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Cerebral Edema (cerebral + edema)
Selected AbstractsLeptomeningeal carcinomatosis from urinary bladder adenocarcinoma: A clinicopathological case studyNEUROPATHOLOGY, Issue 1 2005Kaoru Sugimori We report a 73-year-old male patient with leptomeningeal metastasis from urinary bladder adenocarcinoma. He was presented, with, prominent, hyperactive, delirium, during the course of the disease. Meningeal carcinomatosis was detected 5 days before his death, but the primary site of the malignant tumor could not be determined. Necropsy revealed leptomeningeal infiltration of many adenocarcinoma cells that covered the cerebrum. The leptomeninges of the right middle frontal gyrus, superior temporal gyrus, precentral gyrus and inferior parietal lobe were most severely affected by tumor cell infiltration. Cerebral edema was found to extensively cover the basal part of the temporal lobe. In the cerebrum, tumor cells were clustered in the perivascular spaces and had invaded localized areas of the frontal lobe. Vascular cell adhesion molecule (VCAM)-1 expression was detected in the small vessels of the cerebral upper cortical layers and of temporal subcortical u-fibers. Numerous astrocytes positive for cytokeratin AE1/AE3 were found in the frontal and temporal lobes. Meningeal carcinomatosis from urinary bladder adenocarcinoma is extremely rare and up-regulation of the adhesion molecules in the meningeal adenocarcinoma was confirmed. [source] Cerebral edema in diabetic ketoacidosis: an underestimated complication?PEDIATRIC DIABETES, Issue 2 2006Mark A. Sperling No abstract is available for this article. [source] Orthostatic Headaches in the Syndrome of the Trephined: Resolution Following CranioplastyHEADACHE, Issue 7 2010Bahram Mokri MD Objective., To draw attention to the syndrome of the trephined as a potential cause for orthostatic headaches without cerebrospinal fluid (CSF) leak. Background., Orthostatic headaches typically result from CSF leaks but sometimes may occur in conditions without any evidence of CSF leakage. Methods., A 37-year-old right-handed woman became comatose after a motor vehicle accident with cerebral contusions and massive left cerebral edema. A large frontoparietal craniectomy was carried out. In 5 months, she made good neurologic recovery. Freeze-preserved bone flap was placed back. In several weeks she was functionally near normal. Two years later, she began to complain of orthostatic headache and gradually additional manifestations appeared including progressive gait unsteadiness, imprecise speech, cognitive difficulties, and an increasing left hemiparesis along with progressive sinking of the skull defect and shift of the midline and ventricular distortion. She underwent removal of resorptive sinking bone flap and construction of an acrylic cranioplasty. Results., At 6-month follow-up, there was complete resolution of the orthostatic headaches, remarkable neurologic improvement along with resolution of midline shift and ventricular distortion. Conclusion., The syndrome of the trephined is yet another cause of orthostatic headaches without CSF leak. [source] Oxygen resuscitation does not ameliorate neonatal hypoxia/ischemia-induced cerebral edemaJOURNAL OF NEUROSCIENCE RESEARCH, Issue 9 2010Diana Carolina Ferrari Abstract Neonatal hypoxia/ischemia (HI) is a common cause of cognitive and behavioral deficits in children with hyperoxia treatment (HHI) being the current therapy for newborn resuscitation. HI induces cerebral edema that is associated with poor neurological outcomes. Our objective was to characterize cerebral edema after HI and determine the consequences of HHI (40% or 100% O2). Dry weight analyses showed cerebral edema 1 to 21 days after HI in the ipsilateral cortex; and 3 to 21 days after HI in the contralateral cortex. Furthermore, HI increased blood-brain barrier (BBB) permeability 1 to 7 days after HI, leading to bilateral cortical vasogenic edema. HHI failed to prevent HI-induced increase in BBB permeability and edema development. At the molecular level, HI increased ipsilateral, but not contralateral, AQP4 cortical levels at 3 and up to 21 days after HI. HHI treatment did not further affect HI-induced changes in AQP4. In addition, we observed developmental increases of AQP4 accompanied by significant reduction in water content and increase permeability of the BBB. Our results suggest that the ipsilateral HI-induced increase in AQP4 may be beneficial and that its absence in the contralateral cortex may account for edema formation after HI. Finally, we showed that HI induced impaired motor coordination 21 days after the insult and HHI did not ameliorate this behavioral outcome. We conclude that HHI treatment is effective as a resuscitating therapy, but does not ameliorate HI-induced cerebral edema and impaired motor coordination. © 2010 Wiley-Liss, Inc. [source] Application of intensive care medicine principles in the management of the acute liver failure patientLIVER TRANSPLANTATION, Issue S2 2008David J. Kramer Key Points 1Acute liver failure is a paradigm for multiple system organ failure that develops as a consequence of sepsis. 2In the United States, systemic inflammatory response, sepsis, and septic shock are common reasons for intensive care unit admission. Intensive care management of these patients serves as a template for the management of patients with acute liver failure. 3Acute liver failure is attended by high mortality. Although intensive care results in improved survival, the key treatment is liver transplantation. Intensive care unit intervention may open a "window of opportunity" and enable successful liver transplantation in patients who are too ill at presentation. 4Intracranial hypertension complicates the course for many patients with acute liver failure. Initially, intracranial hypertension results from hyperemia, which is cerebral edema that reduces cerebral blood flow and eventuates in herniation. The precepts of neurocritical care,monitoring cerebral perfusion pressure, cerebral blood flow, and cortical activity,with rapid response to hemodynamic abnormalities, maintenance of normoxia, euglycemia, control of seizures, therapeutic hypothermia, osmotic therapy, and judicious hyperventilation are key to reducing mortality attributable to neurologic failure. Liver Transpl 14:S85,S89, 2008. © 2008 AASLD. [source] Checkpoints and pitfalls in the experimental neuropathology of circulatory disturbanceNEUROPATHOLOGY, Issue 1 2003Toshihiko Kuroiwa In neural tissue injury many pathological processes are common to different neurological disorders, including cerebral ischemia. Because ischemia has a fundamentally simple impact on neural tissue, good laboratory modeling can help improve the general understanding of the neuropathological processes involved. Summarized here are some basic principles that should be followed to ensure that cerebral ischemia studies are reproducible and informative: (i) selection of an appropriate model of cerebral ischemia in an appropriate species (although rodents are widely used for genomic studies, the use of larger animals, with brain structures macroscopically similar to those of humans, is appropriate for many studies, e.g. of white matter lesions or the pathophysiology of cerebral edema); (ii) correct maintenance of physiological parameters, including body temperature, systemic blood pressure, and blood gas tensions, under appropriate general anesthesia; (iii) selection of an appropriate method of cerebral blood flow (CBF) monitoring (decisions include whether or not the experiment requires real-time monitoring, in vivo measurement, and CBF mapping); (iv) appropriate timing of drug application in therapeutic studies (many drugs that are effective when given immediately after a short period of ischemi are ineffective in clinical trials, probably because of longer periods of ischemia and delayed drug delivery in clinical settings); and (v) multiparametric evaluation of therapeutic effect (with the recent increase in diagnosis of cases of mild stroke, measurement of mortality and infarct size have proven to be insufficient for the evaluation of therapeutic effect). Use of mild ischemia models and batteries of neurological tests for individual neurological functions, such as motor, somatosensory, and visual function, are becoming important in experimental ischemia research. In histological evaluation, assessment of the extent of both selective neuronal loss and the infarct will become mandatory. Regional analysis of each brain structure and coordination of the results with the apparent neurological dysfunction is a promising approach. [source] Anesthetic management of staged separation of craniopagus conjoined twins,PEDIATRIC ANESTHESIA, Issue 3 2006MICHAEL GIRSHIN MD Summary We present a case of successful separation of craniopagus conjoined twins. The procedure was staged to permit each child to develop adequate independent cerebral venous drainage and to prevent deleterious, perioperative cerebral edema. Surgical hemorrhage, blood product delivery, and hemodilution were minimized. [source] Strategies to diminish the danger of cerebral edema in a pediatric patient presenting with diabetic ketoacidosisPEDIATRIC DIABETES, Issue 4 2006Mitchell L. Halperin First page of article [source] Frequency of sub-clinical cerebral edema in children with diabetic ketoacidosisPEDIATRIC DIABETES, Issue 2 2006Nicole S Glaser Abstract:, Symptomatic cerebral edema occurs in approximately 1% of children with diabetic ketoacidosis (DKA). However, asymptomatic or subclinical cerebral edema is thought to occur more frequently. Some small studies have found narrowing of the cerebral ventricles indicating cerebral edema in most or all children with DKA, but other studies have not detected narrowing in ventricle size. In this study, we measured the intercaudate width of the frontal horns of the lateral ventricles using magnetic resonance imaging (MRI) in children with DKA during treatment and after recovery from the DKA episode. We determined the frequency of ventricular narrowing and compared clinical and biochemical data for children with and without ventricular narrowing. Forty-one children completed the study protocol. The lateral ventricles were significantly smaller during DKA treatment (mean width, 9.3 ± 0.3 vs. 10.2 ± 0.3 mm after recovery from DKA, p < 0.001). Children with ventricular narrowing during DKA treatment (22 children, 54%) were more likely to have mental status abnormalities than those without narrowing [12/22 vs. 4/19 with Glasgow Coma Scale (GCS) scores below 15 during therapy, p = 0.03]. Multiple logistic regression analysis revealed that a lower initial PCO2 level was significantly associated with ventricular narrowing [odds ratio (OR) = 0.88, 95% confidence interval (95% CI) = 0.78,0.99, p = 0.047). No other variables analyzed were associated with ventricular narrowing in the multivariate analysis. We conclude that narrowing of the lateral ventricles is evident in just over half of children being treated for DKA. Although children with ventricular narrowing did not exhibit neurological abnormalities sufficient for a diagnosis of ,symptomatic cerebral edema', mild mental status abnormalities occurred frequently, suggesting that clinical evidence of cerebral edema in children with DKA may be more common than previously reported. [source] Progressive cerebral edema associated with high methionine levels and betaine therapy in a patient with cystathionine ,-synthase (CBS) deficiencyAMERICAN JOURNAL OF MEDICAL GENETICS, Issue 1 2002Reza Yaghmai Abstract Cystathionine ,-synthase (CBS) deficiency, the most common form of homocystinuria, is an autosomal recessive inborn error of homocysteine metabolism. Treatment of B6-nonresponsive patients centers on lowering homocysteine and its disulfide derivatives (tHcy) by adherence to a methionine-restricted diet. However, lifelong dietary control is difficult. Betaine supplementation is used extensively in CBS-deficient patients to lower plasma tHcy. With betaine therapy, methionine levels increase over baseline, but usually remain below 1,500 ,mol/L, and these levels have not been associated with adverse affects. We report a child with B6-nonresponsive CBS deficiency and dietary noncompliance whose methionine levels reached 3,000 ,mol/L on betaine, and who subsequently developed massive cerebral edema without evidence of thrombosis. We investigated the etiology by determining methionine and betaine metabolites in our patient, and several possible mechanisms for her unusual response to betaine are discussed. We conclude that the cerebral edema was most likely precipitated by the betaine therapy, although the exact mechanism is uncertain. This case cautions physicians to monitor methionine levels in CBS-deficient patients on betaine and to consider betaine as an adjunct, not an alternative, to dietary control. © 2002 Wiley-Liss, Inc. [source] Blood,brain barrier breakdown and repair by Src after thrombin-induced injuryANNALS OF NEUROLOGY, Issue 4 2010Da-Zhi Liu PhD Objective Thrombin mediates the life-threatening cerebral edema that occurs after intracerebral hemorrhage. Therefore, we examined the mechanisms of thrombin-induced injury to the blood,brain barrier (BBB) and subsequent mechanisms of BBB repair. Methods Intracerebroventricular injection of thrombin (20U) was used to model intraventricular hemorrhage in adult rats. Results Thrombin reduced brain microvascular endothelial cell (BMVEC) and perivascular astrocyte immunoreactivity,indicating either cell injury or death,and functionally disrupted the BBB as measured by increased water content and extravasation of sodium fluorescein and Evans blue dyes 24 hours later. Administration of nonspecific Src family kinase inhibitor (PP2) immediately after thrombin injections blocked brain edema and BBB disruption. At 7 to 14 days after thrombin injections, newborn endothelial cells and astrocytes were observed around cerebral vessels at the time when BBB permeability and cerebral water content resolved. Delayed administration of PP2 on days 2 through 6 after thrombin injections prevented resolution of the edema and abnormal BBB permeability. Interpretation Thrombin, via its protease-activated receptors, is postulated to activate Src kinase phosphorylation of molecules that acutely injure the BBB and produce edema. Thus, acute administration of Src antagonists blocks edema. In contrast, Src blockade for 2 to 6 days after thrombin injections is postulated to prevent resolution of edema and abnormal BBB permeability in part because Src kinase proto-oncogene members stimulate proliferation of newborn BMVECs and perivascular astrocytes in the neurovascular niche that repair the damaged BBB. Thus, Src kinases not only mediate acute BBB injury but also mediate chronic BBB repair after thrombin-induced injury. ANN NEUROL 2010;67:526,533 [source] High cortical spreading depression susceptibility and migraine-associated symptoms in Cav2.1 S218L miceANNALS OF NEUROLOGY, Issue 1 2010Arn M. J. M. van den Maagdenberg PhD Objective The CACNA1A gene encodes the pore-forming subunit of neuronal CaV2.1 Ca2+ channels. In patients, the S218L CACNA1A mutation causes a dramatic hemiplegic migraine syndrome that is associated with ataxia, seizures, and severe, sometimes fatal, brain edema often triggered by only a mild head trauma. Methods We introduced the S218L mutation into the mouse Cacna1a gene and studied the mechanisms for the S218L syndrome by analyzing the phenotypic, molecular, and electrophysiological consequences. Results Cacna1aS218L mice faithfully mimic the associated clinical features of the human S218L syndrome. S218L neurons exhibit a gene dosage,dependent negative shift in voltage dependence of CaV2.1 channel activation, resulting in enhanced neurotransmitter release at the neuromuscular junction. Cacna1aS218L mice also display an exquisite sensitivity to cortical spreading depression (CSD), with a vastly reduced triggering threshold, an increased propagation velocity, and frequently multiple CSD events after a single stimulus. In contrast, mice bearing the R192Q CACNA1A mutation, which in humans causes a milder form of hemiplegic migraine, typically exhibit only a single CSD event after one triggering stimulus. Interpretation The particularly low CSD threshold and the strong tendency to respond with multiple CSD events make the S218L cortex highly vulnerable to weak stimuli and may provide a mechanistic basis for the dramatic phenotype seen in S218L mice and patients. Thus, the S218L mouse model may prove a valuable tool to further elucidate mechanisms underlying migraine, seizures, ataxia, and trauma-triggered cerebral edema. ANN NEUROL 2010;67:85,98 [source] Frequency of sub-clinical cerebral edema in children with diabetic ketoacidosisPEDIATRIC DIABETES, Issue 2 2006Nicole S Glaser Abstract:, Symptomatic cerebral edema occurs in approximately 1% of children with diabetic ketoacidosis (DKA). However, asymptomatic or subclinical cerebral edema is thought to occur more frequently. Some small studies have found narrowing of the cerebral ventricles indicating cerebral edema in most or all children with DKA, but other studies have not detected narrowing in ventricle size. In this study, we measured the intercaudate width of the frontal horns of the lateral ventricles using magnetic resonance imaging (MRI) in children with DKA during treatment and after recovery from the DKA episode. We determined the frequency of ventricular narrowing and compared clinical and biochemical data for children with and without ventricular narrowing. Forty-one children completed the study protocol. The lateral ventricles were significantly smaller during DKA treatment (mean width, 9.3 ± 0.3 vs. 10.2 ± 0.3 mm after recovery from DKA, p < 0.001). Children with ventricular narrowing during DKA treatment (22 children, 54%) were more likely to have mental status abnormalities than those without narrowing [12/22 vs. 4/19 with Glasgow Coma Scale (GCS) scores below 15 during therapy, p = 0.03]. Multiple logistic regression analysis revealed that a lower initial PCO2 level was significantly associated with ventricular narrowing [odds ratio (OR) = 0.88, 95% confidence interval (95% CI) = 0.78,0.99, p = 0.047). No other variables analyzed were associated with ventricular narrowing in the multivariate analysis. We conclude that narrowing of the lateral ventricles is evident in just over half of children being treated for DKA. Although children with ventricular narrowing did not exhibit neurological abnormalities sufficient for a diagnosis of ,symptomatic cerebral edema', mild mental status abnormalities occurred frequently, suggesting that clinical evidence of cerebral edema in children with DKA may be more common than previously reported. [source] Applying circular posterior-hinged craniotomy to malignant cerebral edemasCLINICAL ANATOMY, Issue 3 2002H. Traxler Abstract Malignant brain edemas are often fatal, regardless of whether they are treated conservatively with sedation, blood pressure management, mannitol-therapy, hyperventilation and hypothermia, or non-conservatively with routine trepanation. Unfortunately, temporal trepanation may result in significant brain damage through herniation of the cerebrum at the edges of the trepanation openings. In one case of a 26-year-old male with severe head injury, a circular posterior-hinged craniotomy (CPHC) was performed after an ineffective unitemporal trepanation for evacuation of an acute subdural hematoma. This ultimately successful operation prompted experimental and morphologic investigations on a new surgical procedure for lowering intracranial pressure (ICP). In 12 of 15 human cadavers, an experimentally ICP was lowered by a CPHC with between 9,21 mm of frontal elevation of the calvaria. Using computer simulation, the frontal elevations of the calvaria were "virtually" performed on 3D reconstructions from CT scans of skulls, and the intracranial volume gained was measured with a computer software program. The volume increase of the cranial cavity showed a relatively constant relation to the cranial capacity and was increased by 6.0% (±0.4%) or 78 cm3 with a 10 mm elevation and by 12.4% (±0.7%) or 160 cm3 with a 20 mm elevation. There were no significant differences with skulls of different ages or ethnic origin; however, a significant effect of gender (F = 7.074; P , 0.013) on the gained volume in percent of the cranial capacity for the 20 mm elevation was observed. This difference can be explained by the inverse relationship between volume increase and cranial capacity (r = ,0.507; P , 0.004). Clin. Anat. Month:173,181, 2002. © 2002 Wiley-Liss, Inc. [source] | |||||||||||||