Background and Purpose-The mechanisms for clinical deterioration in patients with ischemic stroke are not completely understood. Several proinflammatory cytokines are released early after the onset of brain ischemia, but it is unknown whether inflammation predisposes to neurological deterioration. We assessed the implication of interleukin (IL)-6 and tumor necrosis factor (TNF)-␣ in early neurological worsening in ischemic stroke. Methods-Two hundred thirty-one patients consecutively admitted with first-ever ischemic cerebral infarction within the first 24 hours from onset were included. Neurological worsening was defined when the Canadian Stroke Scale (CSS) score fell at least 1 point during the first 48 hours after admission. IL-6 and TNF-␣ were determined in plasma and cerebrospinal fluid (CSF; nϭ81) obtained on admission. Results-Eighty-three patients (35.9%) deteriorated within the first 48 hours. IL-6 in plasma (Ͼ21.5 pg/mL; OR 37.7, CI 11.9 to 118.8) or in CSF (Ͼ6.3 pg/mL; OR 13.1, CI 2.2 to 77.3) were independent factors for early clinical worsening, with multiple logistic regression. The association was statistically significant in all ischemic stroke subtypes as well as in subjects with cortical or subcortical infarctions. IL-6 in plasma was highly correlated with body temperature, glucose, fibrinogen, and infarct volume. CSF and plasma concentrations of TNF-␣ were also higher in patients who deteriorated, but the differences observed did not remain significant on multivariate analysis. Conclusions-In addition to participating in the acute-phase response that follows focal cerebral ischemia, IL-6 levels on admission are associated with early clinical deterioration. The association between IL-6 and early neurological worsening prevails without regard to the initial size, topography, or mechanism of the ischemic infarction. (Stroke.

Background-Mechanisms involved in stroke progression are incompletely understood. Ischemic brain injury is characterized by acute local inflammatory response mediated by cytokines. Anti-inflammatory cytokines act in a feedback loop to inhibit continued proinflammatory cytokine production. We assessed the implication of interleukin (IL)-10 and IL-4 in deteriorating ischemic stroke. Methods-Two hundred thirty-one patients with ischemic stroke within the first 24 hours from onset were included.Neurological worsening was defined when the Canadian Stroke Scale score fell at least 1 point during the first 48 hours after admission. Anti-inflammatory cytokines were determined in plasma obtained on admission. Results-Eighty-three patients (35.9%) worsened within the first 48 hours after stroke onset. Significantly lower concentrations of IL-10 were found in patients with neurological worsening (PϽ0.05), but IL-4 levels were similar in patients with or without deterioration. Lower plasma concentrations of IL-10 (Ͻ6 pg/mL) were associated with clinical worsening on multivariate analysis (odds ratioϭ3.1, 95% CIϭ1.1 to 8.9) independently of hyperthermia, hyperglycemia, or neurological condition on admission. Further analysis disclosed that early worsening was independently associated with lower IL-10 plasma levels in patients with subcortical infarcts or lacunar stroke but not in patients with cortical lesions. Conclusions-Anti-inflammatory

Background and Purpose-The relevance of elevated blood pressure in acute ischemic stroke and its most appropriate management are unresolved. We aimed to evaluate the rate of functional recovery with relation to early blood pressure management in patients with ischemic stroke. Methods-Four hundred eighty-one consecutive ischemic stroke patients were admitted to the Neurology Service within 20.9Ϯ10.5 hours of symptoms onset as part of the Barcelona Downtown Stroke Registry, including 235 patients who received oral antihypertensive agents within Ͻ24 hours after stroke onset. Demographic, clinical (Mathew scale), and CT scan findings were collected prospectively. Mean arterial pressure (MAP) was recorded before hospital arrival and at 7 AM on days 1, 2, and 7 of hospitalization. The primary end point was complete functional recovery at day 7 defined as a score of 0 to 1 on the modified Rankin scale. Results-Two hundred fifty-two patients achieved complete recovery on day 7. Using logistic regression, independent predictors of complete recovery included mild impairment at stroke presentation, lack of history of hypertension, and absence of brain edema on CT scan. Also, a 20% to 30% drop in MAP on day 2 after stroke onset almost tripled the odds of full recovery (odds ratio, 2.9; 95% CI, 1.3 to 6.3). MAP tended to normalize after stroke in all subjects, more rapidly if hypotensive agents were administered. Brain edema was also less frequent in patients with a greater drop in blood pressure. Despite the fact that a drop in MAP Ͼ30% from baseline was observed in 49 patients, this preceded worsening stroke in only 4 patients. Conversely, worsening stroke occurred in 51 patients despite stable blood pressure. Conclusions-These results suggest that complete recovery in ischemic stroke is facilitated by a moderate blood pressure reduction when brain edema develops, most likely as the result of a more adequate cerebral perfusion pressure. Conversely, stroke worsening due to pharmacological hypoperfusion is exceptional. (Stroke. 1998;29:1850-1853.)

Infarction size and clinical severity in alert patients with nonseptic embolic stroke carries no additional bleeding complications after early anticoagulation. If anticoagulants are deemed necessary, treatment delay seems unjustified. However, rigorous monitoring of the aPTT is strongly advised to keep the level at 1.5 to 2 times control values.