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At least 523 records · Page 29Linked to original sources
PubMed1993

Progressive brain compression. Changes in vital physiological variables, correlated with brain tissue water content and brain tissue displacement. Experimental MR imaging in dogs.

Continuous recording of vital physiological variables and sequential MR imaging were performed simultaneously during continuous expansion of an epidural rubber balloon over the left hemisphere in anaesthetised dogs. Balloon expansion led to a progressive and slightly nonlinear rise in intracranial CSF pressures and a fall in local perfusion pressures. Changes in systemic arterial pressure, pulse rate, and respiration rate usually appeared at a balloon volume of 4% to 5% of the intracranial volume (reaction volume), together with a marked transtentorial pressure gradient and MR imaging changes consistent with tentorial herniation. Respiratory arrest occurred at a balloon volume of approximately 10% of the intracranial volume (apnoea volume), which was associated with occlusion of the cisterna magna, consistent with some degree of foramen magnum herniation. Increase in tissue water was observed beginning at approximately the reaction volume, presumably due to ischaemic oedema, due to the fall in perfusion pressures.

Animals↗
PubMed2000

Development of an antibody against a 40,000 mol. wt brain injury-derived neurotrophic peptide-binding protein and identification of a 40,000 mol. wt brain injury-derived neurotrophic peptide-binding protein in hippocampal neurons.

Brain injury-derived neurotrophic peptide is a 13-amino acid peptide derived from a 15,000 mol. wt neurotrophic factor released from sites of mechanical injury in neonatal rat brain. This peptide promotes survival of septal cholinergic neurons and mesencephalic dopaminergic neurons, and protects hippocampal neurons from glutamate-induced neurotoxicity. In this study, we have developed a monoclonal antibody against a brain injury-derived neurotrophic peptide-binding protein by immunizing mice with septal synaptosomes from five-week-old rat brain. Monoclonal antibodies were screened for inhibition of the binding of a 125I-labeled analogue of brain injury-derived neurotrophic peptide to rat brain synaptosomes. The monoclonal antibody 6A22 suppressed the biological activity of brain injury-derived neurotrophic peptide and abolished the protective effect of the neurotrophic peptide against glutamate-induced neurotoxicity. This monoclonal antibody recognized a 40,000 mol. wt brain injury-derived neurotrophic peptide-binding protein, which was also identified by cross-linking experiments. Immunohistochemical studies showed that the 6A22 antibody bound to the cell surfaces of a subpopulation (about 60%) of hippocampal neurons in culture. These results are consistent with the possibility that the 40,000 mol. wt protein belongs to brain injury-derived neurotrophic peptide receptors.

Animals↗
PubMed1996

Delayed posttraumatic brain hyperthermia worsens outcome after fluid percussion brain injury: a light and electron microscopic study in rats.

The morphological consequences of delayed posttraumatic brain hyperthermia (39 degrees C) after fluid percussion brain injury were assessed in rats. Sprague-Dawley rats anesthetized with 4% halothane and maintained on a 70:30 mixture of nitrous oxide:oxygen and 0.5% halothane underwent moderate (1.5-2.0 atm) traumatic brain injury with the injury screw positioned parasagittally over the right parieto-occipital cortex. At 24 hours after traumatic brain injury, the rats were reanesthetized and randomized into two groups in which either a 3-hour period of brain normothermia (36.5 degrees C, n = 18) or hyperthermia (39 degrees C, n = 18) was maintained. Sham-operated controls (n = 10) underwent all surgical and temperature-monitoring procedures. After the 3-hour monitoring period, the rats were allowed to survive for 3 days for light microscopic analysis or were injected with the protein tracer horseradish peroxidase and were perfusion-fixed 15 minutes later for light and electron microscopic analysis. At 4 days after traumatic brain injury, delayed posttraumatic hyperthermia (n = 12) significantly increased mortality (47%) and contusion volume (1.7 +/- 0.69 mm3, mean +/- standard error of the mean), compared to normothermia (n = 12) (18% mortality and 0.13 +/- 0.21 mm3 contusion volume) (P < 0.01, analysis of variance). At 15 minutes after the 3-hour hyperthermic period, the area of hemorrhage and horseradish peroxidase extravasation overlying the lateral external capsule was significantly increased (2.52 +/- 0.71 mm2, mean +/- standard error of the mean, versus 0.43 +/- 0.16 mm2) (P < 0.01), compared to normothermic rats. Examination of toluidine blue-stained plastic sections demonstrated a higher frequency of abnormally swollen myelinated axons per high microscopic field with hyperthermia. For example, numbers of swollen axons within the sixth layer of the right somatosensory cortex, corpus callosum, and internal capsule were 7.3 +/- 1.3, 4.2 +/- 1.4, and 3.0 +/- 1.2 axons (mean +/- standard error of the mean) with normothermia, respectively, compared with 24.7 +/- 12.1, 33.1 +/- 4.2, and 27.3 +/- 3.1 axons with hyperthermia, respectively (P < 0.01). An ultrastructural examination of the swollen axons demonstrated a severely thinned myelin sheath containing axoplasm devoid of cytoskeletal components. These experimental results indicate that posttraumatic brain hyperthermia might increase morbidity and mortality in patients with head injury by aggravating axonal and microvascular damage.

Animals↗
PubMed1997

Agrin accumulates in the brain microvascular basal lamina during development of the blood-brain barrier.

The blood-brain barrier (BBB) is an essential feature of the microvasculature in neural tissues. Agrin, a synapse organizing molecule at the neuromuscular junction, also accumulates on brain microvasculature and may be involved in BBB formation and function. We investigated the developmental expression of agrin at rat and chick brain capillaries by immunohistochemistry and immunoblotting. Anti-agrin immunoreactivity (IR) completely ensheathes all observed microvessels labeled with anti-von Willebrand factor in adult brains of both species. Brain microvascular agrin IR codistributes with anti-laminin IR, consistent with agrin localization in the microvessel basal lamina. On microvessels in testis and thymus, tissues which also contain blood-tissue barriers, the pattern of IR is indistinguishable from brain microvessels. In contrast, little or no agrin IR is observed on capillaries in muscle and other tissues. During chick and rat development, agrin accumulates on brain microvessels around the time the vasculature becomes impermeable. Differential staining and electroblotting suggest that the agrin isoforms expressed on brain microvessels lack the 8- and 11-amino acid sequences that confer on agrin high potency in acetylcholine receptor clustering. Taken in context with the organizing role of agrin in synaptogenesis, these results indicate that agrins may function as important players in the formation and maintenance of cerebral microvascular impermeability.

Agrin↗
PubMed2000

Mannitol for acute traumatic brain injury.

BACKGROUND: Mannitol is sometimes dramatically effective in reversing acute brain swelling, but its effectiveness in the on-going management of severe head injury remains open to question. There is evidence that in prolonged dosage mannitol may pass from the blood into the brain, where it might cause reverse osmotic shifts that increase intracranial pressure. OBJECTIVES: To assess the effects of different mannitol therapy regimens, of mannitol compared to other intracranial pressure (ICP) lowering agents, and to quantify the effectiveness of mannitol administration given at other stages following acute traumatic brain injury. SEARCH STRATEGY: The review drew on the search strategy for the Injuries Group as a whole. We checked reference lists of trials and review articles, and contacted authors of trials. SELECTION CRITERIA: Randomised trials of mannitol, in patients with acute traumatic brain injury of any severity. The comparison group could be placebo-controlled, no drug, different dose, or different drug. Trials where the intervention was started more than eight weeks after injury, and cross-over trials were excluded. DATA COLLECTION AND ANALYSIS: The reviewers independently rated quality of allocation concealment and extracted the data. Relative risks (RR) and 95% confidence intervals (CI) were calculated for each trial on an intention to treat basis. MAIN RESULTS: Overall there were few eligible trials. There were no trials comparing different doses, or type of administration. One trial compared ICP-directed therapy to 'standard care' (RR for death= 0.83; 95% CI 0.47;1.46). One trial compared mannitol to pentobarbital (RR for death = 0.85; 95% CI 0. 52;1.38). No trials compared mannitol to other ICP lowering agents. One trial tested the effectiveness of pre-hospital administration of mannitol against placebo (RR for death=1.59; 95% CI 0.44;5.79). REVIEWER'S CONCLUSIONS: There are insufficient data to recommend one form of mannitol infusion over another. Mannitol therapy for raised ICP may have a beneficial effect on mortality when compared to pentobarbital treatment. ICP-directed treatment shows a small beneficial effect compared to treatment directed by neurological signs and physiological indicators. There are insufficient data on the effectiveness of pre-hospital administration of mannitol to preclude either a harmful or a beneficial effect on mortality.

Brain Injuries↗
PubMed2001

Speech and language therapy for dysarthria due to non-progressive brain damage.

BACKGROUND: Dysarthria is a common sequel of non-progressive brain damage (typically stroke and traumatic brain damage). Impairment-based therapy and a wide variety of compensatory management strategies are undertaken by speech and language therapists with this patient population. OBJECTIVES: To determine the efficacy of speech and language therapy interventions for adults with dysarthria following non-progressive brain damage. SEARCH STRATEGY: This review has drawn on the search strategies developed for the following Cochrane Groups as a whole: Stroke, Injuries, and Infectious Diseases. Relevant trials were identified in the Specialised Registers of Controlled Trials (see Review Group Details for more information). We also searched the trials register of the Cochrane Rehabilitation and Related Therapies Field. The Cochrane Controlled Trials Register, MEDLINE, EMBASE, CINAHL, PsycLIT, and Linguistics and Language Behavior Abstracts were electronically searched. Hand-searching of The International Journal of Language and Communication Disorders and of reference lists from relevant articles and conference proceedings was also undertaken. Colleagues were approached to identify other possible published and unpublished studies. Date of most recent searches: May 2000. SELECTION CRITERIA: Unconfounded randomised controlled trials. DATA COLLECTION AND ANALYSIS: One reviewer assessed trial quality. Two co-reviewers were available to examine any potential trials for possible inclusion in the review. MAIN RESULTS: No trials of the required standard were identified. REVIEWER'S CONCLUSIONS: There is no evidence of the quality required by this review to support or refute the effectiveness of Speech and Language Therapy interventions for dysarthria following non-progressive brain damage. There is an urgent need for good quality research in this area.

Adult↗
PubMed1997

Influence of ischemia and reperfusion on the course of brain tissue swelling and blood-brain barrier permeability in a rodent model of transient focal cerebral ischemia.

Brain swelling is a serious complication associated with focal ischemia in stroke and severe head injury. Experimentally, reperfusion following focal cerebral ischemia exacerbates the level of brain swelling. In this study, the permeability of the blood-brain barrier has been investigated as a possible cause of reperfusion-related acute brain swelling. Blood-brain barrier disruption was investigated using Evans Blue dye and [14C]aminoisobutyric acid autoradiography in a rodent model of reversible middle cerebral artery (MCA) occlusion. Acute brain swelling and cerebral blood flow (CBF) during ischemia and reperfusion were analyzed from double-label CBF autoradiograms after application of the potent vasoconstrictor peptide endothelin-1 to the MCA. Ischemia was apparent within ipsilateral MCA territory, 5 min after endothelin-1 application to the exposed artery. Reperfusion, examined at 30 min and 1, 2, and 4 h, was gradual but incomplete within this time frame in the core of middle cerebral artery territory and associated with significant brain swelling. Ipsilateral hemispheric swelling increased over time to a maximum (>5%) at 1-2 h after endothelin-1 but was not associated with a significant increase in the ipsilateral transfer constant for [14C]aminoisobutyric acid over this time frame. These results indicate that endothelin-1 induced focal cerebral ischemia is associated with an acute but reversible hemispheric swelling during the early phase of reperfusion which is not associated with a disruption of the blood-brain barrier.

Aminoisobutyric Acids↗
PubMed2006

Photodynamic therapy increases brain edema and intracranial pressure in a rabbit brain tumor model.

The objective of this study was to evaluate the effect of a single photodynamic therapy (PDT) on brain edema and intracranial pressure (ICP) in a rabbit model of brain tumor. A total of 57 adult New Zealand rabbits were assigned to 3 groups: the PDT group, the tumor group, and the tumor plus PDT group. Rabbits in the PDT group (n = 9) received PDT but no tumor implantation; rabbits in the tumor group (n = 18) received VX2 carcinoma implantation but no PDT; rabbits in the tumor plus PDT group (n = 30) received tumor implantation with subsequent PDT 16 days later. Brain edema and ICP levels were then evaluated. We found that ICP in the PDT group was 7.43 +/- 0.50 mmHg. After tumor implantation, ICP increased rapidly (18.43 +/- 1.10 mmHg, 21 days later). PDT alone did not increase ICP, but compared with that in the tumor group, ICP increased significantly in the tumor plus PDT group (9.55 +/- 1.32 vs. 13.31 +/- 1.13 mmHg, p < 0.01) 24 hours after treatment. Brain water content in the tumor group increased rapidly after tumor implantation. PDT again increased perineoplastic brain edema 24 hours after treatment (81.09 +/- 0.97% vs. 78.32 +/- 0.49%, p < 0.01). It should be noted that PDT alone did not induce brain edema. In conclusion, PDT causes transient brain edema and increases ICP in a rabbit brain tumor model.

Animals↗
PubMed1991

Increased capillary permeability in rat brain induced by factors secreted by cultured C6 glioma cells: role in peritumoral brain edema.

To investigate whether brain tumors secrete a factor(s) responsible for peritumoral brain edema, we studied the effect of conditioned medium from cultured C6 glioma cells on rat brain capillary permeability. Three different fractions of conditioned medium were obtained. SUP-N was a culture supernatant incubated 4 hours in serum-free medium. SUP-C was the 60-100 fold concentrated fraction obtained by dialysis-concentration of SUP-N; it contained 950 micrograms/ml of protein greater than 10 k-daltons from 3 x 10(8) cells. SUP-L was a water-dispersible lipid fraction from SUP-N; the major components of SUP-L were neutral lipids and free fatty acids. The supernatant fractions and their corresponding control solutions were infused into normal rat brain, and capillary permeability was determined using quantitative autoradiography by measuring the unidirectional entry constant, K (micrograms l/g.min), of 14C-alpha-aminoisobutyric acid (14C-AIB) into brain tissue. SUP-C and SUP-L significantly increased capillary permeability of normal brain; the effect of SUP-C was more intense and extensive than that of SUP-L. The highest mean K value (Kmax) of SUP-C was 10.83 +/- 0.99 and that of the control was 2.53 +/- 0.22 (p less than 0.001). The Kmax of SUP-L was 5.61 +/- 0.23 and that of the control was 2.67 +/- 0.36 (p less than 0.01). A time-course study after infusion of SUP-C demonstrated that more than 1.5 hours is required for the supernatant fraction to open the barrier and that the effect of SUP-C was reversible. The increase of capillary permeability induced by SUP-C was significantly inhibited by pretreatment of rats with dexamethasone (10 mg/kg, ip) 1 hour before intracerebral infusion of SUP-C (Kmax (untreated): 8.30 +/- 0.82, Kmax (treated): 1.33 +/- 0.64, p less than 0.001). These results indicate that experimental brain tumors secrete at least two different diffusible factors responsible for capillary endothelial leakage in normal brain. One is a protein of molecular weight greater than 10 k-daltons, whose effect is inhibited by glucocorticoids, and the other is a waterdispersible lipid.

Animals↗
PubMed1985

The effect of acute lithium administration on brain monoamine synthesis and the precursor amino acids tyrosine and tryptophan in brain and plasma in rats.

The effect of a single i.p. injection of lithium chloride on brain monoamine synthesis and tyrosine and tryptophan levels in brain and plasma in rats was studied. Acute lithium administration was found to decrease brain tyrosine levels, which most likely was due to decreased plasma tyrosine levels. Brain tryptophan levels were mainly unaffected whereas plasma tryptophan leves were slightly decreased at 8 hours after lithium administration. Brain catecholamine synthesis was decreased at 4 hours and increased at 48 hours after the injection of lithium. Brain 5-hydroxytryptamine (5-HT) synthesis was decreased at all time intervals after the injection of lithium. It is concluded that the effects of acute lithium administration on brain monoamine synthesis are not mainly due to its effect on brain tyrosine and tryptophan levels in rats. Furthermore acute lithium administration appears to affect 5-HT synthesis to a greater extent than it affects catecholamine synthesis.

Animals↗
PubMed1978

Brain energy metabolism in global brain oedema.

Different degrees of severity in global brain oedema were induced by varying amounts of water intoxication (50, 100, 150, and 200 ml Aqua dest./kg b.wt. intravenously) in groups of six cats, which were functionally nephrectomized. Animals loaded with physiological saline and sham-operated served as controls. Two hours following the water load, the tissue concentrations of CrP, ATP, ADP, AMP, pyruvate, glucose, and lactate were determined by optical enzymatic analysis. The results show disturbances in brain energy metabolism dependent on the severity of the brain oedema. The high energy compounds and in consequence the ATP/ADP-ratio, and respectively the energy charge potential, fall in direct relationship to the severity of the brain oedema. Lactate and lactate-pyruvate ratio increase. The energy source of the cell, glucose as well as pyruvate, significantly falls in the group with severe brain oedema. The results of the brain energy metabolism were compared with our previous study concerning the brain water content, rCBF and CPP in global brain oedema (Meinig et al. 1973). The results show that the disturbances of energy metabolism are directly related to the rCBF and are not dependent on CPP over a wide range.

Adenosine Diphosphate↗