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OBJECTIVE: Microvascular decompression (MVD) is the only curative treatment modality for hemifacial spasm (HFS). Although generally considered to be safe, this surgical procedure is surrounded by many risks and possible complications. The authors present the spectrum of complications that they met in their case series, the possible causes, and the strategies recommended to minimize them. METHODS: The authors reviewed a prospectively maintained database for MVDs performed from 2005 until 2021 and extracted relevant data including patient demographics, offending vessel(s), operative technique, outcome, and different complications. Descriptive statistics with uni- and multivariable analyses for the factors that may influence the seventh, eighth, and lower cranial nerves were performed. RESULTS: Data from 420 patients were obtained. Three hundred seventeen of 344 patients (92.2%) with a minimum follow-up of 12 months had a favorable outcome. The mean follow-up (standard deviation) was 51.3 ± 38.7 months. Immediate complications reached 18.8% (79/420). Complications persisted in only 7.14% of patients (30/420) including persistent hearing deficits (5.95%) and residual facial palsy (0.95%). Temporary complications included CSF leakage (3.10%), lower cranial nerve deficits (3.57%), meningitis (0.71%), and brainstem ischemia (0.24%). One patient died because of herpes encephalitis. Statistical analyses showed that the immediate postoperative disappearance of spasms and male gender are correlated with postoperative facial palsy, whereas combined vessel compressions involving the vertebral artery (VA) and anterior inferior cerebellar artery can predict postoperative hearing deterioration. VA compressions could predict postoperative lower cranial nerve deficits. CONCLUSIONS: MVD is safe and effective for treating HFS with a low rate of permanent morbidity. Proper patient positioning, sharp arachnoid dissection, and endoscopic visualization under facial and auditory neurophysiological monitoring are the key points to minimize the rate of complications in MVD for HFS.

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The role of intercalatus nucleus of Staderini (INS), the most caudal of the perihypoglossal nuclei, is much debated. Last research seems to suggest that this nucleus plays a role as a vertical eyes movements integrator. The few clinical reports present in the literature that describe isolated lesions of the INS have described patients presenting in acute with up-beating vertical spontaneous nystagmus. Isolated acute lesion of INS is, in fact, much rare, and, without other neurological signs, is exceptional. We present a case of acute isolated vertigo with no other neurological signs or symptoms, due to INS ischemia provoked by vertebral artery stenosis. The patient presented with spontaneous vertical up-beating nystagmus that showed at videonystagmographic recording, a clear exponential decay of angular slow-phase velocity, that is considered a typical sign of neural integrator impairment. This case seems to represent a further confirm that INS is part, as a vertical-to-position neural integrator, of the neural circuit controlling the vertical eyes movements.

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Vertebrobasilar insufficiency can lead to devastating brainstem and posterior cerebral infarction without timely treatment.1 A 56-year-old man with a history of hypertension, hyperlipidemia, and diabetes mellitus presented to the clinic with right hemiparesis due to previous left cerebral hemispheric stroke. He also harbored a giant asymptomatic parieto-occipital meningioma incidentally diagnosed 2 years ago. Neuroimaging showed old left cerebral infarcts and a tumor that had remained stable in size. Cerebral angiography identified bilateral vertebral artery stenosis near their origin from the subclavian arteries with severe vertebrobasilar insufficiency. There was some collateral flow to the posterior cortex via the internal maxillary and occipital artery branch anastomoses. Despite recommendation, the patient decided to not undergo tumor resection, but opted for a high-flow bypass to the posterior circulation to prevent stroke. We used a saphenous vein graft to perform a high-flow extracranial-to-extracranial bypass revascularization of the ischemic vertebrobasilar circulation (Video 1). The patient tolerated the procedure well and was discharged without new deficits 4-days postoperatively. Most recent follow-up examination at 3 years after surgery revealed a patent bypass graft with no new adverse cerebrovascular events. The tumor remains asymptomatic without change in imaging characteristics. Cerebral bypasses remain useful tools in carefully selected patients for the treatment of complex aneurysms, complex tumors, and ischemic cerebrovascular diseases.2-7 We demonstrate an extracranial-to-extracranial high-flow bypass to revascularize the posterior cerebral circulation using a saphenous vein graft in a patient with vertebrobasilar insufficiency.

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PURPOSE: Despite being rarely reported, ischemic insults resulting from compromising small brainstem perforators following microvascular decompression (MVD) remain a potential devastating complication. To avoid this complication, we have been using indocyanine green (ICG) angiography intraoperatively to check the flow within the small brainstem perforators. We aim to evaluate the safety and usefulness of ICG videoangiography in MVD. METHODS: We extracted retrospective data of patients who received ICG videoangiography from our prospectively maintained database for microvascular decompression. We noted relevant data including demographics, offending vessels, operative technique, outcome, and complications. RESULTS: Out of the 438 patients, 15 patients with a mean age (SD) of 53 ± 10.5 years underwent intraoperative ICG angiography. Male:female was 1:1.14. The mean disease duration prior to surgery was 7.7 ± 5.3 years. The mean follow-up (SD) was 50.7 ± 42.0 months. In 14 patients, the offending vessel was an artery, and in one patient, a vein. Intraoperative readjustment of the Teflon pledget or sling was required in 20% (3/15) of the cases. No patient had any sort of brainstem ischemia. Eighty percent of the patients (12/15) experienced complete resolution of the spasms. 86.7% (13/15) of the patients reported a satisfactory outcome with marked improvement of the spasms. Three patients experienced slight hearing affection after surgery, which improved in two patients later. There was no facial or lower cranial nerve affection. CONCLUSION: Intraoperative ICG is a safe tool for evaluating the flow within the brain stem perforators and avoiding brainstem ischemia in MVD for hemifacial spasm.

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To evaluate the efficacy of magnetic resonance imaging in brainstem stroke, we studied 21 cases of clinically definite brainstem ischemic stroke with brain magnetic resonance imaging (MRI) and conventional computed tomography (CT). MRI demonstrated brainstem lesions in 79% of the cases (16.5 out of 21), while CT revealed 33% (7 out of 21) when cases with suspicious lesions counted as 0.5. Although MRI was done a few days later than CT in most cases, MRI was superior to CT in detecting the number and the size of ischemic lesions, with clear delineation of anatomy and visualization of the status of the blood flow in the vertebral-basilar artery. Disappearance of the flow signal void in the basilar artery can be an important clue in diagnosing occlusion or thrombus of the basilar artery. By delineating the extent and the location of the infarction, MRI findings allowed an interpretation of whether the ischemic vessel is a small basilar branch or a large vessel vertebral or basilar artery.

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The brainstem ischemic injuries were produced by the occlusion of the basilar artery for 6 h in dogs. Gypenoside (150 mg ?kg-1)were intradudinally given at 3 h before the occlusion. We discovered that gypenoside alleviated the ischemic neuronal damage (histopathologically evaluated by the light and electronic microscope), ameliorated the abnormal changes of brainstem auditory evoked potentials (BAEP) (F