Background and Purpose-About one half of those who develop adult-onset moyamoya disease experience intracranial hemorrhage. Despite the extremely high frequency of rebleeding attacks and poor prognosis, measures to prevent rebleeding have not been established. The purpose of this study is to determine whether extracranial-intracranial bypass can reduce incidence of rebleeding and improve patient prognosis. Methods-This study was a multicentered, prospective, randomized, controlled trial conducted by 22 institutes in Japan.Adult patients with moyamoya disease who had experienced intracranial hemorrhage within the preceding year were given either conservative care or bilateral extracranial-intracranial direct bypass and were observed for 5 years. Primary and secondary end points were defined as all adverse events and rebleeding attacks, respectively. Results-Eighty patients were enrolled (surgical, 42; nonsurgical, 38). Adverse events causing significant morbidity were observed in 6 patients in the surgical group (14.3%) and 13 patients in the nonsurgical group (34.2%). Kaplan-Meier survival analysis revealed significant differences between the 2 groups (3.2%/y versus 8.2%/y; P=0.048). The hazard ratio of the surgical group calculated by Cox regression analysis was 0.391 (95% confidence interval, 0.148-1.029).Rebleeding attacks were observed in 5 patients in the surgical group (11.9%) and 12 in the nonsurgical group (31.6%), significantly different in the Kaplan-Meier survival analysis (2.7%/y versus 7.6%/y; P=0.042). The hazard ratio of the surgical group was 0.355 (95% confidence interval, 0.125-1.009). Conclusions-Although statistically marginal, Kaplan-Meier analysis revealed the significant difference between surgical and nonsurgical group, suggesting the preventive effect of direct bypass against rebleeding. Clinical Trial Registration

Background and Purpose-The efficacy of superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis in adult moyamoya disease was evaluated by clinicopathophysiological studies. Methods-Fifteen patients with cerebral ischemic attacks (ischemia group) and 15 patients with intracranial hemorrhages (hemorrhage group) were investigated. Clinicoangiographic features and regional cerebral blood flow (rCBF) of the MCA territory were preoperatively and postoperatively investigated, and cortical arterial pressure (CAP) and anastomotic blood flow (AF) were intraoperatively measured.

Mobile plaque is associated with increased risk of ischemic stroke, but definitions have remained unclear. We have previously reported that carotid ultrasonography can detect the mobile component of the carotid plaque surface, which rises and falls in a manner inconsistent with arterial pulsatile wall motion (Jellyfish sign). However, clinical and pathological features of Jellyfish sign remain unclear. The subjects comprised of 165 patients with carotid plaque and degree of area stenosis ≥50% on ultrasonography. Using magnetic resonance imaging, we quantified intraplaque hemorrhage (IPH) and defined ischemic stroke in each patient. Fifteen surgical specimens were obtained by carotid endarterectomy, and pathological features (area of fibrous cap and intraplaque atheromatous lesion) were compared with ultrasonographic plaque surface movement rate. Carotid plaques with IPH were seen in 78 cases, with Jellyfish sign in 31 cases. Jellyfish sign was not detected in patients without IPH. In these 15 patients, the fibrous cap covered the atheromatous lesion, and cap thickness correlated negatively with Jellyfish-positive plaque surface movement rate. Kaplan-Meier and Cox multiple regression analysis demonstrated that the most important predictor of ischemic stroke during follow-up is Jellyfish sign, not IPH. Stroke events in patients with Jellyfish sign repeated within a short interval after diagnosis. Jellyfish sign on ultrasonography is a sign of high-risk plaque vulnerability, suggesting rupture of the fibrous cap associated with the release of thrombogenic factors into the arterial lumen, and resulting in repeated ischemic stroke during a short interval after diagnosis.

The correlations between changes in blood pressure after admission and hematoma expansion were in vestigated in 118 patients with spontaneous intracerebral hematoma admitted within 24 hours of onset who underwent serial computed tomography. Multiple logistic regression was performed to assess cor relations between hematoma enlargement and clinical characteristics on admission. Hematoma en largement was predominantly correlated with time of onset (p 0.01567), and not well correlated with blood pressure at admission (p 0.07908). Serial changes in blood pressure were investigated in 57 patients admitted within 6 hours of ictus whose blood pressures were monitored every hour from admission. Wilcoxon signedrank analysis was used to determine the relationships between hematoma enlargement and blood pressure. Patients with hematoma enlargement was significantly correlated with increased blood pressure (p 0.0004). Increases in blood pressure after admission may be a factor in hematoma enlargement.

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This study suggests that the MFV at the M1 segment is inadequate for estimation of the severity of VSP extending to vessels more peripheral than the M1 segment. Furthermore, severe VSP extending to more peripheral sites can produce more serious ischemic insults, compared with that localized to basal vessels. Patients with negative TCD results and clinical features suggesting the development of VSP should undergo quantitative investigation of cerebral circulatory parameters, such as the CCT, using intra-arterial digital subtraction angiography.

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A 71-year-old female had vertigo attacks once or twice a day secondary to vertebrobasilar insufficiency. Left carotid angiography revealed persistent primitive hypoglossal artery (PPHA) associated with a large internal carotid artery (ICA) aneurysm and severe stenosis of the ICA. The bilateral vertebral arteries were hypoplastic. The basilar artery was opacified via the PPHA but not via vertebral arteries. Clipping of the aneurysm was performed first because the risk of rupture of the aneurysm was not negligible. One month after clipping, carotid endarterectomy using a T-shaped shunt system was suc cessfully performed. The postoperative course was uneventful and the vertebrobasilar ischemic attacks did not recur. Left carotid angiography demonstrated complete obliteration of the aneurysm and dis appearance of the carotid artery stenosis. Low ICA flow (70 ml/min) and low stump pressure of the PPHA (25 mmHg) strongly suggested low perfusion of the posterior circulation. Carotid endarterectomy may be essential for augmentation of the posterior circulation in patients with PPHA associated with ICA stenosis.