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At least 37 records · Page 2Linked to original sources

PubMed1993

[Extensive subdural hematoma with brain edema and brain death. Sequela of late manifestation of vitamin K deficiency].

After an uneventful pregnancy and birth without vitamin-K-prophylaxis a seven-week-old breast-fed infant showed a subdural hemorrhage caused by vitamin-K-deficiency. Laboratory investigations indicated a subclinical cholestasis. The infant died 3 days later. This case once again provides a strong argument for routine vitamin-K-prophylaxis after birth for all infants.

Blood Coagulation Tests↗

PubMed2000

Attenuation of brain edema, blood-brain barrier breakdown, and injury volume by ifenprodil, a polyamine-site N-methyl-D-aspartate receptor antagonist, after experimental traumatic brain injury in rats.

OBJECTIVE: Traumatic brain injury (TBI) has been shown to induce a significant change in polyamine metabolism. Polyamines and polyamine-dependent calcium influx play an important role in mediating the effects of excitotoxic amino acids at the N-methyl-D-aspartate (NMDA) receptor site. We studied the effects of ifenprodil, known as a noncompetitive inhibitor of polyamine sites at the NMDA receptor, on brain edema formation, blood-brain barrier breakdown, and volume of injury after TBI. METHODS: Experimental TBI was induced in Sprague-Dawley rats by a controlled cortical impact device, functioning at a velocity of 3 m/s to produce a 2-mm deformation. Ifenprodil or saline (10 mg/kg) was injected intraperitoneally immediately after the cortical impact injury and then every 90 minutes until 6 hours after TBI. Blood-brain barrier breakdown was evaluated quantitatively 6 hours after injury by fluorometric assay of Evans blue extravasation. Brain water content, an indicator of brain edema, was measured with the wet-dry method 24 hours after TBI. Injury volume was quantitated from the brain slices stained with 2% cresyl violet solution 7 days after TBI. RESULTS: Blood-brain barrier breakdown was significantly lower in the traumatic cortex of the ifenprodil-treated group than in the saline-treated group (84.4 +/- 26.8 microg/g versus 161.8 +/- 27 microg/g, respectively, P < 0.05). Brain edema was significantly reduced in the cortex of the ifenprodil-treated group relative to that in the saline-treated group (80.9 +/- 0.5% versus 82.4 +/- 0.6% respectively, P < 0.05). Ifenprodil treatment reduced injury volume significantly (14.9 +/- 8.1 mm3 versus 24.4 +/- 6.7 mm3, P < 0.05). CONCLUSION: The polyamine-site NMDA receptor antagonist ifenprodil affords significant neuroprotection in a controlled cortical impact brain injury model and may hold promise for the discovery and treatment of the mechanism of delayed neurological deficits after TBI.

Animals↗

PubMed1992

The role of bradykinin in the etiology of vasogenic brain edema and perilesional brain dysfunction.

The feline infusion model of brain edema was used to evaluate the role of bradykinin in the etiology and pathophysiology of vasogenic brain edema. Bradykinin (3 or 90 ug in 600 microL saline) did not alter normocapnic regional cerebral blood flow (rCBF) nor induce specific changes in either the somatosensory (SEP) or motor (MEP) evoked potentials. The mean increases in ICP (from 4.5 to 16.1 mmHg) and peri-infusion white matter water content (from 69.4 to 79.8 ml/100 g tissue), mean decrease in lumped craniospinal compliance (from 0.040 to 0.014 ml/mmHg) and local histological changes were all similar to those after 600 microL saline infusion. The interstitial bradykinin infusion caused focal blood-brain-barrier (BBB) opening to Evans Blue dye and was chemotaxic for granulocytes. After the infusion there was a global loss of rCBF CO2 reactivity but there was no ischemia at normocapnia. These results show that bradykinin in brain edema fluid, at concentrations greater than those found in neuropathological conditions, can open the BBB of normal cerebral parenchymal capillaries and cause vascular dysregulation. In neuropathological conditions bradykinin may therefore potentiate formation of vasogenic brain edema but does not contribute to perilesional brain dysfunction.

Animals↗

PubMed1999

Ultrastructural pathology of Golgi apparatus of nerve cells in human brain edema associated to brain congenital malformations, tumours and trauma.

The alterations induced by ischemia and anoxia upon smooth endoplasmic membranes are studied in 38 patients with congenital malformations, brain tumours and brain trauma. The effects of vasogenic and cytotoxic brain edema are examined in the Golgi apparatus of nerve and endothelial cells. Samples of cortical biopsies were conventionally processed for transmission electron microscopy. Cortical biopsies were performed according to the basic principles of Helsinki declaration. Slices of 2 to 5 mm were immediately fixed in the surgical room in 4% glutaraldehyde-0.1 M sodium phosphate buffer, pH 7.4 at 4 degrees C, and postfixed in 1% osmium tetroxide in similar buffer. The pathological alterations of the Golgi complex were studied in samples with moderate and severe brain edema. Moderate edema was mainly found in congenital malformations and severe edema in brain trauma and tumours. In some severely edematous neurons, observed in hydrocephalus associated to Arnold-Chiari malformation, small vesicular type Golgi complexes and atrophic ones were observed, characterized mainly by partial or total disappearance of stacked Golgi cisternae and presence of congregated vesicular profiles. In brain trauma and tumours the Golgi complex showed enlargement and fragmentation of the stacked cis- medial- and trans-Golgi cisternae and vacuolization of trans-Golgi network. In addition, an increased formation of Golgi and coated vesicles was observed in the cis- and trans-Golgi regions. Most Golgi and clathrin coated vesicles were observed throughout the cytoplasm suggesting an increased vesicular transport. In severe edema the nerve cell plasma membranes appeared fragmented, presumably due to an interference of the protein insertion process into the plasma membrane. In brain trauma, a hypertrophic Golgi complex was observed in some nerve cells and endothelial cells of cortical capillaries, with increased formation of Golgi and coated vesicles. The ischemia and anoxia associated to the vasogenic and cytotoxic brain edema induced enlargement, fragmentation and disappearance of stacked Golgi cisternae.

Adolescent↗

PubMed1990

Effect of atrial natriuretic peptide on ischemic brain edema: changes in brain water and electrolytes.

The effects of intraventricularly administered atrial natriuretic peptide (ANP) on the brain water, sodium, and potassium contents in ischemic brain edema were investigated. By use of a three-vessel occlusion model, ischemic brain edema was produced in the rat brain by 15 minutes of global ischemia followed by recirculation. Water content was measured by means of a drying/weighing method; sodium and potassium contents were measured by means of flame photometry. The effects of intraventricular administration of ANP were evaluated by a comparison between the groups given 2 and 5 micrograms of atriopeptin II (treated) and those given 0.9% NaCl (sham-treated). The treated groups showed significant decreases in brain water (P less than 0.02) and sodium (P less than 0.01) contents at 15 and 30 minutes after recirculation, whereas the brain potassium contents remained unaltered. Before ischemia and immediately after 15 minutes of ischemia, intraventricularly administered ANP did not significantly change the brain water, sodium, or potassium contents. There was no significant difference in the effect on the amount of brain water and sodium between the two doses (2 and 5 micrograms). These effects of ANP were thought not to be mediated by primary changes in serum osmolality and sodium and potassium concentrations, because intraventricular administration of ANP did not change them significantly. The present results reveal that, in ischemic brain edema, ANP may act directly on the central nervous system to inhibit brain water and sodium accumulation.

Animals↗

PubMed2000

Mild hypothermia delays the onset of coma and prevents brain edema and extracellular brain glutamate accumulation in rats with acute liver failure.

Mild hypothermia is effective in the prevention of brain edema associated with cerebral ischemia and traumatic brain injury. Brain edema is also a serious complication of acute liver failure (ALF). To assess the effectiveness of hypothermia in ALF, groups of rats were subjected to hepatic devascularization (portacaval anastomosis, followed 48 hours later by hepatic artery ligation), and body temperatures were maintained at either 35 degrees C (hypothermic) or 37 degrees C (normothermic). Mild hypothermia resulted in a significant delay in the onset of severe encephalopathy and in reduction of brain water content compared with normothermic ALF rats (control [n = 8] 80.22%; ALF-37 degrees C [n = 8] 81.74%; ALF-35 degrees C [n = 8] 80.48% [P <.01 compared with ALF-37 degrees C]). This protective effect was accompanied by a significant reduction of cerebrospinal fluid (CSF) (but not plasma) ammonia concentrations (CSF ammonia: control: 0.05 mg/dL; ALF-37 degrees C: 1.01 mg/dL; ALF-35 degrees C: 0.07 mg/dL, P <.01 compared with ALF-37 degrees C). In vivo cerebral microdialysis studies revealed that mild hypothermia resulted in a significant reduction of extracellular glutamate concentrations in the brains of rats with ALF (control: 1. 06 micromol/L; ALF-37 degrees C: 2.74 micromol/L; ALF-35 degrees C: 1.49 micromol/L [P <.01 compared with ALF-37 degrees C]). These findings suggest that: 1) mild hypothermia is an effective approach to the prevention of the central nervous system consequences of experimental ALF; and that 2) the beneficial effect of hypothermia is mediated via mechanisms involving reduced blood-brain transfer of ammonia and/or reduction of extracellular brain glutamate concentrations. Mild hypothermia may be an effective approach to delay the onset of brain edema in patients with ALF awaiting liver transplantation.

Ammonia↗

PubMed1999

Does growth hormone augment brain edema caused by brain injury? A study with a freeze brain injury model in the rat.

OBJECTIVE: Because of the known sodium and water retention associated with growth hormone (GH) therapy, it is crucial to evaluate the safety of GH after brain injury. To clarify this issue, we investigated whether GH affects brain edema in a rat brain freeze-injury model. METHODS: Male Wistar rats (n = 29) were divided into four groups according to the substance injected (GH vs. normal saline) and whether the brain was injured or not. The subcutaneous injections of GH (0.8 IU/kg) or saline were given 24 hours apart. In the injury groups, after the second injection, an aluminum rod (4-mm diameter) cooled to -50 degrees C was placed on the exposed dura mater in the right parietal region for 4 minutes, under anesthesia. At 4 hours after the insult, brain and skeletal muscle were excised and their water content was measured by drying. RESULTS: Freeze injury of the brain caused an increase in water and sodium content in skeletal muscle. GH injection augmented this edema in skeletal muscle. Freeze injury of the brain also caused an increase in water and sodium content in the injured hemisphere of the brain. GH injection did not exacerbate this edema in injured brain tissue. Neither freeze injury nor GH injection caused brain edema in the noninjured hemisphere or in the cerebellum. CONCLUSION: GH administration did not augment brain edema caused by brain injury in our model.

Animals↗

PubMed1984

Resolution of brain edema in severe brain injury at controlled high and low intracranial pressures.

A series of 87 patients with severe brain injury were studied. Intracranial pressure (ICP) monitoring and external ventricular drainage were used to control ICP at high and low levels. Clearance of ytterbium-169-labeled diethylenetriaminepentaacetic acid (169Yb-DTPA), Evans blue dye, and ventricular cerebrospinal fluid protein was measured at the two ICP levels over consecutive periods of 4 hours to confirm clearance of brain edema. The results support the hypothesis that brain edema is in part absorbed in the cerebrospinal fluid via transventricular flow.

Adolescent↗

PubMed1996

Dextrorphan reduces infarct volume, vascular injury, and brain edema after ischemic brain injury.

Focal cerebral ischemia confined to the cerebral cortex in the right middle cerebral artery (MCA) territory was induced by temporary ligation of the MCA and both common carotid arteries (CCAs). Reperfusion was initiated by releasing all three arterial occlusions after 90 min of ischemia. Infarct volume was morphometrically measured after triphenyltetrazolium chloride staining 24 h postischemia. Blood-brain barrier breakdown was assessed 4 h postischemia by measuring vascular permeability to fluorescein isothiocyanate-conjugated dextran (FITC-D), a macromolecule tracer. Ischemic brain edema was measured based on percent water content, 24 h postischemia. Dextrorphan (DX) 20-10 mg/kg given ip 15 min before ischemia reduced infarct volume in a dose-dependent manner with an apparent U-shaped dose-response curve; best protection was observed at 30 mg/kg. Posttreatment at 30 min, but not 60 min, was still effective. DX (30 mg/kg, given 15 min before ischemia) also reduced the postischemic increase in vascular permeability and brain edema in the right MCA cortex. Results from this study support the idea that NMDA receptor activation contributes to blood-brain barrier breakdown and brain edema after ischemic insults

Analysis of Variance↗

PubMed1988

Mediators of brain edema and secondary brain damage.

Progress is our understanding of the roles of vasogenic and cytotoxic brain edema in secondary brain damage can be expected from studies of the ability of biochemical factors to open the blood-brain barrier, derange the microcirculation, and cause cell swelling and necrosis. Mediator compounds are considered to form or to become released in an area of primarily damaged brain (necrosis) and to enter the cerebral parenchyma through the broken blood-brain barrier from the intravascular space. Many biochemical factors must be considered. We suggested three criteria for determining the roles of mediators: a) they must inflict brain tissue damage, b) they must occur in pathologic concentrations or in compartments not normally present, and c) specific inhibition should attenuate secondary brain damage. These requirements are met by the kallikrein-kinin system and by glutamate. In the case of arachidonic acid and its many metabolites, the concept is difficult to test because fatty acids may be active only if not bound to proteins, and therapeutic inhibition might be difficult. A variety of mediators may enhance each other in a cascade manner by various initiating reactions that might be amenable for pharmacologic inhibition.

Animals↗

PubMed1994

Peritumoral brain edema associated with pediatric brain tumors: characteristics of peritumoral edema in developing brain.

The incidence and clinical significance of peritumoral brain edema in pediatric patients is not well understood. The purpose of this study is to clarify the clinical significance of peritumoral brain edema in pediatric patients. Seventy seven pediatric patients (under 15 year old) with brain tumor were studied by MRI. The volume of peritumoral edema and brain tumor were measured by integration of the cross-sectional area on serial MRI. The severity of brain edema was expressed by the ratio of edema volume to tumor volume. The results were compared with that of 408 adult patients with brain tumor. Incidence of the brain edema associated with supratentorial tumors is lower in pediatric group than in adult. Severity of brain edema is also less extent in the pediatric group. Forty two percent of supratentorial gliomas in pediatric group showed peritumoral edema. On the other hand, 63% of adult group showed peritumoral brain edema. In general, pediatric brain tumors rarely associated with marked peritumoral brain edema which observed in the adult group. However, intraventricular or paraventricular tumors with obstructed hydrocephalus showed remarkable brain edema in pediatric group. Low incidence and less severity of peritumoral edema are caused not only by histological bias of tumors, but also by the biological nature of developing brain.

Adolescent↗

PubMed1984

The role of brain edema in epileptic brain damage induced by systemic kainic acid injection.

Edema formation and blood-brain barrier permeability was studied in animals with epileptic seizures induced by subcutaneous injection of kainic acid. Brain edema was most pronounced between 3 and 24 h after kainic acid injection. It was reflected by massive swelling of perineuronal and perivascular astroglia. Three hours after kainic acid perivascular astroglia swelling resulted in disturbance of local microcirculation in the affected brain areas. In addition, compression of drainage veins by the edematous brain induced focal perivenous hemorrhages similar to herniation damage in human brain edema. Tracer studies with sodium fluorescein, Evans blue, albumin and horseradish peroxidase revealed only a mild increase in the permeability of cerebral vessels, topographically unrelated to areas of brain edema. This finding indicates the presence of cytotoxic brain edema in kainic acid-induced epileptic brain damage. Treatment of brain edema with dexamethasone did not influence the incidence and severity of kainic acid-induced epileptic brain damage. However, in 54% of animals injected with kainic acid, lesions were completely prevented by treatment of brain edema with mannitol. The present results indicate that brain edema plays an important role in the pathogenesis of epileptic brain damage following systemic kainic acid intoxication. It is suggested that in this model of limbic epilepsy the brain edema is due to the massive ionic imbalance elicited in the affected brain regions by the kainic acid-induced persistent neuronal excitation.

Animals↗

PubMed1982

[Unilateral inferior temporal lobectomy with hippocampectomy for acute ischemic brain edema].

Intractable brain edema with hippocampal gyrus herniation through the incisura of the tentorium is a fatal complication of the main cerebral artery occlusion and severe vasospasm following subarachnoid hemorrhage. We presented 10 operative cases of ischemic brain edema, 3 due to middle cerebral artery occlusion, 2 due to internal carotid artery occulsion and 5 due to severe vasospasm, discussing the surgical indication and prognosis in severe ischemic brain edema cases. Internal decompression by frontal and anterior temporal lobectomy with extensive craniectomy was done in 4 cases and hippocampectomy with extensive craniectomy in 5 cases with hippocampal herniation. Of the 8 survivors, one was fully independent, five required assistance and two totally disabled in activity of daily living. Patients with ischemic brain edema due to main cerebral artery occlusion showed better recovery by internal decompression with hippocampectomy than those with vasospasm. From above results, inferior and medial temporal lobectomy including the hippocampal gyrus to relieve peduncle compression, blockage of cerebrofluid circulation proved life saving in patients with severe ischemic brain edema.

Acute Disease↗

PubMed2000

Neuroprotective effects of citicoline on brain edema and blood-brain barrier breakdown after traumatic brain injury.

OBJECT: Cytidine 5'-diphosphocholine (CDPC), or citicoline, is a naturally occurring endogenous compound that has been reported to provide neuroprotective effects after experimental cerebral ischemia. However, in no study has such protection been shown after traumatic brain injury (TBI). In this study the authors examined the effect of CDPC on secondary injury factors, brain edema and blood-brain barrier (BBB) breakdown, after TBI. METHODS: After anesthesia had been induced in Sprague-Dawley rats by using 1.5% halothane, an experimental TBI was created using a controlled cortical impact (CCI) device with a velocity of 3 m/second, resulting in a 2-mm deformation. Four sham-operated control animals used for brain edema and BBB breakdown studies underwent the same surgical procedure, but received no injury. Brain edema was evaluated using the wet-dry method 24 hours postinjury, and BBB breakdown was evaluated by measuring Evans blue dye (EBD) extravasation with fluorescein 6 hours after TBI. The animals received intraperitoneal injections of CDPC (50, 100, or 400 mg/kg two times after TBI [eight-10 animals in each group]) or saline (eight animals) after TBI. Traumatic brain injury induced an increase in the percentage of water content and in EBD extravasation in the injured cortex and the ipsilateral hippocampus. No significant benefit from CDPC treatment was observed at a dose of 50 mg/kg. Cytidine 5'-diphosphocholine at a dose of 100 mg/kg attenuated EBD extravasation in both regions, although it reduced brain edema only in the injured cortex. In both regions, 400 mg/ kg of CDPC significantly decreased brain edema and BBB breakdown. CONCLUSIONS: This is the first report in which dose-dependent neuroprotective effects of CDPC have been demonstrated in the injured cortex as well as in the hippocampus, a brain region known to be vulnerable to injury, after experimental TBI. The results of this study suggest that CDPC is an effective neuroprotective agent on secondary injuries that appear following TBI.

Animals↗

PubMed1988

Neuropharmacologic control of cerebral capillary permeability: current implications for therapy of vasogenic brain edema.

Vasogenic brain edema occurs as a result of a diverse spectrum of central nervous system pathology. The fundamental physiologic abnormality of vasogenic brain edema is an increase in cerebral capillary permeability. It is hypothesized that the recent development of new, potent, synthetic vasopressin antagonists will make it possible to impede the formation of vasogenic brain edema by the intraventricular administration of such agents with the subsequent inhibition of the neural control of brain capillary permeability by the locus ceruleus. The action of the vasopressin antagonists should be synergistic with the anti-edema effects of central alpha-adrenergic blockade produced by phentolamine. The combination of these two modes of therapy is expected to produce an increase in intracranial pressure which will require additional forms of medical therapy to control, in spite of the overall decrease of brain parenchymal water content.

Blood-Brain Barrier↗

PubMed2000

Reduced brain edema after traumatic brain injury in mice deficient in P-selectin and intercellular adhesion molecule-1.

Platelet (P-) selectin and intercellular adhesion molecule-1 (ICAM-1) mediate accumulation of neutrophils in brain. However, the mechanisms regulating neutrophil accumulation and damage after traumatic brain injury (TBI) are poorly defined. We hypothesized that mice deficient in both P-selectin and ICAM-1 (-/-) would have decreased brain neutrophil accumulation and edema, and improved functional and histopathological outcome after TBI compared with wild-type (+/+). In Protocol I, neutrophils and brain water content were quantified at 24 h after TBI. No difference in brain neutrophil accumulation was observed between groups; however, brain edema was decreased in dual P-selectin and ICAM-1 -/- (P < 0.05 vs. +/+ mice). In Protocol II, after TBI, tests of motor and memory function and histopathology were assessed over 21 days. No difference in motor or memory function or histopathological damage was observed between +/+ and -/- mice. A role for adhesion molecules in the pathogenesis of brain edema independent of leukocyte accumulation in brain is suggested.

Animals↗

PubMed1990

Brain edema, autoregulation, and calcium antagonism. An experimental study with nimodipine.

We investigated the effects of the calcium entry blocker nimodipine on cerebral autoregulation, BBB, and vasogenic edema in animal experiments. In the first series of rats, ICBF was measured with H2 clearance using a balanced multiwire surface electrode. Variations in blood pressure (SAP), which was measured via femoral catheter, were induced by infusion of norfenefrine (pressure increase) and by hemorrhage (pressure decrease). The effect of SAP on the cerebral microcirculation was evaluated. In control animals receiving nimodipine, a typical autoregulation plateau was found. In rats treated with nimodipine infusion (12-14 micrograms/kg/min), 1CBF was considerably elevated at all blood pressure levels above 50 mm Hg, and in the steep 1CBF/SAP correlation, the autoregulation plateau was almost suspended. In a second series of randomized rats, the effect of nimodipine on BBB was investigated after Evans blue infusion. When a SAP of 180 mm Hg systolic was maintained for 6 min, a diffuse Evans blue staining was seen in 70% of the nimodipine animals (break-through of BBB). In the third series of rats, the effect of nimodipine on cold injury edema was investigated. Nimodipine (1 mg i.p.) considerably decreased the SAP; Edema formation measured by water and Na+ content 24 hr after trauma was then reduced. However, if the decrease in SAP was in part prevented by norfenefrine application, the rats receiving nimodipine developed significantly more edema. Brain water and sodium contents were markedly increased in both hemispheres. The results indicate an interference of nimodipine with cerebral autoregulation, and a BBB disruption may occur at lower SAP. If the BBB is impaired, nimodipine may considerably intensify edema formation. Nimodipine and similar calcium entry blockers should therefore only be used with caution in acute brain damage.

Animals↗

PubMed2003

Effects of magnesium administration on brain edema and blood-brain barrier breakdown after experimental traumatic brain injury in rats.

In this study, we examined the effects of magnesium sulfate administration on brain edema and blood-brain barrier breakdown after experimental traumatic brain injury in rats. Seventy-one adult male Sprague-Dawley rats were anesthetized, and experimental closed head trauma was induced by allowing a 450-g weight to fall from a 2-m height onto a metallic disk fixed to the intact skull. Sixty-eight surviving rats were randomly assigned to receive an intraperitoneal bolus of either 750 micromol/kg magnesium sulfate (group 4; n = 30) or 1 mL of saline (group 2; n = 30) 30 minutes after induction of traumatic brain injury; 39 nontraumatized animals received saline (group 1; n = 21) or magnesium sulfate (group 3; n = 18) with an identical protocol of administration. Brain water content and brain tissue specific gravity, as indicators of brain edema, were measured 24 hours after traumatic brain injury. Blood-brain barrier integrity was evaluated quantitatively 24 hours after injury by spectrophotometric assay of Evans blue dye extravasations. In the magnesium-treated injured group, brain water content was significantly reduced (left hemisphere: group 2, 83.2 +/- 0.8; group 4, 78.4 +/- 0.7 [P <.05]; right hemisphere: group 2, 83.1 +/- 0.7; group 4, 78.4 +/- 0.5. [P <.05]) and brain tissue specific gravity was significantly increased (left hemisphere: group 2, 1.0391 +/- 0.0008; group 4, 1.0437 +/- 0.001 [P <.05]; right hemisphere, group 2, 1.0384 +/- 0.001; group 4, 1.0442 +/- 0.005 [P <.05]) compared with the saline-treated injured group. Evans blue dye content in the brain tissue was significantly decreased in the magnesium-treated injured group (left hemisphere: group 2, 0.0204 +/- 0.03; group 4, 0.0013 +/- 0.0002 [P <.05]; right hemisphere: group 2, 0.0064 +/- 0.0009; group 4, 0.0013 +/- 0.0003 [P <.05]) compared with the saline-treated injured group. The findings of the present study support that beneficial effects of magnesium sulfate exist after severe traumatic brain injury in rats. These results also indicate that a blood-brain barrier permeability defect occurs after this model of diffuse traumatic brain injury, and magnesium seems to attenuate this defect.

Animals↗