Abstract

Spasmodic dysphonia (SD) is a voice disorder characterized by abnormal intermittent spasms of intralaryngeal muscles that result in voice breaks during speech. In the adductor variant of spasmodic dysphonia (ADSD), spasms of the adductor muscles cause strangled voice breaks and a strained-strangled voice quality. In the abductor variant (ABSD), spasms of the posterior cricoarytenoid muscle (PCA) cause breathy voice breaks and a breathy voice quality. Patients with SD typically have no other associated chronic medical problems or handicaps and are highly functioning individuals. The voice breaks lead to a significant difficulty in daily communication. Therefore individuals with SD perceive their voice significantly limits them functionally, physically, and emotionally. Successful treatment of vocal spasms thus leads to a dramatic improvement in the patient’s perception of health and social functioning. The ideal treatment for any disease is a single noninvasive therapy that results in a permanent cure without associated complications. Such ideal treatment does not exist for most medical disorders, and SD is no exception. One main hurdle toward achieving a cure for SD is that the cause and pathophysiology of SD remain unclear. There are no animal models for this disorder. What we know from laryngoscopic and electromyographic exams is that voice breaks in SD are associated with abnormal electrical activity of the laryngeal nerves, resulting in increased muscle movements [1]. SD is thus classified as a focal dystonia that affects the larynx. However, we do

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