Background and Purpose-Mild alterations in temperature have prominent effects on ischemic cell injury and stroke outcome. Elevated core body temperature (CBT), even if mild, may exacerbate neuronal injury and worsen outcome, whereas hypothermia is potentially neuroprotective. The antipyretic effects of acetaminophen were hypothesized to reduce CBT. Methods-This was a randomized, controlled clinical trial at 2 university hospitals. Patients were included if they had stroke within 24 hours of onset of symptoms, National Institutes of Health Stroke Scale (NIHSS) score Ն5, initial CBT Ͻ38.5°C, and white blood cell count Ͻ12 600 cells/mm 3 ; they were excluded if they had signs of infection, severe medical illness, or contraindication to acetaminophen. CBT was measured every 30 minutes. Patients were randomized to receive acetaminophen 650 mg or placebo every 4 hours for 24 hours. The primary outcome measure was mean CBT during the 24-hour study period; the secondary outcome measure was the change in NIHSS. Results-Thirty-nine patients were randomized. Baseline CBT was the same: 36.96°C for acetaminophen versus 36.95°Cfor placebo (Pϭ0.96). During the study period, CBT tended to be lower in the acetaminophen group (37.13°C versus 37.35°C), a difference of 0.22°C (95% CI, Ϫ0.08°C to 0.51°C; Pϭ0.14). Patients given acetaminophen tended to be more often hypothermic Ͻ36.5°C (OR, 3.4; 95% CI, 0.83 to 14.2; Pϭ0.09) and less often hyperthermic Ͼ37.5°C (OR, 0.52; 95% CI, 0.19 to 1.44; Pϭ0.22). The change in NIHSS scores from baseline to 48 hours did not differ between the groups (Pϭ0.93). Conclusions-Early administration of acetaminophen (3900 mg/d) to afebrile patients with acute stroke may result in a small reduction in CBT. Acetaminophen may also modestly promote hypothermia Ͻ36.5°C or prevent hyperthermia Ͼ37.5°C. These effects are unlikely to have robust clinical impact, and alternative or additional methods are needed to achieve effective thermoregulation in stroke patients.

Background and Purpose-The feasibility, safety, and efficacy of intravenous tissue plasminogen activator (t-PA) for patients with acute ischemic stroke in clinical practice need to be assessed. Methods-We initiated a prospective open-label study at a university hospital and two community hospitals in Houston, Tex, immediately after the publication of the National Institute of Neurological Disorders and Stroke (NINDS) t-PA study. A total of 30 patients, age 32 to 90 years, were treated with 0.9 mg/kg of intravenous t-PA (maximum dose, 90 mg) within 3 hours of acute ischemic stroke between December 1995 and December 1996. Results-Six percent (6%) of all patients hospitalized with ischemic stroke received intravenous t-PA at the university hospital and 1.1% at the community hospitals. The rates of total, symptomatic, and fatal intracerebral hemorrhage were 10%, 7%, and 3%. Thirty-seven percent (37%) of patients recovered to fully independent function. The average time from stroke onset to emergency department arrival was 57 minutes; emergency department arrival to computed tomography scan 41 minutes; and computed tomography scan to administration of treatment 59 minutes. Conclusions-When treatment guidelines are carefully followed in an urban hospital setting, intravenous t-PA for acute ischemic stroke is feasible and shows safety and efficacy comparable to the results of the NINDS study. (Stroke. 1998;29:18-22.)

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Hemorrhage is the major complication of IV recombinant tissue plasminogen activator (rt-PA) treatment for stroke. We report three patients with mild or indistinct cardiac symptoms prior to thrombolysis in whom hemodynamically significant cardiac tamponade occurred after treatment with rt-PA. Acute ischemic stroke patients may have undetected myocardial or pericardial disease that may pose a risk for hemopericardium and life-threatening tamponade after treatment with rt-PA.