Articles: brain-injuries.
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Journal of neurotrauma · Mar 1999
Effects of six weeks of chronic ethanol administration on the behavioral outcome of rats after lateral fluid percussion brain injury.
This study examined the effects of 6 weeks of chronic ethanol administration on the behavioral outcome in rats after lateral fluid percussion (FP) brain injury. Rats were given either an ethanol liquid diet (ethanol diet-groups) or a pair-fed isocaloric sucrose control diet (control diet groups) for 6 weeks. After 6 weeks, the ethanol diet was discontinued for the ethanol diet rats and they were then given the control sucrose diet for 2 days. ⋯ Histologic analysis of both diet groups after behavioral assessment revealed comparable ipsilateral cortical damage and observable CA3 neuronal loss in the ipsilateral hippocampus. These results only suggest that chronic ethanol administration, longer than six weeks of administration, may worsen behavioral outcome following lateral FP brain injury. For more significant behavioral and/or morphological change to occur, we would suggest that the duration of chronic ethanol administration must be increased.
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Critical care medicine · Mar 1999
Quinolinic acid in the cerebrospinal fluid of children after traumatic brain injury.
To measure quinolinic acid, a macrophage-derived neurotoxin, in the cerebrospinal fluid (CSF) of children after traumatic brain injury (TBI) and to correlate CSF quinolinic acid concentrations to clinically important variables. ⋯ A large and progressive increase in the macrophage-derived neurotoxin quinolinic acid is seen following severe TBI in children. The increase is strongly associated with increased mortality. Increased CSF quinolinic acid concentration on admission in children with shaken infant syndrome could reflect a delay in presentation to medical attention or age-related differences in quinolinic acid production. These findings raise the possibility that quinolinic acid may play a role in secondary injury after TBI in children and suggest an interaction between inflammatory and excitotoxic mechanisms of injury following TBI.
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Journal of neurotrauma · Mar 1999
Regional changes in cerebral extracellular glucose and lactate concentrations following severe cortical impact injury and secondary ischemia in rats.
Traumatic brain injury (TBI) causes the brain to be more susceptible to secondary insults, and the occurrence of a secondary insult after trauma increases the damage that develops in the brain. To study the synergistic effect of trauma and ischemia on brain energy metabolites, regional changes in the extracellular concentrations of glucose and lactate following a severe cortical impact injury were measured employing a microdialysis technique. Three microdialysis probes were placed in center of the impact site, in an area adjacent to the impact site, and in the contralateral parietal cortex, and perfused with artificial cerebrospinal fluid (CSF) at 2 microl/min. ⋯ The impact injury resulted in a three- to fivefold global increase in dialysate lactate concentrations, with a corresponding fall in dialysate glucose concentration by 50% compared to no change in lactate or glucose concentrations in sham-injured animals (p < .0001 for both lactate and glucose). The secondary insult resulted in a second increase in dialysate lactate and decrease in dialysate glucose concentration that was significantly greater in the animals that had suffered the impact injury than in the sham-injured animals. Ischemia and traumatic injury have synergistic effects on lactate accumulation and on glucose depletion in the brain that probably reflects persisting ischemia, but may also indicate mitochondrial abnormalities and inhibition of oxidative metabolism.
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Semin Pediatr Neurol · Mar 1999
ReviewThe pursuit of effective neuroprotection during infant cardiac surgery.
Advances in infant cardiac surgery have resulted in a dramatic decline in mortality rates; however, neurological morbidity remains an important concern. The effectiveness of a number of interventional strategies to prevent or minimize brain injury during open heart surgery are currently being investigated. This article provides an overview of two approaches: (1) interventions to enhance intraoperative cerebral oxygenation so as to prevent hypoxic-ischemic insults, and (2) the application of cerebral rescue therapies to attenuate the cascade of brain injury. Infant cardiac surgery provides a controlled environment in which to apply these neuroprotective approaches, so as to optimize the quality of life of these vulnerable children.
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We studied specific aspects of speed performance in neuropsychological tests and functional and vocational long-term outcome among moderate or severe traumatic brain injury (TBI) patients admitted to a rehabilitation programme. A group of 140 patients with mild, moderate or severe TBI was followed up for a minimum of 5 years in a rehabilitation programme. Severity of TBI was estimated using the Glasgow Coma Scale (GCS) scores on emergency hospital admission. ⋯ Simple reaction times did not differ significantly between the GOS scores at the end of follow-up, and neither did they predict capacity or incapacity for employment. Our data suggest that the Stroop and PB tests can help estimate functional outcome, as measured by the GOS, among patients with initially moderate or severe TBI and who were referred to a rehabilitation programme. The same tests could also be useful in predicting long-term vocational outcome.