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We aimed to determine the sensitivity of CT perfusion (CTP) for the diagnosis of cerebral infarction in the acute stage. We retrospectively reviewed patients with ischemic stroke who underwent brain CTP on arrival and MRI-diffusion weighted image (DWI) after hospitalization between October 2008 and October 2011. Final diagnosis was made from MRI-DWI findings and 87 patients were identified. Fifty-five out of 87 patients (63%) could be diagnosed with cerebral infarction by initial CTP. The sensitivity depends on the area size (s): 29% for S < 3 cm(2), 83% for S ≥ 3 cm(2) - < 6 cm(2), 88% for S ≥ 6 cm(2) - < 9 cm(2), 80% for S ≥ 9 cm(2) - < 12 cm(2), and 96% for S ≥ 12 cm(2) (p < 0.001). Sensitivity depends on the type of infarction: 0% for lacunar, 74% for atherothrombotic, and 92% for cardioembolism (p < 0.001). Sensitivity is not correlated with hours after onset. CT perfusion is an effective imaging modality for the diagnosis and treatment decisions for acute stroke, particularly more serious strokes.

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The optimal technique of microvascular decompression (MVD) for trigeminal neuralgia (TN) caused by venous conflict remains unclear. The objectives of this study are to characterize the offending veins identified during MVD for TN and to evaluate intraoperative technique applied for their management. From 2007 till 2019, 308 MVD surgeries were performed in 288 consecutive patients with TN, and in 58 of them, pure venous conflict was identified. In 44 patients, the offending vein was interrupted, as was done for small veins arising from the cisternal trigeminal nerve (CN V) or its root entry zone (REZ) causing their stretching (19 cases), small veins on the surface of REZ (9 cases), transverse pontine vein (TPV) compressing REZ or distal CN V (12 cases), and superior petrosal vein (SPV) using flow conversion technique (4 cases). In 14 other cases, the offending vein was relocated, as was done for the SPV or the vein of cerebellopontine fissure (8 cases), TPV (3 cases), and the vein of middle cerebellar peduncle (3 cases). Complete pain relief after surgery was noted in 49 patients (84%). No one patient experienced major neurological deterioration. Postoperative facial numbness developed in 14 patients (24%), and in 8 of them, it was permanent. In 14 patients, MRI demonstrated venous infarction of the middle cerebellar peduncle, which was associated with the presence of any (P = 0.0180) and permanent (P = 0.0002) facial numbness. Ten patients experienced pain recurrence. Thus, 39 patients (67%) sustained complete pain relief at the last follow-up (median, 48 months), which was significantly associated with the presence of any (P = 0.0228) and permanent (P = 0.0427) postoperative facial numbness. In conclusion, in cases of TN, small offending veins arising from REZ and/or distal CN V and causing their stretching may be coagulated and cut. In many cases, TPV can be also interrupted safely or considered as collateral way for blood outflow. The main complication of such procedures is facial numbness, which is associated with the venous infarction of middle cerebellar peduncle and long-term complete pain relief.

Background:Neurovascular-compression syndrome (NCS) is described as a prominent pathological contact between cranial nerves and vessels. Trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia are typical clinical entities associated with NCS. On the other hand, the hyoglossal nerve is rarely affected by NCS.Case Description:We present a case of hypoglossal nerve palsy (HNP) secondary to vertebral artery (VA) compression. A 47-year-old man presented to our hospital with a 1-month history of dysarthria and dysphagia. Neurological examination revealed left HNP, with an intact swallowing reflex and no oropharyngeal or palatal weakness. Magnetic resonance imaging (constructive interference in steady state) revealed left hypoglossal nerve compression by the V4 segment of the left atherosclerotic VA. He underwent microvascular decompression (MVD) surgery. Intraoperatively, the VA was compressing the hypoglossal nerve. The left VA was moved and attached to the dura matter using a polytetrafluoroethylene (Teflon®) sheet and fibrin glue. Postoperatively, the patient exhibited gradual recovery of HNP in 3 months without dysfunction of lower cranial nerves.Conclusion:In patients with isolated HNP, vascular compression should be considered as a cause of these symptoms, and subsequent MVD can lead to resolution.