Both transcranial Doppler ultrasound and magnetic resonance angiography noninvasively identify 50 to 99% intracranial large vessel stenoses with substantial negative predictive value. The Stroke Outcomes and Neuroimaging of Intracranial Atherosclerosis trial methods allow transcranial Doppler ultrasound and magnetic resonance angiography to reliably exclude the presence of intracranial stenosis. Abnormal findings on transcranial Doppler ultrasound or magnetic resonance angiography require a confirmatory test such as angiography to reliably identify stenosis.

Background and Purpose-Statins may be beneficial for patients with acute ischemic stroke. We tested the hypothesis that patients pretreated with statins at the onset of stroke have less severe neurological effects and a better outcome.

We describe an analysis of 227 patients with lacunar infarcts; 177 were inpatients and the remaining 50 were outpatients. The group comprised 11% of all inpatients with cerebrovascular pathology and 16% of all consecutive inpatients with brain infarcts studied at the Department of Neurology of the Hospital de la Santa Creu i Sant Pau. The main risk factors identified in these patients were arterial hypertension in 164 (72%), diabetes mellitus in 64 (28%), and heart disease in 58 (26%). The most common clinical syndromes were pure motor hemiparesis in 125 (55%), pure hemisensory stroke in 42 (18%), the sensorimotor deficit syndrome in 34 (15%), ataxic hemiparesis in seven (3%), and the dysarthria-clumsy hand syndrome in four (2%); atypical syndromes were observed in 15 patients (7%). Lacunes were demonstrated by computed tomography in 100 patients (44%) and by magnetic resonance imaging in 35 (78%) of the 45 patients in which it was applied. Magnetic resonance imaging was significantly better (p< 0.001) than computed tomography for imaging lacunes, especially those located in either the pons (p<0.005) or the internal capsule (/xO.001). After the acute phase, mild or no neurologic disability was detected in 178 patients (78.4%), moderate disability persisted in 48 patients (

We found unequivocal evidence of active cell proliferation in the ipsilateral subventricular zone following an acute ischemic stroke in our patients.

Background and Purpose-Symptomatic intracerebral hemorrhage (ICH) is a major complication of thrombolysis in patients with acute ischemic stroke. We analyzed whether baseline hemostatic markers could predict symptomatic ICH (SICH). Methods-In a multicenter study of patients treated with intravenous tissue plasminogen activator (t-PA) within 3 hours of stroke onset, we analyzed the following variables: demographic data, vascular risk factors, blood glucose at admission, time from the onset of symptoms to t-PA infusion, blood pressure, neurological deficit measured by the National Institutes of Health Stroke Scale (NIHSS) score, early signs of ischemia on the baseline computed tomography (CT) scan, and protocol deviations. In blood samples, the following markers of coagulation/fibrinolysis were measured before treatment: fibrinogen, prothrombin fragments 1ϩ2, Factor XIII, Factor VII, ␣ 2 antiplasmin, plasminogen activator inhibitor-1 (PAI-1), and thrombin-activatable fibrinolysis inhibitor. ICH was classified according to the European Cooperative Acute Stroke Study (ECASS) II criteria. SICH was defined as a parenchymal hematoma-1 (PH1) or PH2 type, associated with an increase in Ն4 points on the NIHSS score appearing within 36 hours after infusion. Results-We studied 114 patients. Mean age was 68.4Ϯ12.7 years, and 61% were men. The median baseline NIHSS score was 14. Mean time to treatment was 153Ϯ33 minutes. Eight patients had SICH (7%), and 18 patients (15.7%) had asymptomatic ICH. None of the baseline markers of coagulation/fibrinolysis were associated with SICH. In the multivariate analysis, only NIHSS on admission was an independent risk factor for SICH. Conclusions-None of the hemostatic markers analyzed in our study predicted symptomatic cerebral hemorrhage in patients with ischemic stroke treated with t-PA. (Stroke. 2006;37:996-999.)