Hemifacial spasm is a syndrome involving involuntary contraction of the muscles that are innervated by the ipsilateral facial nerve. It is important to distinguish this process from other types of facial spasm, such as psychogenic facial spasm, facial tic, facial myokymia, blepharospasm, and tardive dyskinesia. (1) Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) are sensitive studies that often show vascular compression of the root exit zone of the ipsilateral facial nerve. (1-5) Other underlying processes, such as space-occupying lesions, should be ruled out in patients with associated atypical symptoms.
The most common cause of hemifacial spasm is neurovascular compression of the facial nerve at its root exit zone. This compression can be caused by vascular loops that may involve the posterior inferior cerebellar artery, the anterior inferior cerebellar artery, and the vertebral artery. The location of the compression and its clinical correlation are of utmost importance because some studies have shown that asymptomatic control subjects had some degree of incidental neurovascular compression of the facial nerve, although it was rarely seen in the anterior root exit zone. (2) Also, patients with hemifacial spasm frequently experience progressively worsening involuntary contractions of the facial muscles that can lead to closure of the eye and interfere with daily activities such as driving; they can be socially embarrassing, as well. (6) Over a period of months, these contractions may spread from the periorbital area to other muscles of the ipsilateral facial nerve.
Common treatments for hemifacial spasm are botulinum toxin injections and microvascular surgical decompression. Surgical decompression is the most definitive treatment, but it is not without risk of permanent complications. (7,8) Botulinum toxin treatment is less risky, but it is less effective, it is costly, and it requires repeated injections. (6,9-11) Patients with hemifacial spasm who are not candidates for surgery or botulinum toxin may be treated with pharmacologic agents such as gabapentin and carbamazepine; several small studies have shown that these drugs may reduce the number and severity of spasms. (9,12-14)
We evaluated a 37-year-old woman who had an 8-month history of painless twitching in the left periorbital area. The twitching had progressively worsened over a few months prior to consultation, to the point that she had become unable to open her left eye. This symptomatology was considered to represent a classic case of hemifacial spasm. The patient was placed on medical therapy, which included carbamazepine, but to no avail. Thereafter, MRI and MRA revealed that a portion of the left vertebral artery was compressing the area of the facial nerve and indenting the brainstem at the pontomedullary junction (figure). Given the failure of the medical therapy, we performed surgical decompression of the facial nerve. The twitching was alleviated by more than 50% within 24 hours of the surgery and by more than 75% at discharge. At the 6-month follow-up, the spasm had almost completely resolved.
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Enrique Palacios, MD, FACR; Jack Breux, MD; Jorge E. Alvernia, MD
From the Department of Radiology (Dr. Palacios), the Department of Medicine (Dr. Breaux), and the Department of Neurosurgery (Dr. Alvernia), Tulane University Hospital and Clinic, New Orleans.
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|Title Annotation:||IMAGING CLINIC|
|Author:||Palacios, Enrique; Breaux, Jack; Alvernia, Jorge E.|
|Publication:||Ear, Nose and Throat Journal|
|Article Type:||Case study|
|Date:||Jul 1, 2008|
|Next Article:||Anterior glottic web.|