No abstract

Hemifacial spasm induced by intracranial aneurysm is a rare clinical condition. A 45-year-old male patient presented with a 3-year history of progressive involuntary twitching movement on right face. On radiological study, a dilated vascular lesion compressing the brain stem was found at the junction of vertebral artery and posterior inferior cerebellar artery. On operative field, we found the posterior inferior cerebellar artery and the fusiform aneurysm compressing root exit zone of facial nerve. Microvascular decompression was performed and the facial symptom was relieved without complications.

Voltage-dependent anion channel (VDAC) is the main protein in mitochondria-mediated apoptosis, and the modulation of VDAC may be induced by the excessive release of extracellular glutamate. This study examined the role of glutamate release on VDAC-mediated apoptosis in an eleven vessel occlusion model in rats. Male Sprague-Dawley rats (250–350 g) were used for the 11 vessel occlusion ischemic model, which were induced for a 10-min transient occlusion. During the ischemic and initial reperfusion episode, the real-time monitoring of the extracellular glutamate concentration was measured using an amperometric microdialysis biosensor and the cerebral blood flow (CBF) was monitored by laser-Doppler flowmetry. To confirm neuronal apoptosis, the brains were removed 72 h after ischemia to detect the neuron-specific nuclear protein and pro-apoptotic proteins (cleaved caspase-3, VDAC, p53 and BAX). The changes in the mitochondrial morphology were measured by atomic force microscopy. A decrease in the % of CBF was observed, and an increase in glutamate release was detected after the onset of ischemia, which continued to increase during the ischemic period. A significantly higher level of glutamate release was observed in the ischemia group. The increased glutamate levels in the ischemia group resulted in the activation of VDAC and pro-apoptotic proteins in the hippocampus with morphological alterations to the mitochondria. This study suggests that an increase in glutamate release promotes VDAC-mediated apoptosis in an 11 vessel occlusion ischemic model.

This result suggests that the effect of acupuncture might be closely associated with modulation of the brain glutamate release in the ischemic condition.

Hemifacial spasm (HFS) is almost always induced by vascular compression but in some cases the cause of HFS are tumors at cerebellopontine angle (CPA) or vascular malformations. We present a rare case of hemifacial spasm caused by epidermoid tumors and the possible pathogenesis of HFS is discussed. A 36-year-old female patient presented with a 27-month history of progressive involuntary facial twitching and had been treated with acupuncture and herb medication. On imaging study, a mass lesion was seen at right CPA. Microvascular decompression combined with mass removal was undertaken through retrosigmoid approach. The lesion was avascular mass and diagnosed with an epidermoid tumor pathologically. Eventually, we found a offending vessel (AICA : anterior inferior cerebellar artery) compressing facial nerve root exit zone (REZ). In case of HFS caused by tumor compression on the facial nerve REZ, surgeons should try to find an offending vessel under the mass. This case supports the vascular compression theory as a pathogenesis of HFS.