Spasmodic dysphonia, whether and where: results of seven years of research.
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.
Finitzo
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Dallas Center for Vocal Motor Control, University of Texas 75235.
Freeman
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F
D000328:Adult; D000368:Aged; D001306:Auditory Pathways / Q000503:physiopathology; D001921:Brain / Q000503:physiopathology*; D005072:Evoked Potentials, Auditory; D006801:Humans; D007830:Larynx / Q000503:physiopathology*; D008875:Middle Aged; D014832:Voice Disorders / Q000503:physiopathology*