or in repeating fairly lengthy sentences, reciting verses and strings of digits, re-narrating a story just heard, and the like; in all such situations speech is normal. The aphasia we shall now discuss is restricted to one situation (if the syndrome is sufficiently selective), i.e., when the patient composes discourse unaided. Quite some time ago this symptom was noted and named "transcortical motor aphasia", being associated with ruptured pathways between Broca's area and other frontal regions lodging the "conceptual centres" (see the WernickeLichtheim classification in Chapter II, § 2). It was established that this disorder occurs when a lesion affects the left frontal lobe and is lodged anteriorly to Broca's area (Luria, 1947,1962; Luria and Tsvetkova, 1968).

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When this type of patient tries to compose spontaneous discourse (spoken or written), he is either unable to start or is able only to utter irrelevant stereotyped phrases. Luria (1962) illustrates this syndrome by a case where the patient was asked to write a story about the North where he had spent a number of years. After long pondering, he wrote the sentence: "There are bears up north". Urged to write more, he added a second clause to this "story" which runs (in free translation) "which is something I would like to call to your attention". These patients lack an active attitude and do not initiate speech; they generally complain of "emptiness in the head" and inability to phrase in words, the information they want to express. As a result they spend long hours in silence, without verbal contact with the environment, merely answering questions addressed to them. In his earlier work on aphasia, Luria (1947) suggested that this form of aphasia is a disorder of inner speech, i.e., a consequence of the patient's inability to plan an utterance. This was thought to be a kind of disorder of verbal thinking involving loss of the ability to programme a text spontaneously in the mind. Support for this hypothesis was the evidence that the patient could be helped to overcome this handicap through reeducative procedures aiding him to lay down a plan on paper. For instance, the patient was asked to note down on separate cards those bits of information about a given topic as they came to mind. Once the patient had made notes on a number of such cards, a plan was worked out for an expanded utterance, based on ordering the cards in a suitable way. Another way in which the patient was significantly helped to formulate a story was to supply him beforehand with a list of words and expressions serving to link together lexical words or word groups, such as "once", "then", or "because". With these external "props" the patient could manage to write a story on some topic which otherwise would have been an impossibility for him (cf. Luria, 1948). The above facts illustrate the specificity of the disorder called dynamic aphasia. The technical side of speech production remains intact, but the process of generating the content of discourse is impaired. Luria, and more recently his collaborator Tsvetkova (1969), have associated their research on dynamic aphasia with the inner speech theory of Yygotsky (1956). Vygotsky's conception was that inner speech is characterized by predicative properties; in other words, it is restricted to those words that state something about some object. It may be inferred from this that the inner plan for an utterance is largely restricted to the predicative part, i.e., the verb. The question then arises whether the mechanism behind dynamic aphasia may not involve a peculiar difficulty with using verbs, if they constitute the basis for inner speech. Tsvetkova tried to verify this hypothesis in a study in which she compared the ability to actualize nouns and verbs in patients with dynamic aphasia. The patients, with eyes closed, were required to produce as many nouns as they could in 60 seconds' time; then similarly verbs. A striking difference was found in the production of nouns and verbs: the mean number of nouns per minute was 10.3 and of verbs about 2.7. Individual differences were insignificant. Tsvetkova also noted that

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the patient in unaided attempts to formulate discourse had difficulty in producing words standing for actions; either he omitted the verbs or placed them at the end of the sentence, contrary to the rules for Russian. Tsvetkova made another interesting observation concerning the ability to formulate sentences in patients with dynamic aphasia. As mentioned earlier, such patients could on the whole produce simple sentences; for example, they could answer questions, especially when the question contained words which might be employed in the answer; or they could reproduce stories they had just heard. The trouble mounted however when the patient had to compose a sentence with a subject and predicate based, for example, on a simple picture of a horse drawing a cart. He would usually restrict himself to itemizing the objects in the picture (horse... cart) without building a complete sentence. Tsvetkova made use of an external schema for constructing the sentence, which was a row of blank cards. The patient was asked to point to the cards from left to right as he produced the words making up the sentence. This external schema was found to be extremely helpful to the patient in forming complete sentences. A moment earlier the patient would have been powerless to combine two words in a sentence; now by touching the cards one after the other he could produce a wellformed sentence composed of 3 or 4 words. Applying this method, the patient was even able to utter ex-situational sentences. For instance, when asked to tell what trucks are used for in the countryside, the patient produced: "So ... seed ... no". He was then handed some blank cards which he laid down before him; pressing his finger on each card in turn, he now answered as follows: "Trucks ... carry ... grain ... to the barn". Lucki (1965) made similar observations about the role of external schemas in constructing spoken texts in a study of aphasics with dominant frontal lobe damage. He describe^ a patient with a severe speech disorder which in the initial phase affected production of phonemes and words. Later during therapy these difficulties abated and work was undertaken to arouse active speech in the patient. For this purpose the therapist used a picture of a farmyard scene. Asked to prepare a story on this topic the patient produced the following utterance: "Here is the barn. And there are cows in the barn. A cat and dog are waiting for some milk. A man is taking the milk to the dairyhouse. Chicken and ducks... and geese are eating oats. That's all". Encouraged by this successful performance, the therapist then asked the patient to prepare a story for the next therapy session on the subject of "dyngus" 6 (this occurred shortly before Easter). The patient was also given the farmyard picture he had already described as an aid to practice his previous story. At the next session the patient spoke as follows: "Here is a house, and there are girls in the house, and boys are trying to throw water over them. And the girls are scared of the water. And the boys ran off home. They (the boys) were scared of the water". Only after he had finished talking did the therapist note that he had placed before him the picture used at the 6

"Dyngus" is a traditional Polish holiday, Easter Monday, mainly celebrated in the countryside where boys try to throw water over the girls who escape as best they can.

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previous session. The therapist tried to remove it, whereupon the patient protested. It turned out that he was using the picture as an external schema to organize his story about "dyngus", as evidenced both in the construction of the story itself and in his outward behaviour. Mentioning the house, he pointed to the barn, mentioning the boys, he pointed to the domestic fowl, and so on. Without this prop he would have had far greater difficulty in carrying out his task. More study is required before the phenomena just described can be clarified. But it is already amply clear that the frontal lobe region anterior to Broca's area, damage to which is responsible for such symptoms, must play a role in the organization of the complex processes involved in the formulation of more extensive texts. These phenomena also suggest that this region has special importance for inner speech, i.e., for the ability to lay down a plan for the utterance. Relevant to this question are the results published by Milner (1964, 1967) on "verbal fluency" in patients with left frontal lobe lesions. This author studied two groups of patients who had undergone curative surgery for epilepsy (without aphasia), the epileptogenic foci having been situated in various parts of the brain. Of numerous experimental tests applied by Milner, one task required the patient to write down as many words as he could beginning with "S" in 5 minutes; afterward he was to write as many 4-letter words as/' he could beginning with "C" in 4 minutes. Two groups of patients with different locus of cerebral damage were compared as to the combined score of the two tests. Table IX shows the results in two successive trials, one a few weeks after surgery, the other several years later. TABLE IX Mean number of words in verbal fluency tests for groups of patients with different locus of postoperative lesions (based on Milner, 1964,1967). Results for 1964 ("early" group) Locus of excision

Left frontal Left temporal Left parietal Right frontal Right temporal

number of patients

mean score in word fluency test

7 7

35.4 57.6

4

56.8

—

—

—

—

Results for 1967 ("later" group) number of patients

mean score in word fluency test

6 18 4

28.7 49.3 44.3

—

12

—

58.4

There are two points worth noting in Table IX. Firstly, in both groups of patients a clearcut statistically significant difference has been reported by the author between verbal fluency scores of patients with left front damage and those with lesions elsewhere (despite the small number of subjects). In other words, patients with left frontal damage, but who do not show clinical symptoms of aphasia, sustain a consid-

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erable loss of verbal fluency, that is, ability to produce words according to a given feature. Secondly, this phenomenon is found not only in the immediate postoperative period ("early" group of 1964) but is also after several years ("later" group of 1967). The change thus appears to be stable and specific to damage in the left frontal region outside of the speech area. It is rather a difficult matter to interpret these findings, since the tasks applied were too specific and abstract to admit of more general conclusions. We can note some correspondence between the above findings and an observation made by Luria (1947, 1962) and Tsvetkova (1969); these authors noted that patients with dynamic aphasia have serious trouble in producing automatic strings of words in reverse order. Patients who could easily count to 10 or 20, could not count backward. This task also calls for certain abstract operations and internal manipulation of well-fixed verbal material. Perhaps these two tasks require specific metalinguistic operations in inner speech and for this reason are disordered when this locus is damaged.

F. OTHER DISORDERS OF SPEECH PRODUCTION DUE TO FRONTAL LOBE DAMAGE: "SUBCORTICAL MOTOR APHASIA"; DISORDERS DUE TO LESIONS IN THE SUPPLEMENTARY MOTOR SPEECH AREA

Our review of the various forms of speech production disorders caused by lesions in the anterior portions of the speech area should include certain others as well. Primarily we shall mention the form known as "subcortical motor aphasia", which is said to be connected with disruption of the pathways connecting Broca's area and the articulatory apparatus. This form of aphasia was postulated as far back as Wernicke-Lichtheim's classification (see Chapter II, § 2) and later became the subject of ardent discussion among workers in the aphasia field (cf. Brain, 1965). At first the debate hinged around the question whether this disorder could be singled out as a specific form of aphasia, later the disputed question was locus of damage responsible for it. There was also some difference of opinion as to whether this could be taken as a variant of aphasia or simply a disturbance of the dysarthric type. The distinctive feature of this speech disorder is that, while particular processes involved in speech appear to be intact, the patient is unable to speak (some authors call this "pure verbal mutism") or, if he speaks, his talk is profoundly deformed. At the same time these distortions are unlike those of typical dysarthria in that the organs of the oral cavity function normally (see Section A above). Also, in contradistinction to the motor aphasias described earlier, the patient with "pure verbal mutism" does not display writing disorders; he is also able to determine the number of sounds and syllables in a word, and the number of words in a sentence, evidence that inner speech may be preserved. This form of aphasic patient is extremely rare; we have few exact studies of the mechanisms behind this disorder. As to the anatomical base there is little data which would permit a demarcation of the structures

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involved. In Brain's view (1965), the hypothesis associating them with subcortical lesions remains unverified. The situation is clearer when we come to consider the role played in speech production by the "supplementary" motor area for speech. Penfield and Roberts (1959; see also Chapter IV, § 2, Fig. 14), who employed the method of electrical stimulation of the cortex during surgery, found that the medial surface of the left frontal lobe anterior to the motor representation of the legs, when stimulated evokes perturbation in the speech of the patient similar to that observed when other parts of the speech area are stimulated. This is evidence that this region, which the authors have named the supplementary speech motor area, has its own share in the cerebral regulation of speech. At the same time they found that surgical ablation of the supplementary speech area in the dominant hemisphere produces a transient aphasia of several weeks duration, clearing almost totally. Penfield's data, first published in the early fifties, aroused lively interest; only then did it come to light that clinicians had long noticed speech derangements associated with damage or stimulation of this region without ascribing significance to their observations (cf. Chusid et al., 1954; Tonkonogi and Ag'ejeva, 1961; Tonkonogi, 1968). Briefly, these observations can be summarized as follows: When the supplementary motor speech area in the dominant hemisphere is stimulated, as for instance when an adjacent tumour exerts pressure, epileptic seizures occur which typically interrupt vocalization or produce multiple repetition of words, syllables or phrases uttered at the onset of the attack. Lesions or ablations of this area produce aphasic disorders whose symptomatology differs in patients with cerebral vascular disease and those which are postoperative cases; in the latter group, the symptoms clear relatively rapidly but in the former, disorders are more persistent, probably due to involvement of a wider area. Tonkonogi (1968) observed three patients with damage of vascular origin in this region and concluded that the resultant disorders could be associated with lesions affecting other cerebral areas as well. In any event, the facts amassed so far demonstrate convincingly that this portion of the dominant frontal lobe also participates in cerebral speech regulation although the specific mechanisms involved need clarification. Konorski (1961) has suggested that the function of this region is to cross-switch the motor stimulatory patterns; the loss of this function when the field is damaged produces a strong tendency for perseveration. *

#

*

The above discussion of speech disorders originating in stimulation or injury to the supplementary motor speech area of the dominant hemisphere ends this review of speech production disorders associated with anterior damage of the brain. Lesions situated in the anterior parts of the dominant hemisphere, as observations demonstrate, evoke symptoms of which the most striking are disturbances of speech production.

5. CEREBRAL MECHANISMS O F SPEECH P R O D U C T I O N

U7

However, similar disturbances are likewise observed when the posterior parts of the speech area are damaged, i.e., in the various forms of sensory aphasia where the receptive side of speech is predominantly affected (see Chapter VI). We shall now turn to a brief discussion of this aspect of matters.

§ 5. CEREBRAL MECHANISMS OF SPEECH PRODUCTION IN THE LIGHT OF ITS DISORDERS DUE TO DOMINANT HEMISPHERE DAMAGE: LOCUS IN POSTERIOR DIVISIONS

It was pointed out earlier in this chapter (in § 1) that every motor activity, not excepting speech production, depends upon an inflow of sensory information about the conditions of performance and about the course of performance itself. The latter kind of information is particularly important since it enables the course of an activity to be tested against the plan, on which attainment of the intended result depends. It also is the basis for introducing corrections in the event of any deviation from the plan that would jeopardize a successful outcome of that activity. In speech production this type of feedback information (afferentation) is supplied in the main by two kinds of sensory information: signals about the position and movements of the articulators, and auditory input of one's own speech. When we discussed efferent and afferent motor aphasia (in §4), we learned about those disorders of speech production which depend—on the basis of data hitherto available—on disturbances of analysis and synthesis of sensory feedback information arriving from the articulators during the act of speaking. No less severe disturbances in speech production, but of a different origin, occur when analysis and synthesis of auditory sensation is disrupted. Since speech reception in general is deranged, the patient is deprived of normal auditory afferentation or feedback while he is in the act of speaking. We find these speech production disorders occurring in various forms of sensory aphasia associated with injury to the posterior parts of the speech area 7 . The simplest form of speech production disorder in sensory aphasia is literal paraphasia, or the substitution of one speech sound for a phonetically similar one. We have already said that literal paraphasia occurs in afferent motor aphasia as well; now we shall see that there is a basic difference between the sound substitutions in these two forms of aphasia. In afferent motor aphasia, the substitutions are symptomatic of disorder in the differentiation of similar patterns of articula7 An experimental model simulating the condition of the person suffering from perturbed perception of his own speech has been applied for the study of delayed auditory feedback', by means of a special apparatus the subject hears his own utterance with a slight delay (a fraction of a second). Numerous experiments have demonstrated that such a delay causes distinct disruptions in speaking, reading and repeating, as manifested in a slowdown of speaking rate, inability to adjust speaking rate at will, and so on (Chase, 1958; Lenneberg, 1967). Therefore even slight interferences in the reception of one's own speech suffice to upset productive operations. In sensory aphasia, receptive speech disorders are much more severe, hence it is not surprising that speech production disorders are also more clearly marked in these cases.

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tory movement; the phonemes affected are similar in manner of articulation. On the other hand, in sensory aphasia, substitutions are symptomatic of disordered phonemic hearing; they concern those phonemes phonetically similar in acoustic features. Omitting the question of how to diagnose these two forms of literal paraphasia, we note that in sensory aphasia (or more strictly, acoustic aphasia, as in Luria's terminology, associated with lesions in Wernicke's area, to be discussed in Chapter VI, § 3B), we are dealing with unstable auditory word-patterns, as shown by the fact that the patient not only displays literal paraphasia but also gropes for the correct sound so that the whole word is deformed (Luria, 1947, 1962). Broadly speaking, lesions of the posterior third division of the superior temporal gyrus of the dominant hemisphere (Wernicke's area) cause disintegration or derangement of the acoustic patterns of speech sounds and words without which correct production is impossible. This explains the frequent symptom that patients speak in stereotyped expressions (fixed articulatory habits) producible without auditory feedback afferentation. Examples of such expressions are: "Okay ... listen you... let's see now ... so long kid". Sometimes there are symptoms of "verbal salad" when the patient speaks fluently and without the articulatory groping typical of motor aphasia but strings together loosely connected words without intelligible meaningful relations between them or with a topic. Here is an example of such a text: A patient suffering from severe sensory aphasia of vascular origin was shown a set of pictures; in the first a little girl is running, in the second she is falling down, and in the third she is crying. The patient says (in free translation): "Well miss... there was a person (noun with wrong case— ending suggesting instrumentality) who was riding along with a little girl (masculine gender ending to noun and adjective) here on ... (nonsense word), on a boy, what was her name, and here was some tiny ... (nonsense word, plural form), very little ones, and here is a little boy still fast, sort of young, with that little girl". Then the examiner pointed to the first picture and asked: "What is she doing?" The patient answered: "Oh yes, it was still in a black, navyblue, blue, her little legs, green kind of, then they made some legs, young young, sweet little girl, nice tree, a lovely little bit of something, here her was wider, that was narrower" (observation noted by M. Nowakowska, translated from Polish8). In this example of "verbal salad", the words are typically unrelated. Also present are "jargon-aphasia" and agrammatisms, other features typical of sensory aphasia. Even though not paraphasias, the words were frequently in the wrong grammatical form. Jargon-aphasia, or speech deforma8

The original version of this observation is: "Prosze pani, a wi?c to by! czlowiekiem, kt6ry sobie jezdzil przy malym dziewczynem, tutaj na poleSli, na chlopcem, jak ona si? nazywala, a tu bylo malenkie obieszczki takie mate, tu chlopczyk malutki jeszcze szybki, taki mlody, dziewczynk^ takq". The examiner pointed to the first picture and asked: Co ona robi? "A tak, to bylo w takim czarnym jeszcze, granatowym, niebieskim, nogi swoje male, zielone takie, p6zniej zrobione s^ nogi, mlodziutkie, dziewczyneczka, ladne drzewo, takie jaSniutkie, Sliczniutkie kawaleczek, tu bylo jej szerszej, to bylo wi?siej".

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tions based on production of "non-words" (not in the lexicon of the language) is particularly interesting because it throws light on the sensory determination of speech production. These phenomena have not yet been well clarified. They are not exclusively assoc i a t e with receptive speech disorders because there are known to be exceptions to the rule. For instance, Kinsbourne and Warrington (1963) describe two patients with jargon-aphasia, only one of whom displayed major disturbances of speech reception, while the other showed clear symptoms of "verbal salad" with comprehension preserved. These authors interpreted these states by Alajouanine's hypothesis which associates jargon-aphasia with disturbances in evaluation of one's own speech, or perception of flaws in speaking, i.e., the disorder called anosogrtosia. The present author has also observed several cases of intact receptive speech with jargon-aphasia. Therefore the mechanism responsible for this symptom is not solely a disorder of analysis and synthesis of auditory feedback associated with sensory aphasia. Probably other mechanisms are also involved, such as disorders of auditory verbal memory, which is incurred with lesions of the dominant temporal lobe (see Chapter VI, § 3). Some interesting possibilities arise for the interpretation of these symptoms in relation to other symptoms of speech production disorders with temporal lobe lesions in the dominant hemisphere. These are called contaminations or fusions. Very often the patient will produce "words" made up of parts of several words, either those just produced or associated in some way with the context of the utterance or with the next word to be produced. This type of "word" differs from "jargon words" in that their components are recognizable. However, this difference is likely to be superficial and may be a matter of degree of disorder. Both jargon words and fused words probably originate in the same pathophysiological mechanism: jargon words are totally distorted while the elements of fused words are at least partially identifiable. If the patient trying to name an electric light bulb (¿arowka) produces *r§baszka, we have no way of knowing how this neologism came about. But if a patient has been trying to say the word for teakettle (czajnik) and next tries to name a hen (kura) and produces *kuszczek, then we can reasonably attribute the origin of this neologism to a combination of the latter word with a perseverating fragment of the word "czajnik" which the patient had just been trying to produce. The pathophysiological mechanism responsible for the production of this neologism would then be perseveration. Probably there are more such pathological mechanisms manifested when the left temporal lobe is damaged. Abov'yan, Blinkov and Sirotkin (1948) collected a large number of contaminations in aphasic speech of Russian patients and analyzed them for their causes. They found that contaminations originated from the following sources: combinations of the word to be produced with a perseverating element of a previously produced word, as in the foregoing examples; combinations * See footnote Chapter III, page 55.

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of the word to be produced with a semantically similar one [e.g., "*butylok" is a combination of "butylka" (bottle) and "puzyriok" (small bladder); "*varchatki" combines the words "variezki" (mitten) and "pierchatki" (glove)]; combinations arising from situational associations such as words signifying an action and its object [e.g., instead of "skovoroda" (frying-pan), "*skrazana", combining the former and "zariat na..." (fry on...)]. Another common origin of contaminations is phonetic similarity between the word to be produced and one that is interjected [e.g., "kolbasa" (sausage) and "sosiski" (frankfurter) give a contamination "*kolbasiski"; also "gospital" (hospital) and "vospitatel" (tutor) give "*gospitatel"]. And so, in addition to perseveration, semantic and phonetic similarity are factors responsible for contamination; in such cases the word selection process is deranged. The patient actualizes not only the word-pattern he wants but also one or more other word-patterns related to the former by contiguity, thereby producing a blend of word-fragments. Similar facts have been observed by Solov'ev (1948) in conduction aphasia. Disorder of word selection is a frequent result of lesions in the dominant temporal region but does not always give the symptom of jargon or contamination. There is another typical symptom, i.e., groping for the auditory-motor pattern of a word, observable especially when the patient has to name some object. For example, one patient with focal damage in this region, but with intact comprehension, tried to name a bicycle (in Polish: "rower"). He produced: "ryba (fish) ryb... o jezu (O Christ)... *rywa ... *weru ... *wernuf... ja wiem (I know) ... re ... *wer ... *wertu... widzisz (you see)... wie (know... *wiew (author's observation). This example illustrates two phenomena. One is a typical symptom of temporal lesions in the dominant hemisphere: the patient produces "ryba", which is a verbal paraphasia; the patient skates around, as it were, and slides off from the correct auditory-motor pattern to one of a similarly sounding word. The other phenomenon is that the patient, knowing he has produced the wrong word, gropes for one that sounds right: first, fragments of "ryba" perseverate and then are transformed into a neologism. Sometimes a patient will manage to approximate the word he wants. For example, a patient who tried to say "wentylator" (ventilator), produced the following: "*ferni... *serninatop ... *wertynatop ... *wentynator". These are good examples to show that, without the articulatory difficulty typical of motor aphasia, speech production is still severely deformed, the pathological basis being a disruption of the process of selection by which word patterns are actualized. Since the injured region is connected with the auditory analyzer, probably these disruptions affect the actualization of the auditory word-patterns. This hypothesis is supported by other data to be discussed in the next chapter. One more very curious phenomenon connected with damage of the left temporal lobe is relevant at this point. The difficulties described in actualizing auditory wordpatterns do not apply equally to all word classes. For reasons as yet unclarified, they affect mainly nouns (cf. for example Goodglass et al., 1966). The following example illustrates this clearly. The patient studied underwent surgical ablation of cerebral

6. CONCLUSIONS

121

tumorous tissue in the superior anterior portion of the left temporal lobe. The lesions did not cause receptive speech disorder but considerably disrupted speech production as manifested mainly in "forgetfulness" of words. The patient was asked to reproduce a story 9 just told him. His version of the tale was (in free translation): "The black one made himself white and went for a meal over to these—they're everywhere around buildings. He was hungry but he couldn't talk like them—he talked like the black ones—so it didn't work out and he had to jump out because those—there are lots of them in Warsaw—could see he didn't speak like those white ones" (author's observation). If the reader did not know the tale, the patient's version would be incomprehensible; but a comparison of the former with the version in the footnote shows that the patient understood it and, to reproduce the story, substituted the names of the leading characters by circumlocutory descriptions. The patient himself admitted he could not recall the names in the story. This same difficulty was strikingly present in other test performances. The cleavage between the ability to produce nouns and words of other classes has also been observed in cases of left parietal lesions, or "semantic" aphasia. It has furnished a theme for lively debate in respect to the relation between language and thought, the use of general concepts, and so on. We shall return to this subject later in Chapter VII. To summarize the foregoing material, it has been clearly demonstrated that speech production depends to a very large degree upon the auditory processes connected with the left temporal region. Our-present knowledge is not sufficiently consolidated to permit an interpretation of the mechanisms connected with the auditory sphere regulating speech production. We may only hypothesize that there are two kinds of mechanisms: one kind is associated with speech reception including one's own, and the auditory feedback afferentation necessary for the normal speech flow; the other is connected with the storage and actualization of auditory word patterns, which, once disturbed, block the selection of words as components of utterances.

§6. CONCLUSIONS

We have reviewed the main forms of disorders affecting speech production. There are some other forms of this general type, more related to the questions to be raised in Chapter VII, viz., on the relation of speech and the cognitive processes, and these 9

This is a tale of the crow who decided to paint himself white in order to dine on the pigeons, but once inside the pigeons' nest his caw betrayed him and he was thrown out by the pigeons. The original version of this observation is: "Jeden czarny na bialo si? zrobil, na bialo poszedl najeác si? do tych, którzy sqi wsz^dzie kolo domów, poszedl i chcial jeác, ale nie powiedzial tak jak one, tylko tak jak te czarne, po prostu nie udato mu si? i wyskoczyl, bo te, których w Warszawie jest mnóstwo, zauwazyly ze on nie odezwal si?, jak te biale".

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will be discussed in that chapter. The material included in the present chapter, however, demonstrates conclusively that the cerebral regulation and programming of speech production is a complex process embracing many differently located structures within the dominant hemisphere. The "motor speech centre", such as was visualized in the classical conceptions, does not exist; rather we postulate a complex functional system underlying speech production, composed of various centres in the speech area of the dominant hemisphere. This does not mean, however, that speech production is the product of the brain as a whole, understood as an equipotential or functionally undifferentiated structure. On the contrary, each of the regions under discussion has its own special part to play in speech production to ensure the flow of speech in one or another of its aspects; the best evidence for this are the above facts showing that, when different localities are injured, the resulting disorders differ qualitatively one from the other. As was earlier mentioned, our present knowledge of the functional system of speech production is incomplete; many fundamental problems require further study. But, from the facts we already possess, a clear outline is emerging of a cerebral construction which determines normal speech production. Let us attempt to summarize the findings of neuropsychological research presented above from the following viewpoint: What can we now say about the localization and functional significance of the particular links in the functional system of speech production within the brain? First and foremost, it has been ascertained that the cerebral regulation of speech production is associated with the normal function of both anterior and posterior parts of the speech area in the dominant hemisphere. In one sense we can say that this regulatory activity is a function of the entire speech area. However, from the data presented, the different component parts of the speech area play their own various roles in regulating speech production; each contributes in its own specific way to an integrated regulation. In the broadest terms, the following parts of the cerebral functional system of speech production can be distinguished: — The inferior division of the postcentral region (the parietal "lid") has probably the function to analyze and synthesize arriving somesthetic information from the articulators, which is needed to posture them correctly in order to produce the different speech sounds. This structure plays a crucial role in forming the most elementary linguistic units, the speech sounds. — The inferior division of the premotor region (Broca's area) has probably the function of ensuring the organization of speech production in respect to timing at the word level (the linkage of speech sounds into word arrangements), as also on the sentence level (combining words into grammatical sequences). This region therefore plays a vital role in arranging simpler units into more complex ones, and ensuring the smooth, "melodic" and automatic flow of this process. — Anterior to Broca's area are the frontal lobe structures whose boundaries are not yet strictly fixed; their functions appear to be connected with the substantive

6. CONCLUSIONS

123

aspect of sentence construction. This includes, on the one hand, actualizing the appropriate words, and on the other, constructing the schemas or programmes of utterances. From the facts reported above, there are grounds to think that this region is of particular importance for the processes of inner speech. — The supplementary motor speech area, located on the medial surface of the frontal lobe, participates unquestionably in the cerebral regulation of speech production, but in a manner not yet clearly defined. Most probably, this region plays a vital role as well in the dynamic organization of speech flow. — Temporal lobe structures probably determine two aspects: one is the analysis and synthesis of auditory feedback afferentation during speech production, which is indispensable for its smooth flow; the other aspect is the storage and selective actualization of auditory word patterns needed as components of utterances. In anticipation of discussions to follow in the next chapters, we recall here that, in addition to the structures listed above, there are other structures that also share in the regulation of speech production; these are located at the parieto-temporo-occipital junction and their role is associated with the semantic aspect of word selection (see Chapter VII) and with grammatical combination of words (see Chapter VI, § 4 A). In conclusion, mention should be made of those questions which remain unresolved, controversial and pending further study. Apart from the more particular problems indicated above (locus and function of the particular parts of the functional system under discussion), there are two primary questions of more general significance. One is the role of subcortical structures in regulating speech production, the other the interaction of the regions already identified. Available data on these two questions do not suffice for drawing precise conclusions. In Chapter IV (see § 2), certain observations were reported on the role of the deeper cerebral structures in speech production. Aphasic research has also provided grounds for hypotheses which attribute certain aphasic disorders to subcortical damage (see above § 4 F). But these facts show that further research is needed to verify the hypothesis that speech production is linked not only with cortical structures in the speech area of the dominant hemisphere, but also with structures lodged in the deeper portions of the brain. There are insufficient grounds for this assertion at present. Still less neuropsychological research has been directed to the question of the collaboration of the various parts of the functional system of speech production. That such interplay must occur is implied in the fact that the processes involved in speech production terminate in creation of a text which could not have arisen without collaboration of this kind. However we know little of the regularities and localization of the neural pathways by which this collaboration is effected. In other words, despite our relatively good knowledge of the elements composing the functional system of speech production, we do not yet possess a good understanding of the functioning of this system as an integrated whole. This question therefore belongs to the realm of problems urgently calling for resolution.

CHAPTER VI

CEREBRAL MECHANISMS OF SPEECH RECEPTION

§ 1. INTRODUCTORY REMARKS

In the foregoing chapter we were concerned with data about speech production and its cerebral regulation. The point was made early in that chapter that we must exercise caution in separating the expressive and receptive processes involved in speech, in particular when dealing with their brain mechanisms. The best example of the need for a relative approach is the particular speech production abnormality examined in the final section of Chapter V, which is associated with auditory deficiency resulting from temporal lobe damage in the dominant hemisphere. The same care must be applied when dealing with the cerebral mechanisms of speech reception. As we shall see, there are good grounds for believing that this activity is not purely receptive and sensory in character but is in large part dependent on phenomena occurring in the auditory sphere. When we speak, certain acoustic events are produced which are perceived by others as speech. There arrives at the receiver's ear a stream of acoustic phenomena or a series of sounds. The basic unit of this flow is the speech sound (or phoneme). Each phoneme speech sound has a number of acoustic features, such as pitch, duration, voice, and others. Studies of acoustic features of phonemes (Jakobson and Halle, 1956) have demonstrated that some of these features play a special role in the communication process; they have been called "distinctive features", since they guide the listener in his discrimination of speech sounds, and therefore of word meanings. In the Polish language, one of these distinctive features is "voicing" (absence or presence of voice), for example, in dorn (house) and torn (volume). The same feature differentiates the English words ban and pan. One of the ways that languages differ one from the other is in respect to the distinctive features of their phonemes. For instance, in English or in Polish, as in many other non-tonal languages, the tonal features of phonemes, which are associated with fundamental pitch, play no role in the communication process, since they are not utilized to discriminate speech sounds. On the other hand, in tonal languages, such as Chinese or Thai, pure tonal elements act likewise as distinctive features, which means that the fundamental frequency of a sound has the function of differentiating word meanings. Thus, to understand an utterance in a tonal language, one must be able to detect differences

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125

in speech soupds in terms of their fundamental pitch, just as comprehension of English or Polish involves the ability to distinguish between voiced and unvoiced sounds as a common distinctive feature. The particular auditory adaptation to the specific properties of a language's phonological system is known as "phonemic hearing" (Luria, 1947, 1962, 1967). Observation and experimental studies (Leont'ev, 1959) have shown that phonemic hearing is not an innate function but is formed during ontogenesis through the action of the phonemic system of the native language upon the auditory system. This explains the characteristic difficulties of the second language learner in perceiving the differences between words that are similar in sound but different in meaning. If features other than those of the native language are critical in differentiating between words, speech reception in a foreign language does not flow economically; it is in a sense disturbed, because the hearer has not developed a phonemic ear for the given language. A basic prerequisite for normal speech reception is phonemic hearing adapted to that language. The process involved is one of complex auditory analysis and synthesis. But speech reception is not simply perception of the sounds of a language. Words are the meaningful elements of any text; they are linguistic signs. The essential part of speech reception is to interpret meanings of words and of larger units of the text. The relation between sound and meaning is highly complex. On the one hand, the sound of a word determines its sense, as we have already seen; sometimes minimal alterations in sound produce radical changes in meaning. On the other hand, there is the phenomenon called "transparency" of a word for its meaning. Words in use are carriers of meanings. In language communication, the physical and sensory vehicle of meaning, which is the sound, is normally a background event; we are rarely aware of it. All our attention is focussed on the semantic aspect of words; only under special conditions does the word lose its meaning, in which case its sound comes into the foreground (Rubinshtein, 1964). In perceiving a linguistic sign, we do not automatically become aware of its material form. The preponderant influence of word meaning (as opposed to word sound) stands out clearly when a person is faced with a perceptual task requiring attention to the acoustic aspect of words. In one experimental variant (Maruszewski and Nowakowska, 1970), secondary school pupils were asked to judge the phonetic similarity of pairs of words reproduced from tape. Of 50 pairs, 20 were controls and the remainder were 3 sets of 10 pairs composed of items having the same degree of acoustic similarity. These items were either words or nonsense syllables, paired so that for each member only one phoneme differed in one distinctive feature (voicing). The sets of pairs had different semantic aspects: the first set was composed of 10 pairs of nonsense syllables (e.g., *taf-*daf; *bugo-*pugo-; *sugona-*zugona); the second set was words paired with nonsense syllables (e.g., dach-*tach; noga-*noka, paliwo-*palifo); and the third set consisted of word pairs. In all cases the same principle * See footnote Chapter III, page 55.

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held of minimal phonetic difference (one distinctive feature). The subjects used a 7-degree rating scale, as follows: Very dissimilar, Dissimilar, Fairly dissimilar, Don't know, Fairly similar, Similar, Very Similar. Table X shows the results of these ratings, percentages being given for the combined two extreme positions at each end of the scale (i.e., Very Dissimilar and Dissimilar together, as also Very Similar and Similar). TABLE X Extreme similarity and dissimilarity ratings (in percentages1) for 3 sets of paired words and nonsense syllables, each set composed of pairs having the same degree of acoustic similarity, but differing on the semantic aspect6 (Maruszewski and Nowakowska, 1970). Set I II III

Decidedly dissimilar ratings0

Decidedly similar ratings0

r 1.7] Ll9.3 19.7.

[55.3] 1.41.3 36.7

a Percentages are based on 300 (30 subjects, each rating 10 pairs per set) b Bracketings indicate statistically significant difference on the level of 0.01. 0 Very Dissimilar and Dissimilar combined; Very Similar and Similar likewise.

The influence of the semantic aspect of words, or word-like items, is shown very clearly in Table X. Although the degree of acoustic similarity does not differ within the three sets of pairs, the subjects gave most accurate estimates when dealing with nonsense syllables (Set I) and were less accurate where meaning entered in. When one member of the pair (Set II) or when both members (Set III) were meaningful words, the impact of this fact upon the judgement of phonetic similarity was so strong that it camouflaged that similarity. There was a statistically significant increase in the number of decidedly dissimilar ratings as well as a decrease in the number of extreme similarity judgements. The semantic side of the word appreciably affects the perception of its phonetic side. This fact serves to underline the error inherent in limiting the research area of speech reception to sound perception alone. A necessary component of this process is reception of the meaning of any spoken text, which is, ultimately, the essential thing in communication.

§ 2. GENERAL CHARACTERIZATION OF SPEECH RECEPTION. ASSOCIATED PHYSIOLOGICAL AND PSYCHOLOGICAL PROBLEMS

So far we have outlined the two more general aspects of speech reception, viz., the perception of the sound component of speech and the reception of meaning, or

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127

the semantic interpretation of words. Hirsh (1964) has attempted to describe in more detail the processes involved in speech reception. In this description, the following abilities or capacities are considered prerequisites for perception of speech and language. Firstly, audibility, or detectability, of speech sounds. Essential to speech reception is a sound intensity higher than the threshold of hearing. If intensity is below the sensitivity level of an individual's auditory system, speech sounds are either not detected at all, or are wrongly heard, as in cases of deafness or loss of auditory acuity when pathology of the auditory analyzer results in changes of sensitivity properties. Secondly, discriminability of speech sounds. Good hearing is not sufficient for speech reception; another necessary condition is the ability to discriminate speech sounds, which is by no means the same thing as hearing them. Speech sounds differ on many acoustic dimensions. To be able to distinguish between them in terms of the distinctive features for a given language (see first section) is the next prerequisite for speech reception. Thirdly, recognition. To be able to distinguish between two words does not in itself imply that one is able to recognize them in isolation. In normal speech reception, a necessary condition is the ability to identify the inflowing elements by matching them with the words stored in memory as part of the individual's vocabulary. Recognition involves a correspondence between the present perceived stimulus and the memory trace, or image, of the word. Fourthly, comprehension. While the three above conditions—audibility, discriminability and recognition—are necessary, they still are not sufficient to understand what one hears. The mechanisms underlying comprehension processes are highly complex. Hirsh notes the fact that ordinary verbal communication is a production of strings of speech sounds and words comprising sentences and larger units of speech, sometimes very lengthy. To understand a sentence, one must retain in mind the sequence of its component elements in order to identify their interrelations on which depends the meaning of the whole. Complex perceptual and intellectual operations are performed in the decoding of the meaning of a text. In Hirsh's description, we again face the problem of different levels, or facets, of the processes involved in speech reception. Three levels of organization can be distinguished as parts of the entire process: perceptual, memory, and conceptual (intellectual). We shall now turn to an examination of these three levels of speech reception, bearing in mind that they have not been equally well studied.

A. SPEECH SOUND PERCEPTION. THE MOTOR THEORY OF SPEECH RECEPTION

Speech reception is based on perception of speech sounds, or phonemes, as the constituents of every spoken text. This capability clearly rests upon the efficient functioning of both peripheral and central parts of the auditory system, i.e. the

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auditory receptor located in the inner ear, the afferent pathways, the subcortical and the cortical auditory centres. But, in fact, does only the auditory system participate in this process? This question has been raised in the light of experimental findings on speech sound perception coming from the Haskins Laboratories in New York (Liberman, 1957; Cooper, Liberman, Harris and Grubb, 1958). This research group developed a technique for producing synthetic speech. As we know, any natural speech sound can be converted into a "visible" display on paper or photographic film by means of an apparatus called the spectrogram (Mitrynowicz-Modrzejewska, 1963. See Fig. 19). This spectrographic technique has been widely used for the acousKH2 012-

•h*

3-Ì 45-

1

.

Ir |r

b

Fig. 19. Spectrograms of the Polish vowels /u/, /o/, /a/, /e/, /y/ and /i/ (Mitrynowicz-Modrzejewska, 1963).

tic analysis of speech sounds. But when construction was started on a speech synthesizer, this type of spectrogram turned out to be too complex for the machine to handle. Artificial spectrograms were then constructed, which are simplifications of natural spectrograms with secondary components omitted (Fig. 20). A graphic pattern of a syllable is drawn, and then converted into sound by the machine. In this way, by changing certain characteristics of the graphic pattern, the properties of synthesized sound can be manipulated with great precision. Liberman's group used this method in a series of experiments to ascertain the critical acoustic features of the speech sounds of American English which serve the hearer as cues for their recognition1. A number of important findings were made, including the fact that listeners tend sometimes to assign sounds to the same category, although very considerable changes were introduced into the graphic patterns. To illustrate, the upper half of Figure 20 presents graphic patterns for the consonant /g/ together with each of seven vowels. In the first four of these patterns, regardless of the second-formant changes (the upper contour), the sound starts with a vibrational frequency of about 3000 cps. But, starting with the fifth, there is a large and abrupt change in the acoustic pattern: 1 The basic technique is to feed the graphic pattern into the machine which converts it into synthetic speech sounds; the listener then judges which sounds these are, or distinguishes between sound sequences, etc.

2. GENERAL CHARACTERIZATION OF SPEECH RECEPTION

129

Frequency in cps

gi

ge

g£

ga

gO

go

gu

Fig. 20. Artificial spectrograms of syllables composed of the consonant /g/ and seven vowels, with the corresponding articulatory positions shown schematically (Cooper et al., 1958).

the second formant starts at a lower frequency than the preceding ones. Despite this fact, listeners invariably identified the consonant as /g/. Thus we find an invariance in the perception of sound despite acoustic discontinuity. But, as these investigations show, on the articulatory side there is no such break; the arrangement of the articulatory apparatus varies very little for all vowel combinations with the consonant /gJ (see lower half of Fig. 20). This implies that large and abrupt changes in the physical properties of acoustic stimuli occur concomitantly with minimal shifts in articulation and with perceptual invariance. This fact, along with other observations, strongly suggested to the authors that speech is perceived by reference to articulation through the overlearning of articulatory patterns. This is advanced as the explanation for attributing the same identity to very different acoustic phenomena. Articulatory movements and their proprioceptive (somesthetic) feedback afferentations are mediating factors in the perception of acoustic stimuli constituting speech sounds. The above hypothesis has been formalized as follows (Lane, 1965): Rv

SA I

Rd t

where R v is a vocal response from a sender, generating an acoustic stimulus (SA), which leads to a covert articulatory response (RVl), whose proprioceptive feedback (SP) leads to the discriminative response (RD). The Haskins group recognizes that, for the adult with his tremendous experience both in talking and listening, speech perception is not necessarily based on explicit mimicry but is somehow short-circuited

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into implicit mimicry, or response as if to proprioceptive return. The important point for these authors is that the perceptual operations, however mechanized, are mediated by articulation. The motor theory of speech perception has been criticized by Lane and his collaborators (Lane, 1965; Cross, Lane and Sheppard, 1965). Their investigations demonstrate that the phenomena described by the advocates of the motor theory of speech reception are not peculiar to speech perception but involve more general discriminatory functions not necessarily built upon a long history of connections with the initiating responses. There are other findings which also raise doubts about the hypothesis reported above; these derive from observations of patients with profound articulatory defect, but with a command of speech reception (Lenneberg, 1962, 1967). Evidence has thus been furnished that lack of mediating articulation need not be an obstacle to the development of normal speech sound perception. Despite these reservations, the work of Liberman's group remains clear testimony to the possible mediating role of the articulatory system in the receptive processes of speech, though it cannot be granted that in the normal state it is a necessary condition. As we shall have occasion to see later in discussing functional abnormalities associated with brain lesions, the hypothetical role of the articulatory apparatus in speech reception finds further substantiation in pathology.

B. TEMPORAL AND SEQUENTIAL FACTORS IN SPEECH RECEPTION. VERBAL MEMORY

It has frequently been emphasized that the text, which is the product of the processes involved in oral speech production, invariably comprises a sequential flow of units, differing in degree of complexity, with a given temporal order determined by the rules of the language system. This applies to sounds comprising words, words comprising sentences, and sentences as parts of larger units of text. Speech reception, therefore, involves the inflow of an ordered string of elements, each of which, from the simplest to the most complicated, constitutes a temporal pattern, or a time-dependent set of ordered events. This fact elevates the problem of timing and sequential organization to one of the great theoretical issues for understanding speech mechanisms in general, and those controlling speech reception in particular. Hirsh (1967) distinguishes two quite different roles of the time factor in speech reception. One has to do with the basic measure of every auditory process, i.e., the duration of any acoustic event, including speech. The other concerns the listener's capacity to receive very long, and in many respects variable, patterns of acoustic events comprising the text. This ability must depend upon the listener's capacity to determine in some way the order of the units he hears and to establish which conform to regularities of the language and what meaning these units have.

2. GENERAL CHARACTERIZATION OF SPEECH RECEPTION

131

If one consider the most elementary acoustic phenomena in speech perception, many examples may be found to show that minimal changes in duration of a single acoustic feature can produce a perceptible change of identity, entailing a change in the meaning of the word, the sentence and the entire text. Another important temporal-sequential aspect of speech reception is segmentation of the speech flow into its units, i.e. finding the junctures at which one word ends and another begins. Subjectively we experience speech as a series of clearly separated words, but an acoustic analysis informs us that objective breaks between words do not often occur. One can readily see that fixing word boundaries is an operation in itself by listening to speech in an unknown language; we often experience it as an unstructured stream of sound and are quite unable to decide how many words, or what kind of words, comprise it. Thus normal speech reception involves breaking down a text into its component units, or segmenting it into temporal parts. The next question of importance is the serial order of acoustic events. Speech reception requires a very precise judgement as to which of two successive stimuli precedes the other. It has been found that a normal listener can estimate accurately the succession of two distinct auditory stimuli given at an interval not less than 50-60 msec. Aphasic patients, however, require more time between acoustic stimuli to make this judgement, sometimes in excess of one second which is about 20 times that needed for normal perception. Nonetheless, no correlation has been established between these acoustic patterning difficulties and the degree of abnormality of speech reception, although the contrary might be expected. That is to say, some patients may display considerable deficiency in discriminating acoustic sequences, but still show good comprehension, whereas other patients with evident disorders of comprehension deviate insignificantly from the norm in the time required to judge sound successions (Efron, 1963,1967). This discrepancy complicates the situation when we attempt to interpret the role of serial ordering of acoustic phenomena in speech reception. Most likely we could find two responsible factors for this state of affairs: first, we should probably find that artificial and overly simplified experimental tasks were used to study the complex acoustic phenomena comprising speech sounds; secondly, the cases under study were treated as homogeneous groups with no clearcut differentiation made of the pathophysiological and pathopsychological mechanisms underlying the speech disorders. From other sources it is known that, in certain aphasic forms, difficulties in retention of the serial order of perceived elements is the cause underlying many disorders both "of speech production and reception (see below, § 3 C). So far we have dealt with processes which account for the perception of a temporally ordered series of acoustic events; but, as mentioned earlier, this does not exhaust the processes necessarily involved in speech reception. An utterance is ordinarily made up of a number of elements given successively, but to decode its meaning the relations between these elements must be accounted for; these relations are often referred to as logico-grammatical. To begin with, the listener

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must be capable of retaining in mind the earlier parts of the text until he has heard the later parts in order to grasp the meaning of the whole. For example, the following sentence could not be understood without retaining all, or nearly all, the words that comprise it (citation translated from Polish, after Shugar, 1969): "The matches the children were playing with yesterday have been hidden so that they won't find them again." As we shall show in a moment, the process of interpreting the meaning of this sentence is highly complex, requiring a number of operations, applications of grammatical rules, and so on. The prerequisite for reception of such a sentence (assuming that the earlier described processes have occurred normally) is retention of all its elements; forgetting any of them before the whole is decoded would preclude an interpretation or, at the least, would lead to a faulty one. Thus verbal memory, or the capability of retaining an incoming text for a given interval of time, constitutes another prerequisite for normal speech reception. The process of retention must be highly accurate; not only must the elements be remembered but also their sequential order, for to confuse the order of elements could disrupt the receptive processes. The role of memory in speech reception processes is prominent also in the recognition of the components of a text, as earlier mentioned. For a speech sound, word or structure to be recognized, there must be access to the corresponding pattern which is stored in memory. The loss or deformation of these patterns will of necessity produce profound disorders of speech reception.

C. SPEECH RECEPTION. THE DECODING OF MEANINGS

The receptive processes we have discussed up to this point are in themselves sufficient for an accurate reproduction of a heard text. As demonstrated in the case of the patient with an isolated speech area syndrome (Geschwind et al., 1968; see also Chapter IV), and in descriptions of echolalia incurred in certain brain diseases (such as Pick's disease), there are situations when a patient can repeat long sentences by ear without the least sign of comprehension. Such performance testifies to the accuracy of the operations involved in the perception and retention of utterances; the absence of comprehension, however, suggests that other processes are necessary which in this case are either absent or disturbed. The problem of processes involved in decoding meanings of received texts is one of the most complex in the whole domain of research into speech and language. As of today there is no formulation, even the broadest (apart from the statement itself of the importance of the problem), which would be backed by all those engaged in research on this problem. In dealing with this issue, then, we shall select for discussion certain hypotheses which will serve as examples of attempts to elucidate this difficult problem. One such hypothesis was formulated by Chomsky (1967a, b) in his theory of

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linguistic competence, or of the innate knowledge of language as a determinant of the capacity to create and understand speech. According to Chomsky, every sentence possesses both surface and deep structure. The surface structure represents the sequence of minimal sound and lexical units, the immediate constituents of the sentence. In the sentence cited above (Shugar, 1969), the immediate units at the level of surface structure are the minimal sound units: /S/, /a/, /m/, /ae/, and so on, and also the minimal units of meaning into which they combine: 5a, maetp, iz, 5a, etc. But by analyzing the surface structure, according to Chomsky, we may not always arrive at the semantic interpretation of the sentence. The meaning of a sentence depends on its deep structure, which usually differs from the surface structure (as is most evident in complex sentences); therefore to understand the meaning of the sentence we must analyze its deep structure. This is well exemplified in ambiguous sentences, interpretable in more than one way. One of Chomsky's examples is the following: "What disturbed John was being disregarded by everyone". This sentence can be understood as: "What disturbed John was the fact that everyone disregards him" or as: "Everyone is disregarding the thing that disturbs John". The same surface structure bears two quite different semantic interpretations. Which one is appropriate depends on two factors: the context in which this sentence occurs, and the operations involved to reach the deep structure. Among the rules required for encoding and decoding sentences, particularly important are the rules of transformation. In the sentence about the children and the matches, several simpler sentences are presumably included: "Yesterday the children played with the matches", "The matches were hidden somewhere", and "The children won't find them again". These sentences were combined into one sentence by rules of transformation. In turn, these sentences are transformations of still simpler sentences. For example, the sentence "The children won't find the matches again" is a negative transformation of the sentence: "The children will find .the matches again". To arrive at the meaning of a complex sentence, such transformations have to be effected in reverse, thus breaking the sentence down into its more elementary sentence components. This type of analysis leads to a formal model for encoding and decoding sentences. We shall not explore in greater detail whether this model is an adequate interpretation of the processes occurring during speech, but we mention it to illustrate the point that the whole process by which an utterance is received, and its meaning grasped, embraces a number of intellectual components which "process" what is heard, these components being separable from the perceptual and memory components of that process. Chomsky's proposal is an eminent example of the trend searching into the relations between the structural and semantic aspects of the sentence. Another approach is by way of examining how a sentence acquires meaning out of its component meaningful units. Each word lifted out of its context has many "senses". Which of these possible ones should be assigned to the word in a given context depends on

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the other words making up that context. Consider a word like "dog". A Polish dictionary (Skorupka et al., 1968) lists its possible senses depending on context of use. We read: "domesticated animal of the family of the same name; chained dog; hunting dog; draft dog; watchdog; house dog; homeless dog; stray dog; faithful as a dog; vicious as a dog"; and so on. Once in context, a word loses its ambiguous character, totally or at least partially. In other words, the context determines which of a word's senses is being used at the moment. This is one facet of the process; the other is complementary to it, i.e., the meaning of the word component determines in some way the meaning of the whole sentence. "He was treated like a dog" and "He was treated like a friend" have essentially different meanings. Therefore the reverse process occurs: the meaning of particular words gives rise to the meaning of the whole sentence. We still know very little about the mechanisms of these processes, but it is certain that in speech reception the decoding of the semantic component of the utterance is a complex process, which might be described as arriving at a closed, internally consistent, semantic pattern: closed, because each component is assigned only one of its possible meanings; internally consistent, because the senses assigned to the particular elements cannot be mutually contradictory (in the light of practical experience and accepted usage in the given culture). The foregoing remarks, as we have forewarned, serve only to illustrate the problem which we have described as the intellectual or conceptual aspect of speech reception, i.e., the level at which the meaning of a received text is decoded. The present state of research on this subject does not, unfortunately, lay a sufficiently firm base for more detailed interpretations or hypotheses. Attention to this aspect—which is of central importance—should lead to a more profound penetration into the essentials of many pathological phenomena.

§ 3. CEREBRAL MECHANISMS OF SPEECH RECEPTION IN THE LIGHT OF ITS DISORDERS DUE TO DOMINANT HEMISPHERE DAMAGE: LOCUS IN THE TEMPORAL LOBE

In line with our treatment of speech production disorders, we shall not be concerned in this chapter with those abnormalities which originate in peripheral impairment, i.e., in the auditory receptor or the afferent pathways transmitting impulses to the central nervous system. Although deafness in all its forms provides one of the most obvious examples of defective speech reception, it does not serve as a basis for interpreting the cerebral mechanisms specifically related to speech reception, the cause for such deficiency being a more general perceptual abnormality affecting all acoustic stimuli; this aspect will be left aside in further discussion. Our attention will be directed rather to those disorders in which perception of acoustic stimuli is basically intact but reception of verbal stimuli is selectively disordered; these are aphasic disorders. Analysis of these various disorders has permitted the isolation of several

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syndromes of sensory aphasia, caused in all likelihood by different locus of lesion in the brain and consequently by disorders of different programming mechanisms. We now proceed to their discussion.

A. PURE WORD

DEAFNESS

Pure word deafness (known also as subcortical sensory aphasia, peripheral sensory aphasia, or phonemic deafness) is characterized by severe or total loss of speech comprehension, oral speech repetition and dictated writing, but with preserved hearing, speaking, spontaneous writing, and reading. The patient hears the voice but recognizes neither individual sounds as speech sounds, nor sound sequences as words. One patient described his condition thus: "Voice comes, but no words. I can hear, sounds come, but words don't separate. There is no trouble at all with the sound. I can hear, but I cannot understand it" (case description by Hemphill and Stengel, cited after Brain, 1965). Although this form of aphasia is relatively uncommon, many authors have observed it (cf. for example Goldstein, 1948; Kleist, 1962; Kogan, 1962; Brain, 1965; Geschwind, 1965). There is no unified opinion as to the exact locus of the causal cerebral lesion nor to the explication of the underlying mechanism. But, for all practical purposes, there is agreement that the damaged area associated with pure word deafness lies in the middle segments of the superior convolution of the left temporal lobe. Some authors have observed this syndrome in cases of unilateral lesions, while others have noted it in cases of bilateral damage; still others express the opinion that the fundamental cause is a subcortical lesion. Various suggestions have been advanced to explain the mechanisms behind this syndrome. The earliest was formulated by Lichtheim (see Chapter II, §2), who considered that pure word deafness (or, as he called it, subcortical sensory aphasia) was caused by a rupture of the pathways connecting the auditory centre in the gyrus of Heschl and Wernicke's area. The patient hears acoustic stimuli but cannot identify them because the auditory impulses do not reach Wernicke's area where auditory word patterns are stored. Since the latter area is intact, the patient can speak and write normally. Geschwind (1965) suggested an interesting modification of this explanation. He proposed that pure word deafness is caused by subcortical damage localized so as to spare Wernicke's area but to destroy the pathways connecting it with the auditory regions in both right and left hemispheres. If the left auditory region is also destroyed, then the patient receives auditory stimuli only through the right hemisphere; the latter, however, cannot transmit impulses to Wernicke's area. Still other explanations have been offered by Goldstein and Kleist. According to Goldstein (1948), pure word deafness (or "peripheral sensory aphasia" in his terminology) is due to partial damage of the cortical area of acoustic perception which does not disturb acoustic perception in general but "de-differentiates" complex

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acoustic phenomena displayed best in speech sound perception (acoustic speech "gestalts"). In turn, Kleist (1962) restricts word deafness to those disorders in which the word cannot be comprehended as a phonemic sequence, and loses its function as a "monitor" of the utterance. This is related anatomically to the posterior third of the first temporal convolution. These latter two explanations of the syndrome do not, however, appear to sufficiently discriminate it from disorders associated with lesions in Wernicke's area itself, which we shall shortly deal with. Since pure word deafness is a rare form of aphasia, as already mentioned, the data hitherto collected do not yield a convincing picture for any of the suggested interpretations.

B. PHONEMIC HEARING DISORDERS. ACOUSTIC APHASIA

We have just discussed the syndrome called pure word deafness, whose typical symptom is disorder or loss of recognition of speech sound patterns, leading to comprehension failure and inability to repeat and write by ear. In acoustic aphasia, associated with lesions in Wernicke's area, the symptoms may be similar, but there is a fundamental difference between these two aphasic syndromes. Processes which are preserved in pure word deafness, permitting speaking, nondictated writing and reading, are disturbed in cases of acoustic aphasia. It has therefore been assumed that different pathophysiological mechanisms underlie these two forms of speech disorder. Acoustic aphasia was first described by Wernicke in 1874 (see Chapter II, § 2) and is produced by a lesion in the posterior third of the first superior temporal gyrus of the dominant hemisphere (Figure 21). The fundamental defect in this case is total or partial loss of comprehension of spoken texts. In the most severe cases no verbal contact of any kind can be established with the patient; all repetitions of a command fail to evoke any response. In milder cases the patient can grasp simple questions and commands after several repetitions, but lengthier or more rapidly spoken utterances tend to confuse him. Profound abnormalities are displayed in attempts to repeat or write from dictation; often these efforts fail completely. Oral speech is also considerably distorted (see Chapter V, § 5) due to distortion of sound sequences comprising words, reduction of speech to stereotyped phrases, "verbal salad", and the like. Similar difficulties occur in writing and reading. Acoustic aphasia was first called sensory aphasia 2 ; initially it was thought to result from loss of "mnestic auditory images" of words stored in Wernicke's area and necessary for recognizing words in sound sequences. Loss of these memory 2 Today the term "sensory aphasia" is used in a broader sense to cover various forms of speech reception disorders. For this reason it seems appropriate to introduce Luria's term "acoustic aphasia" to signify the particular form of sensory aphasia discussed here. Luria sometimes also uses the term "acoustic-gnostic aphasia".

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area (Luria, 1947).

traces would prevent identification of words, therefore comprehension. With this view of the matter, sensory aphasia was treated as a manifestation of a general deficit of intellect, or dementia (see Chapter II, § 3). More recent investigations into the mechanisms of speech disorders in acoustic aphasia, particularly by Luria (1947, 1962), but also by others, have led to the conclusion that the fundamental mechanism involved is a disorder of complex auditory analysis and synthesis which manifests itself particularly as a disturbance of phonemic hearing, i.e., disorder in perception of phonemes as a specific category of complex auditory stimuli. In other words, acoustic aphasia is the result of disturbances arising from the inability to discriminate and recognize speech sounds. Patients afflicted with this form of aphasia have no difficulty in discriminating the simpler acoustic stimuli but have severe trouble with all complex stimuli in this modality, not only verbal. To illustrate, Kabelyanskaya (1957, cf. Stolyarova-Kabelyanskaya 1961) experimented with sensory aphasic patients with left temporal lesions by forming motor responses to a series of pure tones presented in varying serial

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order. For instance, when the patient heard the series of tones ABCD, he was to perform a simple motor response, and when the same tones were presented in a different order (e.g., CDBA, ACBD, DBCA), he was to refrain from responding. Two groups of patients were compared for performance. One group had severe comprehension disorders associated with deficient discrimination of phonemes; these were acoustic aphasia cases. They had great difficulty in learning the motor response to a given stimulus pattern, especially in learning to discriminate between patterns, particularly when the middle elements were switched, in other words to differentiate ABCD as a positive stimulus and ACBD as a negative stimulus. The other group of patients, which could discriminate speech sounds normally but had severe comprehension disturbances, gave a much superior performance though with some deviation from the normal. Neither group, it should be added, had any difficulty in performing similar tasks with visual stimuli. Analogous results have been obtained by others using different research techniques (Traugott, 1946, 1959; Kaidanova, 1954; Kaidanova and Meierson, 1961; Tonkonogi and Kaidanova, 1963). In view of the fact that discrimination of pure tone patterns presents grave difficulties to acoustic aphasics, it is not surprising that these difficulties are aggravated when the need arises to discriminate the much more complex auditory stimuli of speech sounds. This explains why speech reception is so severely impaired in acoustic aphasia. While this type of aphasia may differ in intensity, the typical feature remains the inability to differentiate speech sounds. In milder cases, this difficulty may be noted only with respect to pairs of phonemes differing in one distinctive feature, that is, oppositional phonemes such as /b/ and /p/. In such cases, the patient has no trouble in differentiating between words or syllable sequences composed of clearly separable sounds, but when faced with the task of distinguishing between minor phonetic differences the aphasic disorder is manifested in full force. If, for example, the patient is asked to point to objects as they are named, he can perform this task perfectly so long as the objects do not have acoustically similar names. When he is to show "coat", and among the pictures before him there is one of a goat, the patient will be confused and will indicate one or the other at random. Disrupted phonemic hearing, which is the fundamental defect in acoustic aphasia, inevitably produces secondary disturbances. The patient cannot grasp spoken texts, since the words are blurred and indistinct; for example, he cannot judge whether he hears "hat" or "had" or "head", on which the interpretation of the whole text depends. For the same reason the patient can neither repeat properly nor write from dictation. Other secondary effects of disordered phonemic hearing involve speech production, since precise control over articulation, as well as over writing not only from dictation but also in free composition, is lost (see Chapter V, §5). Furthermore, it is most likely that, due to lability of the auditory word-patterns,

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the semantic aspect is also affected. When the patient tries to name objects, his speech becomes paraphasic, i.e., he may replace the correct word by a phonetically similar one (for instance, room—tomb). Or he may perseverate in the search for a lost word. One patient, observed by the present author, tried thus to name a carrot (in Polish, marchew): He said:..."mar... mar ... in Russian it is morkva ... marche... mar... no I can't". The interpretation of acoustic aphasia as resulting from disorders of acoustic analysis and synthesis, particularly in speech sound reception, is now almost universally accepted. Some terminological discrepancies still remain 3 . Points under dispute touch only upon the relation of this form to other forms of sensory aphasia. We have so far outlined the differences between acoustic aphasia and pure word deafness; now we pass on to other forms which, differentiated in terms of specific symptoms, are thought to be the effects of disorders of other cerebral mechanisms.

C. SENSORY APHASIAS UNRELATED TO PHONEMIC HEARING DISORDERS. TRANSCORTICAL SENSORY APHASIA AND CONDUCTION APHASIA AS CONTRASTED WITH LURIA'S ACOUSTICMNESTIC APHASIA

Acoustic aphasia results from a lesion in Wernicke's area in the left temporal lobe. At times, however, only the adjacent area is damaged, leaving Wernicke's area intact. In this event, different speech reception disorders occur, which for many years have been the subject of controversies. The question has been raised whether they do in fact constitute separate syndromes connected with a particular locus; there have also been different interpretations as to the responsible mechanisms. We begin with a description of these disorders. Transcortical sensory aphasia was postulated by the early investigators of aphasia in their diagrams (see Lichtheim's scheme, Fig. 4 on page 25). It was conceived as the effect of ruptured pathways connecting Wernicke's area with other cortical regions associated with the "higher" intellectual functions. The symptoms should be comprehension loss with intact speech perception. Evidence for the latter was to be correct repetition performance, which depended upon formal connections between Wernicke's and Broca's areas. It seems quite possible that transcortical sensory aphasia can constitute a distinct and specific syndrome, although it is rarely found in the pure form. The characteristic symptom in a patient is a relatively good repetition of texts accompanied with severe comprehension loss. The most glaring example of this syndrome is the description by Geschwind et al. (1968), cited in Chapter IV, § 2, of a patient with isolated speech area. There are other descriptions of cases where repetition is preserved and compre3

For example, Konorski (1968) suggests the term verbal-auditory agnosia for this type of speech disorder.

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hension deranged (cf. for example Goldstein, 1948; Stolyarova-Kabelyanskaya, 1961; Geschwind, 1965 a). However, this syndrome has been variously interpreted. Reference has already been made to an anatomical explanation, according to which the responsible factor is isolation of Wernicke's area from other cortical regions. It has also been suggested that transcortical sensory aphasia is simply a mild form of acoustic aphasia. Still another explanation has been advanced by Luria, but we shall postpone discussion of it until we have presented another postulated form of aphasia, called "conduction aphasia". Conduction aphasia was also taken into account in the classical conceptions. The typical symptom was disturbed repetition of spoken texts with intact comprehension, supposedly caused by a rupture of the pathways connecting Wernicke's and Broca's areas. Thus with Wernicke's area intact the patient could receive texts correctly and understand them, but he would be unable to repeat them due to lack of means to transmit impulses from this area to the motor speech region. The controversy over conduction aphasia has focussed mainly around the issue whether this is actually a distinct syndrome, i.e., the product of separate pathological mechanisms. Weisenburg and McBride (1935) suggested that conduction aphasia is a stage of recovery from sensory aphasia, during which comprehension returns, due to the takeover of this function by the nondominant hemisphere, but repetition remains as severely disturbed as before. In Luria's view (1947, 1962) this condition (disturbed repetition with normal comprehension) can arise in milder forms of afferent motor aphasia or in acoustic-mnestic aphasia. Solov'ev (1948) took the position that conduction aphasia is evoked by pathology of auditory word patterns. On the other hand, many authors accept conduction aphasia as a distinctive syndrome, although their attempts to clarify the responsible mechanisms differ. Apart from the classical anatomical version reported above, there are a number of other explanations. For instance, Goldstein (1948) identified conduction aphasia with a disorder he called "central aphasia" and which is caused by disturbances of inner speech. His descriptions of this syndrome, however, diverge in fundamental ways from those generally accepted. This question appears to be one of the knotty problems in aphasia classification. In our present discussion of those types of speech reception disorders which are not caused by disordered phonemic hearing, we revert now to Luria's conception, mentioned earlier (Luria, 1947,1962; Luria and Rapoport, 1962), concerning acoustic-mnestic aphasia. Luria's view is that lesions of the middle segments of the convexital portion of the left temporal lobe, and the deeper-lying structures of this lobe, produce a set of symptoms characterized by an evident deficit in reception of lengthier texts, phonemic hearing remaining intact. These patients have no trouble repeating single words, but fail to reproduce a simple phrase of two or three words, not to mention longer sentences. The same difficulty occurs in comprehension of spoken texts. Capable of carrying out short instructions, these patients lose the thread of more expanded utterances. Naming is also disordered, particularly when the patient is required to name several successively indicated objects; perseveration results, i.e.,

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after naming the first object correctly, the patient will use that name for the next object. Experiments with patients afflicted with this form of aphasia led Luria to conclude that the fundamental defect responsible for these symptoms is pathology of memory processes in the auditory modality, particularly affecting auditory word patterns. The pathophysiological mechanism underlying speech reception disorders primarily, and speech production disorders secondarily, consists of lability changes in the preservation of traces of verbal material. Although Luria's interpretation seems most adequate to explain the events occurring when areas adjacent to Wernicke's area in the dominant hemisphere are injured, some questions remain open for further study. Primarily we have to account for the twofold nature of symptoms discussed. In some situations there are symptoms of lability, or pathological distortion of new traces resulting from immediately perceived texts, as when the patient fails to repeat a series of 3 words although he can repeat each of them apart, or when he can carry out simple commands but fails with combinations of such commands. We seem to be dealing here with a sort of "span" restriction on short-term memory probably associated with the pathological accumulation of retroactive and proactive inhibition influences (Klimkovsky, 1966; Luria et al., 1967). But these same patients also display symptoms of disturbances to long-term memory traces necessary for the activation of processes involved in speech production, as manifested in jargon, contamination, and other abnormalities of word selection (see Chapter Y, § 5). Another question awaiting further clarification concerns the specific pathophysiological mechanisms responsible for these disorders: whether they are related to a heightened tendency for extinction of auditory traces, or whether there are other mechanisms involved, such as increased inertia of the trace, accumulation of inhibition, loss of selectivity in the reproduction of memory traces, etc. (Luria et al., 1967). N o purpose would be served by delving more deeply into these questions; it should be amply clear that lesions in the regions bordering on Wernicke's area in the temporal lobe of the dominant hemisphere constitute additional causes for speech reception abnormalities, and therefore these regions can be expected to subserve the normal function in some way. At the same time, the established fact that abnormal receptivity is not, in this case, linked with phonemic hearing deficit testifies to some difference in function between these temporal lobe regions and Wernicke's area. The most likely hypothesis is that these functions are associated with the memory aspect of speech reception. Other evidence supporting this conclusion can be adduced from investigations of verbal memory disorders in cases of temporal lobe damage in the dominant hemisphere which in principle does not lead to aphasia. D. VERBAL MEMORY DISORDERS ASSOCIATED WITH LEFT TEMPORAL LOBE DAMAGE

So far, disorders of brain mechanisms involved in speech reception have all been of a clearly aphasic character, severely crippling the ability to communicate with

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the outside world. Another pertinent source of information, one of considerable import to our discussion, is the study of patients whose brain damage does not produce unequivocal symptoms of aphasia but causes other changes which have been revealed by special techniques. These are patients under treatment for focal cerebral seizures by surgical removal of the epileptogenic focus in the temporal lobes. Ordinarily these operations do not encroach on the speech area, and for this reason aphasia occurs only temporarily in the early post-operative period as the result of such reversible changes as cerebral edema, and subsequently clears completely; from a clinical standpoint these are not regarded as aphasic symptoms. Such patients have been investigated by Milner's group (Milner, 1958, 1962,1967; Milner and Kimura, 1964; Milner et al., 1965). Highly ingenious experimental tasks were developed to test patients with postoperative lesions in the anterior portion of both right and left temporal lobes; these yielded information about the differentiation of functions of the two neural structures and their specific roles in the regulation of higher functions, as compared with other cerebral structures. Milner tested various aspects of the memory processes, viz. free recall, recognition, verbal and nonverbal learning (Milner, 1968). The basic finding from these experiments was that the left temporal lobe (more precisely, in the dominant hemisphere) is necessarily involved in normal verbal memory, while the right temporal lobe (in the nondominant hemisphere) participates in normal nonverbal memory processes. We shall report, below, on some of the experiments from which this conclusion was drawn. Kimura, a collaborator of Milner's, developed a special experimental task to study nonverbal memory, called the Recurring Nonsense Figure test. The subject is presented with 160 cards, each showing an unfamiliar geometric figure or unfamiliar graphic pattern difficult to name (Fig. 22), In each set of 20, 8 designs recurred, mixed at

Fig. 22. Example from Recurring Nonsense Figure Test used by Kimura (after Milner, 1967).

random among 12 designs appearing only once in the whole series of 160. The cards were presented one at a time to the subject, whose task was to distinguish between drawings which he had seen before and those appearing for the first time. Two patient

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groups, one with left and the other right temporal lobe damage, and a normal control group were tested in this manner. The results showed that, while the left temporal lobe group did not differ from the controls, the right temporal lobe group gave a statistically significantly higher number of false positive answers. The reverse situation was found when analogous verbal tasks were used, i.e., when short words, syllables, or 3-digit numbers were presented on the cards. In this version of the test, called the Recurring Card Test, patients with right temporal lobe excisions did not differ from the normal group, while patients with left temporal lobe damage gave appreciably poorer results. These findings are presented in Table XI, from which TABLE XI i Results» of the Recurring Card Test in two patient groups, one with left, the other with right temporal lobe damage, as compared with a control group (Milner and Kimura, 1964). Statistically significant differences are underlined.

Localization of lesion

Right temporal Left temporal Normal

Early post-operative scores (2.5 weeks)

Follow-up post-operative scores (1 to 5 years)

No. of cases

Nonverbal test

Verbal test

No. of cases

Nonverbal test

Verbal test

22 12 11

25.6 34.0 38.9

45.6 29.4 47.1

7 10 11

29.9 38.8 38.9

45.1 35.7 47.1

a , Results are based on subtraction of the number of wrong positive answers (cards treated as already seen) from the total number of correct answers.

it is evident that the verbal memory deficit, following removal of the anterior portion of the temporal lobe in the dominant hemisphere, is not restricted to the auditory modality but affects the visual as well. Thus, lesions thus localized produce broader disorders of verbal memory. In another study (Milner, 1967) visual and oral presentations were compared for effect on learning verbal material in patients with similarly localized lesions. Two tasks were used: one was to retell a short prose passage, and the other to learn 10 paired word associates. In the Auditory version, the material was spoken and respoken, while in the visual version, the material was read and rewritten. Delayed recall was tested by requiring the subject to perform the task after a 40-minute interval occupied with other testing. Pre- and post-operative testing were compared. The results of these delayed recall tests are presented in Table XII, which shows that both auditory and visual retention of verbal material differs appreciably in patients with epileptogenic foci in left or right temporal lobes, the differences reported as statistically significant. Found in the pre-operative period, they increase following operation. Note that, while right temporal lobe excision produces no de-

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TABLE XH Delayed verbal recall of auditory and visual material in pre-operative and early post-operative tests of 2 groups of patients, one with left and the other right, temporal lobe lesions. Means for both tasks (correctly retold texts together with correct word associates) (Milner, 1967). Localization of damage Left temporal Right temporal

No. of cases 21 23

Auditory presentation

Visual presentation

Pre

Post

Pre

Post

11.2 14.8

6.6 15.7

13.2 17.1

9.6 17.2

terioration, and may even improve performance (see scores for auditory tasks) 4 , left temporal lobe excisions considerably worsen performance in verbal recall, regardless of which mode of presentation is used. These and numerous other data provide solid substantiation for the hypothesis that the left temporal lobe plays some specific role in verbal memory processes. It is pertinent to note that investigations of patients with extra-temporal lobe lesions demonstrated that verbal memory deficit is specific to temporal lobe damage, i.e., is not found in cases of damage in other cerebral areas. Milner's findings provide additional confirmation of the hypothesis that the neural structures adjacent to Wernicke's area in the temporal lobe of the dominant hemisphere possess the peculiar function of ensuring the mnestic aspect of speech reception 5 . §4. CEREBRAL MECHANISMS OF SPEECH RECEPTION IN THE LIGHT OF ITS DISORDERS DUE TO DOMINANT HEMISPHERE DAMAGE: EXTRA-TEMPORAL LOCUS In our discussion of speech reception mechanisms, we have so far concentrated on those disorders which arise from damage in the temporal lobe of the dominant hemisphere. Both clinical observation and experimental research have yielded unequivocal evidence that this lobe subserves exceedingly important functions in normal speech reception. However, speech reception does not depend solely on the cerebral mechanisms connected with the temporal lobe, since lesions elsewhere in the brain * Probably this improvement is due to the fact that at times removal of the epileptogenic focus from the right temporal lobe may help to normalize functions in the intact left temporal lobe which has been, prior to operation, under the pathological influence of discharges connected with focal activity in the homologous right lobe. Improvement of immediate recall subsequent to unilateral temporal lobe excision has already been reported (cf. StQpien and Sierpinski, 1961). 5 This hypothesis may require some modification. An unpublished study (Maksymczuk, 1969) demonstrated that sequential learning presented particular difficulties to patients with left temporal lobe damage, while simultaneous learning was more difficult for patients with right temporal lobe lesions. Since verbal material has a sequential character, the suggestion can be advanced that the verbal memory abnormalities described by Milner as accompaniments of left temporal lobe damage may be related to more general disturbances of sequential learning.

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may also produce abnormalities of speech reception. Clearly there are other relations involved in the cerebral control of receptive processes, where extra-temporal structures enter in. We shall now review the data supporting this statement and certain ensuing hypotheses. A. SPEECH RECEPTION DISORDERS DUE TO LESIONS IN THE PARIETO-OCCIPITAL REGION. SEMANTIC APHASIA

Speech reception disorders hitherto discussed have been identified as deficits in speech sound perception or in reception of lengthier texts, the latter being due to verbal memory abnormalities with pathological lability of the memory traces of verbal material. We find a different form of speech reception disorder in cases of lesions located in the parieto-occipital portions of the dominant hemisphere. Patients with such lesions have no difficulty in respect to phoneme perception, memory processes, or reception of structurally simple texts even when they are of some length. The abnormalities specific to this locus of damage pertain to comprehension of texts requiring complex mental "processing", in other words, comprehension of complex logico-grammatical constructions (Head, 1920, 1926; Luria, 1947, 1962, 1967; Maruszewski, 1966). Consider such linguistic constructions as inflections marking possession, instrumentality, etc., prepositions denoting spatial relations ("Put the matches on the notebook" versus "Put the notebook on the matches"), attributive constructions ("brother's father" versus "father's brother"), and so on. The meaning of the whole phrase depends not only upon the meaning of individual words but also upon the relations between them expressed by case-endings, prepositions, word order, and such devices. It will not do to merely understand "father" and "brother" in order to grasp the distinction between a phrase meaning "uncle" and one meaning "father". Similarly, understanding each of the words "show", "notebook" and "pencil" will not suffice to grasp the whole instruction "Show the notebook with the pencil". There must be a kind of mental "processing", or decoding of meaning, of all essential elements and of their logical and syntactic relations. It is the ability to perform such mental operations that is disturbed in the event of a lesion in the parieto-occipital region of the dominant hemisphere, and the symptoms produced are those of semantic aphasia. In this, type of aphasia, patients not only have naming difficulties (see further in Chapter VII, § 3 D) but have characteristic problems in understanding "nonsequential" constructions, those that can be understood only by grasping the logical and syntactic relations contained in it. Patients can comprehend such words as "circle", "under", and "cross", but fail in carrying out the following instruction: "Draw a circle under a cross"; they will draw first a circle and then under it draw a cross. When asked to "Point to the notebook with the pencil", ("with" meaning "by means of") the patient will tend to respond by showing both notebook and pencil at the same time. Patients with semantic aphasia also fail to understand gram-

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matically complex sentences, having difficulty with syntactic structure and not with length. Such a patient may be able to repeat fairly long sentences and show that he understands them by answering appropriately to lengthy questions, provided there is no cross-reference among the components. For instance, he can repeat correctly "Father and mother went to the theatre and the old nurse and the children stayed at home"; he can also answer "Who went to the theatre?" and "Who stayed at home?" But the same number of words combined in a syntactically complex sentence is totally incomprehensible to such a patient. Not only will he fail to give appropriate answers to questions based on such a sentence, but he will have difficulty even in repeating it. An example would be the following: "An engineer from the Central Office came to deliver a report at the enterprise where Smith is employed" 6 . Such a patient could not sort out who was to deliver the report, where, and what Smith had to do with it. A more adequate explanation of the mechanisms underlying the symptoms we have described is obviously required. In Luria's opinion, the fundamental defect lies in simultaneous synthesis, which depends for normal operation on the parietooccipital regions; where the dominant hemisphere is concerned, this refers to simultaneous synthesis of verbal material. Accepting this viewpoint, the causes for the loss of ability to understand "nonsequential" constructions should be sought in the loss of simultaneous retention of several interdependent elements and the inability to sort out their relations. These difficulties are part of more general abnormalities of simultaneous synthesis, manifested diversely in failures to grasp spatial relations, the characteristic symptom of lesions in this area. Evidence that the spatial factor plays a role in semantic aphasia may be adduced from such disorders as acalculia (disorders of arithmetical operations), defective spatial orientation, and other symptoms often accompanying these speech disorders.

B. SPEECH RECEPTION DISORDERS DUE TO DAMAGE IN THE ANTERIOR DIVISIONS OF THE SPEECH AREA

We have repeatedly stressed that the separation of speech production from speech reception is a strictly relative affair, there being complex interdependencies between these two major processes. In Chapter V, § 5, we discussed those speech production disorders which accompany lesions in the posterior portions of the dominant hemisphere, producing receptive disturbance as the major symptom. We shall now review data concerning speech reception disorders in cases of lesions in the anterior parts of the brain, where the dominant symptoms are diverse disturbances of speech production, as discussed above. 6

Translated from the Polish more literally, this sentence would have the following word order: "To the institution where Smith is employed came an engineer from die Central Office to deliver a report".

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The thesis that certain receptive disorders co-occur with motor aphasia, where the main disorder lies in speech production, has now been universally accepted, and a number of terminological adjustments reflect this fact. (See for instance the term "predominantly expressive aphasia" introduced by Weisenburg and McBride, 1935). Although motor aphasia patients manage well, on the whole, to follow speech in everyday situations, it has been demonstrated both clinically and experimentally (cf. Boiler and Vignolo, 1966) that in more difficult situations these patients show a clear deficit of speech reception. For instance, they fail to comprehend longer instructions or high-level verbal tasks (such as: "He was not an unhappy man"); a rapid conversation involving several speakers also poses difficulties for them. Several hypotheses have been advanced to explain these phenomena. In Luria's opinion (1947, 1962), the above-described disturbances of speech comprehension in motor aphasia cases have various underlying causes, depending on the form of aphasia. In afferent motor aphasia, for example, articulatory defects may lead to a secondary disturbance in the auditory perception of speech sounds, since articulation is a major factor in the discrimination of such sounds (see above, § 2 A, for a discussion of the motor theory of speech reception). Such perceptual disorders create minor difficulties in comprehending words and their combinations in sentences. But where efferent motor aphasia or dynamic aphasia is involved, Luria proposes that a disorder of inner speech is responsible for comprehension losses, i.e., interference in decoding those texts which must be rehearsed internally for the necessary transformations to be executed. The hypothesis of inner speech disorder has also been advanced by others (cf. for example Brain, 1965; Boiler and Vignolo, 1966), i.e., loss of internal reverbalization of complex messages as the underlying cause of speech reception disorders in motor aphasia. But in practical terms there is no experimental support for this claim, which is most often encountered in general theorizing about the role of inner speech in speech reception processes. As a hypothesis of theoretical interest, it awaits experimental confirmation. Before terminating this review of the various forms of speech receptivity disorders, mention should be made of certain comprehension losses which are apparently due to pathological changes in the dynamics of nervous processes, called "perseveration of set" (Maruszewski, 1966). In some cases of widespread cerebral damage, a rather strong tendency has been found to perseverate in behaviour, manifested as a persistent continuation of the immediate task. These patients have serious difficulties in grasping instructions calling for actions of a type different from those which they have been performing. If, for instance, a patient has been performing a test of naming objects pointed out to him, he may require a lengthy interval to shift to a task where he is to point out objects as they are named by the examiner. The patient tends to repeat the instruction issued, without sign of comprehension. When the perseverating set to speak is broken, and the patient succeeds several times in performing the task required (pointing out objects as they are named), he will then be unable to return

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to the former task which he had been correctly performing, viz., naming objects shown to him; he will continue to point to the objects before him. In this case, impairment of comprehension, or of speech reception, appears to be of a highly specific nature, associated with a pathological inertia of set. The perseverating set for a task which has been just performed creates a blockage in perception of the arriving instruction, although in principal the patient can hear and understand it (since in other test situations he can hear and understand instructions on the same level of complexity). This type of disorder is apparently connected mainly with lesions in the anterior portions of the dominant hemisphere. Similar symptoms, though less pronounced, are observed in patients with frontal lobe lesions; in such cases, aphasic disorders may not even occur. Behind these phenomena lies an inability to deal with instructions formulated so that the actions called for are ordered differently from the sequential order of linguistic elements. This has been exemplified in the tests, described earlier, where "nonsequential constructions" are used in instructions. Patients suffering from frontal lobe lesions have no difficulty in carrying out instructions as long as the order of objects named corresponds to the order of their presentation in performance. Thus, in contrast to patients with semantic aphasia, who cannot carry out commands with "nonsequential" construction regardless of order of elements, patients with frontal lobe damage perform perfectly on instructions such as: "Show—with the pencil—the notebook" (grammatical word order in Polish); they will pick up the pencil and use it to point to the notebook; or "Draw—under the cross—a circle", in which case they will draw a cross first and under it a circle. But, once the order is changed, these patients make faulty performances. For instance, when asked: "Show the notebook with the pencil", the patient will take the notebook and use it to show the pencil; or when asked: "Draw a circle under a cross", he will first draw a circle and then under it a cross (Luria, 1947, 1962; Maruszewski, 1966). The patient fails, in these cases, to grasp the instruction, but not because of perceptual difficulties, memory failure or inability to establish the relations between the elements (since he can grasp the relation once the elements are placed in a different sequential order). This disorder is presumably connected with a loss of capacity to abstract from the behavioural sequence imposed by the word order, or to evade the influence of "surface structure". Dependency upon purely external physical properties of signals is a typical symptom of frontal lobe damage (Luria, 1962; Maruszewski, 1962, 1966).

§ 5. CONCLUSIONS

The above discussion of symptoms of frontal lobe damage terminates this review of the various disorders of speech reception processes and conclusions drawn from their analysis which throw some light on the cerebral mechanisms underlying them.

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Similarly as for processes involved in speech production, it is proper to state that no single "sensory speech centre" exists in the brain which can be considered responsible for the normal reception of voiced speech. The latter is associated with many anatomically and functionally diversified structures located within the dominant hemisphere, which together compose the functional system of this activity. Though many aspects require additional clarification, present knowledge entitles us to venture an answer to the question as to what cerebral structures are responsible for normal speech reception. Observations and experimental research with aphasic patients have yielded data, reported above, substantiating the thesis that the functional system of speech reception embraces the following divisions of the speech area in the dominant hemisphere: — The posterior division of the superior temporal convolution (Wernicke's area), whose function is the analysis and synthesis of complex auditory stimuli, particularly speech sounds. It is therefore a necessary structure for identification of the elementary units of speech, that is, for normal phonemic hearing. — Additional temporal lobe structures in the dominant hemisphere, lying adjacent to Wernicke's area. Opinions differ widely as to their role, but the best substantiated hypothesis appears to be that these structures ensure the mnestic aspect of speech reception, that is, serve a major function in normal processes of retention of verbal material necessary for effective speech reception. Future research should reveal the functional differentiation of these structures, but present knowledge justifies the inference that different portions of the temporal lobe subserve this function to unequal extents and possibly in different ways. — The parieto-occipital region. This structure undoubtedly plays an essential role in decoding the complex logico-grammatical constructions of utterances without which shifts of meaning based on "nonsequential" linguistic order cannot be grasped. — Anterior divisions of the speech area, sharing in cerebral regulation of speech reception. The necessary information for a better formulation of their functions is lacking. One hypothesis of major interest associates inner speech with these regions as the essential element for integrating the decoding processes during speech reception. — Frontal lobe regions lying outside the speech area, understood in the narrow sense. Necessarily involved in normal speech reception, they appear to ensure the ability to make rapid switches in the perception of received texts, as well as to transcend the "suggestion" of the surface structure in order to reach the deep structure and therefore the semantic interpretation of the text. The conclusions we have listed above are, as may readily be seen, not very precise, and some are no more than hypotheses awaiting verification. The latter mainly concern a sharper delineation of the functions of particular structures; as to their participation in speech reception control, this has been demonstrated beyond shadow of doubt. At this point we again revert to the matter of separating the cerebral mechanisms

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in control of production and reception of speech. As we compare those structures mentioned in the discussion of speech production, and those listed above, we find that the same structures are involved. In this sense, these broad processes are both the function of the entire speech area, which justifies the reservation made at the start of Chapter V that the distinction between speech production and speech reception is arbitrary. However, the fact is that the various regions of the speech area do not share uniformly in the control of these two broad processes; some regions are essential for regulating speech production while others serve the major role in receptive speech control. This reflects the internal functional differentiation of the speech area: made up of a set of interacting structures differing both in function and in relative share of responsibility for the particular processes involved in speech.

CHAPTER VII

SPEECH AND COGNITIVE PROCESSES IN THE LIGHT OF APHASIA RESEARCH

§ 1. INTRODUCTORY REMARKS

The interrelationship between cognition and speech, or thought and language, has long been the subject of inquiry by scholars of many disciplines, and continues to occupy a prominent place in current literature. The underlying reason is the striking coincidence of two phenomena: man is the only species capable of communicating through language, and at the same time that species whose cognitive and intellectual abilities are developed to a degree unknown in the animal world. This is the source of the highly plausible assumption that man's mental capacities and, indeed, the growth of human thought, are strictly related to these linguistic abilities (see Chapter I, § 1). Attempts have been made to establish what it is that language use contributes to the human cognitive processes, particularly to the thinking operations. Such studies follow various directions, including both developmental change and mature functioning, and employ diverse methods of formal analysis. It is also widely anticipated that aphasia research may provide at least some of the key answers. A cursory examination appears at first sight to justify such expectations. We have before us a subject who, as a result of brain damage, is deprived of the use of language. How do the intellectual processes of such a person function? In the event that the aphasic patient does not differ from the normal language user, this constitutes evidence—as anticipated by many authors—that thought and speech are not interdependent. But, if speech disorders are accompanied by evident disturbances of cognitive functions, then this could mean that speech is an essential factor in man's kind of thinking, or the human manner of cognizing reality. One may even go a step further: by examining what type of disturbances occur in the mental processes, we could conceivably ascertain what specific role speech serves in the thinking process, what language contributes to thought and cognition. The foregoing and other analogous assumptions, while in fact naive, have evoked a lively interest in aphasia research amongst those concerned with this problem, and have instigated aphasia investigators themselves to try and resolve them. The prospects seem tempting enough, since among the manifold symptoms of aphasia, some at

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least appear to invite theoretical reflections of this nature. A great deal has been written on topics related to this question, based on observations and experimentation with aphasia patients. But anyone who entertains the hope of finding clearly substantiated data, or of deriving some unequivocal conclusions, from' such publications, is due for a sad disappointment. It is the reverse which prevails: the relation between speech and thought in aphasia patients is one of the most intractable problems and, in the final analysis, one of the least investigated of all the problems in aphasia; furthermore, the multiform hypotheses and interpretations proposed on this subject belong among the least credible. There are several reasons for this state of affairs. To begin with, it is unsophisticated to make the assumption that aphasia creates a favourable situation for the study of the language-thought relation, and this because of two circumstances. A state of aphasia is practically never tantamount to a total loss of speech. Even in the most severe forms of this disorder, some aspects of speech, albeit residual, are preserved, as is most clearly demonstrated during rehabilitation when latent capacities are unblocked in the patient (Maruszew'ski, 1965, 1966). An aphasic patient is not someone deprived of speech; he is a person whose speech processes have been disordered to a greater or lesser degree. Therefore, when we study thinking processes in aphasic patients we cannot conclude that the changes noted are due simply to the absence of the speech processes; they might equally well be explained as the effect of speech disturbances. On the other hand, even normal thinking processes in aphasics do not comprise evidence of their independence of speech; possibly the preserved residues of speech processes are sufficient to ensure the normalcy of the thinking processes. A further point is that speech disturbances do not ordinarily constitute the sole symptom of brain damage. A lesion always disrupts a number of higher functions, apart from speech disorders. One reason for this is that the brain is practically never damaged selectively: the damage is rarely limited to a functionally homogeneous region of the brain, but commonly embraces several neighbouring areas (see Chapter III, § 2). If one of these areas plays a particular role in the speech processes, and another in some cognitive process, the co-occurrence of speech disorder and cognitive disturbances cannot then be deemed the result of interdependencies between speech and cognitive processes; rather, it is the product of damage in two distinct but adjacent regions sharing in the cerebral regulation of these functions. Another argument for the claim that a lesion always disturbs a number of higher functions derives from the currently accepted view, supported by steadily growing evidence, that one and the same area of the brain can constitute a link in several distinct functional systems and participate in the cerebral control of a number of higher functions; once one link is damaged, all the functions concerned are disturbed. In this event there is no basis to conclude that one, as against another, is more necessary for the normal functioning of the remainder. This is the type of difficulty we are confronted with in attempting to utilize aphasia research for resolving problems associated with the interrelationship between speech

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and cognition. These might be called the objective difficulties, since they result from the complexities inherent in the actual state of affairs. Intermeshed with these are other difficulties that can be termed subjective, since they relate to the state of research methodology and to theories about these questions. In this latter respect, broad differences of outlook exist on the relation of speech and thought ; it is sufficient to leaf through a few of the more recent philosophical or psychological studies on the subject to become aware of the diverse speculations advanced by representatives of the different schools in respect to the role of language and speech in the cognitive processes. These discrepancies are fully reflected in aphasia research, in all manner of interpretations of its manifold symptoms. Many authors are inclined to seize upon only those symptoms of aphasia which fit their favourite theory derived from broader study or speculation, and to ignore the rest. This has led to many conceptualizations of aphasic symptoms which have more in common with current theoretical debate than with aphasia itself. One may easily delude oneself that one or another finding in aphasia research confirms a given viewpoint, whereas in fact the investigator's presuppositions have led him to a fragmentary treatment of the phenomenon involved in aphasia. We must add to this complex picture those difficulties associated with the methods used to examine patients and with interpreting findings. Consider the peculiar position of the aphasic patient with his reduced ability to communicate with other people: communication is, after all, an indispensable condition for exact experimentation. Techniques of investigation designed for normal subjects may not yield conclusive evidence when used with these patients. As a result, the literature devoted to aphasia abounds with reflections on the topic of the speech and thought relation, but a critical examination of them inclines us towards utmost caution in accepting any conclusions to be drawn from them. In the light of the above considerations, our attempt to present what aphasia research has contributed to our understanding of the interrelationship between speech and cognition must be conducted with particular care as concerns the formulation of conclusions. With this in mind we shall proceed in a somewhat different manner from that followed in the previous chapters in presenting our material. We begin with a brief discussion of those aphasic symptoms which superficially appear instructive from the viewpoint of our present problem; the main kinds of interpretations will then be presented, and finally some findings of specific investigations will be reported which have provided additional arguments for one particular explanatory theory. The reader will then see for himself how much the experts differ in their views on the problem of the speech-thought relation in aphasic patients. § 2. NAMING DISORDERS IN APHASIA. CONTROVERSY ABOUT AMNESTIC APHASIA

Among the numerous symptoms of speech disorder caused by brain damage, one has aroused particular interest in the context of discussion over the speech and

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thought relation. This is naming disorder, or more broadly, the impairment of the ability to employ words as names for objects and events. The simplest test for studying this symptom is to confront the patient with an object or picture and ask him to name it. This task creates severe difficulties for the patient: either he fails to produce a name or he produces various utterances but not the appropriate word. This symptom is known by diverse terms: anomia, amnestic aphasia, nominal aphasia, and others. Attention was first focussed on the sheer inability of the patient to produce the correct name. More recently, emphasis has shifted to the variants of this disorder; the inability to name may assume different forms. To interpret the mechanisms underlying naming disorders, the qualitative behavioural differences of a patient, varying with conditions and circumstances, should be accounted for (Goldstein, 1948; Lopatkiewicz, 1961; ¿arski, 1964; Geschwind, 1967c). A classification of naming disorders has been presented in greater detail elsewhere (Maruszewski, 1966). At present we shall broadly describe the main kinds of defective naming by aphasics when requested to name objects shown them. Type I: Naming inability is at times accompanied by signs, verbal or gestural, that the object is recognized. For instance, one patient confronted with the picture of a plum, said: "... those are ... uh ... tsk! ... I really know ... ye gods!" Another patient, shown the picture of a squirrel, said: "What's it called! I know the name— 1 know what that is but 1 can't say it." Type II: Descriptions or circumlocutions instead of naming the object shown, usually about the purposes served by the object or the actions performed with it, its origin, features, spatial-temporal location, or even personal reminiscences about the object. For instance, on seeing a cake of soap: "Yeh! ... I asked my folks to bring me some, mine's nearly gone..." Shown the picture of a bear: "That's what's supposed to be sleeping now..." (test made in winter). Electric light bulb: "That's this... over there to that... how's it go? ... you screw it in and the light comes on... what a laugh ... for that tree, no, for electric light... oh well, you just buy it and screw it in." Type III: Word paraphasia, or name substitution. In semantic paraphasia, the patient produces the name of an object belonging to the same semantic sphere or to some common broader category, as for example: instead of skis, skates; instead of owl, parrot; alternately, the name produced may have some other association, as for example: instead of sheep, milk; instead of chisel, handle. In verbal paraphasia caused by perseveration, the patient replaces the right name by a word previously uttered in connection with some other object. Or, a verbal paraphasia may be a phonetically similar name, for example, instead of "marchew" (carrot), the patient says: "mm...myde... on the farm they call it mydelko (soap) ... maybe mydelniczka (soapholder), what you eat like a vegetable ... m...mydelnica (soapwort)". Other forms of verbal paraphasia may have no apparent association with the object or the immediate

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situation; probably they are idiosyncratic in origin or uncommon associations as, for example, instead of chair, doctor; instead of mushroom, "that's a kind of book". Type IV: Distorted auditory-motor pattern of the word. The patient attempts to produce the name of the object, but deforms the sound of it. Sound paraphasia includes substitution of phonemes [as in gruszka (pear)—*gluszka], addition or omission of sounds in the word [instead of zeszyt (notebook)—*gzekszyk], or complete distortion as when the sound sequence is groped after or in the case of jargonaphasia (see Chapter V, § 5). The fourth type of misnaming performance is usually strictly linked with particular speech production disorders described earlier, being merely their symptoms manifested in given situations. But the first three types, while occurring in various forms of motor and sensory aphasia, can also occur selectively, without any accompanying disorder of speech production. This fact has aroused great interest: in such a situation the patient can articulate a word correctly but experiences sudden difficulty in retrieving the wo/d as a name. One gets the impression that the word-name, as verbal symbol of the object, is inaccessible to the patient for reasons other than simply a disorder of speech production. Debates over this latter symptom hinge upon three questions. One question is whether this is a distinctive and separable symptom, a specific form of aphasia, or whether it is an accompaniment to other forms of aphasia. Another question is the locus of damage responsible for naming disorders, while the third pertains to the mechanisms underlying these disorders. In this section we shall deal with the two former questions and postpone the third to the next section. Naming disorders were noted as early as the 18th century. Towards the close of the 19th century Kussmaul (1879) introduced the term "amnestic aphasia", thus recognizing naming disorder to be a distinct syndrome caused by brain damage. But the question whether amnestic aphasia should be treated thus is still disputed (cf. Markova, 1961; Osgood and Miron, 1963; ¿arski, 1964; Brain, 1965). Many authors approach naming disorders as one of the symptoms manifested in different forms of aphasia involving diverse loci of damage. Others incline to ,the belief that amnestic aphasia is one of the stages of recovery. Few support Kussmaul's claim for amnestic aphasia as a separate syndrome. This cleavage in opinion is apparently the outcome of diverse interpretations of the same symptom, which we shall take up shortly. But it is also linked with the question of locus of lesion responsible for these symptoms. Here as well opinions collide; but since it has been easier to verify this point, it can now be stated with fair certainty which cerebral areas have major importance for normal naming processes. ¿arski (1964) has collected some very interesting data on this matter. He studied naming disorders in aphasics where locus of lesion was defined during neurosurgical operations. Amongst patients with damage in the posterior speech area, 2arski distinguished 5 groups displaying different symptoms of naming disorder, each with a different locus of lesion.

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The first group consisted of patients with damage in the left parieto-temporooccipital junction. These patients could not retrieve names but displayed no other symptoms such as literal paraphasia, verbal paraphasia, or perseveration. In the second group, there were patients with lesions of the infero-anterior portion of the left parietal lobe including the parietal lid. Their symptoms included naming difficulties and literal paraphasia. The third group comprised patients with left temporal lobe damage in the first, second and third convolutions. These patients displayed word-finding difficulty, and in addition word paraphasia, perseveration and jargon. The fourth group included those patients whose lesions embraced more than one of the three demarcated areas. Their disorders were the appropriate combinations of the above described symptoms. The fifth and final group was made up of patients with destruction of practically the entire posterior portion of the speech area. Their naming disorders were profound; often there was a total absence of effort to retrieve names. Thus, according to ¿arski's data, naming disorders are produced by lesions in each of the three posterior portions of the speech area he had distinguished. But a qualitative analysis of these disorders shows that the sub-areas mentioned have different roles in controlling the naming processes, being functionally differentiated. If the infero-anterior portion of the left parietal lobe is involved, naming disorder is accompanied with literal paraphasia, which — as earlier stated in Chapter V, § 4 B — is a symptom of afferent motor aphasia. There can be two explanations for naming disorders with this locus: it is either a secondary symptom of speech production disorders, or a result of the effects of adjacent focal damage in the parietotemporo-occipital junction. Similarly, with lesions in the left temporal lobe, the author observed that naming disorders were linked with symptoms of word paraphasia, jargon and perseveration. These latter symptoms are typical of speech production disorders in cases of temporal lobe lesions, and so naming disorders with this locus of lesion can, too, be either a secondary effect of specific speech production disorders or the result of dysfunction in adjacent areas. The parieto-temporo-occipital junction in fact seems to play an essential and highly specific role in the naming processes. When this region is damaged, no symptoms of speech production disorders are found of the type caused by lesions of other parts of the speech area. That is to say, naming disorders in such cases occur as if in their pure form (2arski's first group). This observation accords with the findings of numerous other investigators. The hypothesis seems well substantiated that the junction of these three lobes (parietal, temporal and occipital) comprises a brain structure serving an essential function in the cerebral naming mechanisms. As we shall shortly see, this region has some anatomical peculiarities as well which differentiate it from other parts of the speech area. This latter fact has become the basis for certain hypotheses explaining the mechanisms of the nominative function and their disturbances in the event of damage to this area.

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§ 3. MAJOR INTERPRETATIONS OF APHASIC NAMING DISORDERS

In the foregoing section we dealt with a highly specific aphasic symptom observed mainly when lesions are incurred at the junction of the parietal, temporal and occipital lobes, viz., the patient, with speech production on the whole intact, has severe difficulties in actualizing names. Clearly this fact opens up enticing theoretical vistas. Naming brings into focus, as it were, all the fundamental problems associated with the role of speech in human cognitive processes and thought. By employing a word as the name of a particular object, we are using it as a symbol for a given category of objects which at the same time reflects the concept behind that category. By employing a name we are thereby performing an act of abstraction and generalization, we express our specific manner of reflecting the world—generalized, categorized, abstract. At the same time, establishing the name of an object is the necessary condition for grasping its properties and for selecting a rational way of reacting towards it. Many investigators have noted this specific nature of naming and the role of names in cognition of reality. But a summary of this vast literature would far overstep the bounds of this monograph; we shall restrict this discussion to the views of two authors. Vygotsky (1956, 1962, cf. Leont'ev and Luria, 1959) founded his theory of the specific human thinking process almost entirely on the tenet that words and wordmeanings play an essential role in thinking. According to Vygotsky, the word is the precondition for formation of the human way of reflecting reality. When the child begins to speak and to follow the example of his surrounding world of persons by naming the objects around him, he thereby separates these objects from the accidental, concrete associations with immediately perceived situations; as he employs word-names, he proceeds to class objects according to their essential features, according to covert associations and relations not necessarily revealed by direct perception. In this manner categories and general concepts are created, of fundamental significance for the formation of the child's thinking processes. Once formed, such categories and concepts cause thinking to become general, conceptual, and hence specifically human. The elementary units of thinking are concepts, or word meanings. Lewicki (1957, 1960a, b) has also emphasized this aspect of the question. In his view, by naming an object, a person's verbal reaction takes on both a general and selective nature. Its generality rests on the fact that the person will use this word as a name for every object possessing the characteristic features of a given class of objects. Its selectivity lies in the fact that the word used is the name for only a given class of objects, those possessing certain characteristic features, and is not used to name objects belonging to another class. This manner of reacting admits of the assumption that, in applying a name, a person reflects objects belonging to a given class differently from objects belonging to other classes. That is to say, he is able to isolate or identify by analysis in an object its criterial feature, the orienting indicator

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that determines whether that object will be assigned to one or another class. The prerequisite of the reflecting process is abstracting, or detaching the characteristic features from the entirety of properties of any unique and distinct object. Thus, to use a name is a condensed manifestation of the human cognitive capacity. Similar examples could be cited from many other sources1. The problem of the mechanisms which enable human beings to name objects, and of the effects of this act upon the manner in which the surrounding world is reflected in the human being, is'among the most intriguing in the sciences of man. It is not surprising, therefore, that the finding that brain damage can cause a relatively selective loss of the naming ability has animated a discussion around the interpretation of this fact and its consequences for the structure of cognitive processes in a patient afflicted with this disability. We now turn to a discussion of the major theories that attempt to explain aphasic naming disorders.

A. NAMING DISORDERS AS INDICATIVE OF INTELLECTUAL DEFICIT

One of the main tendencies in interpreting aphasic naming disorders is associated with both antilocalizationist and one-factor theories (see Chapter II, § 3 and 6). In fact, naming disorders have often served as the main argument for these hypotheses. As emphasized earlier, at the core of the one-factor theory lies the presupposition that normal speech is determined by some fundamental factor, a single intellectual function. Various terms have been applied to it: the symbolic function, intelligence, the abstract attitude. Causes of speech disorders, particularly naming disturbances, were sought in a deficit of this general intellectual functions broader than language itself. In the early period of aphasia research, proponents of this view expressed their ideas in rather general terms on the nature of aphasic naming disorder and its underlying intellectual deficit. The first attempt to systematize these descriptions and to formulate a theory was made by Goldstein (1948,1959,1960; Goldstein and Scheerer, 1941; cf. also Maruszewski, 1958; Geschwind 1964b; Luria, 1966a). Goldstein advanced the hypothesis that the prerequisite of normal naming ability is an abstract attitude in the human being. In his investigation into the speech of aphasic patients, Goldstein distinguished two types of disorder. One was the impairment of speech instrumentalities, or the technical side of language use, e.g., speech automatisms such as articulation of speech sounds, application of grammar rules, etc. The other type had to do with 1 Some years ago the trend was to approach these questions in a "physiological" way, by referring to Pavlov's conception of the two signal systems and the substitutive function of the word. But these attempts were charged with generalities and "cerebral mythology", and proponents of this line of research overlooked some of the more fruitful aspects of Pavlov's theory (see Chapter VIII).

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word meanings, characteristic mainly of patients with disorders of the abstract attitude. In the latter event, the patient might be able to utter words, but not to employ them as symbols. The problem did not lie in a disturbance in the appropriate word images, but in an inability to find and use words as names for objects. Instead of naming, the patient would circumlocute (see § 2 above) or use "pseudonames". In Goldstein's view, normal naming must be distinguished from pseudonaming. Normal naming refers to the use of a word in its general sense and thereby the assignment of the object named to a general category. "Pseudonaming" refers to a simple association of a word with a concrete object, the name being the sound complex belonging to that object. Pseudonaming occurs in amnestic aphasia. Goldstein described a patient who named familiar objects and colours correctly but the latter only when "pure" colours were concerned, such as red, blue, etc. When faced with various shades of the same colour, she declined to extend the same name, protesting that it would not be correct to do so. Asked to name some animals the same patient could not utter a word, at first, even though some examples were mentioned. Then she suddenly said: "A polar bear, a brown bear, a lion, a tiger." Her explanation for choosing these names was: "When we enter the Zoological Gardens, we come first to the polar bears, and then to the other animals". Apparently the patient had recalled the names of the animals according to their location in the Zoo, and used the words only as they belonged to the concrete situation retrieved from memory. Similarly when asked to give different female names, she said: "Grete, Paula, Clara, Martha." She explained, when asked why these names, that they all were G's (her family name was G.) and added: "One sister died of a heart complaint." Goldstein's interpretation of the above examples is that they demonstrate the use of "individual" words which fit only a particular situation or a definite object. This view was confirmed in his other observations. A patient was shown a knife together with some other object and asked to name the former. When the knife was shown with an apple, the patient called it "apple parer", when shown with a pencil, "pencil sharpener", when shown with a piece of bread, "bread knife", along with a fork, "knife and fork". Never did the patient use the word "knife" alone. Asked whether she could not have simply said "knife" in all these situations, the patient's prompt answer was no. Another patient of Goldstein's named colours displayed to him as "strawberry red", "sky blue", "like an orange", and so on. Such observations demonstrate, according to Goldstein, that these patients use words not in their general sense, or in their categorial meaning, but as fitted to concrete and unique objects, features and events. This is symptomatic of a defective abstract attitude, which is the ability to detach from the direct sensory perception of the situation and be guided by general concepts. For this patient, objects are not members of classes or categories; they are unique and concrete and as such can be associated to a word. Amnestic aphasia is thus the result of a deficit of the abstract

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attitude; it is the effect of a disorder of categorial behaviour. There are many varieties of this disorder, amnestic aphasia being only one of the symptoms 2 . Goldstein's theory won many supporters and was very influential subsequently in shaping opinion on determinants of aphasic disorders, particularly naming disturbances. But there are a number of serious reservations that may be expressed about this theory; these may be summed up in three points. The first reservation involves the relative rarity of the specific forms of disorders used by Goldstein as evidence of the pathological concreteness of behaviour in amnestic aphasic patients. The literature contains practically no data to confirm Goldstein's observations and the present writer has himself had difficulty in identifying them in his clinical practice. It is therefore highly contestable how frequently they occur and how integral their connection is with naming disorders which, by way of contrast, are very common indeed. The second doubt concerns the interdependency of naming disorders and intellectual deficit, and hinges on the fact that severe intellectual deficiency of a pathologically concrete type can at times be observed in psychiatric cases but it does not ordinarily produce amnestic aphasia unless brain damage is incurred as well (Markova, 1961). Why, then, in the case of brain damage, are these to be taken as responsible for naming disorder? Finally, the notion of "abstract attitude" is itself unclear. Certain of Goldstein's formulations imply that he regards the abstract attitude as a primary factor in brain functioning, which explains abstract behaviour. However, in discussions of various disorders, Goldstein uses the term in a descriptive sense as an abbreviation for a syndrome involving particular behavioural properties that are disturbed after cerebral damage. Difficulties also revolve around the interpretation of amnestic aphasia. Is the claim that the patient with naming disability displays excessive literalness in his verbal behaviour to be taken as a descriptive statement requiring explanation of its causes, or as an explanatory statement in itself? Goldstein tended toward the latter interpretation, therefore his views were not without a flavour of mysticism and invocation of unknown phenomena, typical of which were frequent references to the Gestalt theory in psychology with its cerebral mythology—a product of the contemporaneous state of knowledge on brain functioning. A fairly well-developed theory of amnestic aphasia as symptomatic of an impairment of some general factor has been advanced by Kogan (1962). Kogan regarded amnestic aphasia as one of the stages of recovery from total aphasia, consisting of a complete disconnection between word and object. Characteristic of this stage is the fact that the patient's major difficulty is his inability to actualize the internal meaningful connections between words and objects, or the connections underlying 2

Goldstein and his collaborators developed a number of tests for the study of the disorders of the abstract attitude in brain-damaged cases. They have been discussed in more detail elsewhere (Maruszewski, 1958).

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the naming processes. The word has neither meaning nor symbolic function if it is merely the verbal duplicate of the perceived object. The active employment of words as names is a complex process in speech, involving not only recognition of the object and retrieval of the word name, but also proficiency in performing mental operations applying knowledge possessed about the object and its relations with other objects and events. The act of naming is always the actualization of a system of propositions about the object, judgments embodying knowledge acquired through prior generalization of earlier experience. To name any object means to actualize a proposition which grasps the object in some relation with something else or in terms of one of its features. Kogan signalizes the fact that the task confronting the aphasic patient in naming tests is a highly artificial one, since it requires the patient to name an immediately perceived object. This involves an unnatural linguistic operation, not encountered in the real communicative process, in which usually absent objects are named, objects not perceived at the moment 3 . In amnestic aphasia, understood by Kogan as a stage of recovery from total aphasia, the word-object connection has partially returned. But still the word does not fulfil its generalizing role, since the patient cannot actualize the meaningful relations underlying the word, and for this reason employs it to refer only to very concrete and explicit situations. In line with his interpretation of the mechanism of amnestic aphasia, Kogan developed a rehabilitation method aimed at recovery of normal naming processes. This technique is essentially to "enact" words by inserting them into many different meaningful contexts. As such it amounts to the practical application of his theory aimed at removal of the Causes of naming disorder (see Fig. 23). Thus both Goldstein's and Kogan's theories consider naming disorder in amnestic aphasia as the symptom of a general intellectual deficit, or a particular kind of dementia. Although many of the cited statements sound probable and seem intuitively acceptable, their empirical verification remains an open question. Both authors tend to base their views on observations of an anecdotal and isolated kind, which perforce 3 Jakobson (1956a) has written similarly on this problem. He sees the aphasic defect in the "capacity of naming" as properly a loss of metalinguistic function, i.e., the ability to talk about language. What we ask of a patient in placing before him an object and prompting him to name it, is fundamentally, to abbreviate a metalinguistic proposition, in terms of the language being used in the test situation. To name an object thus is, in brief, to say: "In the code we use, the name of the indicated object'is pencil." The fact that the aphasic tries in vain to find the name is symptomatic of substitution disorder. He fails to substitute with an equivalent sign (which in this situation is done by the examiner who indicates the object), the latter being redundant and therefore dispensable. For the aphasic patient with naming disorder, the two signs of the equational predication are separated; if the examiner indicates one, then the patient will avoid its equivalent. All this is symptomatic of impairment of one of the two major linguistic operations, i.e., selection of linguistic entities, and substitution of others in some respects equivalent and in other respects different.

Jakobson's views on naming disorders were modified in his later work (Jakobson, 1956b).

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Fig. 23. Example of a scheme of a word's semantic relations as used by Kogan in the rehabilitation of aphasic patients (Kogan, 1962).

diminishes their value as documentation. For this reason the majority of current aphasia workers treat with reserve the propositions about the intellectual determinants of amnestic aphasia. This attitude is reinforced by the fact that the few attempts to verify certain of these assumptions in controlled experimental conditions have yielded either equivocal results or findings out of keeping with the hypothesis on the existence of some general factor underlying aphasic disorders. Illustrative of the latter type of finding are those reported by Goodglass and Kaplan (1963), who set out to verify the idea of a general intellectual factor (intellectual efficiency) that would determine the use of all kinds of symbols and would be disordered in aphasia. They investigated the ability to use gesture and pantomime in aphasic patients and nonaphasic brain-injured patients as controls. Their argument was: If in fact there exists a general asymbolia, then it ought to show up in the gestural communication of aphasic patients. Although gestural disorders undoubtedly occur in aphasia, it remains to be demonstrated whether there is some common substrate with aphasic disorders or whether, alternately, they are nothing but concomitant symptoms resulting from proximity of areas where lesions produce aphasia and where they produce apraxia. If the first hypothesis is correct, i.e., that gestural deficiency is caused by disorders of a symbolic function common to both speech and

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gestural communication, then it can be expected that (1) gestural deficit should be more severe in aphasic than in nonaphasic brain-damaged patients, (2) severity of aphasia should be correlated with the degree of gestural defect, (3) gestural defect should be limited strictly to the use of gestures as communicative acts, as distinct from other gestural movements such as imitations or object manipulation. The series of tests used in this experiment included 46 different gestural and simple pantomimic acts which the patient was to perform at the examiner's request. Two brain-injured groups, aphasic and nonaphasic, were tested. A careful analysis of the material showed that, while worse performances were recorded with aphasic patients as a group, yet (1) no relation was established between severity of aphasia and gestural performance, (2) no clearcut difference was established between gesture as communicative means and gestural movement as imitation, (3) the nonaphasic group displayed evident disturbances in their performances testifying to a gestural deficit independent of aphasia. On these grounds Goodglass and Kaplan drew the well-reasoned conclusion that gestural impairment in aphasic patients is not symptomatic of a deficiency of the general symbolic function, but is a symptom of apraxia which is related to left hemisphere damage, being independent of aphasia. Frequent concurrence of aphasia and gestural impairment is due to the proximity of the cerebral structures responsible for the normal performance of these types of activities.

B. NAMING DISORDERS AS INDICATIVE OF DEFICIENT PERCEPTUAL FUNCTIONS

One of the possible nonlinguistic mechanisms considered to underlie naming disorders in amnestic aphasia is connected with the perceptual aspect of naming. Undoubtedly, in order to name an object correctly, that object must first be identified ; if the patient has difficulty in perceiving it, this will affect the naming of it. What is involved is not a severe perceptual disorder of the type called agnosia, when object recognition is totally impaired, in which case the patient's inability to name objects is self-evident. Amnestic aphasia may be due to a more subtle derangement of perceptual function, clinically unobservable and therefore not diagnosed as agnosia though disturbing the naming operation (cf. Luria, 1947; Kok, 1967 on "optical aphasia"). Evidence in support of this hypothesis has been forthcoming from a number of experimental studies conducted in various centres. Teuber and Weinstein (1956) used the Gottschaldt Hidden Figure Test in a comparative study of an aphasic group, a nonaphasic brain-injured group, and a normal control group (Fig. 24). The task was to find and mark with pencil a simple figure embedded in various complex figures. In this test situation aphasic patients gave poorer performances than the nonaphasic brain-injured group, who in turn were surpassed by the controls. The authors attributed the visual deficit discovered by this test to be a symptom of a more general disorder in aphasics considered to be defective organization or selection of material,

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Fig. 24. One of the tasks in the Gottschaldt Hidden Figure Test. The subject's task is to find and trace with pencil a simple figure (shown at top) embedded in each of the more complex figures (after Teuber and Weinstein, 1956).

linguistic as well as non-linguistic. The size of the aphasic group studied was too small to establish whether all types of aphasia are alike in this respect or whether it is specific to certain types. The authors tended to believe the latter. Ten years later, Teuber and Weinstein's results were corroborated by Russo and Vignolo (1967). In a series of experiments Kok (1957a, b; 1958; 1959a, b; 1960; 1967) sought to clarify the role of perceptual disorders at the root of amnestic aphasia. Kok developed ingenious techniques to study disturbances of simple generalization and abstraction of visually perceived material and tried to link these impairments with various naming disorders in patients Her method was to form motor conditioned reflexes by verbal reinforcement. For instance, the patient was shown four geometric figures in varying successions; two were positively conditioned stimuli (green circle and green diamond) and two were differential stimuli (red circle and red diamond). At the sight of the former, the patient was to press a rubber bulb and to refrain from pressing at the sight of the latter. When the patient had learned to respond to green and red figures, other red and green shapes were introduced, such as a red triangle or green rectangle. If the patient continued to press the bulb at the sight of green stimuli, regardless of shape, and to withhold response to all red stimuli, this was evidence in Kok's opinion that the subject was capable of simple abstraction and generalization. This experimental model was used with a wide variety of visual features of objects, e.g., shape, size (when the patient was trained to react to large as opposed to small figures regardless of shape, colour, etc); number (when the response was trained to several objects as opposed to a single object); spatial relations (when the response was to a given reciprocal distribution of objects), etc.

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Poor performance on such tests was found only in patients with injury in the left parieto-temporo-occipital junction. Interrelations were found between visual features evoking the greatest difficulties and the kinds of naming disorder. For instance, if colour names were disordered, then the patient had most trouble in abstracting and generalizing the colour features of the perceived material. But if object naming was mainly disturbed, the patient performed normally with the colour tests but lost proficiency on tests calling for generalization of size and shape. Lastly, when use of words representing spatial relations was impaired, then this type of generalization was most severely deranged. Kok's conclusion from these experiments was that naming disorders in cases of injury of the parieto-temporo-occipital junction are caused by a selective deficit of the ability to abstract and generalize the visually perceived features of objects. According to Kok, this ability is a property of perception, resulting from subtle processes of analysis and synthesis within the visual analyzer. Since selective naming disorders (letters, colours, objects, or spatial features) correlate with selective disorders of the abstracting and generalizing ability for these respective features, Kok concluded that the junction area in question must contain separate functional systems for each of the visually perceived features determining both the abstracting and generalizing ability and the naming ability in respect to each of these features. In other words, Kok associated naming disorders in amnestic aphasia with selective disturbances of visual analysis and synthesis, i.e., with subtle forms of agnosia. In line with this conclusion, she attempted to find distinct and separate loci of damage answering to each of these disorders. Kok's research gave rise to the highly interesting hypothesis of perceptual determination of naming disorders. Unfortunately, her conclusions have not been substantiated with the necessary precision; particularly, her data lack statistical elaboration. More recently several studies have attempted to examine her hypothesis. Bisiach (1966) studied naming disorders in aphasic patients by presenting three pictorial versions of familiar objects. The first version was of realistic and easily perceived objects, the second contained objects in vague outline with few features to facilitate recognition, and the third was a "mutilated" version posing perceptual difficulties in identifying the object represented. Patients were found to have least naming difficulty with the first version (whose informational redundancy was the highest). The author concluded from this study that naming disorders are conditioned by factors at the level of interaction between the perceptual and the verbal processes. A similar conclusion was reached by Dudley, Doehring and Coderre (1968) who studied speed of visual perception. Their technique comprised a series of tests in which certain items, or sets of items, were to be identified and underlined each time they occurred among similar ones. These items included simple and complex figures, letters, numbers, nonsense syllables and words (Fig. 25). Three groups were studied: aphasic patients with left anterior or posterior damage, nonaphasic patients with right hemisphere damage, and a control group without brain injury. A statistical

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analysis of the findings showed that, although both brain-injured groups were significantly slower than the control group in identifying visual figures, the aphasic patients with left posterior damage were most severely impaired. This was interpreted as further evidence that a specific perceptual deficit is restricted to this group of aphasic patients. One other study of present interest is De Renzi and Spinnler's (1967) investigation of performances of brain-damaged patients on a series of tasks involving identification and use of colours. Aphasic patients displayed special difficulty in colouring drawings of objects, as compared to other brain-damaged groups (Fig. 26). This impairment did not, however, correlate with colour perception disorder. Since objectcolour association occurs apparently on the perceptual level, and since performance of such a simple task can hardly involve verbalization, De Renzi and Spinnler concluded that colouring difficulty is symptomatic of a more general involvement of

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Fig. 26. Performance of an aphasic patient on colouring drawings (De Renzi and Spinnler, 1967).

mental abilities and related this to Goldstein's conception (see above section A). While the latter point remains an open question, the disorder described in their nvestigation is clearly a perceptually-based one, and their findings concord with those reported above. Taken together, the data we have surveyed do not resolve the question as to the veracity of the hypothesis of perceptual determination of naming disorders involving

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lesions in the posterior speech area; they do, however, provide a fairly firm basis for accepting it as a working hypothesis for further investigations. It is of interest to note that this hypothesis fits into a broader discussion on the determinants of the human naming ability. Lenneberg (1962b, 1967; see also Chapter II § 7) goes to the extreme of asserting that naming is derivative in relation to man's specific perceptual capacities, or the human ways of organizing sensory material. Naming, according to Lenneberg, is the human form of expressing perceptual processes proper to man, his manner of cognizing reality. Categorization is a particular mode of ordering the physical world or dealing with sensory data. Concepts are not so much the completed and stored products of cognitive processes as the process itself, since perceptual data are continuously being organized. Words are labels of processes by which the environment is categorized. In Lenneberg's view, loss of the naming ability reflects specific difficulties in the flow of cognitive processes by which sensory data are organized. The experimental findings we have reported above may be considered as support for this explanation.

C. NAMING DISORDERS AS INDICATIVE OF DISTURBED CROSS-MODAL ASSOCIATION PROCESSES

The parieto-temporo-occipital junction has an important role in the naming processes, as the research reported in § 2 demonstrates. This region also possesses specific anatomical features which have served as grounds for another hypothesis on naming disorders associated with this locus of injury. This hypothesis has bsen most thoroughly elaborated by Geschwind (1964a, 1965), who used clinical observations, comparative anatomical studies of human and animal brain structures (mainly the nonhuman primates), and animal experiments on "crossmodal transfer". A fairly exhaustive review of the latter group of studies can be found in Ettlinger (1967). Geschwind's conclusion was that an anatomically determined capacity for cross-modal associations underlies the human naming ability. This capacity is related to a cortical area, "the inferior parietal lobule" which includes the angular and supramarginal gyri, to a rough approximation, areas 39 and 40 of Brodmann. Not all agree about the existence of this area in the animal brain, but those authors who claim to have found it in nonhuman primates admit it to be incomparably more evolved in humans. It is thought to bs a relatively new phylogenetic development, since this area matures late in ontogenesis (at 3 or 4 years). It is particularly significant that this area lies at the junction of the cortical projection areas for the three major modalities (visual, auditory and somesthetic), and can therefore serve as the anatomical substrate for associations across the three perceptual channels, in other words, cross-modal associations. The above supposition has been confirmed in animal investigations. Lacking this cerebral structure or possessing only a rudimentary form, animals fail to form cross-

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modal associations. The only readily established associations in animals are those between any nonlimbic sensory and the limbic system, the latter controlling the organism's essential functions. In other words the animal can learn only in terms of his biological needs; his associations are built on direct biological reinforcement. Associations between sensory signals and the limbic system permit the animal to react in various biologically purposive ways to those environmental influences that are meaningful in terms of need satisfaction. But associations between stimuli arriving through different sensory modalities and unconnected with biological need cannot, in principle, be formed. If occasionally elementary forms are found to exist under some conditions, these are exceptions to the rule. Characteristic of animals is the inability to form cross-modal associations. To illustrate this statement, we report Ettlinger's (1967) experiment in training monkeys to distinguish visually between a triangle and a disc. If the animal pressed the lever under-the disc, he was rewarded with his favourite food; if he pressed the lever under the triangle, no reward occurred. Once the monkey had learned to perform this task (i.e., to press the lever under the disc), the experiment proper began. These same animals were to distinguish by touch between disc-shaped and triangular blocks; prevented from seeing the blocks, they could only palpate them. Again, only choices of the disc-shaped blocks were rewarded. The investigator's purpose was to establish whether the fact of prior learning to distinguish visually between a disc and a triangle would affect the speed at which the animals learned to discriminate tactually between the round and triangular blocks. The findings were unequivocal: in the new situation the animals behaved as if they were dealing with these two Shapes for the first time in their lives. Their learned discriminations affected only the sensory modality in question. Analogous results have been found in numerous other experiments; only occasionally has some minor learning effect across modalities been noted in stimulus discrimination. By way of contrast, cross-modal associations are formed with extraordinary ease in man. Man's capacity is unique in the animal world in respect to associations of stimuli arriving through different modalities of which none has direct biological significance. A person can, for example, identify visually a disc to be the disc he is feeling at the moment. There are divergencies of opinion as to the reason for this phenomenon. It is often suggested that cross-modality transfer is possible because of verbal mediation. The fact that man can verbalize the stimuli he experiences acts as a "bridge" enabling him to match incoming stimuli from different sensory channels (cf. for example Ettlinger, 1967). Geschwind however criticizes this explanation; according to him, the source of the ability for cross-modal associations lies in the specific properties of the cortical projection junction area for the visual, auditory and somesthetic modalities. Cross-modal associations, from a physiological viewpoint, form the base or substrate of the human capacity to name; names, after all, are polymodal representations of objects of the external world. Injury to this particular area necessarily

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leads to naming disorder since the required associations across stimuli of various modalities cannot be effected, or are impaired. Geschwind illustrates this explanation with the example of selective naming disorders in respect to colours, occurring in the syndrome called pure alexia without agraphia. This syndrome results from damage to the left occipital pole and the posterior part of corpus callosum, or splenium (see Chapter III). This locus of lesion has the effect that visual stimuli can be received only through homologous parts of the contralateral hemisphere. For the patient to be able to name the colour he sees, this information must pass over to the left dominant hemisphere, but since injury affects that part of the commissure containing the neural pathways between the right occipital regign and the left hemisphere, no information arrives at the speech area as to what the right hemisphere "sees" (the latter having no speech centres). Such a situation arises only in colour naming since this is a purely visual feature having no cross associations with other sensory modalities. But in object-naming, impulses originating in the right hemisphere evoke many tactual and auditory associations with the perceived object at the right hemisphere junction area, and since information can be transmitted from right to left hemispheres through the intact anterior parts of the great commissure, the patient retains the ability to name objects. Colournaming disorders are therefore the effect of selective destruction of the pathways connecting the visual area and the speech centre. We have already mentioned in Chapter II (§ 5) that Geschwind's hypothesis has invoked criticism mainly around the notions that an association can be equated to a neural pathway, and that regulatory mechanisms of behaviour can be reduced to cortical interaction by means of transcortical pathways. However, it must be emphasized that the body of fact amassed by Geschwind forms an inherently cohesive whole and must be accounted for within any theory that aspires to elucidate the human naming ability. The importance of the latter point is enhanced by the findings of certain experimental studies aimed at verifying some of the implications of Geschwind's theory. These studies demonstrate clearly the role of the cerebral region in question in the formation and actualization of cross-modal association in man. Butters and Brody (1968) studied disorders of intra- and cross-modal associations in patients with posterior parietal lesions of the dominant hemisphere. Their purpose was to establish whether these patients could form such associations on the basis of matching tasks (matching stimulus patterns in like or unlike sensory modality). In the intra-modal association tests, the patient was to match a complex design on a card to an identical figure selected from among several randomly arranged stimuli (visual-visual matching); or he was to match tactual patterns on raised surfaces (tacks or wires used) to a pattern selected from among other tactual stimuli explored by the finger tips (tactual-tactual matching). The cross-modal tasks involved matching visual designs to an unseen wire pattern (visual-tactual matching); matching a tactual figure to a visual pattern (tactual-visual matching), and, finally, matching a sequence of auditory stimuli (tapping)

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of visual sets of dots (auditory-visual matching). Performance of aphasic patients with posterior lesions in the dominant hemisphere was compared with that of nonaphasic patients with different loci of lesion or injury to the peripheral nervous system. It was demonstrated that patients with dominant anterior damage were unimpaired as a group on all intra- and cross-modal tasks as compared with the nonaphasic control group of brain-damaged patients. But the aphasic patients with dominant posterior lesions displayed clear deficiencies in all cross-modal tasks and in one intramodal test (tactual-tactual). The difficulties in the latter task were ascribed to the perceptual impairment in respect to tactual stimuli specific to damage in the posterior parts of the brain. Using sophisticated data processing techniques, Butters et al. demonstrated that this disorder is not however the cause of the deficiency in performing cross-modal tasks, for even after elimination of the possible effect of tactual difficulties upon cross-modal tasks, the aphasic patients with dominant posterior lesions gave significantly worse performances on these tasks than the other groups. On these grounds the authors interpreted their findings as evidence for the hypothesis of the specific role of the posterior part of the dominant hemisphere in the formation of cross-modal associations. Thus it has been shown that the hypothesis ascribing the cause of naming disorders to lesions at the parieto-temporo-occipital junction (by which cross-modal associations are impaired) has been sufficiently substantiated by observation and experimental research to warrant further examination.

D. NAMING DISORDERS AS INDICATIVE OF IMPAIRED SIMULTANEOUS SYNTHESIS

Naming disorders have been thoroughly analyzed in the studies of Luria (1947, 1962, 1967). In line with his general theory, Luria considers the nominative function to be one of the two key functions of speech, the other being the predicative function (see Chapter V, § 4D). To name an object, event or feature is a complex act, embracing many interactive processes of a more elementary kind. The latter include such processes as finding the appropriate meaning (concept) within the conceptual network, and actualizing the auditory-motor word pattern. For this reason, naming can be disordered by lesions diversely localized and can occur in different aphasic forms. Thus, when the anterior part of the dominant hemisphere is injured, leading to various speech production disorders, it is mainly the predicative function that is affected, while the nominative function remains relatively intact. Any difficulties the patient may have in naming are analogous in kind to those occurring in any attempt to speak. Certain specific difficulties may be noted, involving excessive concretization of word meaning and difficulties in finding names in narrative speech when the patient tries to retrieve the appropriate name without support of immediate perception. Observable naming difficulties also occur in cases of lesions of the dominant temporal regions leading to secondary disorders of speech production (see Chapter

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V, § 5). Behind this naming impairment is an instability of auditory word-patterns and pathological changes in the dynamics of auditory traces, as observed in the groping for the right-sounding word, verbal paraphasias, perseverations, contaminations, jargon, and those descriptive circumlocutions substituting for the name itself. Luria points out that, in such cases, no effect can be achieved by prompting the patient with the first sound in the word; instability of the word-pattern can reach such a point that the patient not only fails to benefit from a prompt but may even fail to recognize the whole word when it is repeated by the examiner. In the above forms of aphasia, naming disorders, mild or severe, are due to motor or auditory impairment. But different causes underlie those naming disorders associated with lesions at the parieto-temporo-occipital junction. Symptomatic of such cases are impaired word comprehension and conceptual disorders. The first thing to note is the absence of distorted auditory-motor word patterns in naming; either the patient will say nothing at all, or he will circumlocute, or he will produce errors typical of semantic (verbal) paraphasia, in evidence of poor selectivity of emerging word meanings. This is one of the symptoms of semantic aphasia (Chapter VI, § 4A). In Luria's interpretation of semantic aphasia and associated naming disorders, reference is made to specific properties of the parieto-temporo-occipital junction as the "overlapping" part of the cortical representations of the main analyzers (visual, tactual, vestibular and auditory). This circumstance accounts for the particular role of this junction in ensuring complex analytic-synthetic activity, both spatial and simultaneous. Referring to the early views of Sechenov and later writings of others including Lashley, Luria points out that sensory information undergoes twofold processing: successive synthesis, i.e., linear combination, and simultaneous synthesis, i.e., grouping. Successive synthesis is typical of the auditory analyzer and the motor analyzer; both receive sequential series of external stimuli. Simultaneous synthesis is typical principally of the visual, tactual and vestibular analyzers, which usually receive external stimuli grouped and simultaneously acting upon various spatial points. In view of the exact locus of cortical representation of the analyzers we may say roughly that the anterior portion of the brain has the function of successive synthesis while the posterior portion has that of simultaneous synthesis (cf. also Luria, 1963). At the junction (the parieto-temporo-occipital region), simultaneous crossmodal synthesis takes place, i.e., synthesis of information arriving from the principal analyzers. This function is necessary for various kinds of normal higher activities, such as spatial perception and orientation, mathematical operations, constructional functions, comprehension of complex logico-grammatical constructions, and, among these, naming. As stated earlier, naming calls for actualizing an appropriate concept, or selecting one meaning from a kind of "meaning network" where previously acquired notions are lodged. It is the process of manoeuvring about in the conceptual network that is disturbed when simultaneous synthesis is impaired. It is as if the patient were unable to "get at" the proper point in the network so that, instead of the concept wanted

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proximal meanings emerge, those "located nearby" and belonging within the same semantic sphere. Typically the patient has the word he needs "on the tip of the tongue", so that prompting (giving him the first sound or sounds) allows him to find it immediately. This is evidence that the patient's particular difficulty is not in actualizing an auditory-motor pattern but in getting at the pattern through its meaning. Characteristic of these disorders is the narrowing of word meaning and blurring of boundaries; these phenomena are at the root of poor selectivity in finding and actualizing meanings, and therefore of word retrieval. The interpretation of naming disorders presented above leaves much to be clarified, as Luria himself acknowledges. We still do not possess clear enough notions to approach it in precise fashion and to particularize these statements. The main argument, however, in favour of its acceptance is that naming disorders, in line with clinical observations, are treated as one symptom of a whole syndrome of disorders with lesions of a particular cerebral region, and also—as already demonstrated with fair accuracy—with impairment of simultaneous spatial synthesis. These are adequate grounds to assume that naming disorders due to damage in the parieto-temporooccipital junction are produced by the same pathophysiological mechanism.

E. CONFRONTATION OF THE VARIOUS INTERPRETATIONS OF APHASIS NAMING DISORDERS. CONCLUSIONS

In the foregoing sections we have presented the major hypotheses advanced to explain the specific symptom in aphasia known as naming disorder. This phenomenon is both complex and multifaceted, as this review shows, and attempts to elucidate it are very divergent. However, it would seem that there is adequate substantiation for formulating a number of conclusions. First and foremost, it is abundantly clear that those ideas inspired by the earlier period of aphasia research pertaining to the existence of special "conceptual centres" somewhere in the brain have no foundation in the light of present knowledge about naming and its disorders. Quite the reverse, there is ample ground for assuming that this function is carried out through the participation of numerous and diverse cerebral structures, of which one of special importance is the parieto-temporo-occipital junction region, in all likelihood due to its borderline position. A second conclusion is that the hypotheses advanced, though divergent as explanatory statements, are not mutually exclusive. Each may possibly embrace one facet of a complex mechanism controlling naming processes, and all may be needed for its full elucidation. For example, Goldstein thought that naming disorders result from a deficit of the abstract attitude. If we are to understand "abstract attitude" as some kind of primitive and undefinable brain factor, or symbolic function, or the like, this interpretation raises doubts, as mentioned earlier. But if we understand the abstract attitude as the entirety of specifically human properties of behaviour and

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cognition, then other authors might agree that patients with naming disorders do in fact suffer a deficit in their ability for such behaviours. But a narrower definition is required as to what is disordered, that is, what component factors comprising the abstract attitude are in this case disordered. Nor do the other conceptions contradict each other. It is easy to accept that naming requires a normally precise perceptual functioning, as well as a constant interaction of the major sensory modalities through cross-modal association, and, additionally, complex forms of simultaneous synthesis to ensure retrieval of appropriate meanings—as the determining factor for actualizing the proper auditory-motor word patterns. Perhaps some other hitherto unknown functions of the brain play some role, together with the above, in conditioning the human ability to name objects, events and features of the environment and describe actions and processes occurring in it. This brings us once again to the conclusion that any interpretation of the naming function must account for its complexity, and every attempt to narrow it to one aspect alone will fail to account for all the interdependencies involved.

§4. DISORDERS OF INTELLECTUAL PROCESSES IN VARIOUS FORMS OF APHASIA

We have focussed attention in the foregoing sections on the disorders of naming and the possible cognitive determinants of these phenomena. A no less striking question is that of the cognitive processes of patients suffering from other aphasic disorders, such as disorders of speech reception and production. This problem is very poorly studied, due largely to the methodological hurdles to be overcome. But some attempts to reach solutions are worthy of note. As a preliminary comment, the point should be made that even severe aphasic speech disorders do not result in dementia in the common sense of the term. The aphasic person does not display features of mental dullness in his daily behaviour. If he is in a position to understand the exigencies of the situation, his conduct is rational and adequate, indicative of an ability to benefit from experience acquired prior to the onset of his disorder. In this context some instructive observations have been amassed in studies of "total aphasic" patients (Kogan, 1962; Maruszewski, 1966). These patients suffer severe disorders of all speech processes so that to all intents and purposes any communication with them—at least at initial contact—is out of the question. Not only does the patient fail to utter the simplest word, but he cannot understand the least command, verbal or nonverbal, by gesture or demonstration. Such a condition can last months and years. The question arises: Is the total aphasic patient capable of human thought? In searching for an answer, a wrong strategy is often used, viz., to demonstrate the differences between the thinking of the severe aphasic patient and that of the normal person. These differences undoubtedly exist. But more interesting findings are forthcoming when the search is directed to the following question: Is it true that

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the thinking of the total aphasic shows no features of specifically human thought, or do his mental processes take place on a level common with the lower species or humans who have never acquired the use of language and the processes involved in speech? The answer to this question is decidedly no. Even in the total aphasic, under facilitating conditions, his thinking can display features proper to human thought. Kogan (1962) has reported some interesting observations on this question. He studied the ability of total aphasic patients to make simple generalizations involving grouping objects in accordance with general categories. Twelve pictures of objects in random order were shown to the patient, each of which paired with another member of the same class (e.g., cow—horse; cucumber—tomato; knife—fork, etc.). Then the examiner slowly showed the patient how to match them in pairs. Out of the 18 total aphasic patients studied, 15 grasped the principle behind the task by the time the third pair was matched; only one could not learn to perform this task correctly and made errors in matching pairs. In another experiment, Kogan taught these patients to group geometric figures according to shape or colour. It goes without saying that these patients behaved differently in carrying out such problem-solving tasks than would normal subjects. But the fact that they could master such tasks demonstrates that, to some degree at least, they had the capacity of specifically human thinking and could use general concepts previously acquired. This circumstance has enormous significance for rehabilitation of total aphasic patients. In some cases a considerable speech improvement ensues when a suitable selection of nonverbal tasks capitalizes upon latent intact capacities in the patient (Sobkow, cit. by Maruszewski, 1966). Thus we find that even total aphasia does not deprive a person of the ability to perform specifically human intellectual operations. In milder forms of aphasia this fact is even more striking. The above statements should not be taken to imply that the aphasic's thinking does not diverge from that of the normally speaking person. While such differences apparently exist, contradictory findings have been forthcoming from experimental studies and no conclusion based on empiric fact has yet been reached (cf. Archibald et al., 1967, for a useful literature review and discussion). Two basic obstacles must first be overcome before the true state of affairs can be ascertained. One is a classification of aphasic patients according to type of lesion and ensuing disorders. Hitherto most studies devoted to intellectual functioning in aphasic patients have ignored this as a necessary condition and have been limited to results obtained on accidental samples of aphasic populations as compared to nonaphasic control groups. The other obstacle is the still unresolved problem of appropriate methods to study the intellectual processes of aphasic patients. The tasks hitherto used in investigations of this kind are either too complex to demonstrate what they are intended to test, and therefore to interpret the errors of performance; or they are too simple so that perceptual or motor functions are apparently more involved than intellectual processes.

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For reasons such as these, the distinctive nature of intellectual activities in aphasic patients is still open to more precise study. To illustrate the manner in which data have hitherto been obtained on this question we report two investigations. Tikofsky and Reynolds (1962) studied nonverbal learning in aphasic patients by means of the Wisconsin Card Sorting Task. Briefly, this task involves sorting a set of picture cards into four marked fields. The first field is marked with a red triangle, the second with two green stars, the third with three yellow crosses and the fourth with four blue circles. The cards also contain the same elements but in different combinations. The patient's task is to discover the experimenter's rule for sorting the cards into the four fields. This rule may be to sort according to colour, shape or number of figures and the subject is to guess which rule is being applied. He is told merely whether he has placed the card properly or not—this being the only kind of information given to the subjects. After 10 correct sortings according to one rule (such as colour), the rule is changed without warning and the experimenter begins to evaluate the subject's performance according to another rule (such as: number of figures). The subject therefore must solve a fairly difficult and artificial type of classification task. Comparison of results from aphasic patients and normal subjects showed a poorer performance by the former in discovering rules, the difference between the groups being statistically significant. The authors concluded from this that aphasic patients are restricted in their ability to solve nonverbal problems. The opposite conclusion was reached by Archibald et al. (1967) in their studies on nonverbal cognitive processes. For their purpose they used four tests: Raven's Coloured Matrices, a modification of Weigl's Colour—Form Sorting Test, a modified cube test and a maze test. Comparisons were made of aphasic patients and nonaphasic brain-injured patients. It was found that only the most severe aphasic group differed significantly from the nonaphasic patients, though this difference was also found with the mild aphasic group. The authors concluded that intellectual disorders may occur in cases of severe aphasia but are not involved in the milder forms of aphasia. In their opinion, in most aphasics speech disorders do not lead to disturbances in performance on nonverbal tasks testing the cognitive functions. Studies of the above type are numerous, but the findings of this kind of investigation do not serve as adequate groundwork for more precise conclusions as to whether specific disorders of cognitive processes do in fact occur in aphasia, and if so, what are their scope, the responsible mechanisms, and differences according to locus of lesion and aphasia type. And so the question of the effect of speech disorders on human cognitive processes remains open.

CHAPTER VIII

SPEECH AND GOAL-DIRECTED ACTIVITY IN THE LIGHT OF NEUROPSYCHOLOGICAL RESEARCH

§1. THE ROLE OF SPEECH IN THE REGULATION OF GOAL-DIRECTED ACTIVITY

"We presuppose labour in a form that stamps it as exclusively human. A spider conducts operations that resemble those of a weaver, and a bee puts to shame many an architect in the construction of her cells. But what distinguishes the worst architect from the best of bees is this, that the architect raises his structure in imagination before he erects it in reality. At the end of every labour-process, we get a result that already existed in the imagination of the labourer at its commencement" (Marx, 1954). The idea expressed by Marx in the first volume of Capital that the specificity of man lies in the ability of planning is today a fundamental tenet of many different psychological theories and interpretations of behaviour in man. Such properties of human behaviour as the capacity to act according to a mentally constructed design, to steer toward the attainment of a deliberately chosen goal, to correct deviations from the pre-set path irrespective of external circumstances, in short, the capacity to direct oneself by an "inner" plan, are unquestionably those properties which—even if observable in rudimentary form in some other species—attain dominance in man alone and typify his behaviour. Associated with this fact are many important theoretical problems; these derive from the questions: What are the psychological mechanisms underlying the emergence of this ability? How is man able to plan an outcome of an action and a way to attain it, how is it that he then pursues his goal to its realization often in the face of external hindrance? Answers to these questions must certainly account for many facets of human psychological processes, but it would seem that of special importance for man's directed activity is the capacity for speech. In this chapter our aim is to report on the research into those behavioural disorders caused by brain damage which shed light, from the pathological angle, upon the role of speech in human behavioural regulation. But first, let us examine the broader context of the problem. Let us start with Pavlov's (1928) theory of "the second signal system". This is unfortunately an imprecise formulation, which has given rise to many misunderstand-

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ings. As mentioned earlier, this theory was once very popular among Pavlov's followers but, partly due to a mechanistic interpretation, was later rejected as a basis for theorizing about speech and its role in human behaviour. Apparently Pavlov's followers, in attempting to validate the theory of the second signal system empirically, focussed upon its less promising theoretical aspects, and were therefore deceived. And yet, this conception embraces certain important hypotheses allowing for a fundamentally different approach from that traditionally made to well-known empirical data. Broadly speaking, the second signal system theory can be stated as follows: In contradistinction to animal species, whose behaviour is guided solely by direct environmental action (i.e., by the "first system of signals from reality"), human behaviour is essentially regulated by the stimuli of the second system of signals from reality, i.e. by verbal stimuli. This is a special system of stimuli which are "signals of signals", or signals which can evoke the same reaction as the direct stimulus1 which it signalizes. At the same time this signal system introduced a new "rule" into the higher nervous functions of man, that of abstraction and generalization. Three categories of stimuli belong to the second signal system: words perceived by ear, words perceived visually (writing), and words received in the form of kinesthetic sensations from the speech organs (words uttered by the speaker). Thus stimuli of the second signal system originate not only from the exterior but also from the interior. The latter point in Pavlov's theory has not aroused great interest, yet here lies a theoretical implication of promise even today. We shall therefore examine more closely the two latter properties of verbal stimuli which Pavlov distinguishes, viz., their substitutive function and their nature as self-initiated stimuli. The function of words as replacements of direct stimuli is an obvious fact, although not so simple as might appear from certain experiments performed by physiologists investigating the higher nervous activities. The lexicon and grammatical rules of any language—as was well known before Pavlov's time—include a stock of elements and rules for their use which permit us to express in verbal form all that surrounds us in our environment. This includes not only objects, events, their features and multifaceted interrelations, but also—as noted by the Polish psychologist Szuman (1955)— actions, processes and changes occurring in the environment. Language allows for exhaustive and dynamic verbal descriptions of situations, immediate, past and desired or expected, with reference not only to the actual situation of the human being but also to his undertakings within that situation, a fact which seems of particular importance. Language as system thus creates the possibility for real situations to be substituted by their verbal descriptions and for practical enterprises to be grasped as 1 Investigators of the second signal system have concentrated on this substitutive function of the verbal stimulus; they demonstrated, for example, that if a conditioned reflex is formed to a red light stimulus, it also appears when the subject is told or shown the words red light.

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verbal expressions of intention. As a result, the command of language enables man to "keep in touch" with currently nonexistent states of reality. He is thereby in a position to plan and undertake actions which correspond not only to directly perceived events (i.e., perceived within the first signal system, in Pavlov's terminology) but also to information about reality—not necessarily current reality—obtained from others in the form of verbal texts 2 . If the substitutive function of the verbal stimulus is understood thus, then it must be accepted that human action is regulated by signals mediated by two main channels, the nonverbal channel transmitting diverse kinds of direct information about current states of reality, and the verbal channel which transforms direct information into verbal texts in accordance with the language system. Without pursuing the question of the complex interdependencies of these two channels, we must stress one fact. Man can act planfully not only because he perceives a given state of affairs, but also because he has been told that a given state of affairs has happened or will happen. Human goal-directed activity is thus in some sense independent of momentary direct external influence. A second individual, by producing a certain text, can evoke behaviour in the hearer which will have no visible connection with the actual surrounding situation. Let us relate the above to Pavlov's second major thesis, viz., that verbal stimuli act not only in auditory and visual forms, but also as kinesthetic sensations originating in the speech organs during the act of speaking. One of the differences between verbal stimuli and those of the first signal system is that the former not only arrive from the exterior but can be produced from within. Direct signals from the external world—the optical, acoustic, chemical and mechanical stimuli emitted by objects—are on the whole irreproducible by man. The means we have to reproduce them, such as pictorial representation, gesture, pantomime, and sound imitation, are at best poor approximations; they are time-consuming and laborious, and the results they give vary greatly across individuals. To all intents and purposes, they are inefficient for transmitting information about perceived states of the world. By contrast, verbal signals can be reproduced rapidly and precisely by our articulatory apparatus. We have at our disposal an organ which serves a twofold purpose: to produce speech addressed to others, and to reproduce what others have addressed to us. Its function, as was shown in Chapter V, is to execute lengthy sequences of extremely complex and highly precise movements, requiring no great expenditure of energy. As with all other kinds of body movement, the movements of the articulators during the act of speaking produce a sensory feedback afferentation, by initiating afferent kinesthetic impulses. 2 An additional and extremely important aspect of the verbal description is that—unlike directly perceived stimuli—it invariably contains the element of generality and abstraction, due to the generalizing nature of the word components (see Chapter VII); this factor underlies the specific property of human activity which Goldstein called "categorial".

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As we speak, we produce not only acoustic stimuli (of the second signal system) received by ourselves as well as others, but also kinesthetic stimuli of the same signal system which only we, as speakers, receive. Since one of the primary functions of verbal stimuli is to replace direct external action, kinesthetic verbal stimuli—products of our own motor reactions—can also serve this function. These stimuli can therefore evoke behaviour in the individual on the same principles as can verbal stimuli produced by others. Thus, through the substitutive function of verbal stimuli, and the capacity for inner generation of such stimuli, human behaviour can to a certain degree attain an independence of immediate external stimulation (of the first signal system), and in fact from all manner of external stimuli; it can be regulated by verbal signals initiated within the speaking organism as a product of the processes involved in speech production. In other words, by learning to speak to others in order to influence their behaviour, man learns to speak to himself and thereby acquires the capacity to stimulate and regulate his own activity. Pavlov's conception of the second signal system opens a perspective towards an explanation of man's specific ability for inner planning and behavioural control on the grounds of physiological mechanisms which are at least partially known. But these are no more than prospects; many questions need a more precise treatment than Pavlov's general formulations permit. They are not however illusory hopes, as psychological research on the regulatory function of speech has demonstrated. The forerunner of such studies was Vygotsky (1956) whose ideas were first formulated as a critique of Piaget's theory of egocentric speech. Piaget (1929) was the first to note that two types of utterances are distinguishable in young children's speech. One he called socialized or communicative speech, addressed to others; these are intelligible utterances conveying perceptions, desires, and the like. The other Piaget called "egocentric" speech, when the child, apparently without desire to influence a hearer, talks to and for himself; these utterances are so constructed that others have difficulty in understanding them. According to Piaget's views at that time, the latter type of speech was a manifestation of insufficient socialization, symptomatic of the child's general egocentrism. As socialization advances, egocentric speech disappears and is replaced by communicable speech. Vygotsky conducted a series of experiments to examine the role of such "egocentric utterances" in the child's activity and concluded that they served an important function in problem-solving. In the early developmental stage, such utterances seem to be verbal trials to gain orientation in a situation; they are descriptions of the situation, aiming at verifying possible uses of objects available for mastering immediate difficulties. At a later developmental stage, egocentric speech contains exsituational elements; the child is no longer bound within the confines of the immediate situation; traces of previously verbalized experience are activated and utilized for solving the present problem. These conclusions enabled Vygotsky to formulate his theory of egocentric speech

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as a derived form of speech. Developing as an offshoot of primary communicative speech for interchange of thought with the environment, the new form of speech has the specific function to orient and plan the child's own activity. Egocentric speech is presumably an intermediary link, or sta'ge, between communicative speech and inner speech; the latter is the most elaborated form of orientational-regulatory speech, and plays an essential role in human action. The decline of egocentric speech observable in ontogenetic development is the outcome of a gradual process by which this type of self-directed utterance becomes internalized, along with a maximal reduction of the phonetic aspect and structural change—mainly intensification of predication. Vygotsky interprets the formation in ontogenesis of inner speech in terms of its orientational-regulatory function in relation to the individual's own activity3. Vygotsky's theory prompted a series of experimental studies on the formation of the regulatory (or directive) function of speech in child development, by Luria and his group (Luria, 1956, 1961; Luria and Yudovich, 1956). It was demonstrated that initially the adult's verbal instructions do not evoke an appropriate reaction in the young child. However, with age the correct response is made to the adult command, in other words, the simple impellent, or initiating, function of child-addressed speech develops. Somewhat later, the "inhibitory function" of receptive speech is shaped: the child, hearing an instruction, is able not only to switch his activity to the appropriate response but can also inhibit an action. Finally the "pre-trigger" function of speech develops. This is the regulatory function proper, or the capacity to delay execution of a verbal instruction and regulate a subsequent course of action in accordance with it (e.g., "When you see the light, squeeze the ball")4. This type of instruction evokes only a direct orienting response in children from eighteen months to two years; they look for the stimulus and also squeeze the rubber ball. By three or three-and-a-half, the immediate response is inhibited, the child retains the instruction in mind, and responds only after the announced signal has occurred. But still the child's own speech does not function as regulator, though the first signs of its development are observable. On the latter point some interesting data were obtained by Tikhomirov (1958). Children of three and three-and-a-half years were instructed as follows: "When the light comes on, squeeze twice". At this age they are still unable to cope with such a task. Even knowing the meaning of the word "twice", the children executed the 3 Similar views have been formulated by Szuman (1955) on the basis of interesting studies on children. Speech, according to this author, is utilized by man both to prepare his plan of action and to guide his activity rationally. 4 These and other experiments discussed in this chapter were conducted by a technique developed in Luria's laboratory. The subject is faced with a display panel of acoustic and optical stimuli (coloured lights and bells of different pitch and sound intensity). The subject holds a rubber bulb in his hand and squeezes it according to instruction. Data are recorded on a paper tape moving at a constant speed.

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task only on the first or perhaps second trial; later, they squeezed the bulb at least 3 to 4 times each time. The instruction was then modified: the children were told to press twice when the light came on, at the same time saying aloud: "One—two". Now they were able to produce the double pressures. But when told to discontinue the "self-instructing", the children's motor reactions once again took on a diffuse character. Why should motor reactions be improved by self-instruction ? Two possible answers, were considered: self-instruction either acts through its semantic or through its structural properties. The form of the instruction (one—two) could be responsible for initiating kinesthetic impulses during articulation of the words; these would act as supplementary afferentation for movements primarily evoked by the visual stimulus. To verify which hypothesis was correct, two different instructions were tried. In one variant, the children were instructed to squeeze the ball twice when the light appeared, saying at the same time: "Squeeze the ball twice". In the other variant, the children were told to make two presses and while so doing to repeat twice a Russian nonsense syllable (tu—tu). The difference in the two variants of the self-instruction is this: In the first, the child's utterance was, semantically, a repetition of the examiner's instruction but in its motor aspect was comprised of an unbroken sequence of movements with temporal properties; in the second, the child's utterance lacked semantic content but its temporal structure corresponded to the action being performed simultaneously. It turned out that the first variant did not improve the child's performance but affected it so that, instead of squeezing several times, he made one prolonged squeeze of the same duration as the utterance itself. In the second variant the double repetition of the syllable "tu" had the same effect as the self-instruction "one—two". At this age, therefore, the semantic aspect of the self-instruction does not yet exert any influence; in Pavlov's terminology, the word does not yet exercise its substitutive function. A turning-point is reached only between the ages of four-and-a-half and five-and-a-half, when the child begins to manifest the ability to absorb a complex verbal instruction, retain it and regulate his course of action in accordance with it. These are only some of the many experimental findings which led Luria to advance the hypothesis that early ontogenetic development of the regulatory function of speech goes through several stages. On the one hand, the directive effect of adult speech addressed to the child develops first as immediately impellent and initiating, later as inhibitory, and finally as a synthesis of pre-impellent and pre-inhibitory effects. On the other hand, the regulatory function of the child's own speech in relation to his behaviour also begins to develop. At first speech supplies merely an additional afferentation by which motor responses are ordered, but gradually the semantic component of the self-instruction comes to the fore along with the development of its role in receiving and executing verbal instructions from the exterior. In this way words begin to "mediate" the child's conduct (Vygotsky, 1956) and become an evocative factor operating from the interior in respect to behaviour.

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The regulatory function of speech must therefore be seen as one of the basic psychological mechanisms by which human activity acquires its planful nature, and is subordinated to an inner design, liberated largely from external influences. There can be no doubt that a significant role in developing this function is served by the efferent kinesthetic impulses originating in the articulators during the act of speaking (and also during "inner" speech), in other words, by the sensory feedback from the speaking apparatus. It is in the light of this statement that particular significance must be ascribed to the observation and empiric study of behavioural disorders, especially disorders affecting the regulatory function of speech in patients with damaged frontal lobes.

2. BEHAVIOURAL DISORDERS AND DISTURBANCES OF THE REGULATORY FUNCTION OF SPEECH ACCOMPANYING FRONTAL LOBE DAMAGE

The specific character of disturbances of voluntary behaviour in a person afflicted with frontal lobe damage—more exactly, the anterior portion called the pre-frontal region—has long aroused the interest of researchers, as an abundant literature testifies (cf. Maruszewski, 1962; Maksymczuk, 1967). These regions are more developed in the human than in the animal brain. Bucy (1935) reported that the prefrontal region constitutes 3.4% in the cat, 6.9% in the dog, 11.3% in the gibbon, 16.9% in the chimpanzee, and 29% in man, in respect to total cortical surface. Along with growth of size, there is also a remarkable development in the complexity of cytoarchitectonic structure and neural pathways leading to other cerebral structures (Polyakov, 1966). These structures presumably play some special role in the regulation of human behaviour. Prefrontal damage leads to two basic kinds of disorder. One involves the cognitive processes and conscious purposive action, the other involves the emotions and the personality structure. But this locus of lesion does not lead to speech disorders nor to disturbances of the elementary sensorimotor functions. One of the most common symptoms of a lesion of the prefrontal region is disturbed voluntary behaviour, or goal-directed activity. The patient's behaviour ceases to bear the imprint of an inwardly formulated plan of action and assumes features of coercive influence of accidental external stimuli. The patient loses the ability to carry through a sequence of logically connected actions leading to a prefixed goal. His behaviour becomes impulsive and constrained by accidental associations evoked by the concrete aspects of the immediate situation. For instance, at the sight of a bell-button the patient will press it, but when the nurse comes to answer the call he cannot tell her why he called her. Luria writes of a patient who went to the railway station and boarded a train headed in the wrong direction. The earlier arrival of this train constituted a concrete situational stimulus to which the patient's action was subordinated (Luria 1962, 1967). Rozinsky (1948) describes the behaviour of a patient on his way to the

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doctor's office, who sat down on every chair along his route and on passing an open cupboard door, walked inside. The interpretation of such behavioural disorders is not as yet fully clear. According to Malmo (1948) two basic explanations of the underlying mechanism can be distinguished. The first ascribes the cause of disorganized purposive behaviour in cases of prefrontal damage to disorders of the planning processes, or the processes of formulating and retaining in mind a plan of action together with the goal set; these are disorders of conscious behavioural control. The patient's behaviour begins to be governed by external stimuli because his internal intellectual control mechanism is deranged. But there is another possible explanation. To pursue an action according to plan, it does not suffice to set the goal and formulate a plan of action; it is also necessary to be capable of carrying through that plan despite all sundry external factors that may arise to hinder its implementation. In other words, a necessary condition for goal-directed activity is the ability to overcome the action of accidental factors which prompt behaviour extraneous or contrary to that required by the plan. Viewed from this angle we can interpret the behaviour of patients with prefrontal damage as manifesting a disorder in this domain. The patient may fully know what he is to do, or what goal he means to attain, but he is totally unable to inhibit actions forced upon him by accidental situational elements. At the present moment we have no conclusive evidence in favour of one or the other interpretation. The majority of data seems to uphold the latter, but other facts speak for the former (Szostek, 1970). Leaving this question open, the fact remains that what is chiefly affected in many patients with prefrontal damage is the directionality of activity and its dependency upon internal mental conditions. This is brought out most clearly in studies of disorders of the regulatory function of speech in such patients. A series of experimental investigations on this problem was conducted in Luria's laboratory (Luria and Homskaya, 1966)5. Meshcheryakov (1966) investigated the execution of simple verbal commands in patients with extensive prefrontal damage. In the first experiment, the patient was requested as follows: "Please raise your arm" or "Please squeeze the rubber ball". In the second, a simple motor conditioned and differential reflex was formed with verbal reinforcement. For example, when a red light was flashed on, the patient was asked to press the ball, but when a green light appeared he was told: "Now don't press it". In the final series, simple verbal instructions preliminary to an action were 5 These studies refer to a specific group of patients undergoing neurosurgery for cerebral tumours. They were studied pre-operatively and again in the early post-operative period, which explains the particularly acute form of the disturbances displayed. In later post-operative stages, once reversible changes had cleared, the same patients would probably have displayed milder disturbances. However, it is unlikely that the basic characteristics gf these disorders would have been altered.

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used, e.g., "When the red light appears, please press the rubber ball but when the blue light comes on, don't press it". In these experiments patients with frontal lobe damage were compared with a group of patients with equally extensive damage elsewhere in the brain. These experiments showed that patients with most acute symptoms of frontal lobe damage failed even to carry out the first series of instructions, although the patients frequently repeated the command verbatim (the patient would echo "Please lift your arm" without executing the movement). At times he did as instructed, but after a few repetitions of the instruction he ceased to react. Thus extensive frontal lobe damage destroys the ability to perform in response to even the simplest muchpractised verbal instruction, though aphasia is not involved and motor proficiency is fully retained. Needless to say, the execution of the more complex instructions was beyond the possibilities of this group. In cases of less extensive damage, the patients responded on the whole correctly to the direct verbal command, but failed to master the preliminary verbal instruction. Characteristic of this group was the ease with which they retained the instruction and correctness of repetition, but when the announced signal appeared, the response was lacking. When verbal reinforcement was applied, there was an occasional correct reaction to the signal, but the patient could not tell, when asked, what he had done when the light came on. Only patients with relatively mild damage could perform correctly to all three types of verbal instruction, and even these followed preliminary instructions with vacillation and uncertainty. In contrast, the control group of patients with equally extensive damage outside the frontal regions had no difficulty in carrying out the verbal instructions in the three experimental series. The conclusion was therefore drawn that severe disorders of performance in response to simple verbal instruction, without possible causal factors in speech or motor disturbances, are associated with this type of extensive frontal damage. In another investigation, Ivanova (1966) studied patients with extensive frontal lobe damage from the aspect of choice reaction formation. The patient was instructed: "When the red light comes on, please press the ball with your right hand; ¡when the green light comes on, press it with your left hand." In another experimental variant, verbal reinforcement was applied in forming the same reactions. The red light was flashed on and the patient was told: "Press with your right hand", or the green light appeared and he was told: "Press with your left hand". The majority of patients with damaged frontal regions were unable to perform the choice reaction according to a preliminary verbal instruction. They could remember the instruction and repeat it when called on to do so, but reacted without regard for its content, often pressing the ball between signals, or automatically pressing with either right or left hand in disregard of the colour of signal. Even in the event that the patient responded correctly after several attempts, his reaction soon became erratic again. However, when direct verbal reinforcement was used consistently, choice reactions could be formed in these patients. But, in contradistinction to normal persons, the

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process of formation was extremely slow and unstable, nor could the patients state the principle by which they reacted to the signals. Such disorders were not found in patients with locus of damage exterior to the frontal lobes. In a further investigation by Homskaya (1966), performances on two different verbal instructions were compared in patients differing in degree of severity of frontal lobe damage. One instruction was similar to that used by Meshcheryakov: the patient was requested to press the ball when the red light appeared and to refrain at the sight of the blue light. The other instruction tasked the patient with regulation of reaction strength according to type of stimulus: to press hard at the sight of the red light and to press gently at the blue light. In respect to the first instruction, performances were similar to those found in Meshcheryakov's experiment with patients having extensive frontal damage. Despite retention of the instruction, the performance was far from correct. On occasion, a correct response occurred after many repetitions of the instruction by the examiner and the patient together. As to the patient group with milder symptoms, performance deviated only slightly from the normal. This divergency in results between the two groups of patients practically disappeared in performance in response to the second instruction, i.e., when the patient had to discriminate between a stronger or weaker reaction in respect to signal quality. Both groups could repeat the instruction correctly but neither could differentiate intensity of pressure. They both reacted to all signals with the same intensity; only occasionally and fleetingly did the second patient group differentiate their reactions. Homskaya also used the method of self-instruction applied by Tikhomirov (see § 1). She instructed the patients to say "Hard" when the red light appeared, and to press hard, and to say "Soft" when the blue light came on, and to press gently. It is remarkable that both groups of patients could perform verbally to this instruction; they uttered correctly "Hard" or "Soft" when the respective lights came on. But their motor reactions remained undifferentiated in intensity (Fig. 27a). In other words, self-instruction exerted no influence upon the motor reaction. Herein lies the fundamental difference between frontal damaged patients and the control group with posterior damage. Many of the latter could perform the task normally; in some cases difficulties occurred in differentiating reaction intensity, conceivably due to somesthetic disturbances. When self-instruction was introduced in these cases, there was a clear compensatory effect: by instructing himself the patient could react correctly to the signals (Fig. 27b). Maruszewski (1963) investigated a group of patients with relatively restricted frontal damage whose performance on most of the tasks reported above deviated minimally from the norm. He applied the "conflict" method, by which the verbal instruction called for a response opposite to that evoked by the signal. For example, the patient was instructed to react to signals of the same colour with varying durations of pressure: to a shorter signal with a longer pressure, to a longer signal with a shorter pressure. Not only did patients with frontal damage have trouble in carry-

2. DISTURBANCES OF THE REGULATORY FUNCTION OF SPEECH

a)

187

without self-instruction

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Fig. 27. Experiment conducted by Homskaya (1966a) (See page 186). a—a patient with severe disturbances caused by frontal lobe damage reacts to the instruction to press with varying strength according to colour of light signals. The upper diagram shows performance without self-instruction, and the lower with self-instruction, b—a patient with extensively infiltrating tumour in the right parieto-temporal region performs the same task. Arrows indicate the incorrect reactions.

ing out this type of verbal instruction but so did patients with other loci of lesion. But a comparison of the two groups for types of erroneous reactions revealed significant differences. Whereas the non-frontal group often displayed difficulties arising from failure to grasp the instruction or from perseveration (Fig. 28a), the frontal group correctly understood the instruction but tended to liken the reaction to the signal (Fig. 28c): disregarding the instruction, the patient would react with longer pressures to longer signals, and shorter pressures to shorter ones. Furthermore, not only did the patients repeat the verbal instruction correctly but also would themselves comment on the inconsistency between their reaction and the instruction. Approximation of reaction length to signal length was most apparent when a signal of the

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2.93

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same duration was repeated several times (Fig. 28b). The patient seemed to gradually submit to the influence of the external stimulus, even though initially he had reacted in accordance to the instruction. This type of error did not occur in non-frontal patients and can be regarded as associated exclusively with frontal damage. The experimental findings we have reported demonstrate that frontal lobe damage in the human being is the source of disturbances in the regulatory function of speech,

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though the intensity of the disorder varies with extent of damage and probably with other factors as well. With intact comprehension and retention of a verbal instruction, and preservation of ability to execute the motor reaction involved, the nonaphasic patient with frontal damage is unable to subordinate even the most elementary motor reaction to the instruction; he is unable to control his movements to accord with simple principles conveyed to him verbally. On the basis of this finding it is tempting to look in this direction for an explanation of disturbances of more complex voluntary actions, referred to earlier, in frontal lobe damage. Such disturbances may possibly be interpreted as manifestations of disorders of the regulatory function of speech, and as the outcome of an impairment of the orienting-directive function of inner speech. There remains the problem to what extent such disturbances as we have been discussing are associated with disruption of the regulatory function itself, and to what extent they are associated with disruption of processes forming internal descriptions of situations and plans of action whose role in guiding more complicated behaviour is incomparably greater. Data presented in, Chapter V (§ 4E) pertaining to inner speech disorders in "dynamic aphasia" (which is associated with lesions lying anteriorly to Broca's area in the left frontal lobe), seem to indicate that, at least in some cases, frontal lobe lesions can also lead to disturbances of the inner speech function of orienting and planning, with ensuing effects upon behaviour. In view of the relative infrequency with which lesions occur with sufficient selectivity in different frontal regions, data at hand are too meagre for a resolution of this question at the present moment. Nevertheless, it seems highly probable that future research will render possible a distinction between two conditions of disordered goal-directed behaviour in frontal damage patients: one condition in which there is derangement of the ability to formulate internally action plans, the other in which correctly formulated plans cannot be implemented through activity. Disturbances of the speech regulatory function have been ascertained in frontal damage patients in respect to other kinds of reactions as well, viz., involuntary reactions accompanying perception of meaningful signals. This research stemmed from experiments on the orienting reflex conducted by Sokolov's group (Sokolov, 1958). It was found that the orienting reflex, appearing when the organism is exposed to new stimuli, embraces several different reactions including vegetative (vascular-motor or galvanic skin reactions) and electric (action potential changes in the brain measured by EEG). With repetition of the stimulus, provided no meaning is conveyed to the subject (it is not a signal to perform an action), these components of the orienting reflex are gradually extinguished, and habituation ensues. But once the stimulus becomes a signal to react voluntarily (for example, by verbal instruction), all components of the orienting reflex are disinhibited. This is exemplified in the following experiment: the subject is situated in a soundproof cabin where vascular reactions are registered by an apparatus attached to the

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arm (the plethysmography Suddenly a loudspeaker in the cabin emits a sound of given pitch and duration. The plethysmograph registers a contraction of the blood vessels lasting several seconds. After an interval the sound is repeated, leading to the same reaction but shorter and less intense. After several repetitions the reaction disappears. At this point the subject is instructed to count the number of sounds, or to press a button each time the sound is heard, or some such order. Once the subject begins to carry out the instruction, the vascular reaction reappears with renewed strength and persists despite repetitions of the stimulus. Sokolov explains this change in the following way: The stimulus has now acquired meaning for the subject, and as such it is a signal which not only evokes a given behaviour but also intensifies the subject's general state of activity, as manifested in the intensification of the orienting reflex with all its components 6 . Thus Sokolov's research pointed up one more aspect of the regulatory function of speech. The verbal instruction affects even the individual's activation. This realization led to the question whether frontal lobe damage causes disturbances of this function as well. Homskaya and her collaborators undertook to study this question (Homskaya, 1966b, 1968; Artemeva and Homskaya, 1966; Baranovskaya and Homskaya, 1966; Simernitskaya and Homskaya, 1966). Studying various aspects of the orienting reflex, these investigators found that patients with frontal lesions differed fundamentally not only from normal persons but also from patients with other loci of brain damage. They demonstrated that, while frontal lobe damage did not on the whole destroy manifestations of the orienting reflex in the case of neutral stimuli (nonsignals) and occasionally even pathologically intensified the reflex, it profoundly disturbed the regulatory effect of verbal instruction on the orienting reflex by altering the properties of this reflex typical of reception of meaningful stimuli (signals). When a verbal instruction is issued to the patient by which the neutral stimulus is transformed into a signal for an action, disinhibition of the vegetative and electrophysiological components of the orienting reflex does not ensue, or else appears in much less persistent form than in normal persons or patients with nonfrontal damage. Thus frontal lobe damage leads to distinct pathological changes in the verbal regulation of activation. In this context it is of interest to note findings reported by Walter (1963, 1966) on investigations of the action potential in the frontal lobes of persons without organic brain damage. The basic experimental procedure was as follows: the subject was shown two successive stimuli, such as a sound and a flash of light, separated by a certain time interval. Simultaneously the subject was instructed to perform a simple act when the second stimulus appeared (light flash), such as to press a button or utter a word. The first stimulus (the sound) was thus a warning 6

Sokolov and his associates have discovered numerous extremely important properties of the orienting reflex, shedding new light on the mechanisms of reception of external stimuli. Their studies, however, fall outside the bounds of this book.

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signal that announced the second at which the reaction was to be made. Its meaning was: "In a moment there will be the sound—then I must press the button." By registering the action potential, it was demonstrated that in this situation an electrical event occurs in the frontal lobes: a specific negative alteration of potential takes place lasting from the moment the first signal is given to the onset of the reaction. These changes occur only when there is a meaningful connection between the two signals, and no changes of the sort can be observed in its absence. Walter concluded that negative potential changes are connected with a specific anticipatory state evoked by the warning signal, which he called the expectancy wave (E wave). Further investigations have applied newer technical apparatus (radiotelemetrics) which register cerebral action potentials at distance while the subject performs quite complex actions. The E wave was found to appear invariably when the subject made a conscious deliberate decision or undertook some action, such as deciding to take a walk, initiate a conversation, throw or catch a ball, start a car or stop it. Furthermore, the E wave was not extinguished as long as the subject displayed interest and intent to perform a given task. In some subjects, the E wave may be registered during months when the same actions are performed. We shall not attempt to enter into the ramifications of these matters, such as the properties of the expectancy wave, or its neurophysiological mechanisms. But it is worth noting Walter's view that the E wave has particular associations with social influences, mainly with those acting through the second signal system. It is the specific reaction of the frontal lobes to semantic signals, signals that convey meaning or information important to the individual. Since this reaction precedes decision-making and initiation of goal-directed action, it may perhaps constitute the electrophysiological index of those processes by which the orienting-regulatory function of speech is realized. *

*

*

The research findings we have surveyed above brought Luria (1966b) to the view that the frontal lobes serve a specific and significant role in regulating goal-directed activity, particularly in ensuring those peculiarly human forms of sensory-motorverbal coordination required for its normal flow. Speech allows for abstraction and generalization of influences received directly from the exterior; it also permits the formulation of designs and the anticipation of future events. At the same time speech secures the drafting of programmes of goal-oriented actions, the matching of what has been achieved against what had been intended and the provision of suitable corrections. This sensory-motor-verbal coordination is disturbed in the event of frontal lobe damage, which is the reason for the behavioural changes displayed by patients with this locus of lesion. Much remains to be clarified in respect to the neurophysiological mechanisms of what is here termed the regulatory function of speech, or the influence exerted by

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speech upon the course of human activity. But the facts adduced allow for certain incontrovertible statements. Firstly, the specifically human properties of behaviour such as man's capacity for planful and goal-directed activity, subject to internal correction, is strictly related to the fact that man is a speaking being, addressing speech not only to others but to himself as well. The second assertion is that the cerebral mechanisms underlying the regulatory effect of man's own speech upon his behaviour are closely associated with the frontal lobes of the brain.

FINAL CONCLUSIONS

Our discussion of the disorders of the regulatory speech function following frontal lobe damage terminates this report of the major findings of neuropsychological research pertaining to the cerebral conditionment of the human ability to communicate through language. In the course of this survey we have more than once been confronted with the complex nature of the problem, the obstacles impeding its study, and the divergent interpretations of empiric findings unavoidable under such conditions. In a sense, this problem remains unresolved, since numerous questions still lack adequate and exhaustive answers. Nonetheless the knowledge available today is sufficient to sketch at least in outline the answer as to the human cerebral properties which account for the unique capacity of man to communicate by language. This answer can be formulated in several more particular statements: 1. Language communication, realized in the form of speech activities, reaches fruition by the interaction of a large number of different neural structures making up the cerebral functional system of speech. Neither the theory of isolated "speech centres" nor the antilocalization conception that associates speech with undifferentiated brain function, find support in neuropsychological research. The fullest and most adequate interpretation of the findings of this research domain lies in the theory of dynamic localization of function, or the model of a functional system as the "cerebral organ" of speech. This theory negates the existence of narrow localizations and correlations between given speech processes and strictly defined cerebral loci. It equally rejects the thesis negating the functional differentiation of cerebral structures. According to this theory, speech is a function of numerous parts of the brain, each responsible for speech in some specific aspect and playing its own part in ensuring the normal control of these processes. 2. The brain possesses a functional asymmetry in respect to regulation of speech processes. The two cerebral hemispheres have an unequal share in speech regulation. One hemisphere, usually the left, is dominant for speech, the other subordinate in this respect, having little or no part in the realization of speech. This asymmetry takes shape during ontogenesis; in the initial period of development it has not been found to exist. 3. Not all neural structures within the dominant hemisphere participate in the regulation of speech processes. This role is assumed by the "speech area", lying more or less in the middle portion of the hemisphere and embracing certain divisions of

194

FINAL CONCLUSIONS

the frontal, parietal and temporal lobes. The speech area may well embrace not only the cortical regions mentioned but also the white matter lying directly beneath them, or equally deeply located cerebral structures. This question remains open for further study. 4. The speech area is functionally differentiated, its component structures having distinct and specific functions in speech regulation. With some oversimplification, it may be stated that the anterior division of this area is of particular importance in regulating the processes involved in speech production, while the posterior divisions have this role in respect to speech reception. Supporting evidence lies in the fact that an anteriorly located lesion in the speech area strikes, in the first place, speech production, while posteriorly located damage affects primarily speech reception. However, this does not imply that the posterior divisions of the speech area have no share in controlling speech production or that the anterior divisions have nothing to do with speech reception. As unequivocally demonstrated by findings reported here on the effects of diverse loci of lesions in the speech area, both production and reception of speech depend upon a normal functioning speech area, that is, all or nearly all of its divisions. 5. From an analysis of the symptoms produced by lesions in the component structures of the speech area, the following demarcations can be made between structures which appear to subserve specific functions in the overall regulation of speech. (a) The inferior division of the postcentral region (the parietal lid) which plays an essential role in constructing the most elementary units of text (speech sounds); in all likelihood it participates as well to some degree in their identification during speech reception. (b) The inferior division of the premotor region (Broca's area) with a particular role in the process of combining simple linguistic units into more complex units, and in ensuring the sequential flow of this process. (c) Frontal lobe structures lying anteriorly to Broca's area, whose role appears to be related to the substantive aspect of utterance formation, and to inner speech. Probably this region, like Broca's area, participates as well in the regulation of speech reception, since the latter process undergoes specific disturbances when these structures are damaged. We are lacking the evidence needed to define their role in speech reception with more precision. (d) The supplementary speech motor area, which has a particularly important role in ensuring the dynamic organization of speech production. (e) The posterior division of the superior temporal convolution (Wernicke's area), essential for auditory recognition of the elementary units of text (speech sounds), i.e. for phonemic hearing which determines normalcy of both speech reception and production. (f) Other temporal lobe structures adjacent to Wernicke's area whose role in speech control is unquestionable but cannot yet be described more precisely. The most

FINAL CONCLUSIONS

195

likely hypothesis is that these regions have some special role in processes of retaining and retrieving auditory memory traces essential for speech reception and production. (g) The parieto-temporo-occipital junction, whose role is highly complex and still poorly understood. Most probably it has connections with many aspects of speech activity but appears primarily to be associated with word selection (names, in particular) in their semantic aspect, and with the encoding and decoding of complex logico-grammatical constructions. 6. In addition to the above structures comprising the speech area in the strict sense, the prefrontal lobe regions have an evident relation with the speech processes. Their role is particularly marked in reference to the ability for rapid switching of semantic content, both in reception and production, the ability to detach from surface structure effect in speech reception, and the ability to regulate activity according to own speech. 7. The final two regions mentioned, i.e., the parieto-temporo-occipital junction and the prefrontal areas, apparently play an essential role in ensuring the interaction of the speech area structures with other cerebral regions, particularly those connected with regulation of cognitive processes and goal-directed activity. 8. The above listed cerebral structures, whose role in the regulation of speech processes is established beyond doubt, must maintain a constant interaction during speech activity. Unfortunately there is insufficient data accessible at this time to establish the anatomical bases which make this collaboration possible and to determine the regularities. Therefore, although we have a fairly accurate knowledge of the particular regions making up the cerebral functional system of speech and their several roles, we are missing a fuller orientation as to the regularities in the functioning of this whole system. This constitutes one of the greatest lacunae in our knowledge about the cerebral mechanisms of speech, one which is urgently in need of empirical research.

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REFERENCES

Walsh E. G. Physiology of the nervous system. 2nd edit. Longmans, Green, London 1964. Walter W. G. The living brain. Norton, New York 1953. Walter W. G. Role of the human frontal lobes in the regulation of activity. In: A. R. Luria and E. D. Homskaya (eds.) Frontal lobes and the regulation of psychologicalprocesses. Moscow University Press, Moscow 1966. (Russian). Weinstein E. A. and Keller N. J. A. Linguistic patterns of misnaming in brain injury. Neuropsychologia, 1963, 1. Weinstein E. A. Affections of speech with lesions of the non-dominant hemisphere. Disorders of Communication, 1964, 42. Weisenburg T. H. and McBride K. E. Aphasia: a clinical and psychological study. New York, Commonwealth Fund. Hildred and Co., Brattleboro 1935. Wepman J. M. Recovery from aphasia. The Ronald Press, New York 1951. Wepman J. M., Bock R. D., Jones L. V. and Van Pelt D. Psycholinguistic study of aphasia, a revision of the concept of anomia. J. Speech and Hearing Disorders, 1956, 21, 4. Wepman J. M. and Jones L. V. Five aphasias: a commentary on aphasia as a regressive linguistic phenomenon. Disorders of Communication, 1964, 42. Wepman J. M., Jones L. V., Bock R. D. and Van Pelt D. Studies in aphasia: background and theoretical formulation. J. Speech and Hearing Disorders, 1960, 25, 41. Zangwill O. L. Cerebral dominance and its relations of psychological function. Oliver and Boyd, Edinburgh 1960. Zangwill O. L. Language and right hemisphere. Paper delivered at the meeting of the Commission on Speech Disturbances, Polish Academy of Sciences, Warsaw 1968. 2arski S. Analiza zaburzen nazywania wystgpujqcych w ogniskowych uszkodzeniach dominujqcej pdlkuli mozgu (Analysis of naming disturbances in cases of focal damage to the dominant hemisphere). Unpublished doctoral dissertation. Institute of Neurosurgery, Polish Acad. Sc., Warsaw 1964.

AUTHOR INDEX

Abov'yan, V. A., 119, 196 Achenbach, K., 204 Ag'ejeva, A. N., 116, 205 Ajuriaguerra, J. de, 51 Akert, K-, 203 Alajouanine, T., 74, 119, 196 Anokhin, P. K., 43, 196 Archibald, Y. M., 80, 175, 176, 196 Arieti, S., 198 Artemeva, E. Yu., 190, 196 Auburtin, 21 Auderska, H., 204

Baranovskaya, O. P., 190, 196 Barton, M., 78, 198 Basser, L. S., 74, 75, 196 Bastian, H. C., 22, 23 Baueretz, A., 200 Bay, E., 36, 196 Beach, F. A., 200 Bein, E. S., 109, 196 Benson, D. F., 196 Benton, A. L., 19, 20, 21, 70, 89, 196, 199 Berko, F. G., 202 Berko, J., 109, 198 Berko, M. J., 202 Bisiach, E., 165, 196 Blinkov, S. M., 119, 196 Bock, R. D.., 206 Bogen, J. E., 198 Boller, F., 80, 147, 196 Bouillard, 20, 21 Brain, R„ 14, 21, 22, 24, 69, 74, 99, 100, 116, 135, 147, 155, 196, 197, 207 Branch, C., 76, 77, 197, 203 Bricker, A. L., 89, 90, 197 Broca, P., 21, 22, 27, 30 Brody, B. A., 170, 197 Brown, J., 37, 38, 197, 207 Bucy, P. G , 183, 197 Butters, N., 170, 171, 197

Carey, P., 199 Carroll, J. B., 204 Charlton, M. H., 60, 197 Chase, R. A., 117, 197 Chomsky, N., 39, 40, 132, 133, 197 Chusid, J. G., 116, 197 Clask, W. E. Le G., 59 Cobb, S., 59, 68, 197 Coderre, L., 165, 197, 208 Cole, M., 27, 197 Cooper, F. S., 128, 197, 207 Critchley, M., 7, 21, 80, 197 Cross, D. V., 130, 197 Curry, F. K. W., 78, 197 Cushing, H., 63, 64

Darley, F. L., 197, 198, 199, 203, 204 Dax, G., 21 Dax, M., 21, 68 de Fouchy, J. P. G., 20 Dejerine, J., 22, 32, 61 de Gutierrer-Mahoney, C. G., 197 De Renzi, E., 166, 167, 208 De Reuck, A. V. S., 199, 203 Diamond, A. S., 14 Doehring, D. G., 165, 197, 208 Doroszewski, W., 8, 197 Dowzenko, A., 101, 197 Dudley, J. G., 165, 166, 197, 208

Efron, R., 131, 197 Eisenson, J., 80, 198 Engels, F., 14, 202 Espire, M. L. F., 71, 204 Ettlinger, G., 168, 169, 198 Exner, S., 22

Fedio, P., 203 Fenuell, E., 204

208

AUTHOR INDEX

Filimonov, I. N., 204 Finkelnburg, L., 27 Freud, S., 22, 31, 198, 207 Frings, H., 2, 198 Frings, M., 2, 198 Fritsch, G., 22, 63 Fusillo, M. G., 32, 198

Galanter, E., 203 Gall, F. J„ 20, 48, 49 Gamska, Z., 57, 89, 90, 198, 207 Gazzaniga, M. S., 80, 82, 198, 204, 207 Gelb, A., 28, 29 Geschwind, N., 22, 28, 29, 32, 33, 61, 65, 78, 79, 85, 86, 87, 132, 135, 139, 140, 154, 158, 168, 169, 170, 198, 199, 207 Gesner, J. A. P., 20 Giannitrapani, D., 78, 198 Goldstein, K., 26, 28, 29, 32, 35, 108, 135,140, 154, 158, 159, 160, 161, 167, 173, 179, 198 Goodgla c s, H., 78, 108, 109, 120, 162, 163, 198, 199 Grubb, P. M., 128, 197, 207 Guiot, G., 88, 199 Halle, M„ 124, 199 Harris, K. S., 128, 197, 207 Head, H., 21, 22, 26, 28, 29, 30, 145, 199 Hebb, D. O., 200 Hecaen, H., 51 Hemphill, R. E., 135 Hertzog, E., 199 Hines, D., 78, 199 Hippocrates, 19 Hirsh, I. J„ 127, 130, 199 Hitzig, E., 22, 63 Hockett, C. F., 2, 3, 94, 199 Homskaya, E. D., 184, 186, 187, 190, 196, 199, 201, 203, 204, 206, 208 Howes, D., 87, 90, 199 Humphrey, G., 98, 199 Ivanova, M. P., 185, 199

Jackson, J. H., 27, 28, 29, 30, 31, 58, 80, 199 Jakimowicz, W., 101, 197 Jakobson, R., 39, 94, 124, 161, 199, 207

Jenkins, J. J., 35, 36, 92, 197, 204 Johnson, S., 20 Jones, K., 199 Jones, L. V., 35, 196, 199, 206 Joynt, R. J„ 19, 20, 21, 196,199

Kabelyanskaya, L. G., 137, 199 Kaidanova, S. I., 138, 200,205 Kaplan, E„ 32, 162, 163, 198, 199 Karesseva, T. A., 201 Keller, N. J. A., 206 Kimura, D., 78, 142, 143, 200, 203 King, R. A., 203 Kinsbourne, M., 119, 200 Klein, B., 199 Kleist, K., 32, 135, 136, 200 Klimkovsky, M., 141, 200, 201 Kogan, W. M., 36, 111, 135, 160, 161, 162, 174, 175, 200, 207 Kok, E. P„ 163, 164, 165, 200 Konorski, J„ 33, 34, 35, 103, 106, 116, 139, 200 Kukuev, L. A., 204 Kussmaul, A., 27, 155, 200 Lane, H., 129, 130, 197, 200 Lansdell, H., 90, 200 Lashley, K. S., 98, 99, 172, 200 Laskowski, E. J., 200 tempicka, Z., 204 Lenneberg, E. H., 8, 9, 10,11, 33, 38,40, 41, 42, 51, 64, 68, 75, 76, 88, 90, 96, 97, 98, 99, 107, 117, 130, 168, 197, 200 Leont'ev, A. N., 5,125,157, 200, 201 Lewicki, A., 157, 201, 202 Lewin, M. G., 59, 67, 68, 86, 204 Levitsky, W., 78, 79, 198, 207 Lhermitte, F., 74, 196 Liberman, A. M., 128, 130, 197, 201, 207 Lichtheim, L., 23, 25, 26, 135, 139 Liepmann, H., 32 Lopatkiewicz, J., 154, 201 Lorge, I., 89, 205 Lucki, W., 113, 201 Luria, A. R., 8, 28, 39, 42, 43, 44, 45, 58, 70, 71, 72, 85, 102, 103, 105, 106, 108, 110, 111, 112, 115, 118, 125, 136, 137, 139, 140, 141, 145, 146, 147, 148, 157, 158, 163, 171, 172, 173. 181, 182, 183, 184, 191, 196, 199, 201, 203, 204, 205, 206, 207, 208

AUTHOR INDEX

Maksymczyk, A., 144, 183, 201, 202 Malmo, R. D., 184, 202 Marie, P., 26, 27, 29, 30, 36, 106 Margules-Lavergne, M. P., 197 Markova, E. D., 155, 160, 202 Maruszewski, M., 17, 18, 28, 35, 42, 47, 54, 56, 100, 102, 104, 105, 125, 126, 145, 147, 148, 152, 154, 158, 160, 174, 175, 183, 186, 188, 202, 208 Marx, K., 14, 177, 202 McBride, K. E., 140, 147, 206 McCleary R. A., 33, 202 McKinney, I. P., 78, 202 Mecham, M. J., 74, 202 Meierson, J. A., 138, 200 Meshcheryakov, A. I., 184, 186, 203 Meyers, R., 196 Mierzejewska, H., 104, 202 Miller, G. A., 93, 96, 100, 203 Milner, B., 76, 77, 114, 142, 143, 144, 197, 203, 208 Miron, M. S., 92, 155, 203 Mitrynowicz-Modrzejewska, A., 10, 12, 95, 96, 97, 128, 203, 207 Molina, P., 199 Money, J., 198 Monrad-Krohn, 111 Moore, R. Y„ 33, 202 Morgan, C. T., 200, 203 Mountcastle, V. B., 197, 203 Myers, R. E., 33, 203

Nielsen, J. M., 32, 203 Nissen, H. W., 200 Nowakowska, M., 118, 125, 126, 202 Nowiñski, C., 202 O'Connor, M., 199, 203 Ojemann, G. A., 88, 203 Orbach, J., 78, 203 Osgood, C. E., 92, 155, 203 Patten, D. H., 196 Pavlov, I. P„ 42, 43, 89, 158, 177, 178, 179, 203 Penfield, W., 22, 33, 34, 64, 70, 84, 87, 88, 107, 116, 203, 207 Piaget, J., 180, 204 Pick, A., 108

209

Pliny, 19 Polder, G. F., 196 Polyakov, G. I., 183, 204 Preobrazhenskaya, N. S., 59, 60, 204, 207 Pribram, K. H., 203 Purnell, J. K., 200

Quadfasel, F. A., 108, 198, 199, 207

Rapoport, M. Yu., 140, 201 Rasmussen, T., 197, 203 Reykowski, J., 202 Reynolds, G. L., 176, 205 Riese, W., 30, 204 Roberts, L., 22, 33, 34, 64, 70, 71, 72, 84, 87, 88, 107, 116, 203, 204, 207 Roginsky, J. J., 59, 67, 68, 86, 204 Rommel, P., 20 Rondot, P., 199 Rosadini, G., 77, 204 Rossi, G. F., 77, 204 Rozinsky, J. B., 183, 204 Rubinshtein, S. L., 125, 204 Ruda, G. B., 110 Russel, R. W„ 71, 204 Russo, M., 164, 204 Rutherford, D. R., 78, 197

Sarkisov, S. A., 204 Saltz, P., 70,199, 204 Scheerer, M., 28, 158, 198 Schell, B., 199 /Sfchmidlin, S., 199 Schmidt, J., 20 Schuell, H., 35, 36, 92, 197, 204 Sechenev, I. M., 172 Segarra, J. M., 198, 207 Sextus Empiricus, 19 Sheppard, W. C., 130,197 Shmidt, E. V., 202, 205 Shugar, G. W., 132, 133, 204 Siegel, G. M., 90, 204 Sierpiñski, S., 143, 205 Simernitskaya, E. G., 190, 204 Sirotkin, M. M., 119, 196 Skorupka, S., 134, 204 Sobków, J., 175

210

AUTHOR INDEX

Sokolov, E. N., 189, 190, 201, 204 Solov'ev, I. M., 120, 140, 204 Spalding, J. J., 20 Sperry, R. W., 80, 82, 198, 204, 207 Spinnler, H., 166, 167, 208 Spionek, H., 61, 69, 70,71, 74, 204, 205 Stengel, E., 135 Sepien, L., 143, 205 Stevens, S. S., 203 Stolyarova-Kabelyanskaya, L. G., 137, 140, 205 Subirana, A., 69, 70, 76, 205 Szostek-Dobrowolska, B., 184, 205 Szuman, S., 178, 181, 205 Taylor, J., 199 Taylor, L. B., 203 Teuber, H. L., 163, 164, 203, 205, 208 Thorndike, W. L., 89, 205 Tikhomirov, O.K., 181, 186, 205 Tikofsky, R. S., 176, 205 Timberlake, W. H., 108, 199 Tkachev, R. A., 23, 202, 205 Tomaszewski, T., 13, 202, 205 Tonkonogi, J . M., 51, 106, 107, 111, 116, 138, 205, 207 Traugott, N. N., 138, 205 Trousseau, A., 19 Tsvetkova, L. S., I l l , 112, 113, 115, 201, 205

Valerius Maximus, 19 Van Buren, J. M., 203 Van Pelt, D„ 206 Vatsuro, E. G., 3, 4, 6, 205 Vignolo, L. A., 147, 164, 196, 204 Virchow, R., 68 Von Bonin, G., 78, 205 von Grafenberg, J. S., 20 Vygotsky, L. S., 15, 42, 112, 157, 180, 181, 182, 205 Wada, J., 76 Wald, I., 60, 205 Walter, W. G., 190, 191, 206 Warren, J. M., 203 Warrington, E. K., 119, 200 Weinstein, E. A., 82, 163, 164, 205, 206 Weinstein, S., 208 Weisenburg, T. H., 140, 147, 206 Weiskrantz, L., 203 Wepman, J. M., 35, 70, 80, 196, 199, 206 Wernicke, C., 22, 23, 27, 32, 136 Winarska, E. H., 110 Yudovich, E. Yu„ 181, 201 Zangwill, O. L., 72, 206 Zarski, S., 52, 154, 155, 156, 206

SUBJECT INDEX

Abstract attitude, 29, 159, 173 Acalculia, 146 Action, features, 13 Agnosia, 32, 163, 165 verbal-auditory, 139 Agrammatism, 39, 109, 118 Agraphia, 22 Alexia, 19, see also Pure alexia without agraphia Anarthria, 27 Anomia, 154 Aphasia acoustic and transcortical sensory aphasia, 139 localization of causal damage, 44, 118, 136 symptoms and mechanisms of disorders, 44, 118, 136-139 acoustic-gnostic, 44, see Aphasia acoustic acoustic-mnestic localization of causal damage, 44, 140 symptoms and mechanisms of disorders, 44, 140-141 afferent motor localization of causal damage, 40, 103, 122 symptoms and mechanisms of disorders, 44, 102-105, 117, 140, 147, 156 Broca, see Aphasia efferent motor caused by right hemisphere lesions, 71-74 causes, 49-53, 101-102 central, 140

efferent motor localization of causal damage, 44, 105-107, 122 milder cases (disorders of sentence construction), 107-111 severe cases (disorders of word formation), 105-107 symptoms and mechanisms of disorders, 44, 105-111, 117, 147 history of research, 19-31 in children, 74-76 in polyglots, 60 jargon, 20, 118-119, 155, 156, 172 motor, 20, 147, see also Aphasia afferent motor, Aphasia dynamic, Aphasia efferent motor, Aphasia subcortical motor nominative (nominal), 28, 154 peripheral sensory, 135 predominantly expressive, 147 research methods, 49-63 semantic localization of causal damage, 44, 145-146 symptoms and mechanisms of disorders, 28, 44, 121, 145-146, 149, 172 sensory, 135, see also Aphasia acoustic, Aphasia acoustic-mnestic, Aphasia conduction, Aphasia subcortical sensory, Aphasia transcortical sensory, Pure word deafness

conduction, 25, 120, 139-140 cortical motor, 24 sensory, 25 dynamic and inner speech, 111-114, 147 and metalinguistic operations, 115 and transcortical motor aphasia 111 localization of causal damage, 45, 111, 122 reeducative procedures and mechanisms of disorders, 112-114 symptoms and mechanisms of disorders, 44-45, 111-115, 122-123, 147

significance of research, 7, 16-17 subcortical motor, 24, 115-116 sensory, 25, 135 syntactical, 28 total, 174-175 transcortical motor, 24, see also Aphasia dynamic transcortical sensory, 25, 139-140 verbal, 28 Apraxia, 32, 162-163 Asemia, 27 Asymboly, 27, 162

212

SUBJECT INDEX

Callosal section, 80-82 Categorial attitude, 29 Cerebral hemispheric dominance and anatomy of brain, 78-79, 83 and language capacity, 68, 88-89 and lateralization of body functions, 69-70, 77-78, 83 and speech disturbances, 21, 70-74, 77, 80-82 methods of ascertaining, 76-78 ontogenetic formation, 74-76, 78, 80, 83, 193 species-specific feature, 68-69, 83, 88 Cerebral organization of brain functions antilocalizationist theories, 18-19, 28-29, 35-38, 45-46, 158, 193 localizationist theories, 18, 21-26, 31-35, 45-46 other theories, 19-21, 29-31, 38-42, 45-46, 48-49 research methods, 47-66, 88 theory of dynamic localization of function, 18, 42-46, 193, see also Functional system Colour-Form Sorting Test, 176 Communication through language psychological research on, 6-7 specific human capacity, 1-3 verbal transmission of species experience, 3-6 Comprehension, see Speech reception Concepts and speech reception, 127, 134 derangement of actualization, 36 finding within the conceptual network, 171-173 general, 4, 159 in Lenneberg's theory, 168 in Vygotsky's theory, 157 Concrete attitude, 29 Conditioned reflex, 164, 178 Contaminations, 119-120, 141, 172 Context, 133-134 Cross-modal associations, 168-171, 174 transfer, 168 Cube test, 176 Deep structure, 133 Delayed auditory feedback, 117 Distinctive features, 124-125, 127, 138 Dynamogram, 110

Dysarthria anatomic base, 101 and aphasia, 101-102 and subcortical motor aphasia, 115 symptoms, 101-102 Echolalia, 132 Egocentric versus communicative speech, 180-183 Expectancy wave, 191 Feedback afferentation, 117-121, 123, 129, 179, 183 Frontal lobe, 148,149, see also Aphasia dynamic, Aphasia efferent motor, Prefrontal area Functional system, 42-46, 121-123, 149, 152, 193 Functions of speech communicative, 5-6, 14-15 impellant, 181 inhibitory, 181 nominative, 171 orientational-regulatory, 181 predicative, 108, 112-113, 171, 181 pre-inhibitory, 182 pre-trigger, 181 regulation of others' behaviour, 14 self-regulation, 14-15, 181-182, 188-189, 190-192, 195 Generalization, 157 generalizing role of the word, 161, 179 of direct exterior influences, 191 of visually perceived material, 164-165 rule of generalization in the second signal system, 178 Goal-directed activity and speech, 177, 183, 191-192 disturbances accompanying pre-frontal region damage, 183-192 specificity of man, 177, 192 Human brain causes of damage, 49-52 interindividual variability, 59-60 species-specificity of anatomical structures, 67-68 of functional organization, 193-195, see also Cerebral hemispheric dominance

SUBJECT I N D E X

Inertia, 148 Inner speech and activity, 181, 189 and disturbances of speech comprehension, 147, 149 disturbances in syndrome of central aphasia, 140 dynamic aphasia, 112-114, 123, 189 features, 112 Isolated speech area, 85-86, 132 Jargon, 141 Kinesthetic stimuli, 179-180, see also Aphasia afferent motor, Apraxia Language and speech, 7-8 definition, 7 Language capacity acquired versus innate, 8-12, 40 connection with the brain, 21-46 species-specific, 1-3, 8, 9, 68, 88-89, 151, 168-169 Lateralization, see Cerebral hemispheric dominance Learning, see also Memory, Language capacitynonverbal in aphasic patients, 176 sequential and simultaneous, 144 Linguistic competence, 40, 133 sign, 125 Maze test, 176 Meaning, 110, 125-126, 132-134, 145, 149, 159, 160-161, 171, 172-173, 174, 189-191 network, 172-173 Memory and speech reception, 127, 132-133, 149 auditory word patterns (memory traces), 141, 145, 172, 195 mnestic auditory images, 136 nonverbal, 142-144 proactive inhibition, 141 retroactive inhibition, 141 verbal, 141-144 verbal auditory, 44, 119, 141-218, 149 Methods (experimental) for ascertaining dominance

213

amytal test, 76-77 dichotic listening task, 77-78 EEG, 78 perception of verbal material in the right and left visual fields, 78 Motor theory of speech reception, 127-130, 147

Naming disorders and type of aphasia and localization of damage, 155-156 Kogan's rehabilitation method, 161-162 mechanisms of disorders, 155, 157-174 type of disorders, 154-155, see also Paraphasia

Orienting reflex, 190

Paraphasia, 20 literal, 103-105 semantic, 154, 172 word (verbal), 120, 139, 154, 156, 172 Patterns acoustic of speech sounds, 118 auditory-motor, 155, 171, 172, 173, 174 auditory word, 44, 118, 120-121, 123, 135, 138 of articulatory movement, 117-118 of speech sound, word, structure, 132 semantic, 134 somesthetic speech sound, 102-105 speech, 99-101 Pavlov's theory of the second signal system, 177-180, 191 Perseveration, 106, 107, 116, 119, 120, 140, 154, 156, 187 of set, 147, 172 Phase length ratio, 108 Phonemic hearing, 44, 118, 124-125, 205-209, 140-141, 149, 194 Prefrontal area, 183-192, 195 Prosody, 110-111 Pure alexia without agraphia, 61-63, 170 Pure word deafness, 135-136

Raven's Coloured Matrices, 176 Recurring Nonsense Figure test, 142 Rehabilitation in afferent motor aphasia, 105 in amnestic aphasia, 161

214

SUBJECT INDEX

in dynamic aphasia, 112-114 in efferent motor aphasia, 109 in total aphasia, 175 unblocking of latent capacities, 152 Research methods for the study of speech-brain relation clinical, 49-63 comparative anatomy, 65 electrical stimulation of the brain, 63-65, 88, 116

Residual expressions (stereotypes), 102, 111

Scanding, 105 Selection disorders in aphasia of meanings, 172-173 of words, 120, 121, 123, 141, 195 Simultaneous synthesis, 44, 146, 171-174 Spatial orientation, 146 Speech area, see also Cerebral hemispheric dominance and speech disturbances, and nondominant (subordinate) hemisphere, 79-83 and speech production, 121-123 and speech reception, 149-150 anterior division, 87, 146, 149, 171, 194 Broca's area, 21-25, 44, 84,105-107, 122, 194 deeper cerebral structures, 24-25, 33, 88, 115, 123, 135 frontal lobe region lodged anteriorly to Broca's area, 45, 111, 194 general description, 83-88, 150, 193-195 middle segments of the superior convolution of the temporal lobe, 135 parietooccipital region, 44, 145-146, 149 parieto-temporo-occipital junction, 123, 156, 168-171, 195 posterior division, 27, 87, 156, 171, 194 posterior temporo-parietal area, 84 premotor region, see Speech area, Broca's area supplementary motor area, 84, 116, 123, 194 temporal region, 149, 156, 171 Wernicke's area, 22-23, 25, 44, 79, 118, 149, 194-195 Speech production articulation, phonation and respiration system, 94-97 as sensorimotor activity, 92-93, 194

brain mechanisms conception of reflex chains, 98-99 hypothesis about existence of speech patterns, 99-100 Lashley's hypothesis, 99 Lenneberg's hypothesis, 99 speech programming mechanisms, 100-101 disturbances of the programming mechanisms (aphasia) disintegration of the acoustic patterns of speech sounds and words (sensory aphasia), 118-121 of somesthetic speech sound patterns (afferent motor aphasia), 102-105 disorders of discourse construction (dynamic aphasia), 111-115 of sentence construction (afferent motor aphasia), 107-111 of speech sound linkage in word formation, 105-107 disturbance of semantic aspect of word selection and grammatical combination of words (semantic aphasia), 44,121,123, 172-173 general description, 101-102 in acoustic aphasia, 117-120,136 in acoustic-mnestic aphasia, 120-121,140-141 in pure word deafness, 135-136 linguistic analysis of the product (text), 93-94 role in goal-directed activity, 179-183 structure of activity, 93-94 Speech reception as interpretation of meanings, 125-126 as sensorimotor activity, 124, 150, 194 auditory system, 127-128 cerebral mechanisms of disorders, see Aphasia acoustic, Aphasia acoustic-mnestic, Aphasia semantic, Aphasia transcortical sensory, Isolated speech area, Pure word deafness; see also Inner speech, Meaning, Memory, Perseveration of set, Thought in aphasia acoustic, 136, 138 acoustic-mnestic, 140 conduction, 140 motor, 146-148 semantic, 145-146 in pure word deafness, 135 in transcortical sensory aphasia, 139

SUBJECT INDEX

linguistic description of speech sounds, 124-125 organization (levels, facets) of activity decoding of meanings, 132-134 general description, 126-127 recognition of components (comparison with stored patterns), 132 retention of elements, 132 sequential and temporal factors, 130-132 speech sound perception, see Motor theory of speech reception, Phonemic hearing Speech (speech activities) anatomic base, see Speech area definition, 8 disturbances, see Aphasia, Dysarthria phylogenesis, 15, 86 programming mechanisms, 102, see Speech production, Speech reception Substitutive function of the word, 178-183 Successive synthesis, 44,172 Surface structure, 133, 195

215

Telegraphic style, 108-109 Thought and aphasia, 151-153, 158, 174-176 and language, 121, 151-153, 157-158 and naming disorders, 157-163 disturbances in dynamic aphasia, 111-114 in Bay's theory, 36 in Jackson's theory, 30 intellectual operations in speech reception, 127, 134, 137, 139, 145 Transparency of word for meaning, 125-126 Verbal fluency loss after left frontal lobe damage, 114-115 lesions in anterior or posterior portion of speech area, 87 mediation, 169 salad, 118, 136 Wisconsin Card Sorting Test, 176 Word blindness, 22

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Fig. Fig.

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Fig. 16—Mitrynowicz-Modrzejewska A. Fizjologia i patologia glosu, sluchu i mowy (Physiology and pathology of voice, hearing and speech). PZWL, Warsaw 1963. Fig. 17—Lenneberg E. H. Biological foundations of language. John Wiley, New York 1967. Fig. 18—Luria A. R. Higher cortical functions in man. Basic Books, New York 1966. Fig. 19—Mitrynowicz-Modrzejewska A. Fizjologia i patologia glosu, sluchu i mowy (Physiology and pathology of voice, hearing and speech). PZWL, Warsaw 1963. Fig. 20—Cooper F. S., Liberman A. M., Harris K. S. and Grubb P. M. Some input-output relations observed in experiments on the perception of speech. 2nd International Congress of Cybernetics, Namur 1958. Fig. 21—Luria A. R. Higher cortical functions in man. Basic Books, New York 1966.

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