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Background The National Institutes of Health Stroke Scale (NIHSS) is the most widespread clinical scale used in patients presenting with acute stroke. The merits of the NIHSS include simplicity, quickness, and agreement between clinicians. The clinical evaluation on posterior circulation stroke remains still a limit of NIHSS. Methods We assessed the application of a new version of NIHSS, the e-NIHSS (expanded NIHSS), adding specific elements in existing items to explore signs/symptoms of a posterior circulation stroke. A total of 22 consecutive patients with suspected vertebrobasilar stroke were compared with 25 patients with anterior circulation stroke using NIHSS and e-NIHSS. Results We compared the NIHSS and e-NIHSS scores obtained by the 2 examiners, in patients with posterior circulation infarct (POCI), using the Wilcoxon test. Patients with POCI evaluated with e-NIHSS had an average of 2 points higher than patients evaluated with classical NIHSS. The difference was statistically significant ( P Conclusions The NIHSS is a practical scale model, with high reproducibility between trained, different examiners, focused on posterior circulation strokes, with the same total score and number of items of the existing NIHSS. The e-NHISS could improve the sensitivity of NIHSS in posterior circulation stroke and could have an impact on clinical trials, as well as on outcomes. Further studies are needed to investigate a larger number of patients and the correlation between the e-NIHSS score and neuroimaging findings.

Objective: To determine whether low low-density lipoprotein cholesterol (LDL-C) but not high-density lipoprotein cholesterol (HDL-C) and triglyceride concentrations are associated with worse outcome in a large cohort of ischemic stroke patients treated with IV thrombolysis. Methods: Observational multicenter post hoc analysis of prospectively collected data in stroke thrombolysis registries. Because of collinearity between total cholesterol (TC) and LDL-C, we used 2 different models with TC (model 1) and with LDL-C (model 2). Results: Of the 2,485 consecutive patients, 1,847 (74%) had detailed lipid profiles available. Independent predictors of 3-month mortality were lower serum HDL-C (adjusted odds ratio [ adj OR] 0.531, 95% confidence interval [CI] 0.321–0.877 in model 1; adj OR 0.570, 95% CI 0.348–0.933 in model 2), lower serum triglyceride levels ( adj OR 0.549, 95% CI 0.341–0.883 in model 1; adj OR 0.560, 95% CI 0.353–0.888 in model 2), symptomatic ICH, and increasing NIH Stroke Scale score, age, C-reactive protein, and serum creatinine. TC, LDL-C, HDL-C, and triglycerides were not independently associated with symptomatic ICH. Increased HDL-C was associated with an excellent outcome (modified Rankin Scale score 0–1) in model 1 ( adj OR 1.390, 95% CI 1.040–1.860). Conclusion: Lower HDL-C and triglycerides were independently associated with mortality. These findings were not due to an association of lipid concentrations with symptomatic ICH and may reflect differences in baseline comorbidities, nutritional state, or a protective effect of triglycerides and HDL-C on mortality following acute ischemic stroke.

A case of a severe necrotizing vasculopathic skin lesions occurred in a 43 year old women affected by multiple sclerosis (MS) submitted to IFNb-lb has been described. A fter two months of therapy the patient presented, in injection sites of the abdomen, arms and legs, numerous ulcers. A biopsy of the lesions was performed and evidenced confluent necro sis of the superficial and deep skin tissue with mild infiltration by inflammatory cells and thrombosis in deep blood vessels. The IFNb-lb was immediately discontinued and therapy with corticosteroids was started. A fter 12 months from the onset of the adverse reaction, the skin vasculopathic lesions cicatrised leaving sclerotic areas on the abdomen. Neutralizing antibodies against IFNb-lb (NA Bs) were strongly positive at the onset of the skin ulcers and slowly decreased until the recovery. A possible role of NA Bs in the development of the skin lesions has been considered.

Intravenous thrombolysis is an effective treatment in acute stroke patients, but it increases the risk of intracerebral hemorrhages. Our aim is to establish if fibrinogen depletion increases the risk of intracerebral hemorrhage after intravenous thrombolysis for acute ischemic stroke.In 104 ischemic stroke patients, treated with intravenous thrombolysis, we assessed the rate of intracerebral hemorrhages documented by computed tomographic scan at 24 hours and within 7 days post-treatment. Fibrinogen levels were determined at 2 hours after therapy: patients were classified as belonging to "low fibrinogen group" if levels decreased to less than 2 g/L and/or by 25% or more. Fibrinogen levels and other known hemorrhagic risk factors were studied using univariate and multivariate analyses.During the first 7 days, an intracerebral hemorrhage was detected in 24 patients (23.1%), and only 6 of these (5.8%) experienced symptomatic bleeding; 41 patients were included in the low fibrinogen group. Among the 24 hemorrhages, 18 occurred in the low fibrinogen group and 6 in the "normal fibrinogen group": the bleeding rate in the low fibrinogen group was significantly higher (43.9%) than that in the normal fibrinogen group (9.5%; odds ratio [OR] 7.43, P.001). Univariate and multivariate analyses revealed that only clinical severity (OR 1.15, P.001) and hypofibrinogenemia (OR 7.47, P.001) were significantly associated with brain bleeding at 7 days and at 24 hours (P = .008).An early fibrinogen reduction seems to increase the risk of intracerebral hemorrhage after rtPA treatment in ischemic stroke. Fibrinogen assessment could be a rapid, inexpensive, and widely available tool to help the identification of patients at higher risk of bleeding.

Background: Aims of the study: to identify with echo color Doppler ultrasound of the supra-aortic vessels and transcranial color-coded duplex sonography (TCCD) various patterns of vessel occlusion within 3 h from stroke onset, to compare each group defined at the admission with clinical findings and outcome, and to study the recanalization process, independent of therapy. Methods: We enrolled 89 consecutive patients (mean age 68.9 years). Ultrasound evaluation was done within 3 h from stroke onset, and was repeated at 3–6 and 24–36 h, at day 5, and at 3 months. At admission, patients were divided into the following groups: internal carotid artery occlusions and stenoses (Results: Each subgroup differed significantly for baseline NIHSS (p < 0.0001), 3-month mortality (p = 0.0235), BI at day 5 (p = 0.0458) and mRS at 3 months (p = 0.0028), even after adjustment for treatment. T and tandem occlusions were the subgroups with the highest NIHSS scores and the poorest outcomes, and the same subgroups had the worst recanalization rates. Conclusions: TCCD in the acute setting of stroke patients allows identification of the presence and site of clots, prediction of outcome and study of the dynamic process of vessel recanalization, in both the acute phase and follow-up.