Aphasia and Deafness

APHASIA AND DEAFNESS' HarryMarkowicz 1.0 Introduction. 1.1 Language Disorders. Language pathology has been a useful area of investigation for the neurologist studying brain function and organization. Until now, linguists have but rarely made use of cases of language disorders to learn about normal and abnormal verbal behavior; Jakobson (1941) is a notable exception. Such cases provide the opportunity to test linguistic models and claims made for their psychological reality. Linguistic research of language pathology can also lead to the cooperation of linguists with other professionals, i.e. neurologists, psychologists, and speech therapists, in the therapy programs designed for individuals who suffer from language disorders. In this paper I propose to investigate the relationship of two separate types of language disorders, namely aphasia and deafness. It is my expectation that each area can contribute to knowledge about the other which is not readily available when they are studied separately or in comparison with normal language behavior. Further areas of research will be suggested as a result of this particular survey of the literature. 1.2 Definitions of Aphasia. An interdisciplinary conference on aphasia offers the following definition of this language disturbance: Aphasia is a nonfunctional impairment of the reception, manipulation, and/or expression of symbolic content whose basis is to be found in organic damage to relatively central brain structure. (Osgood and Miron 1963:8). For the linguist, a definition which limits the scope of aphasia to language disorders, such as Tikofsky's, may be preferable: Sign Language Studies Aphasia is a disruption and/or reduction, resulting from a lesion in the central nervous system, of the abilities necessary to voluntarily use and/or comprehend for the purpose of communication, the elements of a language system (1966: 262-263). Both definitions exclude language (more specifically speech) disorders resulting from muscular impairments caused by cortical and sub-cortical lesions. These impairments, known as apraxiaand dysarthriarespectively, may occur concurrently with aphasia. 2.0 The Functional Organization of the Brain. The organic damage referred to in the above definitions must occur at a time when the individual has already acquired his native language(s) to be diagnosed as aphasia. 2.1 Wernicke's Model. Wernicke, besides discovering and describing the language center named after him, constructed the first model of how language areas may be connected in the brain. This line of study represented on of the major approaches to aphasia, a clinical-neurological approach, in which an attempt was made to relate the patterning of symptoms of speech disturbances to the locations of lesions in the brain (Osgood and Miron 1963:2). Not all researchers agree with this view of strict localization of language in the brain. For example, Lenneberg claims in his BiologicalFoundationsof Language that: The brain functions as a single unit such that there are no identifiable neuroanatomical correlates- either topographical or histological-of specific behavioral function (including language), except the visual cortex (quoted in Whitaker 1970:24). Whitaker, on the other hand, criticizes Lenneberg's position, and along with Luria, claims a firm statistical basis for localization studies: Localizing the structures which are active in the brain during the use of language is by no means an exercise in fanciful Markowicz theorizing. Particular, identifiable language deficits are one of the most powerful tools of the clinical neurologist who must know where a lesion is, its extent and its type. It is true that one cannot invariably "place" a lesion in the nervous system with exact coordinates; in the first place, no two brains are absolutely identical anymore than two people are; secondly, most evidence for localization is statistical in nature as just noted. But before one interprets "statistical" to mean "just better than chance" consider this: in a survey of over 800 patients with gunshot wounds, Luria [19621 determined that a "derangement of phonemic hearing" was localized in the superior temporal gyrus (Brodman areas 52, 41 and 42), posterior region, in 94.7% of those patients injured in this area (1970:28). Thus, while Wernicke's model has been criticized for its oversimplification , it has been useful in predicting the site of lesions on the basis of specific language disorders, as well as in predicting that certain lesions...