Background and Purpose-The prognostic influences of fibrinogen and C-reactive protein (CRP) levels and their relations in ischemic stroke have not been well described. The aim of this study was to investigate and compare the 1-year prognostic influences of fibrinogen and CRP levels on outcome in ischemic stroke. Methods-Fibrinogen and CRP were determined within 24 hours after stroke and related to 1-year outcome in 128 patients with first-ever ischemic stroke. The Kaplan-Meier technique was applied in survival analysis. Multiple logistic regression analysis was used to evaluate the associations between risk factors and outcome. Results-The probabilities of death or new vascular event were 21.1%, 27.9%, and 51.7% (Pϭ0.0172, 2 for trend), respectively, in patients stratified by tertiles of fibrinogen (Ͻ3.78, 3.78 to 6.17, and Ͼ6.17 g/L). The probabilities of a primary end point were 12.1%, 29.7%, and 54.8% (Pϭ0.0004), respectively, after stratification of patient data by tertiles of CRP level (Ͻ5, 5 to 33, and Ͼ33 mg/L). In multiple logistic regression analysis, higher CRP levels (odds ratio, 2.39; 95% CI, 1.28 to 4.49; Pϭ0.0066) and stroke severity on the Canadian Neurological Stroke Scale (odds ratio, 2.37; 95% CI, 1.01 to 5.58; Pϭ0.0472) were independently associated with death or new vascular event.Conclusions-Increased levels of CRP are associated with a worse outcome in patients with ischemic stroke. The increased risk associated with elevated CRP levels is independent of the prognostic influence of fibrinogen.

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Background and Purpose-There is growing evidence of the prognostic importance of C-reactive protein (CRP) in ischemic stroke. However, the independent value of CRP at different stages after stroke has not been established. Therefore, we assessed the prognostic values of CRP in ischemic stroke. We also compared the relation of CRP at admission and discharge with 1-year outcome. Methods-One hundred ninety-three patients were included in a derivation set (nϭ128) and a validation set (nϭ65). Serum CRP was measured, within 24 hours after index ischemic stroke, within 48 to 72 hours, and at hospital discharge. We examined the association between the level of CRP at different stages after stroke and outcome. We adjusted for the possible confounding effect using a multivariate Cox proportional hazard model. Results-A cutoff point of 1.5 mg/dL for CRP at discharge provided optimum sensitivity and specificity for adverse outcome, based on the receiver operator curves.

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the NINDS rt-PA Stroke Trial Study Group. Agreement and variability in the interpretation of early CT changes in stroke patients qualifying for intravenous rtPA therapy. Stroke. 1999;30: 1528 -1533. 3. Schriger D, Kalafut M, Starkman S, Krueger M, Saver J. Cranial computed tomography interpretation in acute stroke: physician accuracy in determining eligibility for thrombolytic therapy.

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Abstract-Background: Global brain atrophy rate calculated from serial MRI scans may be a surrogate marker of Alzheimer disease (AD) progression. Few studies have assessed atrophy in AD over short intervals. Methods: Thirty-eight patients with AD and 19 control subjects had MRI scans at baseline, 6 months, and 1 year. Ventricular change and whole-brain volume loss were calculated directly from the regions manually outlined on registered scans and using the automated (boundary shift integral [BSI]) technique. Sample sizes required to power placebo-controlled treatment trials over 6 months and 1 year were calculated using these techniques. Results: Increased rates of ventricular expansion and whole-brain atrophy were seen in AD compared with control subjects at both 6 and 12 months using manual and automated techniques (p Ͻ 0.001). Using the BSI consistently reduced measurement variability especially for whole-brain change. In clinical trials, at 6 months, significantly fewer patients would be required using the ventricular BSI (VBSI) compared with the brain BSI (BBSI) (e.g., 165 vs 410 per arm to provide 90% power to detect a 20% reduction in rate of change). At 1 year, sample size estimates were smaller than at 6 months, and the advantage of using VBSI instead of BBSI was less marked. Conclusions: In short-interval studies, using the ventricular boundary shift integral instead of the brain boundary shift integral may allow for disease-modifying effects to be demonstrated using significantly smaller sample sizes. This potential benefit must be balanced against the possibility that ventricular volumes may be more likely to be affected by factors other than neurodegeneration. NEUROLOGY 2005;65:119-124 Major efforts are under way to develop diseasemodifying agents for Alzheimer disease (AD); outcome measures that can distinguish diseasemodifying from symptomatic effects are therefore urgently required. Cerebral atrophy may be one such measure: a truly disease-modifying drug would be expected to slow excess atrophy in AD compared with placebo. Rates of global brain atrophy may be calculated in vivo from registered serially acquired MRI scans using either brain volume loss 1-5 or ventricular expansion [4][5][6][7] (table 1). To date, all but one 4 of these studies assessing atrophy rates in AD have done so over periods of Ն1 year. In this study, we assessed direct (boundary shift integral [BSI]) 1,8,9 and indirect (outlining) measures of brain volume and ventricular change in cohorts of patients with AD and normal control subjects studied prospectively over periods of 6 months and 1 year and estimated the effect of using ventricular and brain-based measures of atrophy on sample sizes that would be required in clinical trials over 6 months and 1 year.2 By comparing relative rates of brain and ventricular change in patients and control subjects, we also aimed to evaluate factors influencing the dynamics of whole-brain atrophy.