Elsevier

World Neurosurgery

Volume 125, May 2019, Pages e214-e220
World Neurosurgery

Original Article
Preliminary Study on the Relationship Between Inflammation and Hemifacial Spasm

https://doi.org/10.1016/j.wneu.2019.01.044Get rights and content

Background

Complete pathogenesis of hemifacial spasm (HFS) is unknown. In some patients with HFS, thickened, opaque, and sticky arachnoid membranes have been found during microvascular decompression procedures. This phenomenon indicates a possible relationship between inflammation and HFS. The aim of this study was to explore the role of inflammation in pathogenesis of HFS.

Methods

Levels of interferon-γ, interleukin-2 receptor, interleukin-6 (IL-6), interleukin-8, interleukin-10, and tumor necrosis factor α and white blood cell (WBC), neutrophil, and lymphocyte counts were compared between patients with HFS, patients with lumbar disc herniation, and healthy control subjects. A receiver operating characteristic curve analysis was performed to evaluate the diagnostic significance of peripheral blood inflammatory markers for HFS. All the inflammatory markers were further analyzed by single and multiple logistic regression analysis.

Results

Patients with HFS had greater IL-6, interleukin-8, white blood cell count, and neutrophil count than patients with lumbar disc herniation and healthy control subjects. Area under curve values of IL-6, white blood cell count, and neutrophil count were >0.8. Multiple logistic regression analysis indicated that only interleukin-2 receptor and IL-6 were relevant to HFS.

Conclusions

Inflammation is relative to HFS. IL-6 may be 1 of many factors involved in pathogenesis of HFS.

Introduction

Hemifacial spasm (HFS) is a disease with complex symptoms related to hyperactive motor dysfunction of facial nerve. Although HFS does not directly threaten a patient's life, it causes poor quality of life, a poor social image, and psychological problems.1 It is generally believed that HFS is caused by vascular compression at the root entry zone of the facial nerve. Microvascular decompression (MVD) of the facial nerve has been widely accepted as a standard treatment for HFS.2, 3, 4, 5 However, in addition to compression of the vessel itself, another contributing factor leading to HFS is adhesion and traction to vessel of adjacent arachnoid membranes. Some studies have stated that only complete separation and dissection of arachnoid membranes can result in sufficient MVD for HFS.6, 7, 8, 9 Moreover, thickened, opaque, and sticky arachnoid membranes have sometimes been observed during surgery for HFS. This phenomenon indicates possible influence on vessel or facial nerves by abnormal arachnoid membranes. Inflammation was considered to be the primary cause for the abnormal appearances of arachnoid membranes.10, 11, 12 However, studies specifically investigating the link between inflammation and HFS are lacking. The aims of this study were to describe the differences in preoperative inflammatory markers between patients with HFS, patients with lumbar disc herniation (LDH), and healthy control subjects and to explore the roles of inflammatory markers in the pathogenesis of HFS.

Section snippets

Patients and Healthy Control Subjects

This study was approved by the institutional ethics committee of Xinhua Hospital Affiliated to Medicine School of Shanghai Jiaotong University. Medical records of patients with a diagnosis of HFS and operated on at Xinhua Hospital between June 2016 and March 2018 were collected and retrospectively analyzed. Each record included in the final analysis met the following criteria: 1) The patient did not previously undergo an MVD operation. 2) The patient did not have HFS with a rare cause,

Study Population

After screening, 142 patients with HFS and 70 healthy subjects in the healthy control group were enrolled in the final analysis. Detailed demographic data of the study participants are presented in Table 1. Age range of patients in the HFS group was 24–86 years old, with median age 52 years old. The HFS cohort consisted of 44 men (30.99%) and 98 women (69.01%). The disease course ranged from 0.01 to 27 years (median 3 years). The median age of healthy control subjects was 61 years old; the

Discussion

HFS is mainly caused by pulsatile neurovascular contact at the root entry zone of the facial nerve.13, 14 However, although neurovascular compression has been identified as the primary cause for HFS, there are still several questions that have not been answered sufficiently. During MVD procedures, compression from vessel to facial nerve could also be influenced by some indirect contributing factors, such as adjacent abnormal arachnoid membranes. Sometimes the arachnoid membranes in patients

Conclusions

In this study, we found that inflammation is relative to HFS. IL-6 may be 1 of many factors involved in the pathogenesis of HFS.

Acknowledgments

The authors thank all the individuals who offered help and advice on this study.

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    • Evaluation of pre-operative neuroimaging characteristics in patients with primary hemifacial spasm as a prognostic factor of microvascular decompression

      2020, Clinical Neurology and Neurosurgery
      Citation Excerpt :

      These abnormal arachnoid membranes have sometimes been observed during operation for HFS [13,14,21]. Chen et al. have reported that the inflammatory markers, such as IL-6, were related to the pathogenesis primary HFS [13]. The measurement of area revealed that a smaller CPA cistern might be associated with a higher incidence rate of HFS.

    Conflict of interest statement: The authors declare that the article content was composed in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

    Ming Chen, Min Yang, and Wei-ping Zhou are co–first authors.

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