Hemifacial spasm

Toby C Yaltho MD (Dr. Yaltho of Methodist Sugar Land Neurology Associates received honorariums from Allergan for speaking engagements.)
Joseph Jankovic MD, editor. (Dr. Jankovic, Director of the Parkinson's Disease Center and Movement Disorders Clinic at Baylor College of Medicine, received research funding from Allergan, Allon, Ceregene, Chelsea, EMD Serono, Impax, Ipsen, Lundbeck, Medtronic, Merz, and Teva, and compensation for his services as a consultant or an advisory committee member by Allergan, Auspex, EMD Serono, Lundbeck, Merz, Neurocrine Biosciences, and Teva.)
Originally released March 7, 1995; last updated September 26, 2017; expires September 26, 2020

This article includes discussion of hemifacial spasm and postparalytic hemifacial spasm. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Hemifacial spasm is a peripherally induced movement disorder characterized by repetitive involuntary contractions of muscles innervated by the ipsilateral facial nerve. The author reviews clinical features, etiology, pathogenesis, and treatment of hemifacial spasm.

Key points

 

• Hemifacial spasm is a peripherally induced movement disorder, affecting up to 14.5 per 100,000 persons.

 

• Repetitive clonic or more sustained spasms synchronously affect muscles innervated by the facial nerve.

 

• Compression of the facial nerve at its junction with the brainstem, by vascular or other structures (including neoplasms), appears to cause secondary hyperexcitability of the facial nucleus that seems to underlie most cases of hemifacial spasm.

 

• Routine or specialized neuroimaging studies may be helpful in diagnosing or treating hemifacial spasm.

 

• Botulinum toxin injections into affected facial muscles are highly effective as long-term treatment. In patients who fail botulinum toxin, microvascular decompression of the facial nerve should be considered.

Historical note and terminology

Unilateral facial spasm in association with a left vertebral artery aneurysm was first described by Schultze in 1875 (Schultze 1875). In 1888, Gowers further described the syndrome and differentiated it from other facial movements. He noted the clonic nature, propensity to affect the orbicularis oculi, concomitant stapedius involvement, adult onset, predominance in women, and organic nature of the disorder (Gowers 1888). Later, the syndrome was elaborated by Brissaud (Brissaud 1894; Colosimo and Berardelli 2010) and Babinski (Babinski 1905). The first major clinical review, by Ehni and Woltman, appeared in 1945 (Ehni and Woltman 1945). The now widely accepted association between hemifacial spasm and compression of the facial nerve by vascular structures was proposed in 1947 by Campbell and Keedy (Campbell and Keedy 1947).

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