Hemifacial Spasm Caused by Epidermoid Tumor at Cerebello Pontine Angle

Department of Neurosurgery, School of Medicine, Kyung Hee University, Seoul, Korea.
Journal of Korean Neurosurgical Society (Impact Factor: 0.64). 04/2009; 45(3):196-8. DOI: 10.3340/jkns.2009.45.3.196
Source: PubMed


Hemifacial spasm (HFS) is almost always induced by vascular compression but in some cases the cause of HFS are tumors at cerebellopontine angle (CPA) or vascular malformations. We present a rare case of hemifacial spasm caused by epidermoid tumors and the possible pathogenesis of HFS is discussed. A 36-year-old female patient presented with a 27-month history of progressive involuntary facial twitching and had been treated with acupuncture and herb medication. On imaging study, a mass lesion was seen at right CPA. Microvascular decompression combined with mass removal was undertaken through retrosigmoid approach. The lesion was avascular mass and diagnosed with an epidermoid tumor pathologically. Eventually, we found a offending vessel (AICA : anterior inferior cerebellar artery) compressing facial nerve root exit zone (REZ). In case of HFS caused by tumor compression on the facial nerve REZ, surgeons should try to find an offending vessel under the mass. This case supports the vascular compression theory as a pathogenesis of HFS.

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    • "Offending vessels are most often found on preoperative radiologic evaluation or during surgery; MVD of these offending vessels has yielded successful outcomes in large serial studies1,8). In several rare secondary causes of HFS, including CPA tumors, aneurysms, and AVMs, compression of the facial nerve REZ by altered vasculature is also considered the etiology of HFS5,7,10,13,17,18). "
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    ABSTRACT: Although hemifacial spasm is usually caused by vascular compression around the root exit zone of the facial nerve, it is sometimes brought on by a cerebellopontine angle tumor. We reviewed and analyzed data from past experience with hemifacial spasm induced by cerebellopontine angle tumors. Nine patients of a total 2,050, who had presented with hemifacial spasms associated with cerebellopontine angle tumors between 1986 and 2009, were reviewed. Two vestibular schwannomas, five meningiomas, and two epidermoid tumors were included in this study. Hemifacial spasm occurred on the same side of the lesion in eight patients whereas it occurred on the opposite side of the lesion in one patient. With respect to the pathogenesis of hemifacial spasms, offending vessels were found in six patients, tumor encasement of the facial nerve in one patient, hypervascular tumor compression of the facial nerve without offending vessels in one patient, and a huge tumor compressing the brain stem and, thus, contralateral facial nerve compression in one patient. Hemifacial spasm was resolved in seven patients, whereas in two patients with a vestibular schwannoma and an epidermoid tumor, it improved transiently and then recurred in a month. Each type of tumor had different characteristics with respect to the induction of hemifacial spasm; therefore, it is suggested that neurosurgeons, who are planning surgeries both for the purposes of relieving hemifacial spasm and removal of cerebellopontine angle tumor, should thoroughly prepare appropriate approaches and specific dissecting strategies according to each causative lesion.
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    ABSTRACT: Hemifacial spasm is defined as unilateral, involuntary, irregular clonic or tonic movement of muscles innervated by the seventh cranial nerve. Most frequently attributed to vascular loop compression at the root exit zone of the facial nerve, there are many other etiologies of unilateral facial movements that must be considered in the differential diagnosis of hemifacial spasm. The primary purpose of this review is to draw attention to the marked heterogeneity of unilateral facial spasms and to focus on clinical characteristics of mimickers of hemifacial spasm and on atypical presentations of nonvascular cases. In addition to a comprehensive review of the literature on hemifacial spasm, medical records and videos of consecutive patients referred to the Movement Disorders Clinic at Baylor College of Medicine for hemifacial spasm between 2000 and 2010 were reviewed, and videos of illustrative cases were edited. Among 215 patients referred for evaluation of hemifacial spasm, 133 (62%) were classified as primary or idiopathic hemifacial spasm (presumably caused by vascular compression of the ipsilateral facial nerve), and 4 (2%) had hereditary hemifacial spasm. Secondary causes were found in 40 patients (19%) and included Bell's palsy (n=23, 11%), facial nerve injury (n=13, 6%), demyelination (n=2), and brain vascular insults (n=2). There were an additional 38 patients (18%) with hemifacial spasm mimickers classified as psychogenic, tics, dystonia, myoclonus, and hemimasticatory spasm. We concluded that although most cases of hemifacial spasm are idiopathic and probably caused by vascular compression of the facial nerve, other etiologies should be considered in the differential diagnosis, particularly if there are atypical features.
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