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Introduction: Treatment of elevated blood pressure after acute intracerebral hemorrhage (ICH) is controversial. There is a risk of hematoma expansion with elevated blood pressure, and risk of ischemia with blood pressure control. This study was done to determine the effect of blood pressure control on outcome., Methods: We retrospectively studied 122 patients with ICH. We collected 24-h blood pressure readings on all patients. The Glasgow Coma Score (GCS) at baseline and at 24 h was used to determine neurological deterioration (GCS decline > or = 2). Baseline computerized tomography (CT) scans were reviewed for hematoma volume, intraventricular hemorrhage, and location of hemorrhage. Drops in systolic blood pressure and mean arterial pressures over 24 h were divided in quartiles to determine the risk of neurological deterioration among quartiles. A logistic regression model was used to determine the association between variables of interest and neurological deterioration., Results: Neurological deterioration was observed in 12 patients (10%). Baseline blood pressure and GCS were only two variables significantly different among quartiles of blood pressure drop. Multivariable adjusted analysis for these variables demonstrated significant trend toward reduced neurological deterioration with maximum blood pressure drop (systolic or mean). The risk of neurological deterioration was significantly lower in the quartile of maximum drop of systolic (odds ratio [OR] 0.02, 95% confidence interval [CI] 0.0-0.68) or mean (OR 0.03, 95% CI 0.0-0.98) blood pressure when compared to the quartile with least drop., Conclusion: This study supports that reduction of blood pressure in patients with acute ICH is safe and suggests that aggressive reduction might reduce the risk of neurological deterioration in first 24 h of admission.

Background and Purpose: Dedicated stroke units are associated with improved patient outcomes after acute ischemic stroke in general. However, it is unknown whether the population of critically ill ischemic stroke patients admitted to the neurocritical care unit (NCCU) benefit from primary management by a specialized neurocritical care team (NCT). This study is intended to investigate such benefit., Methods: A retrospective chart review in a large academic university hospital identified 400 patients with acute ischemic stroke admitted to the NCCU, from January 1997 to April 2000, aged 65 +/- 14 years. We examined the short- and long-term outcomes of these patients before and after institution of a specialized NCT. We used logistic regression models to determine independent association between outcome and availability of NCT., Results: The presence of a NCT was associated with a decreased length of NCCU stay (2.9 +/- 2.0 vs. 3.7 +/- 2.9 days, P < 0.01), decreased length of hospital stay (7.5 +/- 4.7 vs. 9.9 +/- 7.6, P < 0.001), and increased proportion of home discharges (47% vs. 36%, P < 0.05). The only independent predictor of in-hospital and long-term mortality was the underlying severity of disease as determined by the APACHE III score., Conclusions: In critically ill acute ischemic stroke patients, institution of a dedicated NCT was associated with a reduction in resource utilization and improved patient outcomes at hospital discharge. Several factors including improved patient care protocols may explain this association.

Objective: New approaches are focusing on using a combination of medication that lyse fibrin and prevent aggregation of platelets to achieve higher rates of recanalization and improved clinical outcomes., Methods: A prospective, nonrandomized, open-label trial evaluated the safety of an escalating dose of reteplase in conjunction with intravenous abciximab (platelet glycoprotein IIb/IIIa inhibitor) in patients with acute ischemic stroke (3-6 h after symptom onset). The primary endpoint was symptomatic intracerebral hemorrhage at 24 to 72 hours, and secondary endpoints were partial or complete recanalization (> or = one grade improvement), early neurological improvement (decrease in National Institutes of Health Stroke Scale > or = 4 at 24 h), and favorable outcome at 1 month (defined by modified Rankin scale < or = 2)., Results: A total of 20 patients (mean age, 65 yr; 13 men) were recruited. Five patients were recruited in each of the escalating tiers of intra-arterial reteplase (0.5, 1, 1.5, and 2 units). Intravenous abciximab (0.25 mg/kg bolus followed by 0.125 mug/kg/min) was successfully administered in 18 out of 20 patients. The safety stopping rule was not activated in any of the tiers. One symptomatic intracerebral hemorrhage was observed in one of the 20 patients (in the 1-unit tier). Partial or complete recanalization was observed in 13 of the 20 patients. Thirteen patients demonstrated early neurological improvement, and favorable outcome at 1 month was observed in six patients., Conclusion: In this study, a combination of intra-arterial reteplase and intravenous abciximab was safely administered to patients with ischemic stroke presenting between 3 and 6 hours after symptom onset.

Objective: To review current advances in the treatment of critically ill neurologic patients, including specialized care by neurointensivists., Design: Review article., Main Discussion and Conclusions: Significant developments in the fields of neurology and neurosurgery have led to improved treatments for the critically ill neurologic patient. The major areas reviewed include neuromonitoring, disease-specific treatments, and specialized neurocritical care units and team. The current trend is for the application of the so-called multimodality neuromonitoring, which includes the use of several monitoring techniques, including intracranial pressure, brain electrophysiology, brain metabolism and oxygenation, and cerebral blood flow, among others. Many new therapies that have been introduced are discussed, including thrombolytic therapy for acute ischemic stroke, induced hypothermia for comatose survivors of cardiac arrest, and endovascular coiling for ruptured cerebral aneurysms. Lastly, the introduction of neurointensivists and neurocritical care units has been associated with reduced hospital mortality and resource utilization without changes in readmission rates or long-term mortality rates.

Background: Intra-arterial thrombolysis (IAT) for peri-coronary angiography (CA) stroke may be safe and efficacious. However, IAT may increase the risk of intracranial hemorrhage (ICH)., Methods: A retrospective study was performed involving 3 university hospitals. All peri-CA IAT-treated cases were identified. Patient demographics, stroke severity, angiographic findings, thrombolytic use, modified Rankin Scale (mRS), ICH, and mortality were determined., Results: A total of 21 patients with post-left CA stroke were treated with IAT (mean age 71.8+/-12.3 years). Arterial occlusion was found in 14 (66.7%) and 7 (33.3%) of the anterior and posterior circulation, respectively. Mean time-to-therapy was 36+/-12 minutes from the time the neurological deficit was noted. mRS < or =2 occurred in 10 of 21 (48%) patients. Patients with younger age and shorter time-to-IAT had more complete arterial recanalization and clinical recovery. Symptomatic ICH occurred in 3 (14%) cases, and 4 (19%) patients died., Conclusions: Peri-CA IAT appears to be feasible and safe without increased risk of symptomatic ICH and death when compared with the previously reported IAT literature.

Although transesophageal echocardiography (TEE) is a well-established tool in delineating the cardiac and aortic sources of emboli in stroke patients, its reproducibility in detecting aortic atherosclerosis (AA) that may lead to stroke is not well documented. The aim of this study is to demonstrate the inter- and intra-observer agreement in diagnosing AA based on the TEE study. During the study period, 2 echocardiographers read 32 TEE studies performed on a group of stroke patients. The AA was estimated by measuring the largest atheroma thickness in millimeters (mm). The intra-observers and intraclass correlation coefficients (ICC) were 0.97 and 0.85, respectively, for the 2 TEE observers. The inter-rater ICC coefficient between TEE readers was 0.91. In conclusion, TEE detected AA and defined high proportions of the morphological characteristics of atheroma with good reproducibility among inter and intra-observers.

Background and Purpose: The effect of vessel patency, following recombinant tissue plasminogen activator (rtPA) administration, on clinical outcome in acute ischemic stroke (AIS) has been controversial. We studied the effect of recanalization following intraarterial (IA) and intravenous/IA (IV/IA) rtPA on clinical outcome in AIS., Methods: Recanalization was classified angiographically as complete (as compared with unoccluded vessel, thrombolysis in myocardial infarction classification [TIMI] 3), none (with no change from prethrombolysis, TIMI 0), and partial (when a change in the flow from baseline was noted, TIMI 1-2). Outcomes were symptomatic intracranial hemorrhage (sICH), 90-day modified Rankin scale (< or = 2 as a good outcome), and 3-month mortality., Results: Ninety-six patients had either combined IV/IA (41) or IA (55) rtPA for AIS during a 7-year period. Any recanalization occurred in 69%; 55% of those had a good outcome versus 23% in the rest (Odds ratio = 3.9; 95% confidence interval [CI] = 1.4-11.2; P = .007). Only 24% had complete recanalization; 74% had a good outcome versus 36% in the nonrecanalization group (OR = 5.1; 95% CI = 1.6-16.8; P = .002). When adjusted to time to therapy and vessel occluded, these results lessened but remained significant. The sICH rate with any recanalization was 7.6% versus 13.3% in patients with persistent clot (relative risk (RR) = 0.6; 95% CI = 0.2-2.0; P = .45). Death occurred in 19.7% of those whose vessels recanalized versus 33.3% in the rest (RR = 0.56; 95% = 0.26-1.19; P = .2)., Conclusion: A total of 24% and 69% of patients had complete and any recanalization, respectively, following endovascular rtPA therapy of AIS. The degree of recanalization was directly related to time to therapy and associated with good clinical outcome without an increase in the rate of adverse effect.

Raised intracranial pressure is a relatively common problem facing the clinician treating neurocritically ill patients. It is a leading cause of death in patients with intracranial pathology. There is a lack of controlled clinical trials evaluating most of the therapies currently available for raised intracranial pressure. The basic pathophysiologic and clinical principles of raised intracranial pressure are discussed and the major treatment options are presented. Patients with raised intracranial pressure should be evaluated immediately with particular attention to airway and hemodynamic status. Controlled hyperventilation and hyperosmolality (using mannitol or hypertonic saline solutions) frequently are administered simultaneously. In patients with refractory elevation of intracranial pressure other therapies such as barbiturate coma and surgical interventions are available.

The authors performed a multicenter prospective observational study to evaluate the feasibility and safety of intravenous antihypertensive protocol for acute hypertension in patients with intracerebral hemorrhage (ICH). Twenty-seven patients with ICH and acute hypertension (mean age 61.37 +/- 14.27; 10 were men) were treated to maintain the systolic blood pressure (BP) below 160 mm Hg and diastolic BP below 90 mm Hg within 24 hours of symptom onset. Neurological deterioration (defined as a decrease in initial Glasgow Coma Scale score > or = 2) was observed in 2 (7.4%) of 27 patients during treatment. Among patients who underwent follow-up computed tomography, hematoma expansion (more than 33% increase in hematoma size at 24 hours) was observed in 2 (9.1%) of 22 patients. Patients treated within 6 hours of symptom onset were more likely to be functionally independent (modified Rankin scale < or = 2) at 1 month compared with patients who were treated between 6 and 24 hours (8 of 18 versus 0 of 9,P = .03). Aggressive pharmacological treatment of acute hypertension in patients with ICH can be initiated early with a low rate of neurological deterioration and hematoma expansion.

Introduction: Subarachnoid hemorrhage is one of the most common entities encountered in neurocritical care units. Knowledge of disease sequelae and their management is paramount for all neurointensivists., Materials and Methods: This study relates the case of a 70-year-old woman with poor grade subarachnoid hemorrhage who underwent endovascular detachable coil embolization of a right internal carotid artery aneurysm. Her hospital course was subsequently complicated by symptomatic carotid stenosis and cerebral vasospasm requiring intervention., Discussion: The discussants present their views regarding five main questions pertaining to management of the patient regarding the choice of endovascular versus surgical aneurysm occlusion, stent-supported angioplasty in a patient with a recent subarachnoid hemorrhage, and treatment options for vasospasm.

Objective: To determine the safety of early percutaneous endovascular carotid angioplasty and stenting (CAS) after an ischemic stroke., Methods: The neurointerventional database was reviewed for patients who underwent CAS after an acute ischemic stroke in two university hospitals. Clinical and radiological data were reviewed. Outcomes were worsening stroke, new stroke, or stroke-related death up to 30 days after the procedure. Procedure-related complications were also documented., Results: A total of 38 patients with 39 procedures were identified. The mean age was 67 +/- 15 years; 31 of 38 patients were Caucasian and 24 were female. Hypertension was found in 21 patients, peripheral vascular disease in 12, diabetes in 13, and coronary artery disease in 18. The median initial National Institutes of Health Stroke Scale score was 8. The carotid artery showed severe to high-grade stenosis in 28 patients, dissection was present in 6, and the rest had an acute occlusion treated with thrombolysis followed by CAS. The mean time from stroke onset to CAS was 55 +/- 34 hours. The mean degree of stenosis at baseline was 86 +/- 11%. In 37 procedures, complete recanalization was achieved, defined as less than 10% residual narrowing; in 2 procedures, the residual stenosis was mild (10-20%). Neurological deterioration occurred after three procedures (7.7%), with minor nondisabling stroke in two and death from intracranial hemorrhage in one., Conclusion: If deemed necessary and in certain circumstances, early CAS seems to be safe after acute ischemic stroke if infarction volume is small and neurological deficit is mild.

Objective: To determine predictors of in-hospital and long-term mortality and length of stay in patients admitted to the neurosciences critical care unit., Design: Retrospective analysis of a prospectively collected database., Setting: Neurosciences critical care unit of a large academic tertiary care hospital., Patients: Adult patients (n = 2381) admitted to our neurosciences critical care unit from January 1997 to April 2000., Interventions: Introduction of a specialized neurocritical care team., Measurements and Main Results: Data obtained from the database included demographics, admission source, length of stay, neurosciences critical care unit and hospital disposition, admission Acute Physiology and Chronic Health Evaluation (APACHE) III score, and principal and secondary diagnoses. The introduction of a neurocritical care team in September 1998 was also collected, as was death at 1 yr after admission. Univariate analysis was carried out using Student's t-test, Mann-Whitney U test, or chi-square test (significance, p < .05). A logistic regression model was used to create a prediction model for in-hospital and long-term mortality. A general linear model was used to determine predictors of length of stay (after log transformation). Independent predictors of in-hospital mortality included APACHE III (odds ratio, 1.07 [1.06-1.08]) and admission from another intensive care unit (odds ratio, 2.9 [1.4-6.2]). The presence of a neurocritical care team was an independent predictor of decreased mortality (odds ratio, 0.7 [0.5-1.0], p = .044). Admission after the neurocritical care team was implemented was associated with reduced length of stay in both the neurosciences critical care unit (4.2 +/- 4.0 vs. 3.7 +/- 3.4, p < .001) and the hospital (9.9 +/- 8.0 vs. 8.4 +/- 6.9, p < .0001). There was no difference in readmission rates to the intensive care unit or discharge disposition to home before and after the neurocritical care team was established. The availability of the neurocritical care team was not associated with significant changes in long-term mortality. Factors independently associated with long-term mortality included female gender, admission from another intensive care unit, APACHE III score, and being moderately disabled before admission., Conclusion: Introduction of a neurocritical care team, including a full-time neurointensivist who coordinated care, was associated with significantly reduced in-hospital mortality and length of stay without changes in readmission rates or long-term mortality.

Background and Purpose: Although long-term outcome determinants in acute ischemic stroke (AIS) patients have been defined, less is known about those predicting hyperacute worsening after thrombolytic therapy (TT). We investigated predictors of short-term clinical worsening (National Institutes of Health Stroke Scale [NIHSS] change > or =4 within 24 hours of admission)., Methods: We studied 201 AIS patients who received TT within 6 hours of symptom onset. We determined baseline demographics, comorbidities, NIHSS at baseline and at 24 hours after TT, head computed tomography scan before and within 24 hours after TT, and angiographic recanalization in patients treated with intra-arterial (IA) thrombolysis. Significance of relationships was evaluated by t test or Wilcoxon signed rank sum test. Logistic regression model (LRM) was fitted to determine independence of significant variables., Results: Of 201 patients, 13% worsened, 39% improved, and 48% remained unchanged 24 hours after TT. Most patients (72%) received IA thrombolysis. Patients who deteriorated, compared with those who improved, were more likely to have complicating intracranial hemorrhage (ICH; P<0.001), absent recanalization (P=0.026), and higher blood glucose (BG; P=0.049). Hyperglycemia (>150 mg/dL) was greater in patients who worsened even in presence of recanalization (P=0.004, odds ratio [OR] 6.47). LRM showed that adjusted OR for increased risk of bad outcome and mortality for an increase of BG by 50 mg/dL is 1.56 and 1.38, respectively., Conclusions: Hyperglycemia and ICH are independent predictors of hyperacute worsening in AIS patients receiving TT. Although recanalization is the purpose of IA thrombolysis, its impact on clinical improvement may not be apparent without strict BG control.

Object: Human albumin is used to induce hypervolemia (central venous pressure [CVP] > 8 mm Hg) after subarachnoid hemorrhage (SAH). Unfortunately, human albumin may increase the mortality rate in critically ill patients; because of this, its use became restricted in the authors' hospital in May 1999. The goal of this study was to determine the effect of human albumin on outcome and cost in patients with SAH before and after this restriction was put into place., Methods: All patients with aneurysmal SAH who were admitted to the authors' institution between May 1998 and May 2000 were studied. Basic demographic information, dosage of human albumin given, length of stay, and the incidence of in-hospital deaths and complications were collected. The authors obtained Glasgow Outcome Scale (GOS) scores at 3 months after SAH (good outcome, GOS > or = 4). Data were analyzed using t-test and chi-square analysis. Logistic regression was used to identify independent associations between use of human albumin and outcome. The authors studied 140 patients: 63 who were admitted between May 1998 and May 1999 (Group 1) and 77 treated between June 1999 and May 2000 (Group 2). Two subgroups of patients were further analyzed. Group 1 patients who received human albumin (albumin subgroup, 37 patients) and Group 2 patients who would have received albumin under the old protocol (that is, those who failed to achieve CVP > 8 mm Hg after normal saline administration; nonalbumin subgroup, 47 patients). Patients in the nonalbumin subgroup were more likely to be male (38% compared with 16%), to experience hypertension (55% compared with 30%), to suffer from hypomagnesemia (49% compared with 5.4%), and to have hydrocephalus (47% compared with 27%). There was a trend for these patients to have more vasospasm (28% compared with 19%, p = 0.2). Patients in the albumin subgroup were more likely to have a good outcome at 3 months., Conclusions: Administration of human albumin after SAH may improve clinical outcome and reduce hospital cost.

Objective: The National Institute of Neurological Disorders and Stroke (NINDS) Recombinant Tissue Plasminogen Activator Stroke Study Group showed that recombinant tissue plasminogen activator (rt-PA) administered intravenously within 3 hours of the onset of ischemic stroke can improve clinical outcome. Intraarterial (IA) thrombolysis has been shown to offer advantages over intravenous (IV) thrombolysis, but experience with this type of therapy within 3 hours of the onset of symptoms has not been reported previously. This study is the first retrospective analysis of a two-institution experience with IA thrombolysis within 3 hours of stroke onset., Methods: A total of 36 patients with angiographically demonstrated occlusions were treated with urokinase or rt-PA within 3 hours of stroke onset. Outcome measures included the percentage of patients with no or minimal neurological disability at 30 to 90 days as measured by the modified Rankin Scale, percentage recanalization, incidence of symptomatic intracranial hemorrhage, and mortality rate. The results were compared with those of the NINDS rt-PA study., Results: The median admission National Institutes of Health Stroke Scale score was 14. Fifty percent of treated patients had a modified Rankin Scale score of 0 or 1 indicating no or little disability at 1 to 3 months compared with 39% of treated patients in the NINDS trial. Recanalization was 75%, symptomatic intracranial hemorrhage was 11% (versus 6.4% with IV rt-PA in the NINDS trial), and the mortality rate was 22% (versus 17% with IV rt-PA in the NINDS trial)., Conclusion: The results suggest that IA thrombolysis administered within 3 hours of stroke onset is a feasible and viable alternative to IV rt-PA on the basis of improved clinical outcomes, high recanalization percentage, and comparable mortality rate and despite increased symptomatic intracranial hemorrhage. Whether IA thrombolysis is superior to IV therapy awaits further study.

The use of HS solutions has been shown to reduce ICP both in animal models and in human studies in a variety of underlying disorders, even in cases refractory to treatment with hyperventilation and mannitol. There are several possible mechanisms of action, and important complications such as central pontine myelinolysis and intracranial hemorrhage have not been reported in the human studies. Different types of HS solutions with different methods of infusion (bolus and continuous) have been used in the past, and so far there are not enough data to recommend one concentration over another. Many issues remain to be clarified, including the exact mechanism of action of HS, the best mode of administration and HS concentration to be given, and the relative efficacy of HS vis-à-vis available treatments, particularly mannitol.

Raised intracranial pressure (ICP) is a major contributor to the mortality of many conditions encountered in a neurologic intensive care unit. Achieving a sustained reduction in ICP in patients with intracranial hypertension remains a challenge. Treatment with hyperosmolar agents is one of the few options that are available, and mannitol is currently the most commonly used agent. However, hypertonic saline solutions have recently emerged as a potentially safer and more efficacious alternative to mannitol.

Hypertension-induced encephalopathy is a recognized pathological process commonly focused in the parietal and occipital lobes of the cerebral hemispheres. The parenchyma of the posterior fossa is infrequently involved. The authors report on two cases of isolated edema of the cerebellar hemispheres, which occurred in the setting of hypertensive crisis and led to complete obstruction of or significant impingement on the fourth ventricle and potentially lethal hydrocephalus. To the best of the authors' knowledge, these are the first reported cases of hypertensive encephalopathy centered in the posterior fossa. Two patients presented with profound decreases in neurological status subsequent to development of malignant hypertension. Imaging studies revealed diffusely edematous cerebellar hemispheres with effacement of the fourth ventricle, causing dilation of the lateral and third ventricles. Following emergency placement of external ventricular drains, control of systemic blood pressure was accomplished, and neurological functioning returned to baseline. Although neurological deterioration resolved swiftly following placement of ventricular catheters and administration of diuretic agents, systemic blood pressure did not fluctuate with the release of cerebrospinal fluid and resolution of increased intracranial pressure. Decrease in systemic blood pressure lagged well behind improvement in neurological status; the patients remained morbidly hypertensive until systemic blood pressure was controlled with multiple parenteral medications. The authors hypothesize that the development of hypertension beyond the limits of cerebral autoregulation led to breakdown of the blood-brain barrier in the cerebellum and development of posterior fossa edema secondary to the focal transudation of protein and fluid. Correction of the elevated blood pressure led to amelioration of cerebellar edema. In the appropriate clinical setting, hypertension as the inciting cause of cerebellar encephalopathy should be considered.

Objective: We sought to determine the long-term stroke-free survival of patients who present with ischemic events related to intracranial vertebrobasilar stenosis., Methods: A retrospective cohort of patients diagnosed with symptomatic vertebrobasilar stenosis on the basis of magnetic resonance angiography and/or conventional angiography was identified at four academic medical centers. Patients' clinical and follow-up information was obtained through hospitalization records, clinic visits, and telephone interviews. Kaplan-Meier analysis was performed to determine the rate of stroke-free survival for a 5-year period. Cox proportional hazards analysis was performed to determine the effect of demographic and clinical factors on stroke-free survival., Results: A total of 102 patients were included, whose mean age was 64 +/- 12 years. Fifty-five (54%) of the patients were men. The mean follow-up period was 15 +/- 15.9 months (range, 1-60 mo). During the follow-up period, 14 (14%) of the patients experienced recurrent stroke. The overall mortality rate was 21% (n = 21). Stroke-free survival, calculated by using the Kaplan-Meier curve, was 76% at 12 months (95% confidence interval [CI], 66-83%) and 48% at 5 years (95% CI, 27-65%). The risk of recurrent stroke was 10.9 per 100 patient-years, and the rate of recurrent stroke and/or death was 24.2 per 100 patient-years. Cox proportional hazards analysis revealed that increasing age (hazards ratio, 1.05; 95% CI, 1.00-1.09) decreased stroke-free survival. Treatment with either antiplatelet agents or warfarin (hazards ratio, 0.018; 95% CI, 0.003-0.11) had a protective effect on stroke-free survival after adjusting for age, sex, race, hypertension, diabetes mellitus, smoking, hyperlipidemia, and lesion location., Conclusion: A low rate of stroke-free survival is observed in patients with symptomatic vertebrobasilar stenosis. Further studies are required to evaluate new medical and endovascular treatment options for this group of patients to improve long-term stroke-free survival.

A 44-year-old man with treated neurosyphilis presented with subclinical status epilepticus (SE) refractory to intravenous high-dose lorazepam, phenytoin, and valproic acid over 4 days. Ketamine infusion was instituted after low-dose propofol sedation with gradual control of electrographic seizures over 72h. Reevaluation 3 months later revealed diffuse cerebellar and worsened cerebral atrophy, consistent with animal models of N-methyl-D-aspartate antagonist-mediated neurotoxicity. Animal studies of prolonged ketamine therapy are required before widespread human use in SE.

Objective: To determine the time interval between symptom onset and neurologic deterioration related to cerebral edema in patients with massive middle cerebral artery infarction. The time period between onset and neurologic deterioration represents the window for surgical intervention., Design: Multicenter retrospective chart review., Settings: Five university-affiliated medical centers., Patients: Fifty-three patients with massive middle cerebral artery infarction who experienced neurologic deterioration defined by a decrease in the Glasgow Coma Scale score of two or more points attributable to mass effect., Measurements and Main Results: A total of 53 patients (mean age, 62 +/- 18 yrs; 25 [47%] were men) with neurologic deterioration were identified by using International Classification of Diseases (9th revision) codes and local registries. Medical records and neuroimaging studies were reviewed by a stroke neurologist or neurointensivist to identify the time of neurologic deterioration. Thrombolytics were used at presentation in 19 (35%) patients. A total of 19 (36%) patients had neurologic deterioration within 24 hrs of symptom onset. By 48 hrs, 36 (68%) patients had manifested clinical deterioration. A few patients had later neurologic deterioration on day 3 (n = 10), day 4 (n = 2), day 5 (n = 2), and day 6 or after (n = 3). A total of 25 (47%) of the 53 patients died during hospitalization. The highest frequency of deaths occurred on day 3., Conclusions: Neurologic deteriorations related to cerebral edema after massive middle cerebral artery infarction occur in most patients within 48 hrs of symptom onset.

Background and Purpose: The objective of this study was to determine the clinical features, angiographic findings, and response to treatment with thrombolytic therapy in patients with ischemic stroke caused by acute occlusion of the distal internal carotid artery., Methods: This is a retrospective case series from a prospectively collected stroke database for patients with acute internal carotid occlusion presenting within 6 hours of stroke onset to evaluate safety, feasibility, and response to thrombolytic therapy. The University Hospital-based brain attack database was reviewed over a 5-year period. Demographics, clinical features, stroke mechanisms, severity, imaging findings, type of thrombolysis, treatment responses, mortality, and long-term outcome using modified Rankin Scale and Barthel Index were determined. The short-term outcome was assessed using the National Institutes of Health Stroke Scale (NIHSS). Acute thrombolytic therapy was administered using recombinant tissue plasminogen activator or urokinase given intra-arterially or in combination with intravenous (IV) routes., Results: Two hundred seven patients treated with thrombolysis between 1995 and 2000 were reviewed, and of these, 101 were studied with cerebral angiography. Eighteen patients were identified with acute ischemic stroke and ipsilateral occlusion of the distal internal carotid artery. Time to treatment was the most powerful predictor of response to thrombolytic therapy (P<0.001). The response to therapy also correlated well with the severity of the initial clinical deficit as judged by the NIHSS (P<0.001). There was no difference in recanalization rate, symptomatic hemorrhage, and NIHSS for IV/intra-arterial (IA) versus IA alone (P=NS). Complete angiographic recanalization was accomplished in 80% of those who received combined IV/IA thrombolysis and in 62% of those who received IA therapy (P=NS). Those with distal occlusions extending to the middle and anterior cerebral arteries were the least likely to respond to thrombolysis. Symptomatic intracerebral hemorrhage occurred in 20% of the patients receiving IV/IA therapy, and in 15% of the IA only (P=NS). At 24 hours, the NIHSS dropped by 3 points in the IA group and 4 points in the IV/IA group (P=NS). Mild disability with independence was found in 77% of the survivors at 3-month follow-up. The mortality rate was 50% in this group despite thrombolysis., Conclusions: Thrombolytic therapy using a combination of IV and IA routes and using the IA-only route may be effective in improving outcome for the patients suffering from occlusion of the distal internal carotid artery. Shorter intervals between onset and treatment seem to be correlated with higher rate of recanalization and improved outcome.

Background: We report the occurrence of fatal intracerebral hemorrhage associated with using a combination of antithrombotic agents, including abciximab, in patients undergoing neurointerventional procedures., Summary of Report: Seven patients (average age 60, range 46 to 73 years) developed fatal intracerebral hemorrhages associated with neurointerventional procedures and the use of intravenous abciximab. The procedures included angioplasty and stent placement in the cervical internal carotid artery (n=4), angioplasty of the intracranial internal carotid artery (n=1), and angioplasty of the middle cerebral artery (n=2). Clinical deterioration was observed within 1 hour of the procedure in 5 patients and 7 and 8 hours after the procedure, respectively, in the remaining 2 patients. All patients had received heparin and clopidogrel; 6 had also received aspirin., Conclusions: Intracerebral hemorrhages can occur after neurointerventional procedures in patients with recent cerebral ischemic events, particularly when aggressive antithrombotic treatment is used.

Objective: To evaluate the reliability of transcranial Doppler ultrasound in detecting symptomatic vasospasm in patients after aneurysmal subarachnoid hemorrhage and monitoring response after hypertensive and endovascular treatments., Design: Retrospective chart review., Setting: Neurosciences critical care unit in a tertiary-care university hospital., Patients: All patients admitted to a neurosciences critical care unit with the diagnosis of subarachnoid hemorrhage between January 1990 and June 1997., Interventions: None, Measurements and Main Results: We reviewed transcranial Doppler ultrasound data of 199 patients; 55 had symptomatic vasospasm. Clinical symptoms and corresponding vascular distributions were identified, as was angiographic vasospasm (n = 35). The sensitivity and specificity of transcranial Doppler ultrasound for anterior circulation vessels were calculated by using a mean cerebral blood flow velocity criterion of >120 cm/sec. Clinical diagnosis of symptomatic vasospasm was used as the standard to determine sensitivity and specificity of transcranial Doppler ultrasound and cerebral angiography. The sensitivity of transcranial Doppler ultrasound for anterior circulation in patients with symptomatic vasospasm was 73% with a specificity of 80%. The sensitivity of cerebral angiography was 80%. For individual vessels, the sensitivity and specificity of transcranial Doppler ultrasound were middle cerebral artery, 64% and 78%; anterior cerebral artery, 45% and 84%; and internal carotid artery, 80% and 77%, respectively. The mean times for symptomatic and transcranial Doppler ultrasound signs of vasospasm presentation were 6.4 +/- 2 and 6.1 +/- 3 days, respectively. In patients without symptomatic vasospasm, the mean time for mean cerebral blood flow velocities >120 cm/sec was 7.0 +/- 3 days (p <.05). Symptomatic vasospasm also was associated with thickness of clot on head computed tomography scan and rapidly increasing mean cerebral blood flow velocities. Transcranial Doppler ultrasound signs of vasospasm improved after endovascular treatment in 30 patients., Conclusions: The reliability of transcranial Doppler ultrasound was better at detecting high mean cerebral blood flow velocities in patients with symptomatic vasospasm related to middle cerebral and internal carotid artery distributions than for anterior cerebral artery distribution. Transcranial Doppler ultrasound was as sensitive as cerebral angiography at detecting symptomatic vasospasm. High mean cerebral blood flow velocities can be apparent before the presence of symptomatic vasospasm. Daily transcranial Doppler ultrasound monitoring could provide early identification of patients with aneurysmal subarachnoid hemorrhage who are at high risk for symptomatic vasospasm and may be helpful at following success of endovascular treatment.

Objective: To determine the feasibility of combined intravenous and intra-arterial thrombolytic therapy for acute ischemic strokes and to evaluate its associated risks, using magnetic resonance imaging as a triage tool. Intravenous treatment followed by intra-arterial infusion may increase the rate of recanalization and lead to better clinical results, with reduced frequency of intracranial hemorrhage., Methods: Our Brain Attack Team evaluated patients who presented within 3 hours after symptom onset. Patients who did not demonstrate improvement and exhibited no evidence of intracranial hemorrhage on head computed tomographic scans were treated with intravenously administered recombinant tissue plasminogen activator (0.6 mg/kg) and underwent emergency magnetic resonance imaging of the head. T2-weighted turbo-gradient and spin echo and echo-planar diffusion- and perfusion-weighted imaging scans were obtained. Patients with evidence of imaging abnormalities indicating acute cortical infarction underwent cerebral angiography. After determination of vessel occlusion, intra-arterially administered urokinase (up to 750,000 units) or intra-arterially administered recombinant tissue plasminogen activator (maximal dose, 0.3 mg/kg) was used to achieve recanalization., Results: We treated 45 patients with this protocol. The mean age was 67 +/- 13 years, and 58% of the patients were women. There was a significant improvement in National Institutes of Health Stroke Scale scores after treatment. There was good correlation between abnormal perfusion-weighted imaging findings and cerebral angiographic findings (complete vessel occlusion). The incidence of symptomatic intracranial hemorrhage was 4.4% in this cohort. Seven patients died in the hospital, and the majority of survivors (77%) experienced good outcomes (Barthel index of >or=95) 3 months after treatment., Conclusion: Our data demonstrate that this protocol is feasible and that combined intravenous and intra-arterial thrombolysis to treat acute ischemic strokes is sufficiently safe to warrant further evaluation.

Extra-cranial arterial dissection accounts for 10% of strokes in young people. Information on safety of thrombolytic administration in this group is limited. The literature, however, does not favor use of thrombolytics for myocardial ischemia when peripheral arterial dissection coexists. Based on the clinical and radiological features, two patients who presented with acute stroke secondary to arterial dissection were considered for thrombolysis. One of them received intra-venous recombinant tissue plasminogen activator (rtPA), and the other patient received intra-arterial rtPA. There were no post thrombolysis complications. This report supports feasibility of administering thrombolytics in acute ischemic strokes resulting from extra-cranial arterial dissection. Future larger studies are necessary to determine the efficacy, safety and long-term outcome in this patient population.

Acute motor-sensory axonal neuropathy (AMSAN) is an axonal variant of Guillian-Barré syndrome (GBS) that presents with acute ascending quadriparesis. This has generally been described in association with Campylobacter jejuni infections or with anti-ganglioside antibodies. Known cases have shown a slow recovery and a poor prognosis. We report a case with clinical and electrophysiological evidence of AMSAN in association with active systemic lupus erythematosus (SLE) and anticardiolipin antibodies but not the other associations, with a rapid response to combination immunosuppressant and intravenous immunoglobulin (IVIg) therapy. The association between AMSAN and SLE has not been previously described. This case illustrates that early recognition and the utilization of electrophysiologic techniques may be beneficial in the diagnosis and management of GBS associated with SLE. Fulminant or rapidly progressive cases should be managed in specialized intensive care units. Combination therapy of immunosuppressants and IVIg may be beneficial in non-vasculitic axonal radiculo-neuropathies associated with SLE, resulting in good outcomes.

Objective: Cigarette smoking has been demonstrated to increase the risk of subarachnoid hemorrhage (SAH). Whether cessation of smoking decreases this risk remains unclear. We performed a case-control study to examine the effect of smoking and other known risk factors for cerebrovascular disease on the risk of SAH., Methods: We reviewed the medical records of all patients with a diagnosis of SAH (n = 323) admitted to Johns Hopkins Hospital between January 1990 and June 1997. Controls matched for age, sex, and ethnicity (n = 969) were selected from a nationally representative sample of the Third National Health and Nutrition Examination Survey. We determined the independent association between smoking (current and previous) and various cerebrovascular risk factors and SAH by use of multivariate logistic regression analysis. A separate analysis was performed to determine associated risk factors for aneurysmal SAH., Results: Of 323 patients admitted with SAH (mean age, 52.7+/-14 yr; 93 were men), 173 (54%) were hypertensive, 149 (46%) were currently smoking, and 125 (39%) were previous smokers. In the multivariate analysis, both previous smoking (odds ratio [OR], 4.5; 95% confidence interval [CI], 3.1-6.5) and current smoking (OR, 5.2; 95% CI, 3.6-7.5) were significantly associated with SAH. Hypertension was also significantly associated with SAH (OR, 2.4; 95% CI, 1.8-3.1). The risk factors for 290 patients with aneurysmal SAH were similar and included hypertension (OR, 2.4; 95% CI, 1.8-3.2), previous smoking (OR, 4.1; 95% CI, 2.7-6.0), and current smoking (OR, 5.4; 95% CI, 3.7-7.8)., Conclusion: Hypertension and cigarette smoking increase the risk for development of SAH, as found in previous studies. However, the increased risk persists even after cessation of cigarette smoking, which suggests the importance of early abstinence from smoking.

Background and Purpose: Limited systemic fibrinolysis and reduced dosage are features of intra-arterial thrombolyis (IAT) that may be advantageous in the treatment of postoperative strokes. However, IAT may increase the risk of surgical bleeding. We sought to determine the safety of postoperative IAT., Methods: This was a retrospective case series from 6 university hospitals. All cases of IAT within 2 weeks of surgery were identified. Demographics, stroke mechanism, stroke severity, imaging and angiographic findings, time between surgery and lysis, thrombolytic agent used, surgical site bleeding, intracranial bleeding, and mortality rates were determined. Death or complications directly related to IAT were determined., Results: Thirty-six patients (median age, 71.5 years; range, 45 to 85) were identified. Median time from surgery to stroke was 21.5 hours (range, 1 to 120). Open heart surgery was done in 18 (50%), carotid endarterectomy in 6 (17%), craniotomy in 3 (8%), ophthalmologic-ear, nose and throat surgery in 2 (6%), urologic-gynecologic surgery in 4 (11%), orthopedic surgery in 2 (6%), and plastic surgery in 1 (3%). The stroke causes were cardioembolism in 24 (67%), large-vessel atherosclerosis in 4 (11%), dissection in 3 (8%), postendarterectomy occlusion in 4 (11%), and radiation arteriopathy in 1 (3%). Median time to angiogram was 2.5 hours (0.1 to 5.5). Occlusion sites were M1 in 19 (53%), M2 in 9 (25%), internal carotid artery in 5 (14%), basilar artery in 2 (6%), and posterior communicating artery in 1 (3%). Thrombolysis was completed at a median of 4.5 hours (range, 1 to 8.0). Tissue plasminogen activator was used in 19 (53%) and urokinase in 17 (47%). Nine (26%) patients died. Surgical site bleeding occurred in 9 (25%) cases (minor in 6, major in 3). The major surgical bleeds were 2 post-craniotomy intracranial hemorrhages and 1 hemopericardium after coronary artery bypass grafting; all were fatal. Six deaths were non-IAT related: 3 caused by cerebral edema and 3 by systemic causes. Major bleeding complications were significantly more common among patients with craniotomy (P<0.02)., Conclusions: Postoperative IAT carries a risk of bleeding in up to 25% of patients but is usually minor surgical site bleeding. Avoiding IAT in intracranial surgery patients may reduce complications. Mortality rate in this series was similar to that reported in prior IAT trials. IAT remains a viable therapeutic option for postoperative strokes.

Background and Purpose: The development of thrombolytic agents for use with compromised cerebral blood flow has made it critical to quickly identify those patients to best treat. We hypothesized that combined diffusion and perfusion MR imaging adds vital diagnostic value for patients for whom the greatest potential benefits exist and far exceeds the diagnostic value of diffusion MR imaging alone., Methods: The cases of patients with neurologic symptoms of acute ischemic stroke who underwent ultra-fast emergent MR imaging within 6 hours were reviewed. In all cases, automatic processing yielded isotropic diffusion images and perfusion time-to-peak maps. Images with large vessel distribution ischemia and with mismatched perfusion abnormalities were correlated with patient records. All follow-up images were reviewed and compared with outcomes resulting from hyperacute therapies., Results: For 16 (26%) of 62 patients, hypoperfusion was the best MR imaging evidence of disease distribution, and for 15 of the 16, hypoperfusion (not abnormal diffusion) comprised the only imaging evidence for disease involving large vessels. For seven patients, diffusion imaging findings were entirely normal, and for nine, diffusion imaging delineated abnormal signal in either small vessel distributions or in a notably smaller cortical branch in one case. In all cases, perfusion maps were predictive of eventual lesions, as confirmed by angiography, CT, or subsequent MR imaging., Conclusion: If only diffusion MR imaging is used in assessing patients with hyperacute stroke, nearly one quarter of the cases may be incorrectly categorized with respect to the distribution of ischemic at-risk tissue. Addition of perfusion information further enables better categorizing of vascular distribution to allow the best selection among therapeutic options and to improve patient outcomes.

Objectives: To review the literature on the use of hypertonic saline (HS) in treating cerebral edema and intracranial hypertension., Data Sources: Review of scientific and clinical literature retrieved from a computerized MEDLINE search from January 1965 through November 1999., Study Selection: Pertinent literature is referenced, including clinical and laboratory investigations, to demonstrate principles and efficacy of treatment with HS in patients with intracranial space-occupying pathology., Data Extraction: The literature was reviewed to summarize the mechanisms of action, efficacy, adverse effects, systemic effects, and comparisons with standard treatments in both clinical and laboratory settings., Data Synthesis: HS has an osmotic effect on the brain because of its high tonicity and ability to effectively remain outside the bloodbrain barrier. Numerous animal studies have suggested that fluid resuscitation with HS bolus after hemorrhagic shock prevents the intracranial pressure (ICP) increase that follows resuscitation with standard fluids. There may be a minimal benefit in restoring cerebral blood flow, which is thought to be mitigated through local effects of HS on cerebral microvasculature. In animal models with cerebral injury, the maximum benefit is observed in animals with focal injury associated with vasogenic edema (cryogenic injury). The ICP reduction is seen for < or =2 hrs and may be maintained for longer periods by using a continuous infusion of HS. The ICP reduction is thought to be caused by a reduction in water content in areas of the brain with intact blood-brain barrier such as the nonlesioned hemisphere and cerebellum. Most comparisons with mannitol suggest almost equal efficacy in reducing ICP, but there is a suggestion that mannitol may have a longer duration of action. Human studies published to date reporting on the use of HS in treating cerebral edema and elevated ICP include case reports, case series, and small controlled trials. Results from studies directly comparing HS with standard treatment in regard to safety and efficacy are inconclusive. However, the low frequency of side effects and a definite reduction of ICP observed with use of HS in these studies are very promising. Systemic effects include transient volume expansion, natriuresis, hemodilution, immunomodulation, and improved pulmonary gas exchange. Adverse effects include electrolyte abnormalities, cardiac failure, bleeding diathesis, and phlebitis. Although unproven, a potential for central pontine myelinolysis and rebound intracranial hypertension exists with uncontrolled administration., Conclusions: HS demonstrates a favorable effect on both systemic hemodynamics and intracranial pressure in both laboratory and clinical settings. Preliminary evidence supports the need for controlled clinical trials evaluating its use as resuscitative fluid in brain-injured patients with hemorrhagic shock, as therapy for intracranial hypertension resistant to standard therapy, as firstline therapy for intracranial hypertension in certain intracranial pathologies, as small volume fluid resuscitation during spinal shock, and as maintenance intravenous fluid in neurocritical care units.

Objective: To determine the short- and long-term outcomes after successful reversal of transtentorial herniation by medical treatment. Although it has been recognized that aggressive medical management can reverse transtentorial herniation, it is believed that overall outcome in such patients is poor., Design: Prospective cohort study., Setting: Neurocritical care unit of a university hospital., Patients: A total of 28 consecutive patients who underwent an episode of transtentorial herniation (defined as decrease in level of consciousness accompanied by pupillary dilation) secondary to a supratentorial mass lesion followed by successful reversal., Intervention: Herniation was reversed by using a combination of hyperventilation, mannitol and hypertonic saline., Measurements and Main Results: The following outcomes were analyzed: risk of second herniation, radiologic evidence of structural damage or vascular compromise related to herniation on post-herniation computed tomographic scan, in-hospital mortality, and long-term functional outcome using Rankin score and Barthel index. A total of 32 episodes of transtentorial herniations were reversed in 28 patients during a 14-month period. The most common precipitating cause were edema (n = 23) or new/expanding intracerebral hematoma (n = 5). After first reversal of transtentorial herniation in 28 patients, a second herniation episode was observed in 16 patients after a mean interval of 88.2 hrs (range, 23-432 hrs); four were successfully reversed. On follow-up computed tomographic scan, hypodense lesion in midbrain (n = 6), temporal lobe contusion (n = 2), posterior cerebral artery (n = 3), and middle cerebral artery (n = 1) infarction were visualized in a minority of patients. The in-hospital mortality was 60% (n = 15) with brain death being the cause of death in 13 patients; care was withdrawn in eight patients. Second episode of herniation (p = .002) and midbrain involvement during herniation (p = .02) were associated with in-hospital mortality. During a mean follow-up period of 11.4+/-4.2 months, two patients died of cerebral neoplasm and human immunodeficiency virus-related sepsis, respectively. Of the 11 survivors, 7 were functionally independent (Rankin score <3 and Barthel index >60)., Conclusions: Although mortality after transtentorial herniation is high, we found a prominent potential for meaningful recovery with aggressive medical reversal of transtentorial herniation. Our study implies that timely medical intervention for reversing transtentorial herniation can result in preservation of neurologic function.

Objectives: To determine the frequency and predictors of successful extubations and tracheostomy in patients with infratentorial lesions requiring mechanical ventilation and to determine the optimal time for tracheostomy based on probability of successful extubation and in-hospital survival according to the duration of translaryngeal intubation., Design: Retrospective chart review., Settings: A neurocritical care unit at a university hospital., Patients: A total of 69 patients with infratentorial lesions who were mechanically ventilated during their intensive care unit stay., Measurements and Main Results: Of the 69 patients who were mechanically ventilated, 23 (33%) were successfully extubated. In logistic regression analysis, both the presence of a Glasgow Coma Scale score >7 at time of intubation (odds ratio, 4.8; 95% confidence interval, 1.2-21.7) and the absence of brainstem deficits (odds ratio, 4.3; 95% confidence interval, 1.3-16.7), were independently associated with successful extubation. After extubation, 11 patients were reintubated; seven were reintubated within the same day because of poor control over secretions, airway spasm, or hypoventilation. Tracheostomy was performed in 23 (33%) patients, of whom 19 were successfully weaned off mechanical ventilatory support over a mean period of 3.7+/-4.0 days after tracheostomy. Patients undergoing tracheostomy had a significantly longer intensive care unit stay (19.1+/-9.0 vs. 8.7+/-6.6 days, p < .01) and total hospital stay (34.8+/-18.7 vs. 20.1+/-9.9 days, p < .01) compared with patients who were successfully extubated. The probability of successful extubation or death before extubation or tracheostomy was 67% on the day of intubation, which decreased to 5.8% after translaryngeal intubation for >8 days., Conclusions: An aggressive policy toward tracheostomy is justified based on the low frequency of successful extubations and high frequency of extubation failures and tracheostomies in patients with infratentorial lesions. The decision regarding tracheostomy should be made on day 8 of mechanical ventilatory support because of the low probability of subsequent extubation or in-hospital death.

Objective: Symptomatic vasospasm after subarachnoid hemorrhage (SAH) is associated with a high incidence of permanent disability and death. For early identification of patients who are at risk for poor outcome, we determined the predictors of outcome in patients with symptomatic vasospasm after SAH., Design: We retrospectively determined the prognostic value of clinical characteristics and computed tomographic scan both at admission and at the time of initiation of hypervolemic and hypertensive therapy., Settings: Neurosciences critical care unit at a University hospital., Patients: A total of 70 consecutive patients who developed symptomatic vasospasm after SAH., Intervention: Treatment with oral nimodipine, hypervolemic therapy, and hypertensive therapy. Angioplasty and intra-arterial papaverine were used in patients with vasospasm resistant to standard treatment., Measurements and Main Results: Poor outcome, defined as Glasgow Outcome Scale Score of 3-5 at 2 months or discharge, was observed in 32 (46%) patients. In the logistic regression analysis, a Glasgow Coma Scale (GCS) score of < or =11 (odds ratio, 11.0; 95% confidence interval, 3.6-39.3) and hydrocephalus (odds ratio, 4.3; 95% confidence interval, 1.2-18.2) at the time of initiation of hypervolemic and hypertensive therapy were significantly associated with poor outcome. Poor outcome was observed in 91% of the patients who had both a GCS score of < or =11 and hydrocephalus compared with 15% of patients with a GCS score of >11 and no hydrocephalus at the time of initiation of hypervolemic and hypertensive therapy. A GCS score of < or =11 was also independently associated with length of intensive care unit stay (F ratio = 18.0; p = .0011) and hospital stay (F ratio = 9.2; p = .0034) after initiation of hypervolemic and hypertensive therapy., Conclusions: The results of this study suggest that outcome in patients with symptomatic vasospasm can be effectively predicted by routinely available information, including GCS score at the time of initiation of hypervolemic and hypertensive therapy. This information can be used for selection and stratification of patients in future treatment studies of patients with symptomatic vasospasm.

Background and Purpose: We sought to evaluate predictors of clinical outcome, angiographic success, and adverse effects after intra-arterial administration of urokinase for acute ischemic stroke., Methods: We designed a Brain Attack program at University Hospitals of Cleveland for diagnosis and treatment of patients presenting within 6 hours of onset of neurological deficit. Patients with ischemia referable to the carotid circulation were treated with intra-arterial urokinase. Angiographic recanalization was assessed at the end of medication infusion. Intracerebral hemorrhage was investigated immediately after and 24 hours after treatment. Stroke severity was determined, followed by long-term outcome., Results: Fifty-four patients were treated. There was improvement of >/=4 points on the National Institutes of Health Stroke Scale from presentation to 24 hours after onset in 43% of the treated patients, and this was related to the severity of the initial deficit. Forty-eight percent of patients had a Barthel Index score of 95 to 100 at 90 days, and total mortality was 24%. Cranial CT scans revealed intracerebral hemorrhage in 17% of patients in the first 24 hours, and these patients had more severe deficits at presentation. Eighty-seven percent of patients received intravenous heparin after thrombolysis, and 9% of them developed a hemorrhage into infarction. Angiographic recanalization was the rule in complete occlusions of the horizontal portion of the middle cerebral artery, but distal carotid occlusions responded less well to thrombolysis., Conclusions: The intra-arterial route for thrombolysis allows for greater diagnostic precision and achievement of a higher concentration of the thrombolytic agent in the vicinity of the clot. Disadvantages of this therapy lie in the cost and delay. Severity of stroke and site of angiographic occlusion may be important predictors of successful treatment.

Background: Hypertonic saline (HS) recently has been introduced as a new form of hyperosmolar treatment in patients with brain injury from diverse causes. We reviewed our experience with the use of continuous hypertonic saline/acetate infusion in patients with cerebral edema attributable to head trauma., Methods: We performed a retrospective chart review of all patients admitted with severe head injury, defined as admission Glasgow Coma Scale score of 8 or less, in the neurocritical care unit of a University hospital. Intravenous infusion of 2% or 3% saline/acetate for treatment of cerebral edema was introduced in the unit in April of 1993. The clinical characteristics, interventions required, and outcomes in patients who received HS were compared with patients who received 0.9% saline infusion only. Multivariate analyses were used to evaluate the impact of HS use on in-hospital mortality and Glasgow Outcome Scale score at discharge., Results: Thirty-six patients with cerebral edema caused by head trauma received infusion of HS initiated within 48 hours of admission for a mean period of 72 +/- 85 hours. Compared with 46 patients who did not receive HS, there were no differences observed in age and admission Glasgow Coma Scale scores. Patients who received HS were more likely to have a penetrating injury (p = 0.07) and a mass lesion on initial computed tomographic scan (p = 0.07). There was no difference between frequency of use of hyperventilation, mannitol, cerebrospinal fluid drainage, and vasopressors between the two groups. The requirement for pentobarbital coma was higher in HS group (n = 7 patients) versus control group (n = 2,p = 0.04). After adjusting for differences between both groups, infusion of HS was associated with higher in-hospital mortality (OR, 3.1; 95% CI, 1.1-10.2)., Conclusion: HS administration as prolonged infusion does not seem to favorably impact on requirement for other interventions and in-hospital mortality in our experience. Further efforts should be directed toward use of HS as bolus administrations or short infusions.

A retrospective study was carried out to evaluate the effect of hypertonic (3%) saline chloride/acetate on various hemodynamic parameters in mildly hyponatremic patients with symptomatic vasospasm following aneurysmal subarachnoid hemorrhage (SAH). We identified 29 hyponatremic (serum sodium < 135 mEq/L) patients who received hypertonic (3%) sodium chloride/acetate as a continuous infusion. Administration of hypertonic (3%) sodium chloride/acetate resulted in higher central venous pressures and positive fluid balance, with a concomitant increase in serum sodium and chloride concentrations without metabolic acidosis. There were no changes in mean cerebral blood flow velocities after infusion of hypertonic (3%) sodium chloride/acetate. We found no reports of congestive heart failure, pulmonary edema, metabolic acidosis, coagulopathy, intracranial hemorrhages, or central pontine myelinolysis in any of these patients. We conclude that hypertonic (3%) sodium chloride/acetate can be administered to patients with mild hyponatremia in the setting of symptomatic vasospasm following SAH without untoward effects. Sample size and limitations of a retrospective analysis preclude conclusions about safety and efficacy of hypertonic (3%) sodium chloride/acetate administration in this patient population. However, our results support justification for a prospective, randomized, double-blind trial of hypertonic (3%) sodium chloride/acetate versus normal saline in patients with symptomatic vasospasm following SAH.

The ability of the magnetic resonance imaging transverse relaxation time, R2 = 1/T2, to quantify cerebral blood volume (CBV) without the need for an exogenous contrast agent was studied in cats (n = 7) under pentobarbital anesthesia. This approach is possible because R2 is directly affected by changes in CBF, CBV, CMRO2, and hematocrit (Hct), a phenomena better known as the blood-oxygenation-level-dependent (BOLD) effect. Changes in CBF and CBV were accomplished by altering the carbon dioxide pressure, PaCO2, over a range from 20 to 140 mm Hg. For each PaCO2 value, R2 in gray and white matter were determined using MRI, and the whole-brain oxygen extraction ratio was obtained from arteriovenous differences (sagittal sinus catheter). Assuming a constant CMRO2, the microvascular CBV was obtained from an exact fit to the BOLD theory for the spin-echo effect. The resulting CBV values at normal PaCO2 and normalized to a common total hemoglobin concentration of 6.88 mmol/L were 42+/-18 microL/g (n = 7) and 29+/-19 microL/g (n = 5) for gray and white matter, respectively, in good agreement with the range of literature values published using independent methodologies. The present study confirms the validity of the spin-echo BOLD theory and, in addition, shows that blood volume can be quantified from the magnetic resonance imaging spin relaxation rate R2 using a regulated carbon dioxide experiment.