Hemifacial Spasm

Hemifacial spasm (HFS) is characterized by intermittent twitching of the muscles supplied by one facial nerve. It is thought to result from compression of the facial nerve at its junction with the brain stem by an aberrant or ectopic posterior fossa artery. Whereas many cases are idiopathic in origin, a review of 539 cases of HFS for which the cause was specified showed that compression by vascular structures was responsible in 94 percent of cases, tumor in 4 percent, and bony or other abnormalities in 2 percent.y Ihe average age-adjusted annual incidence for patients of all ages is 0.78 per 100,000, and the prevalence has been estimated at 14.5 per 100,000 in women and 7.4 per 100,000 in men.y Onset generally occurs between the second and eighth decades of life, the average age at onset being 45 to 51. Onset during infancy is atypical and usually indicates an underlying tumor, anomaly, or other pathology. Women are more commonly affected than men, and Asians have a particularly high risk compared with other populations. Although familial cases have been reported, most are sporadic. Trigeminal neuralgia can be associated with the development of HFS, suggesting that ephaptic transmission may underlie the pathophysiology of these two syndromes.

Clinically, symptoms begin in the periorbital region and spread to the ipsilateral facial muscles during the next few months. Spasm occurs spontaneously, is almost always unilateral, and is exacerbated by voluntary facial movements such as lip pursing, stress, fatigue, anxiety, or a change in head position. Ihe movements often persist during sleep. Stapedius muscle contraction frequently accompanies contraction of the muscles of facial expression and may produce ipsilateral tinnitus. y

HFS must be differentiated from other conditions that cause involuntary facial movements. Blepharospasm and other forms of facial dystonia are almost always bilateral. Postparalytic facial spasms generally reflect either fixed contraction of the facial muscles or synkinesis or both. Ihere is always a history of preceding facial weakness (e.g., Bell's palsy), and spontaneous spasms are generally absent. Spastic paretic facial contracture may be confused with HFS. Ihe involved side is weak and contracted, unlike the situation in HFS, in which the facial muscles are relaxed between twitches. Facial myokymia is characterized clinically by undulating movements of the facial muscles. Facial tics are rapid, stereotyped, and relatively well coordinated movements that may also occur in regions distant from the face. Hemimasticatory spasm involves muscles innervated by both the facial and trigeminal nerves.

In the patient with normal results on neurological examination, including careful attention to brain stem testing (e.g., blink reflex and extraocular motility), further work-up is usually not needed. If, however, neurological abnormalities, such as facial sensory deficits or an abnormal corneal blink reflex, are present, MRI and possibly MR

angiography are suggested. Specific attention to the cerebellopontine angle and brain stem is required to detect possible tumors or arteriovenous malformations.

Although some clinicians treat HFS first with clonazepam, botulinum toxin injection to the involved muscles is now the treatment of choice. y The role of surgical decompression has diminished with the advent of this therapy, but surgery is still performed in some clinical settings. Endoscopic surgical correction may offer a permanent treatment with less morbidity than posterior fossa exploration. Myectomies, nerve sectioning, and phenol injections have essentially been replaced by botulinum toxin injections.

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