Recurrent laryngeal nerve pathology in spasmodic dysphonia.
Since it was first described in 1871, spasmodic (spastic) dysphonia has been considered a disease of psychogenic origin. Unsupported theories of possible organic etiology have appeared sporadically in the literature. In 1976 sectioning of the recurrent laryngeal nerve for patients with this disease was reported with resultant improvement in voice production. This was attempted because the spasmodic dysphonic has, in effect, already compensated vocal cords bilaterally. It was reasoned, therefore, that if one of these was paralyzed the patient would immediately be converted to a state approximating that of well-compensated unilateral vocal cord paralysis which situation, as is well known, usually carries with it a fairly good voice. A controlled study to evaluate the efficacy of this surgical approach has been undertaken at the Cleveland Clinic during the past year. In an attempt to elucidate the possible organic etiology of spasmodic dysphonia, a section of nerve was removed in every case and examined by both light and electron microscopy. Special stains for myelin were also used on the light microscopy specimens. Demyelinization has been found in most of the cases examined by electron microscopy. Possible correlation between this disease entity and other cranial nerve syndromes of unknown etiology is noted. Such conditions as trigeminal neuralgia, glossopharyngeal neuralgia, belpharospasm, hemifacial spasm, and even possibly Bell's palsy may exhibit a similar etiology.
D000328:Adult; D000368:Aged; D005260:Female; D006801:Humans; D007823:Laryngeal Nerves / Q000648:ultrastructure*; D008297:Male; D008875:Middle Aged; D010523:Peripheral Nervous System Diseases / Q000150:complications; D012009:Recurrent Laryngeal Nerve / Q000601:surgery / Q000648:ultrastructure*; D013064:Speech Disorders / Q000209:etiology / Q000473:pathology* / Q000601:surgery