Background and Purpose-Increased mean platelet volume (MPV), indicating higher platelet reactivity, is associated with an increased risk of myocardial infarction. Higher levels of MPV have been found in patients with acute ischemic stroke than in control subjects. Data from smaller studies regarding an association between MPV and stroke severity and outcome have been controversial. If such an association exists, MPV might help to identify patients at increased risk of a severe course of acute cerebrovascular disease. Methods-Within a multicenter, cross-sectional study nested in a cohort, we analyzed the relation between MPV and stroke severity as determined by the modified Rankin Scale after 1 week in 776 patients with acute ischemic stroke or transient ischemic attack. By multivariate logistic regression modeling, we determined the influence of MPV on stroke severity, adjusting for potential confounding factors. Results-Patients within the highest quintile of MPV had a significantly higher risk of suffering a severe stroke, defined as modified Rankin Scale score of 3 to 6, compared with patients within the lowest quintile (odds ratioϭ2.6; 95% confidence interval, 1.6 to 4.1; PϽ0.001). This association remained significant after adjustment for possible confounding factors (odds ratioϭ2.2; 95% confidence interval, 1.2 to 4.0; Pϭ0.013). Conclusions-Our results indicate that an elevated MPV is associated with a worse outcome for acute ischemic cerebrovascular events independent of other clinical parameters.

Background and Purpose-Headache is a common symptom in acute ischemic and hemorrhagic stroke, but many aspects of its association with other clinical factors are controversial. Methods-We analyzed characteristics of headache symptoms at stroke onset and associations between headache at stroke onset and at several clinical parameters in 2196 patients experiencing ischemic stroke or transient ischemic attack within a multicenter hospital-based stroke registry. Results-Five hundred eighty-eight (27%) patients experienced headache at stroke onset. In a multivariate analysis, headache at stroke onset was positively associated with female sex, history of migraine, younger age, cerebellar stroke (but not with other brain stem locations), and blood pressure values on admission Ͻ120 mm Hg systolic and Ͻ70 mm Hg diastolic. It showed no significant association with stroke severity measured by the modified Rankin Scale at days 5 to 7 after the event, presumed etiology, or time of day. Conclusions-Our results, derived from a large number of systematically documented patients with acute ischemic cerebrovascular events, show no association of headache with stroke etiology or outcome. Our results indicate that the previously described association of headache with vertebrobasilar stroke is mainly because of its association with cerebellar stroke. We could confirm previously described associations of headache at stroke onset with younger age and a history of migraine, implicating a careful evaluation of young patients with a focal neurological deficit and a history of migraine to avoid misclassification as "complicated migraine." (Stroke. 2005;36:e1-e3.)

Background-Compelling evidence suggests that inflammation is fundamentally involved in the pathogenesis of atherosclerosis; however, temporal correlation between inflammation and morphological features of atherosclerosis progression has not been demonstrated unequivocally. Methods and Results-We prospectively studied 1268 consecutive patients who were initially asymptomatic with respect to carotid artery disease. Patients underwent serial carotid ultrasound investigations at baseline and after a follow-up interval of a median of 7.5 months (range 6 to 9 months), with measurement of carotid flow velocities and categorization of carotid arteries as 0% to 29%, 30% to 49%, 50% to 69%, 70% to 89%, or 90% to 99% stenosed or occluded.High-sensitivity C-reactive protein (hs-CRP) and serum amyloid A (SAA) were measured at baseline and follow-up.

Background and Purpose-The role of the factor V Leiden mutation (FVL) and the G20210A mutation of the prothrombin (factor II [FII]) gene for arterial thrombosis is not clear. Methods-We investigated the prevalence of these mutations in 468 patients with an acute stroke or transient ischemic attack (TIA) before the age of 60 years and in a healthy control population individually matched for age and gender. We also analyzed interactions between the mutations, gender, standard vascular risk factors, and stroke risk. Results-The prevalence of the FVL did not differ significantly between patients and control subjects. However, we found a significant interaction between the FVL, smoking, and risk of stroke in women: female smokers without FVL had a somewhat increased risk of stroke of 2.6 (95% CI, 1.5 to 4.6; Pϭ0.001) compared with nonsmoking noncarriers of the FVL. Stroke risk was markedly higher in female smokers who had the FVL (OR, 8.8; 95% CI, 2.0 to 38.0; Pϭ0.004) after multivariate adjustment. No such interaction was observed in men. In contrast, the frequency of the FII G20210A mutation was significantly higher in male patients compared with controls (6% versus 1%; adjusted OR, 6.1; 95% CI, 1.3 to 28.3; Pϭ0.021). In females, the prevalence of the mutation was 3% in both groups. We found no significant interactions of the FII G20210A mutation with other vascular risk factors and stroke risk. Conclusions-Our data indicate a highly increased risk of ischemic cerebrovascular events in women up to 60 years who smoke and have FVL. We also found evidence for an increased risk of stroke/TIA in men who have the FII G20210A mutation but not in women in this age group.

patients and 6560 control subjects from 6 case-control association studies conducted in the United States, Europe, and China. Genotyping was performed using the same immobilized probe typing system and meta-analyses were based on summary logistic regressions for each study. The primary analyses were fixed-effects meta-analyses adjusting for age and sex with additive, dominant, and recessive models of inheritance. Results-Although 7 polymorphisms showed a nominal additive association, none remained statistically significant after adjustment for multiple comparisons. In contrast, after stratification for hypertension, 2 lymphotoxin-alpha polymorphisms, which are in strong linkage disequilibrium, were significantly associated among nonhypertensive individuals: LTA 252AϾG (additive model; OR, 1.41 with 95% CI, 1.20 to 1.65; Pϭ0.00002) and LTA 26ThrϾAsn (OR, 1.19 with 95% CI, 1.06 to 1.34; Pϭ0.003). LTA 252AϾG remained significant after adjustment for multiple testing using either the false discovery rate or by permutation testing. The 2 single nucleotide polymorphisms showed no association in hypertensive subjects (eg, LTA 252AϾG, OR, 0.93; 95% CI, 0.84 to 1.03; Pϭ0.17). Conclusions-These