Background and Purpose-We investigated whether transient ischemic attacks (TIAs) before stroke can induce tolerance by raising the threshold of tissue vulnerability in the human brain. Methods-Sixty-five patients with first-ever ischemic territorial stroke received diffusion-and perfusion-weighted MRI within 12 hours of symptom onset. Epidemiological and clinical data, lesion volumes in T2, apparent diffusion coefficient (ADC) maps and perfusion maps, and cerebral blood flow and cerebral blood volume values were compared between patients with and without a prodromal TIA. Results-Despite similar size and severity of the perfusion deficit, initial diffusion lesions tended to be smaller and final infarct volumes were significantly reduced (final T2: 9.
We assessed the risk and determined predictors of early epileptic seizures (ES) in patients with acute cerebral venous and sinus thrombosis (CVST). A prospective series of 194 consecutive patients with acute CVST admitted to neurological wards in two German university hospitals was analysed for frequency of ES and in-hospital mortality. Demographic, clinical and radiological characteristics during the acute stage were retrospectively analysed for significant association with ES in univariate and multivariate analyses. During the acute stage, 19 patients (9.8%) died. Early symptomatic seizures were found in 86 patients (44.3%). Status epilepticus occurred in 11 patients (12.8%) of whom four died. Amongst patients with epileptic seizures, mortality was three times higher in those with status than in those without (36.4% and 12%, respectively). In multivariate logistic regression analysis, motor deficit [odds ratio (OR) 5.8; 95% CI 2.98-11.42; P < 0.001], intracranial haemorrhage (OR 2.8; 95% CI 1.46-5.56; P = 0.002) and cortical vein thrombosis (OR 2.9; 95% CI 1.43-5.96; P = 0.003) were independent predictors of early epileptic seizures. Status epilepticus was an important source of morbidity and early mortality in patients with CVST in this study. Patients with focal motor deficits, cortical vein thrombosis and intracranial haemorrhage carried the highest risk for ES. Prophylactic antiepileptic treatment may be an option for these patients.
Our results confirm the value of percentage of macrophage area and percentage of MMP-9 area as markers of plaque instability and provide further evidence to support the hypothesis that statins reduce inflammatory responses and thereby stabilize carotid atherosclerotic plaques.
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