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Does arteriosclerosis contribute to hemifacial spasm?

  • Clinical Article - Functional
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Abstract

Background

Hemifacial spasm (HFS) is caused by pulsative vascular compression of the root exit zone (REZ) of the facial nerve. However, the mechanism that causes the offending vessels to compress the REZ has not been clarified. Elongation of intracranial arteries due to arteriosclerosis is one possibility, but such arteriosclerotic changes are not observed very frequently among patients with HFS. The aim of the present study was to investigate whether arteriosclerotic changes would contribute to the pathogenesis of HFS.

Methods

This study included 111 HFS patients, all of whom were Japanese. The prevalence rates of hypertension, hyperlipidemia, and diabetes mellitus were examined as risk factors of atherosclerosis, and the cardio-ankle vascular index (CAVI) was measured as an indicator of arteriosclerotic change. The severity of white matter lesions (WMLs) in HFS patients was measured by magnetic resonance imaging. These data were compared with data from healthy Japanese controls.

Results

The prevalence rates of the risk factors for atherosclerosis in the HFS patients were not higher than those in the general Japanese population. The CAVI scores for the HFS patients were similar to, or lower than those in the healthy controls for all age groups except 60 to 69-year-old men. The severity of WMLs in the HFS patients was not significantly worse than that in the controls.

Conclusions

It is suggested that arteriosclerotic changes are not involved in the pathogenesis of HFS, and that vascular compression syndromes are attributable to anatomical features of the intracranial arteries and facial nerves formed during the prenatal stage.

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Acknowledgments

We would like to thank Drs. Mamoru Niitsu and Kaiji Inoue for diagnosis and helpful comments on the MR images of the patients.

For this work, support was received from a Grant-in-Aid for Young Physicians from Saitama Medical University Hospital Grant Number 24-C-1 (Miki Ohta) and the Japan Society for the Promotion of Science KAKENHI Grant Number 23592105 (Masahito Kobayashi).

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Correspondence to Miki Ohta.

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Comment

Hemifacial spasm due to vascular compression of the facial nerve represents an important neurologic issue that can be effectively treated by microvascular decompression. At the time of surgery many surgeons describe thickened arteries, suggestive of atherosclerotic disease, compressing the root exit zone. This description has persisted in the literature for decades with little solid research into this aspect of the disease.

The authors compared the risk factors hypertension, hyperlipidemia, and diabetes mellitus as well as cardio-ankle vascular indices (CAVI), a measure of global atherosclerosis (Izuhara et al. 2008), and cerebral white matter changes, as a measure of local atherosclerosis (Park et al. 2015), in a series of 111 patients with hemifacial spasm who had undergone microvascular decompression, and compared these factors to the healthy population. They found no significant difference in rates of risk factors or degrees of local or global atherosclerosis between the hemifacial spasm population and the healthy population. Arteriosclerosis is often cited as an etiology for hemifacial spasm and this article provides a fresh perspective on this assumption (Jannetta 1977; Kondo et al. 1981). The authors confirm the findings of the cadaver studies performed by Hosemann (1983).

The authors are to be commended on the fine work in evaluating this important issue. While their work does not elucidate a definite pathophysiologic etiology or risk factor for microvascular compression causing hemifacial spasm, it does lay the groundwork for further study. Further investigations of the association between arteriosclerosis and hemifacial spasm in the elderly population and study of embryological contributions to the genesis of hemifacial spasm are warranted.

Ryan Hofler

Christopher M. Loftus

IL, USA

References

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Izuhara M, Shioji K, Kadota S, Baba O, Takeuchi Y, Uegaito T, Mutsuo S, Matsuda M (2008) Relationship of cardio-ankle vascular index (CAVI) to carotid and coronary arteriosclerosis. Circ J 72:1762-1767

Jannetta PJ (1977) Observations on the etiology of trigeminal neuralgia, hemifacial spasm, acoustic nerve dysfunction and glossopharyngeal neuralgia. Definitive microsurgical treatment and results in 117 patients. Neurochirurgia 20:145-154

Kondo A, Ishikawa J, Konishi T (1981) The pathogeneshis of hemifacial spasm: characteristic changes of vasculatures in vertebro-basilar artery system. In: Sammi M, Jannetta P (eds) The cranial nerves. Springer, New York, pp 494-501

Park JH, Kwon HM, Lee J, Kim DS, Ovbiagele B (2015) Association of intracranial atherosclerotic stenosis with severity of white matter hyperintensities. Eur J Neurol 22:44-52, e42-43

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Ohta, M., Kobayashi, M., Terano, N. et al. Does arteriosclerosis contribute to hemifacial spasm?. Acta Neurochir 158, 181–188 (2016). https://doi.org/10.1007/s00701-015-2628-9

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