Approach Considerations

In most patients with hemifacial spasm, the treatment of choice is injection of botulinum toxin under electromyographic (EMG) guidance. Chemodenervation safely and effectively treats most patients, especially those with sustained contractions. Relief of spasms occurs 3-5 days after injection and lasts approximately 6 months.

Medications used in the treatment of hemifacial spasm include carbamazepine and benzodiazepines for noncompressive lesions. Carbamazepine, benzodiazepines, and baclofen also may be used in patients who refuse botulinum toxin injections. Compressive lesions need to be treated surgically. Microvascular decompression surgery may be effective for those patients who do not respond to botulinum toxin. A study of 246 patients who underwent microvascular decompression surgery found no significant difference in outcomes and complications between patients who had botulinum toxin injections prior to their first surgery and those who did not.^[8]

Botulinum Toxin Injection

The treatment of choice for hemifacial spasm is botulinum toxin injection of botulinum toxin under EMG guidance. Side effects of botulinum toxin injection (eg, facial asymmetry, ptosis, facial weakness) usually are transient. Most patients report a highly satisfactory response. Caution patients that although botulinum toxin ablates the muscular spasm, the sensation of spasm often persists.^{[9, 10]}

Pharmacologic Therapy

Medications may be used in early hemifacial spasm (when spasms are mild and infrequent) or in patients who decline botulinum toxin injection. Use medications in patients with noncompressive lesions and early idiopathic hemifacial spasm. Response to medication varies but can be satisfactory in early or mild cases. The most helpful agents are carbamazepine and benzodiazepines (eg, clonazepam). Often, medication effects attenuate over time, necessitating more aggressive treatment.

Surgical Decompression

Treat compressive lesions surgically. Ectatic blood vessels cause hemifacial spasm by compressing the facial nerve as it exits the brainstem. Surgical decompression of these blood vessels can yield excellent results.^{[11, 12, 13, 14]}A study evaluating the effect of microvascular decompression surgery on idiopathic hemifacial spasm with compression on different zones of facial nerve found that proper detection of offending vessels and complete decompression may increase cure rate.^[15]

Patients with apparently idiopathic hemifacial spasm may benefit from posterior fossa exploration and microvascular decompression. Myectomy rarely is required.

Medication

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