The authors evaluated the 60-Second Test (SST), a brief test of mental concentration, as a supplement to the Glasgow Coma Scale (GCS) for monitoring verbally responsive patients in the neuro-intensive care unit. The SST demonstrated excellent reliability and was abnormal in 79% of patients assigned a top GCS score of 15. However, both tests had poor responsiveness to clinically identified changes in level of consciousness (LOC). The SST is sensitive to subtle alterations in LOC but, like the GCS, may have limitations as a monitoring tool in the neurocritical care setting.

PURPOSE:Carotid endarterectomy (CEA) after acute stroke is generally delayed 6 to 8 weeks because of fear of stroke progression. This delay can result in an interval stroke rate of 9% to 15%. We analyzed our results with CEA performed within 1 to 4 weeks of stroke.METHODS:Records for all patients undergoing CEA after stroke between 1980 and 2001 were analyzed. Perioperative evaluation included carotid duplex scanning or angiography, and head computed tomography or magnetic resonance imaging. All patients with nonworsening neurologic status, additional brain territory at risk for recurrent stroke, and severe ipsilateral carotid stenosis underwent CEA. Patients were grouped according to time of CEA after stroke: group 1, first week; group 2, second week; group 3, third week; group 4, fourth week. Statistical analysis was performed with the chi(2) test, logistic regression, and analysis of variance.RESULTS:Two hundred twenty-eight patients underwent CEA within 1 to 4 weeks of stroke. Perioperative permanent neurologic deficits occurred in 2.8% of patients in group 1 (72 procedures), 3.4% of patients in group 2 (59 procedures), 3.4% of patients in group 3 (29 procedures), and 2.6% of patients in group 4 (78 procedures). There was no relationship between location or size of preoperative infarct and time of surgery. Only preoperative infarct size correlated with probability of neurologic deficit after CEA (P <.05).CONCLUSION:Incidence of postoperative stroke exacerbation is similar at all intervals. The results are within acceptable limits for treatment of symptomatic carotid stenosis. CEA may be performed within 1 month of stroke with similar results at all intervals during this period.

Background— Cognitive dysfunction is a common and disabling sequela of subarachnoid hemorrhage (SAH). Although several clinical and radiographic findings have been implicated in the pathogenesis of cognitive dysfunction after SAH, few prospective studies have comprehensively and simultaneously evaluated these risk factors. Methods— Between July 1996 and March 2000, we prospectively evaluated 113 of 248 consecutively admitted nontraumatic SAH patients alive at 3 months with a comprehensive neuropsychological evaluation. Summary scores for 8 cognitive domains were calculated to express test performance relative to the entire study population. Clinical and radiographic variables associated with domain-specific cognitive dysfunction were identified with forward stepwise multiple regression, with control for the influence of demographic factors. Results— The study participants were younger (P =0.005), less often white (P =0.006), and had better 3-month modified Rankin scores (P =0.001) than those who did not undergo neuropsychological testing. The proportion of subjects who scored in the impaired range (>2 SD below the normative mean) on each neuropsychological test ranged from 10% to 50%. Predictors of cognitive dysfunction in 2 or more domains in the multivariate analysis included global cerebral edema (4 domains), left-sided infarction (3 domains), and lack of a posterior circulation aneurysm (2 domains). Other variables consistently associated with cognitive dysfunction in the univariate analysis included admission Hunt-Hess grade >2 and thick SAH in the anterior interhemispheric and sylvian fissures. Conclusions— Global cerebral edema and left-sided infarction are important risk factors for cognitive dysfunction after SAH. Treatment strategies aimed at reducing neurological injury related to generalized brain swelling, infarction, and clot-related hemotoxicity hold the best promise for improving cognitive outcomes after SAH.

Background: Cognitive dysfunction is the most common form of neurologic impairment after subarachnoid hemorrhage (SAH). Objective: To evaluate the impact of global and domain-specific cognitive impairment on functional recovery and quality of life (QOL) after SAH. Methods: One hundred thirteen patients (mean age 49 years; 68% women) were evaluated 3 months after SAH. Three simple tests of global mental status and neuropsychological tests to assess seven specific cognitive domains were administered. Four aspects of outcome (global handicap, disability, emotional status, and QOL) were compared between cognitively impaired and unimpaired patients with analysis-of-covariance models controlling for age, race/ethnicity, and education. Multiple linear regression was used to evaluate the relative contribution of global and domain-specific cognitive status for predicting concurrent modified Rankin Scale (mRS) and Sickness Impact Profile (SIP) scores. Results: Impairment of global mental status on the Telephone Interview of Cognitive Status (TICS) was associated with poor performance in all seven cognitive domains (all p < 0.0005) and was the only cognitive measure associated with poor recovery in all four aspects of outcome (all p ≤ 0.005). Cognitive impairment in four specific domains was also associated with functional disability or reduced QOL. After accounting for global cognitive impairment with the TICS, however, neuropsychological testing did not contribute additional predictive value for concurrent mRS or SIP total scores. Conclusions: Cognitive impairment impacts broadly on functional status, emotional health, and QOL after SAH. The TICS may be a useful alternative to more detailed neuropsychological testing for detecting clinically relevant global cognitive impairment after SAH.

OBJECTIVE:Guglielmi detachable coil (GDC) embolization may be used to prevent early rebleeding after aneurysmal subarachnoid hemorrhage, but anticoagulation and induced hypertension may increase this risk. We sought to determine retrospectively the relationship between levels of induced hypertension and anticoagulation and incidence of rebleeding in GDC-treated patients. METHODS:Twenty-five consecutive patients with acute (<14 days) subarachnoid hemorrhage who underwent GDC embolization were retrospectively analyzed with regard to percent obliteration of an aneurysm on postprocedure angiogram, the duration and intensity of anticoagulation, the duration and level of induced hypertension, and the frequency of thromboembolic and rebleeding complications. RESULTS:Complete angiographic obliteration of the aneurysm was achieved in five cases (20%). In some cases (n = 2), only the dome of the aneurysm was coiled to allow eventual surgical clipping. Heparin was given to 23 patients (92%) for an average of 6 days (range, 8 hrs to 22 days); the mean dose was 588 units/hr, and the mean partial thromboplastin time was 37 secs. Seven patients (28%) were treated with vasopressors for symptomatic vasospasm for a mean duration of 5 days (range, 8 hrs to 9 days); mean arterial blood pressure averaged 118 mm Hg, and peak systolic blood pressures ranged from 195 to 250 mm Hg. There were no episodes of aneurysm rebleeding. Three patients (12%) suffered intraoperative thromboembolic complications, which in one instance was fatal; two of these cases were associated with subtherapeutic partial thromboplastin time values. CONCLUSION:Induced hypertension (mean arterial blood pressure, 120 mm Hg) and heparinization do not appear to increase the risk of early rebleeding after GDC embolization. In a select group of patients, use of anticoagulation in the immediate perioperative period to prevent thromboembolic complications appears to be safe.

Five cases of presumed nicotine withdrawal delirium among brain-injured patients treated in a neurologic intensive care unit are presented. Each patient had a history of heavy tobacco use and experienced dramatic and sustained clinical improvement within hours of transdermal nicotine replacement. These preliminary observations suggest that nicotine withdrawal may be an under-recognized cause of delirium in patients with acute brain injury.

Background and Purpose-Thick cisternal clot on CT is a well-recognized risk factor for delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH). Whether intraventricular hemorrhage (IVH) or intracerebral hemorrhage (ICH) predisposes to DCI is unclear. The Fisher CT grading scale identifies thick SAH but does not separately account for IVH or ICH. Methods-We studied 276 consecutively admitted patients with an available admission CT scan performed within 72 hours of onset. Demographic, clinical, laboratory, and neuroimaging data were recorded, and the amount and location of SAH, IVH, and ICH on admission CT scans were quantified. The relationship between these variables and DCI was analyzed separately and in combination with multiple logistic regression. Results-DCI developed in 20% of patients (54 of 276). Among SAH variables, thick clot completely filling any cistern or fissure was the best predictor of DCI (P = 0.008), and among IVH variables, blood in both lateral ventricles was most predictive (P = 0.001). These variables had independent predictive value for DCI in a multivariate analysis of CT findings, and both were included in a final multivariate model when evaluated in conjunction with other clinical risk factors: IVH (OR 4.1, 95% CI 1.7 to 9.8), SAH (OR 2.3, 95% Cl 1.5 to 9.5), mean arterial pressure >112 min Hg (OR 4.9, 95% CI 2.1 to 11.4), and transcranial Doppler mean velocity >140 cm/s within 5 days of hemorrhage (OR 3.8, 95% CI 1.5 to 9.5). Similar results were obtained in a repeat analysis with infarction due to vasospasm as the dependent variable. Conclusions-SAH completely filling any cistern or fissure and IVH in the lateral ventricles are both risk factors for DCI, and their risk is additive. We propose a new SAH rating scale that accounts for the independent predictive value of subarachnoid and ventricular blood for DCL.

BACKGROUND AND PURPOSE:Hospital mortality rates of 50% to 90% have been reported for stroke patients treated with mechanical ventilation. These data have raised serious questions about the cost-effectiveness of this intervention. We sought to determine how often stroke patients are mechanically ventilated, identify predictors of 30-day survival among ventilated patients, and evaluate the cost-effectiveness of this intervention.METHODS:We identified mechanically ventilated patients in a population-based multiethnic cohort of 510 incidence stroke patients who were hospitalized between July 1993 and June 1996. Factors affecting 30-day survival were identified in a multiple logistic regression analysis. We calculated the cost per patient discharged alive, life-year saved, and quality-adjusted life-year saved using a zero-cost, zero-life assumption.RESULTS:Ten percent of patients (n=52) were mechanically ventilated. Thirty-day mortality was 65% overall and did not differ significantly by stroke subtype. Glasgow Coma Scale score on the day of intubation (P:<0.01) and subsequent neurological deterioration (P:=0.02) were identified as predictors of 30-day mortality. The cost (1996 US dollars) of hospitalization per patient discharged alive was $89 400; the cost per year of life saved was $37 600; and the cost per quality-adjusted life-year saved was $174 200. Functional status of most survivors was poor; at 6 months, half were severely disabled and completely dependent. In a worst-case scenario of quality of life preferences, mechanical ventilation resulted in a net deficit of meaningful survival.CONCLUSIONS:Two thirds of mechanically ventilated stroke patients die during their hospitalization, and most survivors are severely disabled. Survival is particularly unlikely if patients are deeply comatose or clinically deteriorate after intubation. In our multiethnic urban population, mechanical ventilation for stroke was relatively cost-effective for extending life but not for preserving quality of life.