Eight Japanese early-onset ataxia patients with ARSACS confirmed molecularly were investigated. We performed neurological examination, SACS gene analysis, and MRI in the patients. Hypointensity

lesions in the middle cerebellar peduncles in addition to the pons were observed in T2-weighted and FLAIR images in all eight cases. Although superior cerebellar atrophy was seen in all cases, this MRI finding might not be specific for ARSACS. Upper cervical cord and medulla oblongata atrophy was not observed in 3 of the 7 patients examined. Not only pontine but also middle cerebellar peduncle hypointensity lesions observed in T2-weighted and FLAIR images could be specific findings for ARSACS even in cases with variable clinical phenotypes. www.selleckchem.com/products/nivolumab.html “
“Despite current developments in neuroradiology, the sources of infarctions go undiagnosed in 28% of cases. An embolic source in the setting of minimal stenosis

at the carotid bifurcation has rarely been reported. The authors report a previously healthy 48-year-old woman, without any risk factors for cerebrovascular events, sustained multiple cerebral infarctions in the right LY2157299 anterior and middle cerebral artery territory. Repeated imaging of the heart and cerebral vessels missed a very small abnormality arising from the posterior wall of the internal carotid artery, until it was diagnosed by computed tomographic angiography. This is problematic because by North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria, minimal stenosis

essentially excludes the carotid artery as an embolic Evodiamine source. Despite maximum antiplatelet and anticoagulation therapy, she continued to have neurological deteriortation by progression of her strokes. She underwent standard carotid endarterectomy and sustained no new embolic phenomena. Histopathological examination showed an endothelial hyperplasia with organizing thrombus, which on the posterior wall of the internal carotid artery, is likely a hemodynamically induced on top of preexisting atherosclerotic plaque. “
“Hyperperfusion is a rare but serious complication following cerebrovascular angioplasty and stent placement. Radiographically identifying hyperperfusion before the development of severe sequelae is difficult, as few diagnostic criteria have been established. A 50-year-old woman, initially presenting with 6 weeks of right-sided hemiparesis and dysarthria, was treated for severe stenosis of the left internal carotid and middle cerebral arteries with intracranial angioplasty and placement of a balloon mounted Wingspan Stent (Boston Scientific, Fremont, CA). Continuous transcranial Doppler monitoring after stent placement indicated developing cerebral hyperperfusion. Concurrent angiography revealed markings consistent with dilatations of small arteries in the vascular territory of the stented arteries. Aggressive blood pressure management started in the procedure and continued postprocedure led to an approximately 40% reduction in systolic blood pressure.