Prevalence and severity of neurovascular compression in hemifacial spasm patients

Abstract

Hemifacial spasm is typically caused by vascular compression of the proximal intracranial facial nerve. Although the prevalence of neurovascular compression has been investigated in a cohort of patients with classical trigeminal neuralgia, the prevalence and severity of neurovascular compression has not been well characterized in patients with hemifacial spasm. We aimed to investigate whether presence and severity of neurovascular compression are correlated to the symptomatic side in patients with hemifacial spasm. All patients in our study were evaluated by a physician who specializes in the management of cranial nerve disorders. Once hemifacial spasm was diagnosed on physical exam, the patient underwent a dedicated cranial nerve protocol magnetic resonance imaging study on a 3 T scanner. Exams were retrospectively reviewed by a neuroradiologist blinded to the symptomatic side. The presence, severity, vessel type, and location of neurovascular compression along the facial nerve was recorded. Neurovascular compression was graded as contact alone (vessel touching the facial nerve) versus deformity (indentation or deviation of the nerve by the culprit vessel). A total of 330 patients with hemifacial spasm were included. The majority (232) were female while the minority (98) were male. The average age was 55.7 years. Neurovascular compression (arterial) was identified on both the symptomatic (97.88%) and asymptomatic sides (38.79%) frequently. Neurovascular compression from an artery along the susceptible/proximal portion of the nerve was much more common on the symptomatic side (96.36%) than on the asymptomatic side (12.73%), odds ratio = 93.00, P < 0.0001. When we assessed severity of arterial compression, the more severe form of neurovascular compression, deformity, was noted on the symptomatic side (70.3%) much more frequently than on the asymptomatic side (1.82%) (odds ratio = 114.00 P < 0.0001). We conclude that neurovascular compression that results in deformity of the susceptible portion of the facial nerve is highly associated with the symptomatic side in hemifacial spasm.

Clinical characteristics of patients with young-onset hemifacial spasm: a retrospective analysis of 151 cases

“…Regarding the size of the patient groups, we could assume that YOHFS has female predominance as well as HFS in the general population. However, the overall male-to-female ratio reported in other studies shows a more definite female predominance (1:1.9-2.4) [5,15,16] but YOHFS shows a more balanced male-to-female ratio. These sex differences in YOHFS and HFS in the general population might be because HFS is a facial muscle disorder related to facial expressions and cosmetic issues; as women tend to be more interested in their cosmetic appearance, they may be more likely to visit a clinic regarding facial muscle disorders than men.…”

Facial Nerve Massage for the Treatment of Hemifacial Spasm Refractory to Microvascular Decompression: Outcomes and Complications

“…The MR examinations were completed on a 3T MR scanner (GE Healthcare) and were performed using our cranial nerve protocol, which has been previously described. 9,12,15 The protocol consists of sagittal T1, axial fluid-attenuated inversion recovery, and diffusion-weighted imaging sequences of the entire brain with multiplanar thin-slice steady-state free precession images through the cranial nerves.…”

“…1 Microvascular decompression (MVD) is a procedure that addresses the proposed etiopathogenesis of HFS by relieving neurovascular compression (NVC) along the centrally myelinated portion of the facial nerve, completely relieving spasms in a large majority of patients with a low incidence of morbidity. [2][3][4][5][6][7][8][9][10] Although unaddressed NVC of the facial nerve after MVD accounts for a portion of patients with persistent HFS, [11][12][13] there remains a cohort of patients with HFS who cannot be cured of HFS with revision MVD (ie, despite adequate vascular decompression). The aim of this study was to investigate the outcomes and complications arising from facial nerve massage (FNM) in patients, who had undergone prior MVD, with persistent signs and symptoms consistent with HFS and with postoperative brain MRI confirming adequate decompression of the centrally myelinated portion of the facial nerve.…”

Classical trigeminal neuralgia is associated with gephyrin and sodium voltage-gated channel alpha subunit 8

“…Classical trigeminal neuralgia is characterized by severe, intermittent, and brief paroxysms of pain. Although approximately 80-90% of patients with classical trigeminal neuralgia have MRI-evidence of neurovascular compression of the trigeminal nerve (2,3), the mechanism by which neurovascular compression may cause classical trigeminal neuralgia in these patients remains poorly understood (4). Demyelination of the trigeminal nerve in trigeminal neuralgia patients with and without neurovascular compression has been documented (5).…”