Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Brain Edema”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed1990

A rodent model of infusion brain edema: methodology and pathophysiological effects of saline and protein infusions.

To evaluate the potency of putative secondary mediators of brain edema and their possible contribution to edema related brain dysfunction an infusion model of brain edema was developed in rats. 100 ul of fluid (saline, 20% nonautologous protein) was infused over one hour into the left forebrain white matter through a stereotaxically placed (+1.2 mm ant to bregma, 3 mm lateral and 2.9 mm depth) 25 G needle. Brain tissue hydraulic resistance (Rt), regional cerebral blood flow (rCBF), cortical somatosensory evoked potentials (SEPs) and intracranial pressure (ICP) (intraventricular needle) were monitored during the infusion and rCBF CO2 reactivity (hydrogen clearance), local brain water content (microgravimetry), BBB integrity (Evans Blue 2%) and brain histology (H & E. Solochrome-cyanin) were evaluated after the infusion. Saline infusates caused no physiological dysfunction despite ipsilateral expansion and vacuolation of the subcortical white matter, separation of axonal bundles and a significant decrease (p = 3.8 x 10(-5] in local subcortical tissue specific gravity. Cortical histology and specific gravity adjacent to the infusion locus were normal. Rt significantly decreased (p = 6.5 x 10(-4] during the infusion but there were only minor increases in ICP. Findings with 20% protein infusates were similar despite a focal 65% decrement in the rCBF CO2 reactivity adjacent to the infusion site. This study has shown that a simple and inexpensive model of infusion brain edema can be created in the rat and that it provides a useful model for assessing the physiological effects of mediator compounds in the infusate. Potential applications and methodological improvements for this model are discussed.

Animals↗
PubMed1994

Combined treatment with nicardipine, phenobarbital, and methylprednisolone ameliorates vasogenic brain edema.

Free radicals formed around the edematous areas of the brain can cause lipoperoxidation of the cellular membrane, followed by calcium influx into the cell through calcium channels. These secondary insults may aggravate vasogenic brain edema. Since phenobarbital is a free radical scavenger, methylprednisolone has an antilipoperoxidation effect; and nicardipine is a calcium channel blocker, we hypothesized that combined treatment with phenobarbital, methylprednisolone, and nicardipine would be beneficial in vasogenic brain edema. This hypothesis was tested in Sprague-Dawley rats with a transdural cold-injury on the right parietal cortex. The animals were randomly divided into two groups. Animals in the treatment group were injected intraperitoneally with phenobarbital (4 mg/kg), methylprednisolone (50 mg/kg), and nicardipine (10 micrograms/kg) at 5 min and 8 hours after the cold-injury. The control animals were injected with saline. These animals were sacrificed 24 hours after the injury. The extent of brain edema was assessed by measuring the water content, the inulin distribution volume, and the distribution area of Evans blue in the brain. Our results showed that the water content of the edematous hemisphere was similar in the control and the treatment groups. However, Evans blue distribution area and inulin distribution volume of the treatment group were less than those of the control group by 12% and 31%, respectively. In conclusion, the combined treatment with phenobarbital, methylprednisolone and nicardipine is beneficial in vasogenic brain edema.

Animals↗
PubMed2004

Differential effects of prolonged isoflurane anesthesia on plasma, extracellular, and CSF glutamate, neuronal activity, 125I-Mk801 NMDA receptor binding, and brain edema in traumatic brain-injured rats.

BACKGROUND: Volatile anesthetics reduce neuronal excitation and cerebral metabolism but can also increase intracellular water accumulation in normal and injured brains. While attenuation of neuronal excitation and glutamate release are beneficial under pathological conditions, any increase in edema formation should be avoided. In the present study we investigated duration-dependent effects of the commonly used isoflurane/nitrous oxide (N2O) anesthesia on EEG activity, specific NMDA receptor binding, extracellular, CSF, and plasma glutamate, and cerebral water content in brain-injured rats subjected to short (30 minutes) or prolonged (4 hours) anesthesia. METHODS: Before controlled cortical impact injury (CCI), during prolonged (4-8 hours) or short anesthesia (7.5-8 hours after CCI), and before brain removal, changes in neuronal activity were determined by quantitative EEG analysis and glutamate was measured in arterial plasma. Brains were processed to determine acute and persisting changes in cerebral water content and 125I-Mk801 NMDA receptor binding at 8 and 32 hours after CCI, i.e., immediately or 24 hours after short or prolonged anesthesia. During prolonged anesthesia glutamate was measured via microdialysis within the cortical contusion. CSF was sampled before brain removal. FINDINGS: Prolonged isoflurane (1.8 vol%) anesthesia significantly increased EEG activity, plasma, cortical extracellular, and CSF glutamate, cortical and hippocampal 125I-Mk801 NMDA receptor binding, and cerebral water content in brain-injured rats. These changes were partially reversible within 24 hours after prolonged anesthesia. At 24 hours, CSF glutamate was significantly reduced following long isoflurane anesthesia compared to rats previously subjected to short anesthesia despite an earlier significant increase. Conclusions. The partially reversible increases in EEG activity, 125I-Mk801 NMDA receptor binding, cerebral water content, plasma and CSF glutamate appear important for physiological, pathophysiological, and pharmacological studies requiring prolonged anesthesia with isoflurane. Increases in extracellular cortical and plasma glutamate could contribute to acute aggravation of underlying tissue damage.

Anesthetics, Inhalation↗
PubMed1990

A two-dimensional, finite element analysis of vasogenic brain edema.

The authors constructed a two-dimensional model of vasogenic brain edema, using the finite element method (FEM). The model incorporates the following physical parameters: cerebrovascular hydraulic conductivity, metabolic water production, tissue hydraulic conductivity and compliance, tissue and plasma osmotic and hydrostatic pressures, cerebrospinal fluid hydrostatic pressure and absorption, intracerebral stress, and shift of brain tissue. These parameters, related by partial differential equations, were approximated numerically in time and space by the FEM. The results of computer simulation of brain edema by the FEM were compared with experimental data obtained in a feline cold injury brain edema model. Computer simulation predicted the changes observed in interstitial pressure, extent of edema, intracerebral stress distribution, and shift of brain tissue. The results indicate that the FEM, applied to a model of vasogenic brain edema, can be used to predict the time course and regional distribution of fluid accumulation and the accompanying regional stress and deformation of brain tissue.

Animals↗
PubMed1989

Comparative study of different iron-chelating agents in cold-induced brain edema.

Increasing numbers of reports demonstrate the importance of iron and oxygen free radicals in brain injury and brain edema. We investigated the protective effects of three different ferric and ferrous iron-chelating agents on cold-induced brain edema. Vasogenic brain edema was produced by a cortical freezing lesion. Thirty-eight cats were separated into five groups: Group 1 (N = 8): normal control group without lesion; Group 2 (N = 8): untreated group; Group 3 (N = 8): deferoxamine (extracellular and intracellular ferric iron chelator)-treated group; Group 4 (N = 8): 2,3-dihydroxybenzoic acid (extracellular ferric iron chelator)-treated group; and Group 5 (N = 6): 2,2-bipyridine (intracellular ferrous iron chelator)-treated group. In Groups 3, 4, and 5, each agent was administered intravenously 15 minutes before lesion production and 60 minutes later. Animals in Groups 2, 3, 4, and 5 were killed 6 hours after lesion production. Brain water content in 8 sampling areas was measured by the specific gravity method. Blood-brain barrier disruption was assessed by the spread of Evans blue dye measured by planimetry. Brain water contents and Evans blue dye extravasated areas were significantly reduced in Groups 3 and 5 in comparison to Groups 2 and 4. These data suggest that both ferrous and ferric iron-chelating agents, which can penetrate the cell membrane and, presumably, act intracellularly, are effective in reducing cold-induced brain edema.

2,2'-Dipyridyl↗
PubMed1997

[Protective effects of nimodipine on brain edema induced by pertussis bacilli in rats].

The changes of brain water content and Evan blue(EB) were investigated on the model of infection brain edema induced by Pertussis Bacilli(PB) in 72 rats. Nimodipine was admenistred to show its effect on the PB induced brain edema. The experiment results showed that the water content and EB content in the PB group were significantly increased than those normal group and normal saline group at 30 min, 4 hours and 24 hours after the injection of PB (P < 0.05). Nimodípine could significantly reduce brain water content and EB content, so that brain edema was attenuated. It indicates that nimodipine showed advantage to treatment of PB brain edema.

Animals↗
PubMed1985

Brain edema: ultrasound examination.

Sonographic examination of the brain in 10 patients who had cortical mass lesions was performed. Results were compared with findings of CT. In each case, brain edema surrounded the lesion, and the adjacent white matter had a diffusely echo-genic appearance that corresponded to the area of brain edema seen on CT.

Adult↗
PubMed1993

Effect of brain edema on infarct volume in a focal cerebral ischemia model in rats.

BACKGROUND AND PURPOSE: Infarct volume is one of the common indexes for assessing the extent of ischemic brain injury following focal cerebral ischemia. Accuracy in the measurement of infarct volume is compounded by postischemic brain edema that may increase brain volume in the infarcted region. We evaluated the effect of brain edema on infarct volume determined by triphenyltetrazolium chloride and hematoxylin and eosin stains in a focal cerebral ischemia model in rats. METHODS: In a middle cerebral artery occlusion model in rats, infarction is confined to the cerebral cortex. The infarct was delineated by triphenyltetrazolium chloride stain and, in selected samples, by hematoxylin and eosin stain. We determined infarct size at different times after the ischemic insult (6 hours to 7 days) in relation to the evolution of brain edema by the direct measurement of infarct volume. Indirect measurement to reduce the effect of edema on infarct volume was also conducted in the same brain samples. RESULTS: Direct measurement showed that infarct volume fluctuated with the evolution of brain edema (one-way analysis of variance, p < 0.0001). Infarct volume determined by indirect measurement was independent of the extent of brain edema and remained stable from 6 hours to 3 days after ischemia. There was a good correlation between triphenyltetrazolium chloride and hematoxylin and eosin stains in delineating infarct volume with both direct and indirect measurement. CONCLUSION: Traditional direct measurement of infarct volume is associated with an overestimation of infarct volume during the development of brain edema in the first 3 days after ischemia. This artifact can be reduced with indirect measurement, which is based on noninfarcted cortex volume.

Animals↗
PubMed1990

A mathematical model for vasogenic brain edema.

A two-dimensional model of vasogenic brain edema was constructed using the FEM. The model incorporates the following physical parameters: cerebrovascular hydraulic conductivity, metabolic water production, tissue hydraulic conductivity and compliance, tissue and plasma osmotic and hydrostatic pressures, CSF hydrostatic pressure and absorption, intracerebral stress, and shift of brain tissue. These parameters, related by partial differential equations, were approximated numerically in time and space by the FEM. The results of computer simulation of brain edema by the FEM were compared with experimental data of cold injury brain edema in cats. Computer simulation predicted the observed changes in interstitial pressure, extension of edema, intracerebral stress distribution, and displacement.

Animals↗
PubMed1992

Possible involvement of interleukin-1 in ischemic brain edema formation.

To determine the contribution of interleukin 1 (IL-1) on ischemic brain edema formation, the effect of recombinant human interleukin 1 beta (rhIL-1 beta), or zinc protoporphyrin (ZnPP) as an IL-1 blocker, on brain edema was studied in rats. The animals were subjected to 60 min of ischemia in a middle cerebral artery occlusion model. Immediately after reperfusion, rhIL-1 beta at a dose of 10 ng/2 microliters, or ZnPP at doses of 1 and 10 micrograms/2 microliters were topically applied into lateral cerebroventricle. In rhIL-1 beta-treated rats, ischemic brain edema formation was significantly increased in the dorsal and ventral areas of the caudate putamen 24 h after reperfusion, compared to that of vehicle-treated control rats. Furthermore, in ZnPP-treated rats, brain edema was decreased in both caudate-putamen areas. This suggests that IL-1 plays an important role in pathogenesis for post-ischemic brain edema.

Animals↗
PubMed1983

Induction of brain edema following intracerebral injection of arachidonic acid.

The effects of polyunsaturated fatty acids on brain edema formation have been studied in rats. Intracerebral injection of polyunsaturated fatty acids (PUFAs), including linolenic acid (18:3) and arachidonic acid (20:4), caused significant increases in cerebral water and sodium content concomitant with decreases in potassium content and Na+- and K+- dependent adenosine triphosphatase activity. There was gross and microscopic evidence of edema. Saturated fatty acids and monounsaturated fatty acid were not effective in inducing brain edema. The [125I]-bovine serum albumin spaces increased twofold and threefold at 24 hours with 18:3 and 20:4, respectively, indicating vasogenic edema with increased permeability of brain endothelial cells. Staining of the brain was observed five minutes after injection of Evans blue dye followed by arachidonic acid perfusion. A major decrease in brain potassium content was evidence of concurrent cellular (cytotoxic) edema as well. The induction of brain edema by arachidonic acid was dose dependent and maximal between 24 and 48 hours after perfusion. Dexamethasone (10 mg/kg) was effective in ameliorating the brain edema, whereas a cyclooxygenase inhibitor, indomethacin (10 mg/kg), was not. These data indicate that arachidonic acid and other PUFAs have the ability to induce vasogenic and cellular brain edema and further support the hypothesis that the degradation of phospholipids and accumulation of PUFAs, particularly arachidonic acid, initiate the development of brain edema in various disease states.

Animals↗
PubMed2002

Prolonged unilateral vasodilatation and brain edema in fulminant hepatic failure, associated with symptomatic seizure.

We report prolonged unilateral vasodilatation and hemispheric brain edema in a 49-year-old man with fulminant hepatic failure (FHF). The patient presented with a tonic-clonic seizure caused by a hypertensive subcortical hemorrhage in the left parietal lobe. Serial computed tomography (CT) scans showed progressive darkening of the ipsilateral hemisphere, suggesting hemispheric cerebral infarction, but the patient did not show clinical signs of deterioration. Brain magnetic resonance angiography showed dilation of the large arteries of the left hemisphere. Evaluation of cerebral blood flow 7 days postictus with single photon emission CT revealed marked ipsilateral hyperperfusion. The darkening of the hemisphere was brain edema elicited by hyperperfusion. Brain edema was reversible, disappearing 14 days postictus. Hemispheric brain edema was caused by unilateral cerebral vasodilatation and resultant hyperperfusion. Although brain edema is a major complication in FHF patients and cerebral hyperperfusion is responsible for edema formation, CT findings of these patients almost invariably show a bilateral lesion. Unilateral vasodilatation and subsequent hemispheric hyperperfusion may be due to overproduction of vasodilators, already abundant in the brains of patients with severe hepatic failure, by seizure activity.

Brain↗
PubMed1993

[A case of isolated adrenocorticotropic hormone deficiency with adrenocorticosteroid-responsive brain edema and repeated confusions].

A 60-year-old man developed confusional state with severely abnormal electroencephalogram and brain edema on computed tomography (CT) of brain. Adrenocorticosteroid therapy was dramatically effective for the confusional state and brain edema. The reduction of adrenocorticosteroid induced confusional states, and they disappeared with the increase of adrenocorticosteroid. When brain edema on CT disappeared, T 2-weighted magnetic resonance imagings revealed diffuse high signal in the white matter. A diagnosis of isolated adrenocorticotropic hormone deficiency was made by endocrinological examinations and clinical features. We suggest that brain edema in this patient is due to deficiency of glucocorticoid. High intensity area in the white matter may show the degeneration of the white matter following brain edema.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Meningiomas with brain edema: radiological characteristics on MRI and review of the literature.

OBJECT: Despite their benign characteristics, meningiomas are often accompanied by perifocal brain edema. The aims of this study are to determine what kind of characteristics on magnetic resonance (MR) image are indicative of a meningioma that produces brain edema and to investigate the mechanism responsible for brain edema accompanying meningiomas. METHODS: Fifty-one patients with meningioma were examined by magnetic resonance imaging (MRI), and tumor size, tumor location, shape of tumor margin, peritumoral rim, and signal intensity of tumor on T2-weighted image (T2WI) were compared and correlated with the presence versus absence of brain edema. Surgical histopathology was also examined and correlated with the MRI findings and brain edema. RESULTS: Shape of tumor margin, peritumoral rim, and signal intensity of tumor on T2WI correlated with brain edema on multivariate analyses. CONCLUSION: Invasive pattern of brain-tumor interface and hyperintensity on T2WI were indicative factors of meningiomas producing brain edema.

Brain↗
PubMed2001

Effects of hypothermia on thrombin-induced brain edema formation.

Recent studies have shown that thrombin plays an important role in brain edema formation after intracerebral hemorrhage (ICH). The possible mechanisms of thrombin-induced brain edema formation include blood-brain barrier (BBB) disruption and inflammatory response involving polymorphonuclear (PMN) leukocyte. Animal experiments have revealed that moderate therapeutic hypothermia improves pathological and functional outcome in various models of brain injury. In this study, we examined the effect of hypothermia on thrombin-induced brain edema formation. Effects of hypothermia on BBB permeability and the accumulation of PMN leukocytes were also determined to clarify the protective mechanism of hypothermia in this model. Anesthetized adult rats received an injection of 10 Units of thrombin into the basal ganglia. Animals were separated into the normothermic and hypothermic groups, which were housed in a room maintained at 25 degrees C and in a cold room maintained at 5 degrees C, respectively, for 24 h after the thrombin injection. The brain temperature in rats housed in a cold room reduced temporarily to approximately 30 degrees C and then gradually recovered to 35 degrees C by the end of the observation. Brain water content in the basal ganglia was significantly reduced in rats treated with hypothermia compared to the normothermic rats (84.3+/-0.2 vs. 82.4+/-0.1%; P<0.01). The decrease of brain water content was accompanied with a significant reduction in BBB permeability to Evan's blue dye and in accumulation of PMN leukocytes. This study indicates that hypothermic treatment significantly reduces thrombin-induced brain edema formation in the rat. Inhibition of thrombin-induced BBB breakdown and inflammatory response by hypothermia appear to contribute to brain protection in this model. Hypothermic treatment may provide an approach to potentially reduce ongoing edema after ICH.

Animals↗
PubMed1996

MIB-1 staining index and peritumoral brain edema of meningiomas.

BACKGROUND: Growth rates and tumor aggressiveness of meningiomas are thought to be closely related to brain edema development. However, histopathologic data alone are not consistently accurate predictors of the behavior and clinical course of a meningioma. METHODS: The authors examined 57 histologically proven intracranial meningiomas to identify factors, including growth fractions determined by MIB-1 immunostaining, that may influence the development of meningioma-associated peritumoral brain edema. There were 54 benign, 2 atypical, and 1 anaplastic meningiomas. The MIB-1 staining index (SI) percentage was defined as the number of MIB-1 positive cells divided by the total number of tumor cells in a 1.037-square millimeter area on the slide. The extent of peritumoral brain edema was determined using preoperative magnetic resonance imaging. The extent of edema was classified as Grade 0,1, or 2 (GR0, GR1, or GR2), in order of increasing severity. RESULTS: The MIB-1 SIs of the 57 cases ranged from 0.06-6.8% (median, 0.80%). There were 26 GR0, 20 GR1, and 11 GR2 edema cases. The MIB-1 SI rose in order of increasing edema severity. There was a statistically significant correlation between the MIB-1 SI and the extent of brain edema (P<0.0001), and also between the tumor size and the extent of brain edema (P=0.001). Meningothelial and atypical/anaplastic meningiomas were associated with peritumoral brain edema more often than any other subtype (P<0.005). CONCLUSIONS: Growth fractions, as determined by MIB-1 immunostaining, rise with increasing severity of peritumoral brain edema, indicating a close relationship between tumor aggressiveness and edema development.

Adult↗
PubMed2001

Indomethacin prevents the development of experimental ammonia-induced brain edema in rats after portacaval anastomosis.

Patients with fulminant hepatic failure (FHF) die with brain edema, exhibiting an increased cerebral blood flow (CBF) at the time of cerebral swelling. Mild hypothermia prevents brain edema in experimental models and in humans with FHF, an effect associated with normalization of CBF. To study the effects of alterations of CBF on the development of brain edema, we administered intravenous (IV) indomethacin to rats receiving an ammonia infusion after portacaval anastomosis. This model predictably develops brain edema and a marked increase in CBF at 3 hours of infusion. Brain water was measured with the gravimetry technique; CBF was monitored with both laser Doppler flowmetry and radioactive microspheres, whereas intracranial pressure (ICP) was monitored with a cisterna magna catheter. Coadministration of indomethacin prevented the increase in CBF seen with ammonia alone (110 +/- 19% vs. -2 +/- 9%) as well as the increase in brain water (80.86 +/- 0.12% vs. 80.18 +/- 0.06%) and the increase in ICP. Plasma ammonia and brain glutamine levels were markedly elevated in the ammonia-infused group and unaffected by indomethacin. However, ammonia uptake by the brain was significantly reduced by indomethacin. Levels of 6-keto-PGF(1alpha), a stable metabolite of prostacyclin, were reduced in the cerebrospinal fluid (CSF) of indomethacin-treated animals. As with mild hypothermia, avoiding cerebral vasodilatation with indomethacin will prevent the development of brain edema in this hyperammonemic model. Cerebral vasoconstriction reduces cerebral ammonia uptake and, if selective to the brain, may be of benefit in FHF.

6-Ketoprostaglandin F1 alpha↗