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Objective: To determine the frequency, predictors, and impact on outcome of epilepsy developing during the first year after subarachnoid hemorrhage (SAH). Methods: The authors prospectively analyzed 247 of 431 patients with SAH treated over a period of 5 years who were alive with follow-up at 12 months. Epilepsy was defined as two or more unprovoked seizures after hospital discharge. Results: New-onset epilepsy occurred in 7% (n = 17) of patients; an additional 4% (n = 10) had only one seizure after discharge. Independent predictors of epilepsy included subdural hematoma (OR 9.9, 95% CI 1.9 to 52.8) and cerebral infarction (OR 3.9, 95% CI 1.4 to 11.3). Unlike those without seizures, patients who developed epilepsy failed to experience functional recovery on the modified Rankin Scale (mRS) between 3 and 12 months after SAH. At 12 months epilepsy was independently associated with severe disability (score ≥ 3) on the mRS (OR 10.3, 95% CI 2.5 to 42.0), increased instrumental disability on the Lawton Instrumental Activities of Daily Living scale (OR 4.9; 95% CI 1.1 to 22.2), reduced quality of life on the Sickness Impact Profile (OR 4.5; 95% CI 1.1 to 18.0), and increased state anxiety on the Spielberger Anxiety Inventory (OR 4.8; 95% CI 1.1 to 20.4). Epilepsy was not associated with cognitive impairment, depression, or subjective life satisfaction. Conclusion: Epilepsy occurred in 7% of patients with SAH, was predicted by subdural hematoma and cerebral infarction, and was associated with poor functional recovery and quality of life. Our findings indicate that focal pathology, rather than diffuse injury from hemorrhage, is the principal cause of epilepsy after SAH.

Background and Purpose — Cerebral edema visualized by CT is often seen after subarachnoid hemorrhage (SAH). Inflammatory or circulatory mechanisms have been postulated to explain this radiographic observation after SAH. We sought to determine the frequency, causes, and impact on outcome of early and delayed global cerebral edema after SAH. Methods — We evaluated the presence of global edema on admission and follow-up CT scans in 374 SAH patients admitted within 5 days of onset to our Neurological Intensive Care Unit between July 1996 and February 2001. Using multivariate analysis, we identified predictors of global cerebral edema and evaluated the impact of global edema on outcome 3 months after onset with the modified Rankin Scale. Results — Global edema was present on admission CT scans in 8% (n=29) and developed secondarily in 12% (n=44) of the patients. Global edema on admission was predicted by loss of consciousness at ictus and increasing Hunt-Hess grade. Delayed global edema was predicted by aneurysm size >10 mm, loss of consciousness at ictus, use of vasopressors, and increased SAH sum scores. Thirty-seven percent (n=137) of the patients were dead or severely disabled (modified Rankin Scale 4 to 6) at 3 months. Death or severe disability was predicted by any global edema, aneurysm size >10 mm, loss of consciousness at ictus, increased National Institutes of Health Stroke Scale scores, and older age. Conclusions — Global edema is an independent risk factor for mortality and poor outcome after SAH. Loss of consciousness, which may reflect ictal cerebral circulatory arrest, is a risk factor for admission global edema, and vasopressor-induced hypertension is associated with the development of delayed global edema. Critical care management strategies that minimize edema formation after SAH may improve outcome.

Objective: To determine whether ketamine administration affects markers of inflammation in cardiac surgery with cardiopulmonary bypass (CPB) and to investigate differences between 2 low-dose ketamine regimens. Design: Prospective, randomized, placebo-controlled trial. Setting: Single-center university hospital. Participants: Patients undergoing cardiac surgery with CPB. Intervention: Patients (n = 50) were randomized to 1 of 3 groups: ketamine, 0.25 mg/kg (n = 15); ketamine, 0.5 mg/kg (n = 18);or placebo (n = 17) in a double-blind manner at the time of induction of general anesthesia. Measurements and Main Results: Serum C-reactive protein (CRP) and interleukin (IL)-6, IL-8, and IL-10 were measured at baseline, on intensive care unit (ICU) arrival, and on the first postoperative day (POD 1). Both ketamine doses decreased the serum IL-6 response at ICU arrival and POD 1 compared with placebo (p < 0.05). CRP was lower in the 0.5-mg/kg group than placebo on POD 1 (p = 0.003). IL-10 was lower in the ketamine groups (p = 0.01) at POD 1 compared with placebo; IL-8 levels were not affected by ketamine. Mean arterial pressure and systemic vascular resistance were higher at the end of surgery, arrival in the ICU, and POD 1 in the ketamine groups (p < 0.05). Conclusion: Low-dose ketamine (0.5 mg/kg) attenuates increases in CRP, IL-6, and IL-10 while decreasing vasodilatation after CPB.

Objective: Delayed cerebral ischemia (DCI) due to vasospasm is often undetected by clinical exam in patients with poor-grade subarachnoid hemorrhage (SAH). The purpose of this study was to identify quantitative EEG (qEEG) parameters that are most sensitive and specific for the detection of DCI in stuporous or comatose SAH patients. Methods: Of 78 consecutive Hunt‐Hess grade 4 or 5 SAH patients admitted to our Neuro-ICU over a 2-year period, 48 were eligible for participation and 34 were enrolled. Continuous EEG monitoring was performed from post-operative day 2 to post-SAH day 14. In each patient, 20 artifact-free, 1 min EEG-clips following an alerting stimulus were analyzed: 10 clips were obtained on monitoring day 1 (baseline), and 10 on days 4‐6 (follow-up). In DCI patients, follow-up clips were obtained after the onset of deterioration and before infarction had occurred. Twelve qEEG parameters were calculated using fast Fourier transformation; generalized estimating equations were used to compare ratios of change in qEEG parameters in patients with and without DCI. Results: Nine of 34 patients (26%) developed DCI. The alpha/delta ratio (alpha power/delta power; ADR) demonstrated the strongest association with DCI. The median decrease of ADR for patients with DCI was 24%, compared to an increase of 3% for patients without DCI (ZZ4.0, P!0.0001). Clinically useful cut-offs included 6 consecutive recordings with a O10% decrease in ADR from baseline (sensitivity 100%, specificity 76%) and any single measurement with a O50% decrease (sensitivity 89%, specificity 84%). Conclusions: A decrease in the ADR may be a sensitive method of detecting DCI, with reasonable specificity. This post-stimulation qEEG parameter may supplement the clinical exam in poor-grade SAH patients and may prove useful for the detection of DCI. Significance: Following ADRs may allow earlier detection of DCI and initiation of interventions at a reversible stage, thus preventing infarction and neurological morbidity. q 2004 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

To determine the effect that acute physiologic derangements have on outcome after subarachnoid hemorrhage (SAH) and to design a composite score summarizing these abnormalities.Prospective observational study.Neuroscience intensive care unit in a tertiary care academic center.Consecutive cohort of 413 patients with SAH admitted within 3 days of SAH onset with 3-month modified Rankin Scale scores.None.Among 20 physiologic variables assessed within 24 hrs of admission, four were independently associated with death or severe disability (modified Rankin Scale score, 4-6) at 3 months in a multivariate analysis: arterio-alveolar gradient of125 mm Hg (odds ratio [OR], 4.5; 95% confidence interval [CI], 2.7-7.6), serum bicarbonate of20 mmol/L (OR, 2.9; 95% CI, 1.6-5.6), serum glucose of180 mg/dL (OR, 2.8; 95% CI, 1.6-4.8), and mean arterial pressure of70 or130 mm Hg (OR, 1.7; 95% CI, 1.0-2.9). Based on their proportional contribution to outcome, we constructed the SAH Physiologic Derangement Score (SAH-PDS; range, 0-8) by assigning the following weights for abnormal findings: arterio-alveolar gradient, 3 points; bicarbonate, 2 points; glucose, 2 points; and mean arterial pressure, 1 point. After controlling for known predictors of death or severe disability (age, admission neurologic status, loss of consciousness, aneurysm size, intraventricular hemorrhage, and rebleeding), the SAH Physiologic Derangement Score was independently associated with poor outcome (OR, 1.3 for each point increase; 95% CI, 1.1-1.6). By contrast, the systemic inflammatory response syndrome score and the Acute Physiology and Chronic Health Evaluation II physiologic subscore did not add predictive value to the model.Acute interventions specifically targeting hypoxemia, metabolic acidosis, hyperglycemia, and cardiovascular instability may improve the outcome of SAH patients. The SAH Physiologic Derangement Score may prove useful for rapidly quantifying the severity of important physiologic derangements in acute SAH.

OBJECTIVE Cognitive decline occurs in 25% of patients after carotid endarterectomy (CEA). Elevated serum concentrations of S-100B and neuron-specific enolase (NSE) occur after stroke, and serum S-100B levels at 24 hours are associated with clinical outcome after both stroke and CEA. We hypothesized that we could detect acute elevations in serum levels of these markers obtained intraoperatively from the jugular bulb (JB) and that these elevations would predict cognitive dysfunction postoperatively as measured by neuropsychometric test performance. METHODS Forty-three patients scheduled for elective CEA were assessed with a battery of neuropsychometric tests before and 1 day after surgery. Before the carotid artery was clamped, a 6-French Fogarty catheter was inserted into the facial vein and threaded 6 cm rostrally into the JB. Serum samples were withdrawn from this catheter and simultaneously from a radial arterial catheter (A-line) at three time points: before clamping, 15 minutes into clamping, and after unclamping the carotid artery. Concentrations between groups were compared by analysis of variance and paired t tests. RESULTS Total deficit scores were significantly worse in 13 (30%) of the 43 patients 1 day after surgery. There was a trend toward elevations in JB concentrations of S-100B relative to A-line levels 15 minutes after cross-clamping (11% elevation, P = 0.079, paired t test). In addition, 15 minutes after clamping of the carotid artery, levels of S-100B from the JB were significantly elevated compared with levels at baseline (P = 0.040, one-way analysis of variance). No significant changes were found between any time point in levels of S-100B from the A-line blood or of NSE from either the JB or the A-line. Subtle cognitive decline after CEA was not correlated with intraoperative levels of S-100B or NSE, but there was a weak, statistically nonsignificant, association between a rise in 15-minute S-100B levels and cognitive injury that was not seen with JB samples. CONCLUSION Although intraoperative levels of S-100B and NSE from the JB failed to predict cognitive injury, carotid cross-clamping, independent of injury, seems to be associated with early elevations in S-100B.