Cerebral necrosis following stroke exposes brain antigens to the immune system, potentially initiating an antibody response. The authors measured levels of antibodies to specific neuronal antigens, neurofilaments (NF), and a ubiquitous antigen, cardiolipin (CL), in 45 patients following an acute first-ever stroke, within 48 hours, and 1, 3, and 6 months later. The mean levels of anti-NF antibodies were elevated compared with baseline at 1, 3, and 6, months (p = 0.012, 0.002, and 0.003 by paired t-test). Anti-CL levels did not change significantly.

Our data indicate that SBI do not predict the development of dementia after stroke.

This registry allows the study of the risk factors, natural history, and clinical manifestations of stroke in different ethnic groups.

Despite its low efficacy, aspirin is the most widely used drug for secondary stroke prevention. The reasons why stroke recurs while patients are on aspirin are unknown. We have analyzed a series of patients who had recurrent strokes while on aspirin. Out of 2231 consecutive patients who were admitted to the Tel Aviv Medical Center from May 1988 through December 1992 with the diagnosis of ischemic stroke, 129 admissions were due to recurrent ischemic strokes while the patients were already on aspirin, and these were defined as aspirin failures. The clinical characteristics of those patients in whom aspirin treatment failed were compared with three control groups, each comprising 129 patients who had had only a single ischemic stroke and were then taking aspirin. One control group was matched for aspirin dose and date of first stroke; another control group was matched for age, sex, and date of first stroke; and a third control group was matched for age, sex, date of first stroke, and aspirin dose. Statistical analysis was carried out by two-tailed Student's t test and chi 2 test. The average period until stroke was longer for patients on higher aspirin doses. Patients matched for aspirin dose and date of first stroke did not differ significantly in age (72.4 years in aspirin failures versus 74.2 years in the first control group) and sex (89 versus 94 men, respectively). Matching for age, sex, and date of first stroke but not for aspirin dose demonstrated a trend toward high frequency of aspirin failure in patients taking lower doses of aspirin (chi 2 test for trend = 3.5; P = .06). Comparison of aspirin-failure patients with a control group matched for age, sex, date of first ischemic stroke, and aspirin dose demonstrated that these patients more commonly had statistically significant hyperlipidemia (odds ratio, 2.6; 95% confidence interval, 1.0 to 6.8; P = .04) and ischemic heart disease (odds ratio, 2.3; 95% confidence interval, 1.3 to 3.9; P = .002). We conclude that age and sex do not influence the efficacy of aspirin. Lower aspirin dose in patients with stroke recurrence suggests that aspirin doses of 500 mg daily or more should be used in secondary stroke prevention. Hyperlipidemia and ischemic heart disease are risk factors for stroke recurrence despite aspirin treatment, which requires further clinical and laboratory evaluation.

Background: It is uncertain whether deterioration after acute ischemic stroke is neurological and/or systemic (somatic) in origin. Methods: 442 consecutive patients admitted with first-ever ischemic stroke (FIS) were assessed by the Unified Neurological Stroke Scale (UNSS) at admission, on hospitalization days 1, 2 and 3 and before discharge. Results: Among 71/442 (16.1%) patients deteriorated during hospitalization, the worsening from stroke onset was early (≤72 h) in 67 (94.4%) of them. The majority (57/71, 80.3%) had CT-confirmed cerebral causes and 14/71 (19.7%) had systemic causes. The causes of late deterioration were exclusively systemic. In the logistic regression analysis the initial mean UNSS score was the only significant independent predictor of stroke deterioration (p < 0.0001). Conclusions: Early clinical deterioration in FIS patients results from infarct-inherent mechanisms while late stroke deterioration is due primarily to systemic factors. An initially severe neurological deficit might predict further decline.