Brain Edema

Background The ''white cerebellum'' sign is a rare imaging finding described mainly in children with hypoxic brain injury. Materials and Methods Single case report and review of the literature. Findings We describe a child with acute bacterial meningitis in whom plain CT and MRI showed the white cerebellum sign. The subtle imagings findings were not recognized and a lumbar puncture was performed. Markedly increased intracranial pressure was documented by lumbar puncture and by placement of an intraparenchymal monitor. Contrary to most prior descriptions the patient made a very good recovery. Conclusions The white cerebellum sign is a subtle imaging finding seen in patients with diffuse cerebral edema, such finding may not be as ominous as previously thought.

A three-layered backpropagation neural network was developed to differentiate malignant from benign brain tumors in a group of patients with astrocytic gliomas. The MRI findings of 43 patients were reviewed before biopsy by three neuroradiologists independently. This provided a database made up of 129 patients' records each of which comprised I3 parameters derived from pre-and post-contrast MR images. The network's generalizing ability was then tested to predict the outcome of biopsy in 36 new cases and its performance compared to that of radiologist using ROC analysis. The output of the network with and without radiologists' impression yielded a better diagnostic performance with relative ROC areas of 0.94 and 0.9 1. respectively, compared to 0.84 obtained by radiologist. These results demonstrate that the neural network can effectively differentiate malignant from benign brain tumors.

Introduction: Reconstruction of the cranial vault is performed for various reasons and precise repair of the defect is important. A modified method of cranioplasty is presented using three-dimensional (3D) models and polyethylmethacrylate mixed with hydroxyapatite, cast in a silicone rubber mould. Patient and method: A large custom made cranial implant was produced using data acquired from 3D computer tomography, rapid prototyping and cast in a silicone rubber mould. This plate was then applied to a 53 year-old man who had undergone a decompressive fronto-parieto-temporo-occipital craniotomy. The bone flap had been lost due to infection. The cranioplasty was performed at 1 year after the initial operation. Results: The cranial plate fitted precisely into the defect and needed no correction at the time of surgery. The stability of the reconstruction plate was increased by the presence of thin margins allowed by silicone rubber elasticity. No complications occurred and the final functional and aesthetic results were good. Conclusion: The use of 3D imaging and rapid prototyping allow precise repair of large skull defects, with good aesthetic and functional results. At the same time, silicone rubber moulds permit the production of very thin details needed not only for cosmetic reasons but for reconstruction plate stability as well. r 2006 European Association for Cranio-Maxillofacial Surgery

A method of opening dura for decompressive craniectomies is described. Numerous cuts intersecting in a lattice pattern allow the dura to expand in a gradual and controlled manner minimising the chances of cortical laceration or venous kinking on the craniectomy edge.

Diabetic ketoacidosis in children may cause brain injuries ranging from mild to severe. Whether intravenous fluids contribute to these injuries has been debated for decades. We conducted a 13-center, randomized, controlled trial that examined the effects of the rate of administration and the sodium chloride content of intravenous fluids on neurologic outcomes in children with diabetic ketoacidosis. Children were randomly assigned to one of four treatment groups in a 2-by-2 factorial design (0.9% or 0.45% sodium chloride content and rapid or slow rate of administration). The primary outcome was a decline in mental status (two consecutive Glasgow Coma Scale scores of <14, on a scale ranging from 3 to 15, with lower scores indicating worse mental status) during treatment for diabetic ketoacidosis. Secondary outcomes included clinically apparent brain injury during treatment for diabetic ketoacidosis, short-term memory during treatment for diabetic ketoacidosis, and memory and IQ 2 t...

Concussion (defined as a traumatically induced alteration in mental status, not necessarily with loss of consciousness) is a common form of sports-related injury too often dismissed as trivial by physicians, athletic trainers, coaches, sports reporters, and athletes themselves. While ...

From the Department of Pediatrics and the Division of Emergency Medicine, Department of Internal Medicine, University of California, Davis, School of Medicine, Davis; the Division of Emergency Medicine, Children's Hospital and Health Center, San Diego; the Department of ...

It is largely unknown whether prolonged insonation with ultrasound impacts the ischemic brain tissue by itself. Our goal was to evaluate safety and the effect of high-frequency ultrasound on infarct volume in rats. Thirtytwo Long-Evans rats with permanent middle cerebral and carotid artery occlusions received either 2-MHz ultrasound at two levels of insonation power (128 or 10 mW) or no ultrasound (controls). We measured cerebral hemorrhage, indirect and direct infarct volume as well as edema volume at 24 h. No cerebral hemorrhages were detected in all animals. Exposure to low-power (10 mW) ultrasound resulted in a significantly decreased indirect infarct volume (p=0.0039), direct infarct volume (p=0.0031), and brain edema volume (p=0.01) compared with controls. Highpower (128 mW) ultrasound had no significant effects. An additional experiment with India ink showed a greater intravascular penetration of dye into ischemic tissues exposed to low-power ultrasound. Insonation with highfrequency, low-power ultrasound reduces ischemic brain damage in rat. Its effect on edema reduction and possible promotion of microcirculation could be used to facilitate drug and nutrient delivery to ischemic areas.

OBJECTIVE: The purpose of this study was to validate diffusion-weighted magnetic resonance imaging in the prediction of the evolutive course of brain edema and to establish its pathophysiologic presence in patients with eclampsia/severe preeclampsia. STUDY DESIGN: Seventeen patients with a clinical diagnosis of severe eclampsia/preeclampsia and T2 hyperintense brain lesions on routine magnetic resonance imaging were evaluated at hospital admission and 8 weeks later. RESULTS: Brain edema was reversible in 13 patients and irreversible in 4 patients, as indicated on follow-up magnetic resonance imaging. Sixteen of 17 patients were differentiated accurately into reversible and irreversible groups on the basis of diffusion imaging on hospital admission. Diffusion-weighted magnetic resonance imaging demonstrated a significant increase in water mobility in abnormal regions compared with normal-appearing brains in patients in the reversible group (1.34 ± 0.10 mm 2 vs 0.79 ± 0.08 mm 2 /s 3 10 ÿ3 , P < .001). In the irreversible group, restricted water diffusion was present, which was consistent with cytotoxic edema and early brain infarction in 3 of 4 patients. CONCLUSION: Diffusion-weighted magnetic resonance imaging can predict successfully the evolutive course of brain edema in an acute setting in these patients. Our findings indicate that brain edema is vasogenic, although ischemic/cytotoxic edema was observed less commonly. (Am J Obstet Gynecol 2003;189:1350-5.)

Second impact syndrome (SIS) is a widely feared complication of traumatic brain injury. Although postulated to occur after repeated concussion, the evidence for such a premise is not compelling. This paper reviews the published evidence for and against the existence of this controversial entity. Rather than SIS being a complication of recurrent concussion, it is far more likely that the clinical condition represents "diffuse cerebral swelling," a well-recognized complication of trau-matic brain injury. This condition is more common in children and adolescents, which reflects the known demographics of so-called "second impact syndrome." We propose that clinicians abandon the misleading term second impact syndrome and refer to the syndrome as diffuse cerebral swelling.

BACKGROUND AND PURPOSE: DTI of normal-appearing WM as evaluated by conventional MR imaging in mTBI has the potential to identify important regional abnormalities that relate to PCS. VBA was used to examine WM changes in acute mTBI. MATERIALS AND METHODS: WM was assessed between 1 and 6 days postinjury with voxel-based DTI analyses in 10 adolescent patients with mTBI and 10 age-matched control participants. In addition to the voxel-based group, analysis used to identify brain pathology across all patients with mTBI, 2 voxel-based linear regressions were performed. These analyses investigated the relation between 1) the ADC and PCS severity scores, and 2) ADC and scores on the BSI of emotional symptoms associated with mTBI. We hypothesized that frontotemporal WM changes would relate to symptoms associated with PCS and endorsed on the BSI. RESULTS: Patients with mTBI demonstrated significant reductions in ADC in several WM regions and in the left thalamus. As expected, no increases in ADC were found in any region of interest. All injury-affected regions showed decreased radial diffusivity, unchanged AD, and increased FA, which is consistent with axonal cytotoxic edema, reflective of acute injury. CONCLUSIONS: Whole-brain WM DTI measures can detect abnormalities in acute mTBI associated with PCS symptoms in adolescents. ABBREVIATIONS: AD ϭ axial diffusivity; ADC ϭ apparent diffusion coefficient; Bdb ϭ slope 10 Ϫ9 mm 2 /sec/BSI; Bdp ϭ slope 10 Ϫ9 mm 2 /sec/RPCSQ; Bfb ϭ slope 10 Ϫ3 1/BSI; Bfp ϭ slope 10 Ϫ3 1/RPCSQ; BSI ϭ Brief Symptom Inventory; Ca ϭ calcium; CC ϭ corpus callosum; DTI ϭ diffusion tensor imaging; FA ϭ fractional anisotropy; GM ϭ gray matter; GRP ϭ group; L ϭ left; mTBI ϭ mild traumatic brain injury; NA ϭ no statistical values; MNI ϭ Montreal Neurological Institute; PCS ϭ postconcussive symptoms; r ϭ Pearson product-moment correlation coefficient; R ϭ right; RD ϭ radial diffusivity; RPCSQ ϭ Rivermead Post Concussion Symptoms Questionnaire; SENSE ϭ sensitivity encoding; SPM ϭ statistical parametric mapping; TBI ϭ traumatic brain injury; VBA ϭ voxel-based analysis; WM ϭ white matter

This review focuses on the epidemiology, clinical description, pathophysiology, treatment, and prevention of high altitude cerebral edema (HACE). HACE is an uncommon and sometimes fatal complication of traveling too high, too fast to high altitudes. HACE is distinguished by disturbances of consciousness that may progress to deep coma, psychiatric changes of varying degree, confusion, and ataxia of gait. It is most often a complication of acute mountain sickness or high altitude pulmonary edema. The current leading theory of its pathophysiology is that HACE is a vasogenic edema; that is, a disruption of the blood-brain barrier, and we review possible mechanisms to explain this. Treatment and prevention of HACE are similar to those for the other altitude illnesses, but with greater emphasis on descent and steroids. We conclude the review with several case histories to illustrate key clinical features of the disorder.

Surgeons in abdominal and gynecological fields have pioneered the use of Seprafilm (a chemically modified sodium hyaluronate/carboxymethylcellulose absorbable adhesion barrier, Genzyme Biosurgery, Cambridge, MA, USA) to prevent adhesion but its use outside these specialties is not well documented. The authors have used Seprafilm for craniectomy closure in several patients as a dural substitute and anti-adhesion barrier. During emergent craniectomy, the dura mater is reapproximated and a layer of Seprafilm is placed over the dura as an onlay and anti-adhesion barrier. During subsequent surgery for bone flap replacement, dissection between the dural plane and overlying tissues has been completed easily. There has been minimal adhesion to the underlying Seprafilm/dural layer. The Seprafilm has been incorporated into the surrounding dural plane. No postoperative complications have been noted. Seprafilm's anti-adhesive properties and biodegradable characteristics make it useful as a dural onlay for craniectomy in which a second surgery is planned.

Charles (Chuck) Fleming&#39;s acute illness developed on June 12, 2000 induced by the ingestion of toxic doses of creatine monohydrate and high levels of propylene glycol (PEG). Chuck was taking several medications contained PEG that increased creatine bioavability and caused acute renal failure, severe hypophosphatemia, and ketoacidosis. Chuck&#39;s serum phosphorous level was 0.1 mg/dL (normal range: 2.8-4.9 mg/dL) and his

Background-The goals of this study were to compare ECG at moderate exercise in normoxia and hypoxia at the same heart rate, to provide evidence of independent predictors of hypoxia-induced ECG changes, and to evaluate ECG risk factors of severe high-altitude illness. Methods and Results-A total of 456 subjects performed a 20-minute hypoxia exercise test with continuous recording of ECG and physiological measurements before a sojourn above 4000 m. Hypoxia did not induce any conduction disorder, arrhythmias, or change in QRS axis. The amplitude of the P wave in V 1 was lower in hypoxia than in normoxia. The amplitudes of the R, S, and T waves and the Sokolow index decreased in hypoxia. Under hypoxia, the amplitude of the ST segment decreased in II and V 6 and increased in V 1 , the ST slope rose in V 5 and V 6 , and the J point was lower in II, V 5 , and V 6 . Multivariate regression of hypoxic/normoxic ratios of electrophysiological parameters and clinical characteristics showed a correlation between the decrease in Sokolow index and T-wave amplitude in V 5 with desaturation at exercise. Trained status and low body mass index were associated with a smaller decrease in T-wave amplitude in V 5 and V 6 . Comparison of ECG between subjects suffering or not suffering from severe high-altitude illness failed to show any difference.

A 29-year-old man was found dead lying on the bed in a hotel room in a famous Slovak mountain resort. He had a full-face diving mask on his face, connected through a diving breath regulator to a valve of an industrial (nondiving) high-pressure tank containing pure 100% nitrogen. The breath regulator (open-circuit type) used allowed inhalation of nitrogen without addition of open air, and the full-face diving mask assured aspiration of the gas even during the time of unconsciousness. At autopsy, we found the typical signs of suffocation. Toxicological analysis revealed 94.7% content of nitrogen in alveolar air. Following the completion of the police investigation, the manner of death was classified as a suicide. Within the medico-legal literature, there has been only one similar case of suicidal nitrogen inhalation described (1).

Concussion is defined as a biomechanically induced brain injury characterized by the absence of gross anatomic lesions. Early and late clinical symptoms, including impairments of memory and attention, headache, and alteration of mental status, are the result of neuronal dysfunction mostly caused by functional rather than structural abnormalities. The mechanical insult initiates a complex cascade of metabolic events leading to perturbation of delicate neuronal homeostatic balances. Starting from neurotoxicity, energetic metabolism disturbance caused by the initial mitochondrial dysfunction seems to be the main biochemical explanation for most postconcussive signs and symptoms. Furthermore, concussed cells enter a peculiar state of vulnerability, and if a second concussion is sustained while they are in this state, they may be irreversibly damaged by the occurrence of swelling. This condition of concussion-induced brain vulnerability is the basic pathophysiology of the second impact syndrome. N-acetylaspartate, a brain-specific compound representative of neuronal metabolic wellness, is proving a valid surrogate marker of the post-traumatic biochemical damage, and its utility in monitoring the recovery of the aforementioned "functional" disturbance as a concussion marker is emerging, because it is easily detectable through proton magnetic resonance spectroscopy.

Barometric pressure falls with increasing altitude and consequently there is a reduction in the partial pressure of oxygen resulting in a hypoxic challenge to any individual ascending to altitude. A spectrum of high altitude illnesses can occur when the hypoxic stress outstrips the subject's ability to acclimatize. Acute altitude-related problems consist of the common syndrome of acute mountain sickness, which is relatively benign and usually self-limiting, and the rarer, more serious syndromes of high-altitude cerebral edema and high-altitude pulmonary edema. A common feature of acute altitude illness is rapid ascent by otherwise fit individuals to altitudes above 3000 m without sufficient time to acclimatize. The susceptibility of an individual to highaltitude syndromes is variable but generally reproducible. Prevention of altitude-related illness by slow ascent is the best approach, but this is not always practical. The immediate management of serious illness requires oxygen (if available) and descent of more than 300 m as soon as possible. In this article, we describe the setting and clinical features of acute mountain sickness and highaltitude cerebral edema, including an overview of the known pathophysiology, and explain contemporary practices for both prevention and treatment exploring the comprehensive evidence base for the various interventions. (Prog Cardiovasc Dis 2010;52:467-484) An additional clinical assessment scoring is sometimes used. GI indicates gastrointestinal.

Background. Frameless stereotaxy or neuronavigation has evolved into a feasible technology to acquire intracaranial biopsies with good accuracy and little mortality. However, few studies have evaluated the diagnostic yield, morbidity, and mortality of this technique as compared to the established standard of frame-based stereotactic brain biopsy. We report our experience of a large number of procedures performed with one or other technique.

Intracerebral haemorrhage is an important public health problem leading to high rates of death and disability in adults. Although the number of hospital admissions for intracerebral haemorrhage has increased worldwide in the past 10 years, mortality has not fallen. Results of clinical trials and observational studies suggest that coordinated primary and specialty care is associated with lower mortality than is typical community practice. Development of treatment goals for critical care, and new sequences of care and specialty practice can improve outcome after intracerebral haemorrhage. Specifi c treatment approaches include early diagnosis and haemostasis, aggressive management of blood pressure, open surgical and minimally invasive surgical techniques to remove clot, techniques to remove intraventricular blood, and management of intracranial pressure. These approaches improve clinical management of patients with intracerebral haemorrhage and promise to reduce mortality and increase functional survival.

Traumatic brain injury (TBI) is one of the leading causes of disability and death which begins with the formation of edema as the persistent primary causative factor in TBI. Although medical management of cerebral edema by hypothermia, ventriculostomy, mannitol or hypertonic saline have been effective in treating edema, many of these therapies end up with some neurologic deficits, necessitating novel treatment options for treating post-TBI edema. This study investigated edema reducing effects of recombinant human Erythropoietin (rhEPO) in reducing acute brain edema in the CCI mouse model of TBI. Anti-edema effects of rhEpo in reducing acute brain edema after injury in the CCI mouse model of TBI were assessed by T2 weighted magnetic resonance imaging (T2wMRI) as the accurate detector of brain edema in correlation with Western blot analysis of cerebral aquaporin 4 (AQP4) index as the critical marker of edema. Results show that rhEpo treatment significantly reduced brain edema with con...

Background: Treatment with bevacizumab is associated with substantial radiologic response in patients with glioblastoma (GB). However, following this initial response, changes in T 2 -weighted MRI signal may develop, suggesting an infiltrative pattern of tumor progression. The aim of this study was to differentiate between vasogenic-edema versus tumor-infiltrative area in GB patients. Methods and materials: Fourteen patients with GB were longitudinally scanned, before and during intravenous bevacizumab therapy (5/10 mg/kg every 2-weeks). A total of 40 MR scans including conventional, diffusion, dynamic susceptibility contrast, dynamic contrast enhancement imaging, and MR-spectroscopy (MRS) were analyzed. Classification of non-enhancing fluid-attenuation-inversion-recovery (FLAIR) area was performed based on mean diffusivity, cerebral blood volume and flow maps, and further characterized using multiple MRI parameters. Results: The non-enhancing FLAIR lesion area was classified into: vasogenic-edema, characterized by reduced perfusion and increased FLAIR values; or tumor-infiltrative area, characterized by increased perfusion. Tumor-infiltrative area demonstrated a higher malignant pattern on MRS compared to areas of vasogenic-edema. Substantial reductions of the enhanced T 1 -weighted (58 ± 10%) and hyperintense FLAIR (53 ± 9%) lesion volumes were detected mainly during the first weeks of therapy, with a shift to an infiltrative pattern of tumor progression thereafter, as detected by an increase in tumor-infiltrative area in the majority of patients, which correlated with progression-free survival (week 8: r = −0.86, p = 0.003, week 16: r = −0.99, p = 0.001). Conclusion: Characterization of non-enhancing hyperintense FLAIR lesion area in GB patients can provide an MR-based biomarker, indicating a shift to an infiltrative progression pattern, and may improve therapy response assessment in patients following bevacizumab therapy.

Methanol is a common component of gasoline, antifreeze, washer fluid, perfume, household cleaners and various other industrial products. Acute methanol poisoning produces severe metabolic acidosis, serious neurologic sequelae and rarely imaging findings. In this paper, we describe a 35-year-old man with methanol intoxication who was in a comatose stage. Computed tomography (CT) showed widespread brain edema and hemorrhages localized in the supratentorial region of the temporal lobe, nearly 3 x 1 cm in a crescent shape, in the white matter surrounding the capsula externa and extending to the periventricular white matter and occipital lobes. Temporal lobe hemorrhage in our patient might also have been due to the effect of heparinization during hemodialysis, metabolic and lactic acidosis, or formate.

Brain edema formation is one of the most important mechanisms responsible for brain damage after ischemic stroke. Despite considerable efforts, no specific therapy is available yet. Arginine vasopressin (AVP) regulates cerebral water homeostasis and has been involved in brain edema formation. In the current study, we investigated the role of AVP V1 and V2 receptors on brain damage, brain edema formation, and functional outcome after transient focal cerebral ischemia, a condition comparable with that of stroke patients undergoing thrombolysis. C57/BL6 mice were subjected to 60-min middle cerebral artery occlusion (MCAO) followed by 23 h of reperfusion. Five minutes after MCAO, 100 or 500 ng of [deamino-Pen(1), O-Me-Tyr(2), Arg(8)]-vasopressin (AVP V1 receptor antagonist) or [adamantaneacetyl(1), O-Et-D-Tyr(2), Val(4), Abu(6), Arg(8,9)]-vasopressin (AVP V2 receptor antagonist) were injected into the left ventricle. Inhibition of AVP V1 receptors reduced infarct volume in a dose-dependent manner by 54% and 70% (to 29+/-13 and 19+/-10 mm3 versus 63+/-17 mm3 in controls; P&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.001), brain edema formation by 67% (to 80.4%+/-1.0% versus 82.7%+/-1.2% in controls; P&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.001), blood-brain barrier disruption by 75% (P&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.001), and functional deficits 24 h after ischemia, while V2 receptor inhibition had no effect. The current findings indicate that AVP V1 but not V2 receptors are involved in the pathophysiology of secondary brain damage after focal cerebral ischemia. Although further studies are needed to clarify the mechanisms of neuroprotection, AVP V1 receptors seem to be promising targets for the treatment of ischemic stroke.

Acute liver failure (ALF) is a clinical condition with high mortality. The most common cause of death in ALF is cerebral edema. We present a 12-year-old boy with hepatitis A-related acute liver failure in grade IV hepatic encephalopathy successfully managed in the ICU using continuous hypertonic saline as the preferred osmotherapy.

Present study was carried out to investigate the possible neuroprotective effect of pioglitazone, an antidiabetic agent, peroxisome proliferator-activated receptor γ (PPARγ) agonist on acute phase changes in mice model of cerebral ischemia induced by Bilateral Common Carotid artery Occlusion (BCCAO). BCCAO model was used to induce partial global cerebral ischemia. BCCAO induced significant brain infarct size and edema in saline treated control group along with high increase in oxidative stress showed by increase lipid peroxidation and decreased levels of antioxidants like superoxide superoxide dismutage, catalase, glutathione peroxidase. Pioglitazone (20 mg/kg, orally) administration showed neuroprotective effects by reducing cerebral infarct size significantly as compared to control group. Postischemic seizure susceptibility was also reduced as number of positive responders decreased to a significant number. Brain edema was subsided to a significant level. Pioglitazone reduced the plasma TNFα levels as compared to ischemia group significantly. Pioglitazone treatment also improved all the antioxidants levels showing activity against oxidative stress induced by BCCAO. Pioglitazone showed neuroprotection against ischemic insult suggesting the role of PPAR γ agonist in neuroprotective agents.

Acute cerebral edema in height (EACA) is a malignant form of acute mountain evil (MAM) or "Sorojche" it develops in people who suffer from a mismatch after rapid ascent to altitudes above 3000 meters on the level sea. Pathophysiologic disorder of the encephalopathy is partially known, but the clinical picture is an extension of the MAM, which is characterized by headache, nausea, vomiting, insomnia, dizziness and lassitude or fatigue that is exacerbated by a neurological disorder that manifests itself by ataxia, stupor, coma and even seizures. The background and the pathological examination and laboratory cabinet as TAC or RMN of the brain, chest radiograph, and the arterial blood gases are essential for the diagnosis and treatment. We present a patient of 22 years of age with the above characteristics, neuroimaging findings, treatment and evolution.

The aim of this study is to assess the anticerebral edema effect of glycerol on a large cerebral infarction with magnetic resonance imaging (MRI). Glycerol, which is widely used as an osmotic agent against cerebral edema, could exacerbate brain tissue shift, since it has been suggested that glycerol might shrink a noninfarcted hemisphere and worsen the mass effect after a large hemispheric cerebral infarction. To investigate these issues, changes in a large hemispheric infarction with cerebral edema were studied using MRI before and after glycerol administration. Infarct volumes, normal brain tissue volumes and lateral ventricle volumes, in addition to signal intensities of T 2 -weighted images, were measured in six patients before and after administration of 300 ml of glycerol. Ventricle volumes were significantly increased ( p = 0.0015) and the T 2 signal intensity of the post-treatment ischemic region decreased after glycerol administration. In contrast, no significant differences in either cerebral volume or T 2 signal intensity were seen in the noninfarcted hemisphere before and after administration. Our data suggest that glycerol does not exacerbate the mass effect on a large hemispheric infarction. D