Abstract

This chapter discusses the central language mechanism and its disorders. The exact neurophysiology of the central language mechanism is not completely known, but a model developed by Carl Wernicke over a century ago has proved to be the most valid and reliable construct for the explanation of the wide array of aphasia symptoms seen clinically. The model has gained wide acceptance among neuroscientists, linguists, and speech-language pathologists. There is growing support for the model from neurosurgical data, brain and CT scans, and other neurodiagnostic procedures. Although aphasic classification systems are abundant, the Wernicke model is the source of the most widely used current classification. Aphasias of the perisylvian zone include Broca's aphasia, Wernicke's aphasia, conduction aphasia, and global aphasia. Aphasia syndromes outside the perisylvian speech zone are called transcortical aphasias. These include transcortical motor aphasia, transcortical sensory aphasia, mixed transcortical aphasia, and the isolated speech-area syndrome. Anomic aphasia is usually associated with bilateral lesions or mild involvement of the perisylvian speech area. Other anomic patients show no demonstrable lesions. Aphasia syndromes have often been dichotomized into fluent or nonfluent disorders in terms of spontaneous speech performance. Nonfluent aphasia is usually associated with anterior lesions and fluent aphasia with posterior lesions.

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