By Martha Taylor Sarno
With chapters containing as much as 50 percentage new insurance, this booklet presents an intensive replace of the newest learn and improvement within the quarter of bought aphasia. assurance contains the indications of aphasia, evaluation, neuropsychology, the categorical linguistic deficits linked to aphasia, similar problems, restoration, and rehabilitation. This entire compilation, written by way of the most a professional employees within the box, presents an authoritative textual content and reference for graduate scholars, clinicians, and researchers. Key gains* Chapters comprise as much as 50 percentage new insurance* offers replace of up to date learn within the box* contains writings by way of the main an expert staff within the box* accomplished, exhaustive reference software
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Extra info for Acquired Aphasia (Third Edition)
The lesion method, reinvigorated by progress in imaging, remains a cornerstone of modern aphasiology, but it has been separated from the theoretical accounts traditionally associated with it. , Wernicke's aphasia), with the greatest progress being made in those areas where autopsy findings were inconclusive. Much of the progress has been in a greater appreciation of the complexity and heterogeneity of the anatomical substrates of the basic syndromes. , Ojemann, 1983), have extended beyond the peri-Sylvian area the boundaries of the neural regions believed to function in language.
Nielsen, J. M. (1936). Agnosia, apraxia, aphasia: Their value in cerebral localization. New York: Harper (Hoeber). Ogle, W. (1867). Aphasia and agraphia. St. George's Hospital Reports, 2, 83-122. Ojemann, G. A. (1983). Brain organization for language from the perspective of electrical stimulation mapping. Behavioral and Brain Sciences, 189, 230. Ombredane, A. (1926). Sur le m6canisme de l'anarthrie et sur les troubles associ6s due langage int6rieur. Journal de Psychologie Normale et Pathologique, 23, 940-955.
Although, like virtually all aphasias, some white matter damage was typically present in conduction aphasia, there was also damage to cortex in nearly all cases. The traditional account of the repetition defect of conduction aphasia caused by isolated interruption of white matter connections between Wernicke's and Broca's areas was no longer tenable. Likewise, transcortical motor aphasia (TMA) was a clearly recognized clinical entity but information on its anatomical basis was sparse. On the basis of radionuclide scans and associated neurological signs, Rubens (1975) posited that TMA resulted from lesions in superior and mesial premotor regions.