Articles: brain-injuries.
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Journal of neurotrauma · Oct 1997
ReviewIs high extracellular glutamate the key to excitotoxicity in traumatic brain injury?
Traumatic brain injury (TBI) increases extracellular levels of the excitatory amino acid glutamate and aspartate, and N-methyl-D aspartate (NMDA)-receptor antagonists protect against experimental TBI. These two findings have led to the prevalent hypothesis that excitatory amino acid efflux is a major contributor to the development of neuronal damage subsequent to traumatic injury. However, as with stroke, the hypothesis that high extracellular glutamate is the key to excitotoxicity in TBI conflicts with important data. ⋯ Finally, we introduce the notion that beneficial effects of glutamate receptor antagonists in experimental models of neurological disorders do not necessarily imply the occurrence of excitotoxic processes. Indeed, glutamate-receptor blockade may be protective by reducing the energy demand required to counterbalance Na+ influx associated with glutamatergic synaptic transmission. In other words, glutamate receptor antagonists (and blockers of voltage-gated Na+-channels) may help nervous tissue to cope with increased permeability of the cellular membrane to ions and reduced efficacy of Na+ extrusion, and thus prevent the decay of transmembrane ionic concentrations gradients.
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Journal of neurotrauma · Oct 1997
Progressive atrophy and neuron death for one year following brain trauma in the rat.
Although atrophic changes have been well described following traumatic brain injury (TBI) in humans, little is known concerning the mechanisms or progression of brain tissue loss. In the present study, we evaluated the temporal profile of histopathological changes following parasagittal fluid-percussion (FP) brain injury in rats over 1 year postinjury. Anesthetized 3-4 month-old Sprague-Dawley Rats (n = 51) were subjected to FP brain injury of high severity (2.5-2.9 atm, n = 51) or sham treatment (n = 27). ⋯ In addition, reactive astrocytosis in regions of atrophy and progressive bilateral death of neurons in the dentate hilus was observed for 1 year following injury. These results suggest that a chronically progressive degenerative process may be initiated by brain trauma. Thus, there is a temporally broad window within which to introduce novel therapeutic strategies designed to ameliorate the short and long-term consequences of brain trauma.
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Journal of neurosurgery · Oct 1997
Comparative StudyPatients with retained transcranial knife blades: a high-risk group.
Sixty-six patients with transcranial stab wounds presenting to Groote Schuur Hospital over a 2-year period are reviewed. Two groups were identified, those with retained knife blades at presentation (Group A, 13 patients) and those without (Group B, 53 patients). ⋯ Increased mortality was a result of vascular injury, and in two patients neurological deterioration occurred only after knife blade removal. Possible reasons for these findings are that retained blades tend to be deeply penetrating with a potential for more cerebral and vascular injury, and there is a higher incidence of petrous bone penetration that results in carotid artery injury.
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J. Neuropathol. Exp. Neurol. · Oct 1997
Temporal and regional patterns of axonal damage following traumatic brain injury: a beta-amyloid precursor protein immunocytochemical study in rats.
Diffuse axonal injury (DAI) is an important consequence of human head trauma. This experimental investigation utilized the immunocytochemical visualization of beta-amyloid precursor protein (beta-APP) to document regional patterns of axonal injury after traumatic brain injury (TBI) and to determine the importance of injury severity on the magnitude of axonal damage. Rats underwent moderate (1.84-2.11 atm) or severe (2.38-2.52 atm) parasagittal fluid-percussion (F-P) brain injury or sham procedures. ⋯ At multiple periods after TBI, selective cortical and thalamic neurons displayed increased staining of the perikarya. A significant increase in the overall frequency of beta-APP profiles was documented in the severe vs moderately injured rats at 72 h after TBI. These data indicate that parasagittal F-P brain injury (a) results in widespread axonal damage, (b) that axonal damage includes both reversible and delayed patterns, and (c) that injury severity is an important factor in determining the severity of the axonal response to TBI.