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Nonspastic hemifacial spasm confirmed by abnormal muscle responses.

ABSTRACT: Hemifacial spasm is usually diagnosed by inspection which mainly identifies involuntary movements of orbicularis oculi. Assessing abnormal muscle responses (AMR) is another diagnostic method.We report a case of left hemifacial spasm without detectable involuntary facial movements. The patient was a 48-year-old man with a long history of subjective left facial twitching. On magnetic resonance imaging (MRI), the left VIIth cranial nerve was compressed by the left anterior inferior cerebellar artery (AICA), which was in turn compressed by the left vertebral artery. We initially treated him with botulinum toxin. We were able to record AMR, and hemifacial spasm occurred after AMR stimulation, although no spasm was detectable by inspection. Subsequently, we performed microvascular decompression with transposition of the AICA that compressed the VIIth cranial nerve. His hemifacial spasm resolved by 5 weeks after surgery and was not induced by AMR stimulation.Hemifacial spasm can sometimes be diagnosed by detecting AMR rather than by visual inspection. We propose that such hemifacial spasm should be termed nonspastic hemifacial spasm.

SUBMITTER: Tani S

PROVIDER: S-EPMC5473113 | biostudies-other | 2017

REPOSITORIES: biostudies-other

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Project description: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.

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Nonspastic hemifacial spasm confirmed by abnormal muscle responses.

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