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  • Updated 03.06.2022
  • Released 08.14.1995
  • Expires For CME 03.06.2025

Spasmodic dysphonia

Introduction

Overview

Spasmodic dysphonia is a focal laryngeal dystonia involving the intrinsic musculature of the larynx. The more common type involves the adductor muscles (thyroarytenoid, lateral cricoarytenoid, and interarytenoid) and typically results in strained, strangled effortful speech with breaks in phonation. Abductor spasmodic dysphonia involves the paired posterior cricoarytenoid muscles, which are the only muscles that abduct or open the larynx for breathing, and generally causes breathy speech with voiceless pauses. The task-specific nature of this condition means that the hyperfunctional muscular spasms occur with speech, but voice and function may be normal with other laryngeal activities, such as swallowing, coughing, laughter, yawning, and singing. Spasmodic dysphonia is typically diagnosed by history, listening to the voice, and laryngeal endoscopic videostroboscopy to exclude other disorders. As in other focal dystonias, the mainstay of treatment for spasmodic dysphonia is EMG-guided botulinum toxin injections into the affected musculature. Several causative genes have been identified for some forms of spasmodic dysphonia, although it usually is idiopathic. There has been a renewed interest in the use of deep brain stimulation for the treatment of spasmodic dysphonia.

Key points

• The diagnosis of spasmodic dysphonia is made clinically based on perceptual voice evaluation combined with laryngeal endoscopy.

• EMG-guided botulinum toxin injections into the intrinsic laryngeal musculature have become the mainstay of treatment for spasmodic dysphonia.

• Advances in genetic studies have allowed causative genes to be identified in some individuals.

Historical note and terminology

Spasmodic dysphonia is a focal laryngeal dystonia resulting in task-specific, action-induced spasm of the vocal cords. Historically, Tiberius Claudius Drusus Nero Germanicus, who became emperor of Rome 41 AD, has been suspected to have spasmodic dysphonia (144). It was first described by Traube in 1871 as a “nervous hoarseness” in a young girl and assigned the label of spastic dysphonia (179). The patient only spoke with great effort, and “the laryngoscopic examination revealed spastic closure of the vocal cord, whereby the left arytenoid cartilage shifted in front of the right one while probably also the vocal cords were particularly overlapping of each other” (159). Schnitzler may be the first one to suspect organic etiology, in 1895, in two patients with “cramping of the vocal cord and forced voice” (161), who also had synkinesis of facial muscles and abnormal movements of the arms and legs (92). Schnitzler termed the condition “aphonia spastica” or spastic dysphonia. Due to the lack of other coexisting neurologic deficits, the disorder continued to be considered psychogenic (67; 159; 10). A century later, Aronson pointed out the wax and wane characteristic and proposed the term “spasmodic” instead of “spastic,” which implies rigidity (07; 08). Credit for reviving interest in spasmodic dysphonia as a medical disorder belongs to Dedo with the proposed recurrent nerve resection, which was a bold decision at the time when most of his contemporaries still believed in a psychiatric etiology (40).

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