It has been generally accepted that HFS is caused by a vascular compression of the facial nerve at the root exit zone (REZ)[2, 12]. Vertebral artery (VA) involvement has previously been reported in 4.4−18.4 % of HFS patients[18, 27, 31]. In our case series, patients with VA and non-VA compressed the facial nerve in 59 (18.8%) and 254 (81.2%) cases, respectively. In the VA-involved group, indirect compression by the VA along with the small branches occurred more frequently than direct compression by the VA alone. When compared to non-VA HFS, we found female predominance and left-sided predominance in VA-associated HFS, and the difference was statistically significant. A similar outcome has been proven in extensive research. The left-sided predominance may result from several factors, including the origin of the left VA directly from the aortic arch, a higher percentage of left-dominant VA, and higher flow velocity and volume in the left VA. Compared with the mean duration of patients in the previous studies, the duration in this study is relatively longer, and there was no significant difference between the VA and non-VA group. This phenomenon may be attributed to the fact that most patients decline surgical treatment until their lives are significantly affected by the symptoms.
Since Jenetta’s first vascularonever compression for hemifacial spasm (HFS) in 1966, Microvascular decompression has been widely used in the treatment of vascular nerve syndrome, Safety and efficacy of MVD in HFS have also been verified, with a success rate ranging from 90.9–94.3%[17, 33]. Patients with HFS are often in their 50s. Aging promotes atherosclerosis of vertebral arteries and makes their walls to become more rigid and brittle. Therefore, MVD is considered more difficult and is associated with a worse outcome when compared to MVD for HFS unrelated to the VA. Several studies have investigated the effect of vertebral artery on HFS. The total spasem-free rate does not differ significantly between the VA involved and the non-VA groups which was in line with the results obtained in this study[10, 21, 22]. Meantime, we also found the delay and partial remissions were more frequent in the VA-associated group. The recurrence rate of VA involved groups was comparable to non-VA groups in our study. Some hypotheses have been proposed for the pathogeneses of delayed healing for HFS. Demyelination of the nerve fibers and hyperexcitability of facial motor nucleus are widely acknowdged and edema of the facial nerve may be another risk factors. According to the findings in the operation, most of the vertebral arteries not only make facial nerve displacement but also cause obvious indentation. The facial nerve becomes demyelinated due to the long-term and continuous blood vessel compression. Even if the facial nerve is fully decompressed, it often takes a long time to repair the myelin sheath. It has been reported that delayed cure is associated with the slow reversal of the plastic changes in the facial nucleus . According to the findings in the second surgery, the causes for persistent or recurrent NVC were often associated with Teflon adhesions and secondary granulomas. Vasculature changes are also a frequent causative factor, especially elongated vertebral artery[3, 28]. Therefore, VA-linked HFS may be a risk factor for delay and partial remissions. However, there is no significant difference in recurrence rate between the two groups in our study, it may be related to the insufficient follow-up period.
Although the incidence of permanent complications don’t have difference, postoperative transient nerve complications in HFS with VA were more common than HFS attributed to small vascular compression. The MVD procedures were mainly comlpleted through the narrow space between vessels and nerves. Due to the large VA maybe obscured surgical field, excessive retraction of the cerebellar flocculus and overstretching of the cranial nerves sometimes were need to achieve sufficient decompression, which increase the complications. Thus, MVD might has a higher surgical risk for VA-involved HFS. Adequate evaluation of preoperative imaging may identify neurovascular contacts and reveal more accurate details of the neighbouring structures, and then help surgeon choose the appropriate operative approach. The appropriate craniotomy, full release of arachnoid membrane and effective use of the natural space of the brain sulcus are often important for providing us with more space[19, 30]. Meantime, endoscopic microvascular decompression provide an more clear field of vision for surgeron and is a better alternative for the treatment of hemifacial spasm. Some new surgeical techniques have also been reported to mobilize the VA safely[9, 11, 14, 16, 20, 24]. However, these techniques are not always effective in all cases, particularly in cases with a high number of perforator blood vessels. Minor damages to the small perforator blood vessels that supply brainstem can have catastrophic repercussions. In this situation, intraoperative electrophysiological mornitoring may be an important and usefull auxiliary tool. Because intraoperative electrophysiological monitoring can provide the real-time response and help the surgeon to judge whether decompression is adequate and when to finish surgery. This help surgeon avoid complications caused by unnecessary harassment for surrounding important structures. Therefore, MVD may pose a higher surgical risk for VA-involved HFS. Adequate preoperative imaging evaluation Intraoperative electrophysiological monitoring are needed to assist in the development of better surgical strategies to minimize postoperative complications