Microvascular decompression for hemifacial spasm
Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, United States Journal of Neurosurgery
(Impact Factor: 3.74).
03/1995; 82(2):201-10. DOI: 10.3171/jns.1995.82.2.0201
The authors report the results of 782 microvascular decompression procedures for hemifacial spasm in 703 patients (705 sides), with follow-up study from 1 to 20 years (mean 8 years). Of 648 patients who had not undergone prior intracranial procedures for hemifacial spasm, 65% were women; their mean age was 52 years, and the mean preoperative duration of symptoms was 7 years. The onset of symptoms was typical in 92% and atypical in 8%. An additional 57 patients who had undergone prior microvascular decompression elsewhere were analyzed as a separate group. Patients were followed prospectively with annual questionnaires. Kaplan-Meier methods showed that among patients without prior microvascular decompression elsewhere, 84% had excellent results and 7% had partial success 10 years postoperatively. Subgroup analyses (Cox proportional hazards model) showed that men had better results than women, and patients with typical onset of symptoms had better results than those with atypical onset. Nearly all failures occurred within 24 months of operation; 9% of patients underwent reoperation for recurrent symptoms. Second microvascular decompression procedures were less successful, whether the first procedure was performed at Presbyterian-University Hospital or elsewhere, unless the procedure was performed within 30 days after the first microvascular decompression. Patient age, side and preoperative duration of symptoms, history of Bell's palsy, preoperative presence of facial weakness or synkinesis, and implant material used had no influence on postoperative results. Complications after the first microvascular decompression for hemifacial spasm included ipsilateral deaf ear in 2.6% and ipsilateral permanent, severe facial weakness in 0.9% of patients. Complications were more frequent in reoperated patients. In all, one operative death (0.1%) and two brainstem infarctions (0.3%) occurred. Microvascular decompression is a safe and definitive treatment for hemifacial spasm with proven long-term efficacy.
Available from: Kyung-Il Jo
- "Carter et al.3) reported a pontine vertebral artery (VA) anomaly, and Miwa et al.13) detected atherosclerotic elongation of the VAs. In other studies, no vascular lesions were detected3,4,15,16) and genetic susceptibility in cranial rhizopathies was suggested2,13). Furthermore, progressive atherosclerotic vascular change, accelerated by aging and hypertension (HTN), was hypothesized as a determinant for the clinical appearance of HFS20). "
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ABSTRACT: The purpose of this study was to evaluate the characteristics and surgical outcomes of familial hemifacial spasm (HFS) and to discuss the role of genetic susceptibility.
Between 2001 and 2011, 20 familial HFS patients with ten different pedigrees visited our hospital. The data from comprehensive evaluation of these patients, including clinical, radiological and electrophysiological data and surgical outcomes were reviewed to characterize familial HFS and to compare the characteristics between familial HFS and sporadic HFS.
According to the family tree, the inheritance pattern was difficult to define clearly using these data. Radiologic findings suggested that the vertebral artery (VA) was a more frequent offender in familial HFS than in sporadic cases (35.0% vs. 10.0%, p<0.001). Chi-square test showed that there were no correlation between VA tortuosity and underlying morbidity such as diabetes or hypertension (p=0.391). Eighteen out of 19 patients who underwent microvascular decompression showed no residual spasm. Other features of familial HFS overlap with sporadic cases. These findings suggest that certain genetic susceptibilities rather than hypertension or diabetes may influence vascular tortuosity and HFS development.
In this study, familial HFS seems not so different from sporadic cases. Authors thought familial HFS could have heterogeneous etiology. Further study of familial HFS including clinical, anatomic, genetic, and molecular information may help identify a gene or trait that can provide insight into the mechanisms of sporadic and familial HFS.
Available from: ncbi.nlm.nih.gov
- "Hemifacial spasm (HFS), a syndrome that involves unilateral involuntary twitching and contractions of facial muscles, is caused by vascular compression of the facial nerve at the root exit zone. Microvascular decompression (MVD) has been established as an effective surgical procedure for hemifacial spasm1,18). In patients with HFS, the lateral spread response (LSR), produced by electrical stimulation of one branch of the facial nerves, is recorded from facial muscles after facial nerve stimulation. "
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ABSTRACT: The purpose of this large prospective study is to assess the association between the disappearance of the lateral spread response (LSR) before and after microvascular decompression (MVD) and clinical long term results over two years following hemifacial spasm (HFS) treatment.
Continuous intra-operative monitoring during MVD was performed in 244 consecutive patients with HFS. Patients with persistent LSR after decompression (n=22, 9.0%), without LSR from the start of the surgery (n=4, 1.7%), and with re-operation (n=15, 6.1%) and follow-up loss (n=4, 1.7%) were excluded. For the statistical analysis, patients were categorized into two groups according to the disappearance of their LSR before or after MVD.
Intra-operatively, the LSR was checked during facial electromyogram monitoring in 199 (81.5%) of the 244 patients. The mean follow-up duration was 40.9±6.9 months (range 25-51 months) in all the patients. Among them, the LSR disappeared after the decompression (Group A) in 128 (64.3%) patients; but in the remaining 71 (35.6%) patients, the LSR disappeared before the decompression (Group B). In the post-operative follow-up visits over more than one year, there were significant differences between the clinical outcomes of the two groups (p<0.05).
It was observed that the long-term clinical outcomes of the intra-operative LSR disappearance before and after MVD were correlated. Thus, this factor may be considered a prognostic factor of HFS after MVD.
Available from: Hyuk Jai Choi
- "Although the mechanism of HFS is not yet clearly defined, vascular compression of the facial nerve REZ is generally considered the primary etiology of HFS9,11). 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 the mechanism of hemifacial spasm (HFS) is not yet well established, vascular compression of the facial nerve root exit zone and hyperexcitability of the facial nucleus have been suggested. We report a case of HFS in the setting of coinciding intracranial hemorrhage (ICH) of the pons and proximal ligation of the contralateral vertebral artery (VA) for the treatment of a fusiform aneurysm of the distal VA and discuss the possible etiologies of HFS in this patient. A 51-year-old male with an ICH of the pons was admitted to our hospital. Neuroimaging studies revealed an incidental fusiform aneurysm of the right VA distal to the origin of the posterior inferior cerebellar artery. Eight months after proximal ligation of the VA the patient presented with intermittent spasm of the left side of his face. Pre- and post-ligation magnetic resonance angiography revealed an enlarged diameter of the VA. The spasm completely disappeared after microvascular decompression.
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