No description available.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1951. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Psy. D.)--Wheaton College Graduate School, Wheaton, IL, 2003. / Abstract. Includes bibliographical references (leaves 98-106).

Thesis (Psy. D.)--Wheaton College Graduate School, 2003. / Abstract. Includes bibliographical references (leaves 98-106).

Thesis (Psy. D.)--Wheaton College Graduate School, Wheaton, IL, 2003. / Abstract. Includes bibliographical references (leaves 98-106).

Thesis (Ph. D.)--University of California, San Diego and San Diego State University, 2006. / Vita. Includes bibliographical references (leaves 139-148).

Thesis (M.S.)--University of Florida, 2005. / Typescript. Title from title page of source document. Document formatted into pages; contains 66 pages. Includes Vita. Includes bibliographical references.

Wernicke’s aphasia (WA), an acquired impairment of language comprehension and word repetition, results from a cerebrovascular accident to the left temporoparietal junction. The disorder has been important to the development of neurobiological models of language, however neuropsychological investigations into the nature of the comprehension impairment have been limited. This thesis presents a series of four experiments, investigating the comprehension impairment in WA. Chapter 3, a behavioural neuropsychological study, investigates existing hypotheses of the comprehension impairment in WA: a phonological breakdown, a semantic breakdown, a dual phonological-semantic breakdown. A case series comparison methodology is utilised. Participants with WA are compared to participants from two other clinical, comprehension impaired groups: semantic dementia and semantic aphasia. Semantic dementia and semantic aphasia provide neuropsychological models of semantic breakdown, affecting semantic representations and semantic control respectively. Individuals with WA showed disrupted non-verbal semantic analysis of a similar magnitude to that in semantic dementia and semantic aphasia and of a qualitatively similar nature to that in semantic aphasia. A significantly greater impairment on assessments which required acoustic-phonological analysis was found for individuals with WA compared to semantic aphasia. Overall a dual breakdown in acoustic-phonological and semantic control best accounted for the comprehension impairment in WA. In Chapter 4, direct evidence was sought for a link between acoustic-phonological non-word analysis and auditory comprehension in WA. A novel test of non-word discrimination was created which was perceptually graded so as to provide a sensitive measure in severely impaired participants. Individuals with WA were significantly impaired at non-word discrimination compared to age and hearing matched control participants who performed at ceiling. The degree of non-word discrimination/acoustic-phonological analysis impairment correlated with auditory comprehension in WA. Chapter 5 investigated the extent to which the established acoustic-phonological impairment in WA was grounded in a more fundamental deficit in non-verbal auditory analysis. The capacity to detect structural changes in non-verbal auditory stimuli was measured. Participants with WA had an impaired capacity to detect differences in all but the most structurally simple auditory stimuli, compared to control participants. The degree of this impairment correlated with the degree of auditory comprehension impairment in the WA group. Chapter 6 revisits the semantic impairment observed in WA. Functional magnetic resonance imaging was used to investigate the residual neural networks recruited by individuals with WA, when performing a semantic animate-inanimate judgment task. Large portions of the inferior and anterior temporal lobes bilaterally were activated, regions remote from the lesion in WA. Age matched control participants recruited similar regions; however the activation in WA participants was significantly stronger. This indicated greater reliance on the residual semantic network in WA in response to damage to posterior temporoparietal semantic regions. The results from this series of studies indicated that the primary deficit in WA is one of impaired acoustic analysis and co-morbid damage to a phonological system. Additional disruption occurs to the semantic control network, which regulates the task directed use of semantic representations. A combination of all three factors accounts for the comprehension impairment in WA and it is the relative contributions of each factor that accounts for behavioural variation between individuals.

No description available.

Diss. Linköping : Linköpings universitet, 2007.