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  • Updated 08.16.2020
  • Released 08.14.1995
  • Expires For CME 08.16.2023

Spasmodic dysphonia

Introduction

Overview

Spasmodic dysphonia is a focal laryngeal dystonia. The more common adductor type typically results in strained effortful speech with breaks in phonation. Abductor spasmodic dysphonia generally causes breathy speech with voiceless pauses. The task-specific nature of this condition means that it may normalize with changes in pitch or volume or with other activities, such as laughing or yawning. Several causative genes have been identified in spasmodic dysphonia. In this article, the author discusses risk factors, clinical features, pathophysiology, treatment, and updates on genetic causes.

Key points

• The diagnosis of spasmodic dysphonia is made clinically based on perceptual voice evaluation.

• Botulinum toxin injections 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 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 (149). It was first described by Traube in 1871 as a “nervous hoarseness” in a young girl and assigned the label of spastic dysphonia (185). 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” (165). Schnitzler may be the first one to suspect organic etiology, in 1895, in 2 patients with “cramping of the vocal cord and forced voice” (168), who also had synkinesis of facial muscles and abnormal movements of the arms and legs (97). Schnitzler termed the condition “aphonia spastica” or spastic dysphonia. Due to the lack of other coexisting neurologic deficit, the disorder continued to be considered psychogenic (73; 165; 11). 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 (42).

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