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Background and Purpose —The hyperdense middle cerebral artery sign (HMCAS) is a marker of thrombus in the middle cerebral artery. The aim of our study was to find out the frequency of the HMCAS, its association with initial neurological severity and early parenchymal ischemic changes on CT, its relevance to clinical outcome, and the efficacy of intravenous recombinant tissue plasminogen activator (rtPA) in patients with the HMCAS. Methods —Secondary analysis of the data from 620 patients who received either rtPA or placebo in the European Cooperative Acute Stroke Study I (ECASS I), a double-blind, randomized, multicenter trial. The baseline CT scans were obtained within 6 hours from the onset of symptoms. Functional and neurological outcomes were assessed using the modified Rankin Scale and the Scandinavian Stroke Scale at day 90. Results —We found an HMCAS in 107 patients(17.7%). The initial neurological deficit was more severe in patients with the HMCAS than in those lacking this sign ( P P P P =0.0297). Conclusions —The HMCAS is associated with severe brain ischemia and poor functional outcome. However, it has no significant independent prognostic value when accounting for the effect of initial severity of neurological deficit and of early parenchymal ischemic changes on CT. Patients with the HMCAS may benefit from intravenous rtPA.

Background Fou rire prodromique , described as pathological laughter preceding the onset of an apoplectic attack, is a rare phenomenon. Case Description A 61-year-old man manifested pathological laughter before a sudden right hemiplegia. MRI showed a left lenticular and caudate nucleus infarct with involvement of the external capsule and prerolandic area. MRA revealed a left internal carotid and middle cerebral artery occlusion. Conclusions The clinicoanatomic correlates of this phenomenon are discussed.

Background Ipsilateral sensory motor symptoms associated with carotid artery stenosis are rare, and few reports are available in the literature. Case Description We report the case of a 50-year-old man who presented with right hemiplegia that recurred 14 months later. A left hemisphere watershed infarction was detected. Repeated angiograms showed a left internal carotid occlusion and a right internal carotid stenosis that initially measured 50% and worsened to 80% after the second stroke. Conclusions Repeated quantitative measurements of cerebrovascular reserve demonstrated the hemodynamic mechanism of the strokes and the role of a right internal carotid lesion in causing the recurrence of right hemiplegia.