Diabetic stroke patients are associated with specific patterns of stroke type, etiology, and topography but not with poor functional outcome. There was no interaction between DM and hypertension or age.

Background and Purpose-Hyperperfusion syndrome (HS) after carotid endarterectomy (CEA) has been related to impaired cerebrovascular autoregulation in a chronically hypoperfused hemisphere. Our aim was to provide new insight into the pathophysiology of the HS using magnetic resonance imaging (MRI) studies with diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI). Methods-Five out of 388 consecutive patients presented 2 to 7 days after CEA, partial seizures (nϭ5), focal deficits (nϭ5), and intracerebral hemorrhage (nϭ3). In 4 patients, using sequential examinations, we identified vasogenic or cytotoxic edema by DWI; we assessed relative interhemispheric difference (RID) of cerebral blood flow (CBF) by PWI; and we measured middle cerebral artery mean flow velocities (MCA Vm) by transcranial Doppler (TCD). Results-None of the patients presented pathological DWI hyperintensities, consistent with the absence of acute ischemia or cytotoxic edema. In 2 patients, we found an MRI pattern of reversible vasogenic edema similar to that observed in the posterior leukoencephalopathy syndrome. Middle cerebral artery (MCA) mean flow velocities (Vm) were not abnormally increased at any time. PWI documented a 20% to 44% RID of CBF in favor of the ipsilateral to CEA hemisphere. Conclusions-HS can occur in the presence of moderate relative hyperperfusion of the ipsilateral hemisphere. MCA Vm values may not accurately reflect RID of CBF over the cortical convexity. We suggest that the hemodynamic pathogenetic mechanisms of the HS are more complicated than hitherto believed and that they may be more accurately described by the term "reperfusion syndrome." (Stroke. 2005;36:21-26.)

BackgroundThe optimal timing to administer non–vitamin K oral anticoagulants (NOACs) in patients with acute ischemic stroke and atrial fibrillation is unclear. This prospective observational multicenter study evaluated the rates of early recurrence and major bleeding (within 90 days) and their timing in patients with acute ischemic stroke and atrial fibrillation who received NOACs for secondary prevention.Methods and ResultsRecurrence was defined as the composite of ischemic stroke, transient ischemic attack, and symptomatic systemic embolism, and major bleeding was defined as symptomatic cerebral and major extracranial bleeding. For the analysis, 1127 patients were eligible: 381 (33.8%) were treated with dabigatran, 366 (32.5%) with rivaroxaban, and 380 (33.7%) with apixaban. Patients who received dabigatran were younger and had lower admission National Institutes of Health Stroke Scale score and less commonly had a CHA 2 DS 2‐VASc score >4 and less reduced renal function. Thirty‐two patients (2.8%) had early recurrence, and 27 (2.4%) had major bleeding. The rates of early recurrence and major bleeding were, respectively, 1.8% and 0.5% in patients receiving dabigatran, 1.6% and 2.5% in those receiving rivaroxaban, and 4.0% and 2.9% in those receiving apixaban. Patients who initiated NOACs within 2 days after acute stroke had a composite rate of recurrence and major bleeding of 12.4%; composite rates were 2.1% for those who initiated NOACs between 3 and 14 days and 9.1% for those who initiated >14 days after acute stroke.ConclusionsIn patients with acute ischemic stroke and atrial fibrillation, treatment with NOACs was associated with a combined 5% rate of ischemic embolic recurrence and severe bleeding within 90 days.