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Journal of Speech and Hearing Research Vol.32 541-555 September 1989.
© American Speech-Language-Hearing Association

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Spasmodic Dysphonia, Whether and Where

Results of Seven Years of Research

Terese Finitzo
Frances Freeman

The Dallas Center for Vocal Motor Control

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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