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)-α 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-α were determined in plasma and cerebrospinal fluid (CSF; n=81) obtained on admission. Results —Eighty-three patients (35.9%) deteriorated within the first 48 hours. IL-6 in plasma (>21.5 pg/mL; OR 37.7, CI 11.9 to 118.8) or in CSF (>6.3 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-α 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.

Objective: To identify potential predictors of and factors associated with early neurologic deterioration (END) in primary intracerebral hemorrhage (ICH). Methods: Two hundred sixty-six patients with spontaneous supratentorial ICH admitted within 12 hours of stroke onset were investigated in a multicenter, prospective study. Sixty-one clinical, biochemical, and neuroimaging variables were registered on admission, and 37 clinical and neuroimaging variables were registered at 48 hours. The volumes of the ICH and peripheral edema on admission and at 48 hours were measured on CT scan. Stroke severity and functional outcome were evaluated with the Canadian Stroke Scale (CSS) and modified Rankin Scale. END was diagnosed when the CSS score decreased ≥1 points between admission and 48 hours. With use of logistic regression analyses, baseline variables that predicted END and factors measured after the early acute phase and associated with END were investigated. Results: END occurred in 61 (22.9%) patients. Body temperature of >37.5 °C (odds ratio [OR] 24.5; 95% CI 4.8 to 125), neutrophil count (by 1,000-unit increase; OR 2.1; 95% CI 1.6 to 2.6), and serum fibrinogen levels of >523 mg/dL (OR 5.6; 95% CI 1.9 to 16.2) on admission were independent predictors of END. Among the factors recorded at 48 hours, early ICH growth (OR 4.3; 95% CI 1.3 to 14.5), intraventricular bleeding (OR 2.6; 95% CI 1.4 to 5.0), and highest systolic blood pressure (by 10-unit increase; OR 1.17; 95% CI 1.02 to 1.32) were associated with END in multivariate analyses. Conclusions: Clinical and biologic markers of the inflammatory reaction on admission are predictors of subsequent END, whereas early ICH growth, intraventricular bleeding, and high systolic blood pressure within 48 hours are factors associated with END in patients with spontaneous ICH.

Background and Purpose— Studies on the relation between blood pressure (BP) and stroke outcome have shown contradictory results. We explored the association of systolic (SBP) and diastolic (DBP) BP during acute stroke with early neurological deterioration, infarct volume, neurological outcome, and mortality at 3 months. Methods— We included 304 patients with acute ischemic stroke. SBP and DBP on admission and on the first day were the average values of all readings obtained in the emergency department and during a 24-hour period after patient allocation in the stroke unit. Results— A U-shaped effect was observed: for every 10 mm Hg ≤180 mm Hg of SBP, the risk of early neurological deterioration, poor outcome, and mortality increased by 6%, 25%, and 7%, respectively, whereas for every 10 mm Hg >180 mm Hg, the risk of early neurological deterioration increased by 40% and the risk of poor outcome increased by 23%, with no effect on mortality. Mean infarct volume increased 7.3 and 5.5 cm ³ for every 10 mm Hg ≤180 and >180 mm Hg. A similar pattern was found in patients with DBP ≤100 or >100 mm Hg. These effects disappeared after adjustment for the use of antihypertensive drugs and BP drop >20 mm Hg within the first day, with the latter being the more important prognostic factor of poor outcome. Conclusions— High and low SBP and DBP, as well as a relevant drop in BP, are associated with poor prognosis in patients with ischemic stroke.

Background and Purpose— The optimal management of blood pressure (BP) in acute stroke remains unclear. For ischemic stroke treated with intravenous thrombolysis, current guidelines suggest pharmacological intervention if systolic BP exceeds 180 mm Hg. We determined retrospectively the association of BP and antihypertensive therapy with clinical outcomes after stroke thrombolysis. Methods— The SITS thrombolysis register prospectively recorded 11 080 treatments from 2002 to 2006. BP values were recorded at baseline, 2 hours, and 24 hours after thrombolysis. Outcomes were symptomatic (National Institutes of Health Stroke Scale score deterioration ≥4) intracerebral hemorrhage Type 2, mortality, and independence at (modified Rankin Score 0 to 2) 3 months. Patients were categorized by history of hypertension and antihypertensive therapy within 7 days after thrombolysis: Group 1, hypertensive treated with antihypertensives (n=5612); Group 2, hypertensive withholding antihypertensives (n=1573); Group 3, without history of hypertension treated with antihypertensives (n=995); and Group 4, without history of hypertension not treated with antihypertensives (n=2632). For 268 (2.4%) patients, these data were missing. Average systolic BP 2 to 24 hours after thrombolysis was categorized by 10-mm Hg intervals with 100 to 140 used as a reference. Results— In multivariable analysis, high systolic BP 2 to 24 hours after thrombolysis as a continuous variable was associated with worse outcome ( P <0.001) and as a categorical variable had a linear association with symptomatic hemorrhage and a U-shaped association with mortality and independence with systolic BP 141 to 150 mm Hg associated with most favorable outcomes. OR (95% CI) from multivariable analysis showed no difference in symptomatic hemorrhage (1.09 [0.83 to 1.51]; P =0.58) and independence (1.03 [0.93 to 1.10]; P =0.80) but lower mortality (0.82 [0.73 to 0.92]; P =0.0007) for Group 1 compared with Group 4. Group 2 had a higher symptomatic hemorrhage (1.86 [1.34 to 2.68]; P =0.0004) and mortality (1.62 [1.41 to 1.85]; P <0.0001) and lower independence (0.89 [0.80 to 0.99]; P =0.04) compared with Group 4. Group 3 had similar results as Group 1. Conclusions— There is a strong association of high systolic BP after thrombolysis with poor outcome. Withholding antihypertensive therapy up to 7 days in patients with a history of hypertension was associated with worse outcome, whereas initiation of antihypertensive therapy in newly recognized moderate hypertension was associated with a favorable outcome.

Background and Purpose —The association between hyperthermia and early neurological deterioration, increased morbidity, and mortality in acute ischemic stroke is well known. However, the timing at which the cerebral lesion may be aggravated by high temperature has not been firmly established. The aim of this study was to determine the prognostic value of body temperature measured at different times after onset of stroke. Methods —Axillary temperature was recorded every 2 hours for 72 hours in 260 patients with a hemispheric cerebral infarction of 37.5°C in any of the assessments). Stroke severity was quantified with the Canadian Stroke Scale on admission. The relationship between the highest temperature recorded in each 6-hour interval from stroke onset and stroke outcome (Canadian Stroke Scale and Barthel Index at 3 months) or infarct volume was evaluated by correlation analyses. The importance of the time at which hyperthermia was first detected was assessed by logistic regression analysis. Results —During the first 72 hours, 158 patients (60.8%) had hyperthermia, and in 57.6% of them an infectious cause was identified. Mortality rate at 3 months was 1% in normothermic patients and 15.8% in hyperthermic patients ( P <0.001). The correlation coefficients between the final infarct volume, Canadian Stroke Scale and Barthel Index scores at 3 months, and each temperature recording decreased progressively over time from symptom onset. Hyperthermia initiated within the first 24 hours from stroke onset, but not afterward, was independently related to larger infarct volume (odds ratio [OR]=3.23, 95% CI=1.63 to 6.43; P <0.001) and higher neurological deficit (OR=3.06, 95% CI=1.70 to 5.53; P <0.001) and dependency (OR=3.41, 95% CI=1.69 to 6.88; P =0.002) at 3 months. The infectious origin of hyperthermia was not associated with poorer outcome or greater infarct volume. Conclusions —The relationship between brain damage and high temperature is greater the earlier the increase in temperature occurs. However, only body temperature within the first 24 hours from stroke onset is associated with poor outcome and large cerebral infarcts.