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Hemifacial Spasm and its Treatment
Charles B. Wilson, M.D.
University of California Medical Center
San Francisco, California
Hemifacial spasm is a benign hyperactivity of the muscles enervated by the facial nerve, including the stapedius muscle in the ear that may cause a clicking sound. The spasm begins as an innocent twitching around one eye, and then progresses relentlessly to affect all facial muscles, including the platysma muscle in the neck. Once started, hemifacial spasm may be more or less active over the course of time, but I am unaware of any case in which the spasm went away and stayed away. In other words, once it starts, it does not disappear. For some reason women are affected preferentialy, slightly more often on the left side, and predominately in mid-life although I have treated patients in their teens and eighties.
I know of no effective medical treatment. Botox in expert hands achieves excellent results in the great majority of patients and can be used repeatedly and over long periods of time. Its effects are not enduring, which is its major failing.
With rare exceptions, hemifacial spasm is caused by compression of the facial nerve at its junction with the brainstem by an arterial loop of a normal nearby vessel, usually one of the cerebellar arteries coursing near the origin of the facial nerve. Although the artery often compresses the intimately related eighth nerve, hearing loss is rare despite slight weakening of the facial muscles in long-standing cases. In 5% or fewer cases, the arterial loop is pushed into the origin of the facial nerve by a benign tumor or an aneurysm, and this is the reason for a preoperative MRI scan.
The operation itself involves microsurgical exposure of the facial nerve at its origin from the medulla, identifying the responsible artery, and then gently displacing it away from the point of compression and maintaining the separation with an interposed pad of Teflon. Function of the facial and acoustic nerves is monitored throughout the procedure by needle electrodes inserted into muscles around the eye and mouth and by means of a microphone in the ear to elicit auditory evoked responses in the brainstem.
The operation carries a low morbidity, most patients leaving the hospital on the second or third day postoperatively, Serious complications are rare, the most frequent being, loss of hearing on the same side, but this occurs in less than 10% of patients and usually slight. In more than 500 consecutive cases of microvascular decompressions for hemifacial spasm and trigeminal neuralgia, there has been no surgical fatality. Relief of the spasm following decompression is usually immediate, but in some cases it sputters for a matter of weeks before stopping permanently. Rarely, a delayed facial weakness occurs, but invariably it is temporary and transient. Late recurrence of the spasm is extremely rare in my experience. The occasional early recurrence reflects some technical error or an incorrect diagnosis. Despite the good outcome from surgery, it is an operation that has serious potential risks, and a decision to undergo the procedure should be made with an understanding of its risks as well as the benefits.
Kureshi, SA; Wilkins, RH. Posterior fossa reexploration for persistent or recurrent trigeminal neuralgia or hemifacial spasm: surgical findings and therapeutic implications. Neurosurgery, 1998 Nov, 43(5):1111-1117.
Shin, JC; Chung, UH; Kim, YC; Park, CI. Prospective study of microvascular decompression in hemifacial spasm. Neurosurgery, 1997 Apr, 40(4):730-734.
Payner, TD; Tew, JM Jr. Recurrence of hemifacial spasm after microvascular decompression. Neurosurgery, 1996 Apr, 38(4):686-690.
Barker, FG 2nd; Jannetta, PJ; Bissonette, DJ; Shields, PT; Larkins, MV; Jho, HD. Microvascular decompression for hemifacial spasm. Journal of Neurosurgery, 1995 Feb, 82(2):201-210.
Benign Essential Blepharospasm Research Foundation Conference
September 17 - 19, 1999
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