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  • Updated 04.26.2020
  • Released 03.07.1995
  • Expires For CME 04.26.2023

Hemifacial spasm

Introduction

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 (121). 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 (56). Later, the syndrome was elaborated by Brissaud (17; 29) and Babinski (10). The first major clinical review, by Ehni and Woltman, appeared in 1945 (40). 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 (19).

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