Articles: brain-injuries.
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Case Reports Clinical Trial
[Analysis of mild barbiturate-moderate hypothermia therapy on the authors' 152 cases].
Mild barbiturate-moderate hypothermia therapy was established for severe head injury and cerebrovascular disease. This study was conducted on 152 patients from April 1984 through July 1995. In this study were included patients with Glagow Coma Scale score of less than 8 points but those with serious systemic complications and elderly and infantile patients were excluded. ⋯ This therapy was found to be particularly effective for preventing ischemic neurological damage in the vasospasm stage following SAH and severe head injury in young patients. However, this therapy did not prevent pneumonia, cardiac failure, arrhythmia and hypopotassemia from occurring frequently. We conclude that this therapy is contraindicated in the elderly, i.e., those older than 65 years.
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Psychiatry Clin. Neurosci. · Jun 1997
Temporal and regional profiles of cytoskeletal protein accumulation in the rat brain following traumatic brain injury.
To characterize the cytoskeletal aberration due to traumatic injury, temporal and regional profiles of changes in immunoreactivity of microtubule-associated protein 2 (MAP2), neurofilament heavy subunit protein (NFH) and heat shock protein 72 (HSP72) were investigated after different magnitudes of traumatic brain injury by fluid percussion. The experimental rat brain was perfusion-fixed at 1, 6 and 24 hours after traumatic brain injury. Conventional histological staining has demonstrated that the mildest traumatic brain injury (1.0 atm) induced no neuronal loss at the impact site and that neuron loss was apparent when traumatic brain injury was increased to 4.3 atm. ⋯ Six and 24 hours after the injury, perikaryal accumulation of neurofilament was observed, and the accumulated neurofilament was mostly phosphorylated. These results indicate that the severe traumatic brain injury of 4.3 atm triggers the abnormal accumulation of cytoskeletal proteins in neuronal perikarya, most probably due to an impairment of axonal transport. It is implied that the increased expression of HSP72 may be involved in the protective process of neurons after traumatic brain injury.
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Intracerebral cytokine production is thought to be partially responsible for the brain edema and increased leukocyte adhesion seen after head injury by both a direct effect on vascular permeability and by causing leukocyte activation. Cerebrospinal fluid concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 are elevated after traumatic brain injury. The cerebral endothelium has not been investigated as a de novo source of cytokines after injury. ⋯ HCME subjected to percussion injury secreted significantly more TNF-alpha at 8 and 24 hours and significantly more IL-1beta at 4 and 24 hours compared with uninjured controls (p < 0.05, Student's t test). These data suggest that HCME production of inflammatory cytokines occurs after traumatic brain injury independent of systemic influences. In situ cytokine production by HCME after percussion trauma may mediate the increased cerebral leukocyte accumulation and cerebrovascular dysfunction observed after focal brain injury.
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Neurological research · Jun 1997
Multiparametric continuous monitoring of brain metabolism and substrate delivery in neurosurgical patients.
Brain function and tissue integrity are highly dependent on continuous oxygen supply and clearance of CO2. Aerobic metabolism is the major energy source to normal brain, however, during hypoxia and ischemia, lactate accumulation may sometimes be seen, indicating anaerobic glycolysis after severe head injury. Current monitoring techniques often fail to detect such events which can affect substrate delivery to the injured brain. ⋯ Brain pH was inversely related to brain CO2 for all patients. Brain glucose and lactate in patients with poor outcome were 639 microM l-1 +/- 330, and 1642 microM l-1 +/- 788, whereas patients with good outcome had brain glucose levels of 808 microM l-1 +/- 321 and lactate levels of 1001 microM l-1 +/- 417. Extended neuromonitoring using a combined sensor for brain oxygen, CO2, pH and temperature measurements, as well as a microdialysis probe for glucose and lactate analysis may optimize the management of comatose neurosurgical patients in the future, by allowing a fuller understanding of dynamic factors affecting brain metabolism.
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Brain injury : [BI] · Jun 1997
Substance abuse, traumatic brain injury and neuropsychological outcome.
The neuropsychological performance of 119 patients with severe closed traumatic brain injury (TBI) who had received toxicology screens at the time of trauma centre admission was examined. Three groups were created: normal screen, positive alcohol screen, or positive abused drugs screen (with or without the presence of alcohol). The admitting Glasgow Coma Scale (GCS) score was significantly lower in the positive alcohol screen group than the normal screen group, while the three groups did not differ in length of post-traumatic amnesia (PTA) or years of education. ⋯ Normal screen patients also scored significantly higher than positive alcohol screen patients on FIQ and VIQ indices and all five indices from the Wechsler Memory Scale-Revised. These data suggest the existence of an additive effect of substance abuse on neuropsychological outcome in TBI. Findings have potential implications for both acute management and rehabilitation of TBI.