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Two questions are addressed in this presentation and integration of experimental data from seven years of research. They are (a) is spasmodic dysphonia (SD) a neurologic disorder; and (b) if so, where in the nervous system does the dysfunction have its locus? The conclusion is that SD is a supranuclear movement disorder primarily, but not exclusively, affecting the larynx. For over 50% of the subjects, isolated, multifocal, cortical lesions can be identified, specifically in left frontal/temporal cortex (perisylvian region), medial frontal cortex, and right posterior temporal/parietal cortex. Twenty-five percent have mixed subcortical and cortical pathology. Seven percent manifest subcortical lesions alone. For 16%, neither cortical nor subcortical structural or functional lesions are identified. Three etiologic processes that could produce mild multiple cortical and subcortical lesions are closed head injury, multi-infarct microvascular disease, and exposure to neurotoxins. These processes are discussed with reference to the population studied.
KEY WORDS: spasmastic dysphonia, electrophysiology, neurogenic voice disorder, SPECT, MRI
Submitted on April 4, 1988
Accepted on January 11, 1989
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