Spasmodic dysphonia

Steven Bellows MD (

Dr. Bellows of Baylor College of Medicine has no relevant financial relationships to disclose.

Robert Fekete MD, editor. (

Dr. Fekete of New York Medical College received consultation fees from Acadia, Acorda, Adamas, Amneal/Impax, Kyowa Kirin, Lundbeck, Neurocrine, and Teva.

Originally released August 14, 1995; last updated August 16, 2020; expires August 16, 2023


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 (Rice 2000). It was first described by Traube in 1871 as a “nervous hoarseness” in a young girl and assigned the label of spastic dysphonia (Traube 1871). 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” (Schaefer and Freeman 1987). Schnitzler may be the first one to suspect organic etiology, in 1895, in 2 patients with “cramping of the vocal cord and forced voice” (Schnitzler 1895), who also had synkinesis of facial muscles and abnormal movements of the arms and legs (Kiml 1965). 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 (Heaver 1959; Schaefer and Freeman 1987; Baizabal-Carvallo and Jankovic 2015). A century later, Aronson pointed out the wax and wane characteristic and proposed the term “spasmodic” instead of “spastic,” which implies rigidity (Aronson et al 1968a; Aronson et al 1968b). 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 (Dedo 1976).

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