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Department of Neurology

Houston, Texas

BCM neurologists see patients through the Baylor Clinic and some of the world's leading specialty clinics.
Department of Neurology
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Hemifacial Spasm (HFS)

What is hemifacial spasm?

Hemifacial spasm (HFS) is a neurological disorder manifested by twitching spasms on one side of the face due to involuntary contractions of the eyelid and other facial muscles. It usually begins gradually around one eye and may eventually spread to include the muscles around the mouth and even neck, all on the same side. These muscle spasms are very brief but occur rapidly and repetitively. They are generally not painful, but may impact vision because of forced involuntary eye closure. In contrast to blepharospasm, a form of focal dystonia, which is associated with eyelid spasms involving both eyes (bilateral), HFS involves only one side of the face (unilateral). Very rarely, the other side of the face may become affected in HFS, but the contractions remain asymmetric and independent of each other. The facial spasms are also often noticed by others and can be a source of embarrassment to the patient; sometimes they are wrongly attributed by others as “winking”. HFS can sometimes be triggered by volitional contraction of certain facial muscles, especially puckering the lips or after forcefully closing eyes. Stressful situations or fatigue may also worsen the spasms. Estimates suggest that one in ten thousand people have HFS. It may be somewhat more common in women than men and is more frequently seen in the Asian population.

What causes hemifacial spasm?

HFS usually appears without obvious cause but it is most frequently attributable to a compression of the facial nerve (seventh of the twelve cranial nerves) as it exits from the brainstem. This nerve supplies muscle power to the facial and superficial neck muscles. In most cases the compression is from a hardened displaced (ectatic) blood vessel near the base of the brain. Rarely, aneurysms, brain tumors or trauma may also compress the facial nerve. The compression then causes the nerve to “short circuit” itself and it begins to fire independently. This is referred to as “ephaptic transmission”. As one part of the nerve fires, the signal is misdirected to another part of the nerve causing muscle contractions in different parts, but the same side, of the face.

In some cases, the condition occurs months or even years after an episode of unilateral facial weakness (Bell’s palsy). The involuntary contractions involving muscles adjacent to those that contract voluntarily, termed “synkinesis” and other features usually readily differentiate typical HFS from spasm that occur following recovery from Bell’s palsy. Bell’s palsy is usually caused by a virus which resides in one part of the facial nerve. The nerve later grows back imperfectly resulting in short circuits and spontaneous firing. One complication of Bell’s palsy is increased tearing in the affected eye, termed “crocodile eyes”.

How do you test for hemifacial spasm?

There are electrical nerve tests (EMG) that can demonstrate a facial nerve short circuit. However, an experienced neurologist can usually diagnose the condition by simply observing it and EMG is rarely needed. If atypical features are present (e.g. facial numbness or hearing loss), then neuroimaging tests such as MRI may be useful.

How is hemifacial spasm treated?

Medications used for seizures such as carbamazepine, phenytoin and clonazepam, and muscle relaxing medi­cations such as diazepam, baclofen and trihexyphenidyl are only rarely helpful their use is often associated with adverse side effects. A complicated surgical procedure, sometimes called the “Jannetta procedure”, used in the past is now rarely needed. While the procedure often relieves the involuntary facial spasms, it is a complicated neurosurgical procedure with many risks of complications, including facial weakness, deafness and stroke. Currently, most physicians consider botulinum toxin injections to be the best treatment. This protein is injected directly into the affected muscles. At relatively low doses, it relaxes the affected muscles enough to prevent the spasms without causing paralysis. The improvement occurs within 3-4 days and lasts an average of 4-6 months. Repeat injections are then required at varying intervals depending on each individual’s response. In the hands of a well-trained practitioner, the procedure is very safe. Potential side effects include an eyelid droop (ptosis), facial weakness or increased tearing, all of which resolves over time.

Selected References

  • Defazio G, Abbruzzese G, Girlanda P, et al. Botulinum toxin a treatment for primary hemifacial spasm: a 10-year multicenter study. Arch Neurol 2002;59:418-420.
  • Jankovic J. Botulinum toxin in clinical practice. J Neurol Neurosurg Psychiatry 2004;75:951-7.
  • Kenney C, Jankovic J. Botulinum toxin in the treatment of blepharospasm and hemifacial spasm. J Neural Transm 2007 (in press).
  • Tan EK, Fook-Chong S, Lum SY, Lim E. Botulinum toxin improves quality of life in hemifacial spasm: validation of a questionnaire (HFS-30). J Neurol Sci 2004;219:151-5.
  • Stamey W, Jankovic J. The other Babinski sign in hemifacial spasm. Neurology 2007;69:402-4.
  • Wang A, Jankovic J. Hemifacial Spasm: Clinical correlates and treatments. Muscle Nerve 1998;21:
    1740-1747.

Appendix

Benign Essential Blepharospasm Foundation, Inc.
P.O. Box 12468
Baptist Hospital Doctors Bldg.
3155 Stagg Drive
Beaumont, Texas 77726-2468
Tel: 409-832-0788
Fax: 409-832-0890

For additional information visit http://www.bcm.edu/neurology/pdcmdc/