Central Auditory Disorders and Developmental Aphasia: Is There a Difference? Jon Eisenson

In the first stage of preparation for this paper, I set Even in the absence of firm definitions, the members out to find "hard" definitions for central auditory process­ of our related professions including those of us who are ing, central auditory disorders, and, in keeping with the audiologists, hearing and speech scientists, speech/lan­ title, developmental aphasia. The search led me in several guage pathologists (I much prefer speech/language clini­ directions, occasionally into cul-de-sac lanes, sometimes cians), and pediatric neurologists have been neither along pleasant and nostalgic roads. Every so often, I felt modest nor negligent in devising tests and procedures for much like the legendary horseman who all at once rode the assessment of central auditory processing deficits in off into all possible directions. But firm definitions were children. Some of these are adaptations of approaches elusive. I found myself involved with points of view, mostly used with adults. Keith (1981), in his edited symposium negative, of minimal brain dysfunction, whether or not the Central Auditory and Language Disorders in Children, damage was minimal and the dysfunction appreciable; included numerous references as well as negative precau­ and in keeping with my own biases, explanations of prob­ tions on the evaluation of central auditory disorders. lems in reading when the teaching method required audi­ More recently, Berick et al. (1984) reviewed some of the tory intake and auditory processing for the decoding of a better known tests and procedures. Central auditory visual display. The names of Wernicke and Luria and their function is also a subject of study in dysfluent speech (Hall assumptions about the auditory area of the cortex and & Jerger, 1978; Wynne& Boehmler, 1982).1 assume that phonetic discrimination were recurrent. More recent ref­ earlier studies of delayed feedback in stutterers and the erences were to psycho neurological learning disabilities effect of masking noise on fluency were also concerned as well as to psychological learning deficits. Sometimes with aspects of central auditory functioning and dysfunc­ the difference between the two escaped me. tioning. For entirely personal reasons, I had little difficulty in In a chapter on "Neurologically Based Disorders", arriving at satisfactory definitions of congenital aphasia James Hardy (1978) devoted three pages to discussion and developmental aphasia. At the moment I do not raise that negates notions of minimal brain dysfunction and any question about the possibility of a difference. Person­ developmental aphasia as either viable or particularly ally, I go along with what Eimas (1979) offered as a work­ useful diagnostic entities. Nevertheless, albeit reluctantly, ing (operational) definition of central auditory disorders. Hardy did consider the possibility that there are children Eimas referred to " ... deficiencies in the ability to perceive who may have developmental auditory agnosia and per­ sounds of speech categorically, to analyze and code haps even developmental auditory aphasia. Hardy des­ speech in terms of a phonetic feature code, and to appre­ cribes a six-year-old boy who had normal hearing sensitiv­ ciate and utilize contextual information." Such deficien­ ity when tested with pure tone audiometry, but who could cies, Eimas noted, " ... may be functionally related to the not be tested with speech stimuli. The boy rejected the development of language disorders other than those speech signals and would not respond to them. The rejec­ tion itself is diagnostic. The boy's speech output was associated with reading disabilities." On the positive side, I like to think of central auditory processing much along wholly unintelligible and consisted of combinations of the line of Lasky & Katz (1983) as the way our central tones and noises. His intonation patterns resembled mechanisms receive, perceive, decode and utilize those of questions and possible attempts at explanations. The child scored no better than chance on language test speech·sound signals. It is how and what we do with the speech signals our hearing mechanisms respond to and items presented orally but scored at age level on intelli­ our central mechanisms select for listening and respond­ gence test items not calling for oral/aural communication. ing. At this point we have the implied distinction between As a possible partial explanation of the boy's difficulties, hearing and listening. Hardy suggested the likelihood of "Difficulty in analysis of the sequencing of the language code." Perhaps we cannot provide a firm definition of what Hardy appears to be a spokesman for many of our we are talking about any more than we are likely to find a colleagues who are reluctant to accept either the notion firm definition of cognition. This minor weakness has not of a central auditory disorder or of developmental aphasia prevented the propagation of courses, books, and except, possibly. when the evaluation includes clear, advanced degrees in cognitive psychology. "hard" neurological evidence to confirm brain damage. The arguments are coldly logical rather than psychologi­ Jon Eisenson, Ph.D. cal. Hardy does not accept diagnostic classification of a Emeritus Professor Hearing and Speech Science problem by a process of elimination. He and his col­ Stanford University leagues hold that mislearning related to inattention may be basic to communicative disabilities and that "The child

Human Cammunication Canada/Communication Humaine Canada, Vol. 9, No. 4, 1985 13 may not have learned to attend well enough to discrimi­ there is, it may only be one of preference for terms or of nate among the acoustic patterns of speech" (Hardy, degree of impairment. My preference is developmental 1978). This line of argument has several weaknesses. aphasia. It is a disorder in which the primary impairment First, in the early months of life, surely without being is the processing (decoding and in turn encoding) of oral taught, normal infants show differential responses to language when the symbol-signals are presented at a speech and nonspeech signals as well as an ability to normal rate and not in excessive quantity_ If this sounds respond differentially to phonemes with minimal distinc­ familiar, it is intentional. Processing impairments are evi­ tive feature differences. They need only opportunity and dent in children who are "brain different" either because do not require teaching to attend to speech and to show of pre-natal or congenital brain damage, or because of evidence that speech is a human species-specific behav­ retarded or asynchronous maturation of the regions of ior. The position that, because young brains are endowed the brain involved in speech processing or association with plasticity for control of language functions, only between critical areas. For reasons considered earlier, I bilateral damage to the auditory centers should produce do not need to discuss the possibility that developmen­ dysfunctions such as auditory agnosia and congenital tally aphasic children may not have learned to be attentive aphasia is not persuasive. to speaking persons, or worse, somehow learned to be My concept of cerebral plasticity explains how a inattentive. The drive to hear and to listen is so powerful function, once established and to some degree shared by that the only possibility we need to entertain is that a rare centers in both hemispheres, in the event of damage to few children may stop listening because they have learned one hemisphere cent er for that particular function, may language and the aversive ways of some speakers in their come under the dominant control of the other hemis­ use and abuse of langauge. Until these rare children learn phere.lnitially, we need all the mechanisms with which we when and why they should not listen, and conversely elect are born to establish a function normally and naturally. to be mute, the human species-specific drive for language Further, it is possible that our newer techniques for learning is likely to dominate the behavior of potentially determining brain function and/or damage may soon normal children. provide us with information as to how individual brains Children with developmental aphasia may be pre­ are organized and how disorganization is related to corti­ sumed to show the following: adequate intelligence when cal, subcortical, and possibly subcerebral systems. It may assessed with non-language measures and adequate turn out that we have been looking where it was easy and hearing when assessed, however inadequately, by usual convenient to look and our looking and seeing may have audiometric procedures. They usually do not show early been limited to the instruments and prejudgements we evidence of emotional disturbances and of non-relating chose based on our expectations of what and where we problems and, therefore, should not be confused with would find what we were looking for. children with primary autism. Developmentally aphasic I believe that not enough of our colleagues have been children are almost always born into families whose sufficiently impressed with the reality that almost all hear­ members are themselves normal speakers and who try to ing children learn to speak without being directly taught. provide normal stimulation and opportunities for listening Even children with demonstrated articulatory apraxia, and responding to spoken language. unless turned off and away from speaking persons and The term adequate intelligence does not necessarily speaking situations, are usually able to comprehend imply normal or higher intellectual ability or potential. spoken language. In fact, later in their lives, if articulatory Generally, the acquisition of spoken language is denied apraxia persists and if they are taught appropriately, they only to severely mentally retarded children. It is possible, can also learn to read. as Benton (1978) noted, that "There is also evidence that The difficulties of children who are identified as hav­ many retardates show pronounced impairments in the ing central auditory disorders and those of adults with development of linguistic function that cannot be acquired Wernicke's aphasia are too much alike to be accounted for by their low mental age." Relatively few ignored. The results of many investigations provide children in my investigations of developmentally aphasic potent evidence that the impairments of comprehension children fall into the range ofthe mentally retarded. A few seen in persons with acquired auditory aphasia constitute we studied at the Stanford Institute of Childhood Aphasia a disability of processing speech at the phonemic decod­ were well above average in intelligence even when ing level. The literature on the subject includes such assessed by verbal items. These, of course, were children terms as word deafness, auditory imperception, auditory who had been in therapy for two to three years and were verbal agnosia, sensory aphasia, and cortical deafness. successful in academic studies. One made it to High Whatever this aphasic auditory disorder may be called, School Valedictorian. the primary deficit is in speech sound discrimination for temporally ordered events when the signals are pres­ Differential Features ented at the rate and quantity normally spoken by speak­ ers of that language. Developmentally aphasic children cannot encode speech because of a primary deficit in decoding orallan­ Developmental Aphasia guage. In contrast, children with oral (articulatory) Is there a difference between congenital central audi­ apraxia may have little or no decoding problems unless tory disorder and congenital (developmental) aphasia? If they are also aphasic. Just as normal children decode

14 Human Communication Canada/Communication Humaine Canada, Vol. 9, No. 4, 1985 (comprehend) speech before they begin to speak, child­ aphasia is for the processing of acoustic events which are ren with articulatory apraxia may be competent decoders rapidly changing and which require phonemic and tem­ until the limitations of a one-way communication system poral order resolution. turn them off and away from speech and speakers. Those Stark, Mellits, & Tallal (1983) reported that language who are taught to sign do much better. delayed children are less proficient than normal speaking At this point we need to differentiate between devel­ children on tests of visual sequencing. Do children who opmental aphasia and early acquired (childhood) aphasia. are, or were, aphasic have parallel and comparable diffi­ Children may become aphasic as a result of cerebral culties for the processing of visual events? They probably lesion after they have learned to understand and express do, or would, if the visual events were to be presented so themselves through speech. If the damage is limited to that they are as rapidly changing, as transitory, as one hemisphere, more likely as a result of external trauma instantly fading as are auditory signals, and especially than disease, recovery of most language functions is usu­ those signals that constitute the symbols of speech. In the ally rapid. An interesting early feature of acquired aphasia real, non-experimental world, this is not so. Only speech in children is a period of mutism, an apparent "loss of events fade into the past at the very moment they are ability to initiate speech" (Hecaen, 1976) - Hecaen also presented. Visual events are almost always available for noted that, in the early stages, "Disorders of auditory re-viewing, for second and third looks, without our need­ verbal comprehension appeared in more than a third of ing to call upon short term memory to recall and process the cases." Residual impairments include disturbances in the content. Normally, what we look at, even should we naming and serious cognitive and academic problems be flying at the speed of the fastest moving jet plane, can (Satz & Bullard·Bates, 1981). For example, Cooper & be looked at and re-viewed before it is out of sight. What Ferry (1978) described a syndrome of auditory agnosia we hear and try to listen to and decode for meaning can be associated with acquired aphasia for a group of children reconstructed only from memory, a memory that who were also prone to seizures. Persistent problems requires a knowledge of language to make the guesses included "some degree of dysphasia that may range from reasonably correct and confirmable. Lacking this knowl­ auditory verbal agnosia and no functional verbal commu· edge, developmentally aphasic children are very poor at nicaton to less severe difficulties in ... academic areas such guessing. They are weak at dealing with the assumptions as reading and spelling ... many of the children required and anticipations inherent in the game of linguistic proba· special education." bility. Perhaps, in Chomsky's constructs, developmen­ The literature on early acquired asphasia is burgeon· tally aphasic children lack or are retarded in the estab­ ing (Eisenson, 1984; Satz & Bullard·Bates, 1981). Con· lishment of a "Language Acquisition Device" (LAD). trary to earlier impressions, there is mounting evidence They are also slow in establishing a Speech Auditory that most children who have incurred aphasic impair· Device (SAD). This may very well be their primary retar­ ments in childhood do not recover completely, and they dation. Thus, they start out as SAD LADs. Fortunately, are likely to be left with residual deficits which demand with appropriate training and with maturation, both of continued attention and treatment. Descriptions of the these early deprivations can be overcome. deficits include the presence of impairments strongly A Linguistic Profile of An Aphasic Child suggestive of central auditory disorders. What are developmentally aphasic and dysphasic Primary autism, developmental aphasia, children like in their linguistic acquisitions and produc­ tions when they do begin to decode and encode lan­ and central auditory disorders. guage? Are the differences between these children and Is there a possible relationship among primary aut· normal peers quantitative or qualitative? What are the ism, developmental aphasia, and central auditory dis­ likely "residual" deficits often translated and manifested orders? In the 1950's, Dr. Loretta Bender and I frequently into learning disabilities and slow academic achievement? appeared on the same panel at professional society pro· An important precautionary observation is that children grams. Dr. Bender took the position, from which she did who are labelled as aphasic or dysphasic are members of not vary, that, if there were such an impairment as con­ a hetergeneous population. This may be a result of initial genital or developmental aphasia, it was best regarded as mislabeling or a failure to appreciate that these children a subtype of childhood autism. I took the position that the change in their linguistic profiles as they mature. In part, two syndromes were separate, but that if pushed I could these changes may be an expression of the training and make a case that primary autism was in fact a severe form education to which they are exposed once a diagnosis is of congenital aphasia. I think that I can still argue that made. such is the case. I can also be persuaded that the pres­ Our own findings support the observation of variabil­ ence of echolalia, mutism, and other indications of audi­ ity among children whom we diagnosed and treated as tory deficits together suggest that we are dealing with aphasic from 1963-1973. For example, Stark, Poppen, & variations of central auditory disorders. I have not gone May (1967) found that 5 of 8 aphasic children had difficulty into detail on the more recent studies of developmental in a sequencing task (impaired memory for sequencing), aphasia. However, that information seems to support the but 3 children did as well as the control subjects. Part of view, at least in keeping with my perceptions and prejudi· the problem may be that children with a history of aphasic ces, that the underlying impairment in developmental impairments continue to express uncertainty and anxiety

Human Cammunlcation Canada/Communication Humaine Canada, VoL 9, No. 4, 1985 15 in experimental situations and perform at a less than intentions and purposes of their utterances will be optimal level. This behavior may also account for the achieved. Prutting and Kirchner (1983) are optimistic that difference in expressive language usage reported by it is possible to "teach" linguistic pragmatics to children Morehead & Ingram (1973). Normal preschool and who are retarded in language acquisition. At this time I aphasic children were compared on the basis of Mean share that optimism. Length of Utterance (MLU) according to Roger Brown's stages rather than on the basis of age, I.Q., or parents' References socioeconomic level. In the early stages, there were few Benton, A. (1978). "The cognitive functioning of children with differences between the experimental group (age range developmental dysphasia," in M.A. Wyke (Ed.), Developmental from 3 years to 9:6 years) and the controls (age range dysphasia. New York: Academic Press. from 1:7 years to 3 years). Differences increased at the Berrick J.M., Shubow, G.F., Schultz, M.c., Freed, H., Fourn­ upper stage-levels, permitting an observation that, even ier, S.R., & Hughes, J.P. (1984). Auditory processing tests for with training, aphasic children tended to use shorter children, Journal of Speech & Hearing Research, 49, 318-325. utterances, grammatically less complex constructions, Cooper, J.A. & Ferry, P.C. (1978). Acquired auditory verbal and fewer transformations than did normal children. The agnosia and seizures in childhood. Journal of Speech & Hearing investigators projected that, at about age ten, aphasic Research, 43, 176-184. children really postaphasic or dysphasic children - Eimas, P.D. (1979). On the processing of speech: some implica­ would be at about the level of normal 3-year-olds. More­ tion for language development In C.L. Ludlow & M.E. Doran­ head and Ingram observed that their linguistically deviant Quine (Eds.), Neurological bases of language disorders in child­ children, despite increases in vocabulary, failed to ren: Methods and directions for research. NINCDS Monograph develop - or at least ot use the complex structures No. 22. Washington: U.S. Dept. of Health, Education, and that are there as tokens but which are less frequently Welfare. used by younger normal children at the same mean length Eisenson, J. (1984). Aphasia and related disorders in children of utterance (MLU) levels. They stated: "Clearly, the (2nd ed.). New York: Harper and Row. major differences between normal and linguistically Hall, J.W. & Jerger, J. (1978). Central auditory function in deviant children at comparable linguistic levels were not stutterers. Journal of Speech & Hearing Research, 21, 324-337. in the organization of specific subcomponents of their base syntactic systems. Rather, the significant differences Hardy, J. (1978). Neurologically Based Disorders. In J.F. Curt is et al. (Eds.), Processing and disorders in human communica­ were found in the onset and acquisition time necessary tion. New York: Harper and Row. for learning base syntax and the use of aspects of that system, once acquired, for producing major lexical items Hecaen, H. (1976). Acquired aphasia in children and the onto­ in a variety of utterances." genesis of hemispheric functional specialization. Brain & Lan­ guage, 33, 113-134. As a general observation, relevant to Morehead & Ingram and other investigations conducted at Stanford, Keith, RW. (Ed.) (1981). Central auditory and language dis­ orders in children. Houston: College-Hill Press. we found that severely linguistically delayed children designated as aphasic are quantitatively rather than qual­ Lasky, E.Z. & Katz, J. (1983), Central auditory processing, itatively different from normal children in their linguistic Baltimore: University Park Press. acquisitions and productions. What they acquire, at least Morehead, D. & Ingram, D. (1983). The development of base in relationship to MLU, is essentially the same as acquisi­ syntax in normal and linguistically deviant children. Journal of tions of normal children. However, the linguistically Speech & Hearing Research, 16, 330-352. delayed (post-aphasic) children do not use what they Prutting, C.A. & Kirchner, D.M. (1983). Applied pragmatics. In acquire as creatively as normal children for producing T. Gallagher & c.A. Prutting (Eds.), Pragmatic assessment and varied utterances. This difference, we speculated then intervention issues. Houston: College-Hill Press. may represent a cognitive deficit in representational Salz, P. & Bullard-Bates, C. (1981), Acquired aphasia in child­ behavior, at least as these data are related to findings in ren. In M.T. Sarno (Ed.), Acquired aphasia. New York: Aca­ experimental studies. I suggest that this difference is at demic Press. least in part an expression of apprehension, of fear of Stark, J., Poppen. R., & May, M.Z. (1967). Effects of alteration committing an error, rather than of an irreversible deficit. of prosodic features on the sequencing performance of aphasic In several studies, we found that aphasic children, as well children, Journal of Speech & Hearing Research, 10, 849-855. as those who had progressed enough to be considered Stark, RE, Mellits, E.D., & Tallal, P. (1983). Behavioral attrib­ post-aphasic, took twice as long as linguistically normal utes of speech and language disorders. In c.L. Ludlow & J.A. children to indicate choices in test situations. Cooper, (Eds.), Genetic aspects of speech and language dis­ I wish it were possible to consider recent studies on orders. New York: Academic Press. pragmatics and their implications for aphasic children. Tallal, P. & Piercy, M. (1978). Defects of auditory perception in My conjecture is that most aphasic children will be children with developmental dysphasia. In M.A. Wyke (Ed.), delayed shadows of normal ones in becoming linguistic Developmental dysphasia. London: Academic Press. pragmatists. In this respect they will probably require Wynne, M.K. & Boehmler, KM. (1982). Central auditory func­ more direct teaching to understand the subtleties of tion in fluent and disfluent normal speakers. Journal of Speech pragmatics, and the differences in how to say what needs & Hearing Research, 25, 54-57. to be said in order to enhance the likelihood that the

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