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作者 Beach, Woodford Ascher
書名 Dyspragmia in Wernicke's aphasia and Alzheimer's disease: An investigation in clinical pragmatics
國際標準書號 9780493897066
book jacket
說明 416 p
附註 Source: Dissertation Abstracts International, Volume: 63-11, Section: A, page: 3924
Adviser: Jerrold M. Sadock
Thesis (Ph.D.)--The University of Chicago, 2002
Conversational implicature was assessed in 15 subjects (six with Wernicke's aphasia, five with Alzheimer's disease, and four normal controls) to ascertain if conversational implicature could differentiate the two pathological groups. The data were assessed for violations of the conversational maxims of Quality, Quantity and Relevance, as described by Horn (1984). Violations of the Maxim of Quality proved to be the least frequent type across all subjects, with greater frequencies of violations seen in the Maxims of Quantity and Relevance. Normals produced surprisingly high rates of violation of the Maxim of Relevance. Although normals were differentiated from the subjects with Wernicke's aphasia and Alzheimer's disease in frequency of pragmatic violations, the two experimental groups were not differentiated. At best a gross correlation was seen between severity of Wernicke's aphasia and frequency of pragmatic violations. No such correlation was seen in subjects with Alzheimer's disease Patterns of violations varied from subject to subject and across language elicitation tasks. In a post hoc analysis, potential causes for the violations of conversational implicature were proposed. Both linguistic and nonlinguistic cognitive etiologies were proposed, which are congruent with the known sites of lesion of the pathologies of the patients. Violations of the Maxim of Quality were most often due to miscomprehension, frank errors, and dysnomia. Violations of the Maxim of Quantity were most often due to insufficient information being presented by the subject and dysnomia. Violations of the Maxim of Relevance were most often due to tangentiality and overdetail. These data offer a potential starting place for a neurolinguistic model of dyspragmia. Given that multiple etiologies obtain for the violations, we propose that pragmatics is neurolinguistically multifactorial. This vitiates claims for pragmatics being modular. Further support for its nonmodularity is the wide range of dysfunction within and across subjects. Implications for speech-language pathology include potential for assessment combining cognition and linguistic as well as suggestions that therapy for pragmatic dysfunction could best address the impaired cognitive systems which underlie pragmatics
School code: 0330
DDC
Host Item Dissertation Abstracts International 63-11A
主題 Language, Linguistics
0290
Alt Author The University of Chicago
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