Journal of neurotrauma
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Journal of neurotrauma · Jun 2000
Review Practice Guideline GuidelineThe Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Nutrition.
Data show that starved head-injured patients lose sufficient nitrogen to reduce weight by 15% per week. Class II data show that 100-140% replacement of resting metabolism expenditure with 15-20% nitrogen calories reduces nitrogen loss. Data in non-head injured patients show that a 30% weight loss increased mortality rate. ⋯ The data strongly support feeding at least by the end of the first week. It has not been established that any method of feeding is better than another or that early feeding prior to 7 days improves outcome. Based on the level of nitrogen wasting documented in head-injured patients and the nitrogen sparing effect of feeding, it is a guideline that full nutritional replacement be instituted by day 7.
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Journal of neurotrauma · Jun 2000
Review Practice Guideline GuidelineThe Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Use of barbiturates in the control of intracranial hypertension.
High-dose barbiturate therapy is efficacious in lowering ICP and decreasing mortality in the setting of uncontrollable ICP refractory to all other conventional medical and surgical ICP-lowering treatments. Utilization of barbiturates for the prophylactic treatment of ICP is not indicated. The potential complications attendant on this form of therapy mandate that its use be limited to critical care providers and that appropriate systemic monitoring be undertaken to avoid or treat any hemodynamic instability. When barbiturate coma is utilized, consideration should also be given to monitoring arteriovenous oxygen saturation as some patients treated in this fashion may develop oligemic cerebral hypoxia.
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Journal of neurotrauma · May 2000
Comparative StudyDissociation of cerebral glucose metabolism and level of consciousness during the period of metabolic depression following human traumatic brain injury.
Utilizing [18F]fluorodeoxyglucose positron emission tomography (FDG-PET), we studied the correlation between CMRglc and the level of consciousness within the first month following human traumatic brain injury. Forty-three FDG-PET scans obtained on 42 mild to severely head-injured patients were quantitatively analyzed for the determination of regional cerebral metabolic rate of glucose (CMRglc). Reduction of cerebral glucose utilization, defined as a CMRglc of < or =4.9 mg/100 g/min, was present regionally in 88% of the studies. ⋯ With regards to severity of head injury, this correlation was worst for the severely injured (r = -0.11; p = 0.58) and better for the mildly injured patients (r = 0.50; p = 0.07). In most cases, intraparenchymal hemorrhagic lesions were associated with either focal CMRglc reduction or elevation. It is concluded that the etiologies of CMRglc reduction are likely multifactorial given the complex nature of traumatic brain injury and that the reduction of CMRglc represents a fundamental pathobiologic state following head injury that is not tightly coupled to level of consciousness.
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Journal of neurotrauma · May 2000
ReviewGender differences in acute CNS trauma and stroke: neuroprotective effects of estrogen and progesterone.
Increasing evidence has demonstrated striking sex differences in the pathophysiology of and outcome after acute neurological injury. Lesser susceptibility to postischemic and posttraumatic brain injury in females has been observed in experimental models. Additional evidence suggests this sex difference extends to humans as well. ⋯ Progesterone, on the other hand, has a membrane stabilizing effect that also serves to reduce the damage caused by lipid peroxidation. In addition, it may also provide neuroprotection by suppressing neuronal hyperexcitability. The following review will discuss experimental and clinical evidence for sex differences in outcome after acute brain trauma and stroke, review the evidence implicating estrogens and progestins as mediators of this neuroprotection following acute neurological injury, and finally, address the specific mechanisms by which these hormones may protect the brain following acute neurological injury.
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Journal of neurotrauma · May 2000
Microdialysis-based long-term measurements of energy-related metabolites in the rat brain following a fluid percussion trauma.
The aim of the study was to evaluate an experimental approach based on a fluid percussion rat trauma model in combination with the microdialysis technique for the analysis of cerebral interstitial biochemical alterations following head trauma, and to test the hypothesis that the previously observed acute accumulation of lactate and increase in the lactate pyruvate ratio may persist for several days following trauma. We analyzed how lactate, pyruvate, and glucose were altered in the cortex adjacent to the contusion and in the contralateral side of the brain following a traumatic brain injury. The results were compared with those from sham-operated animals. ⋯ We conclude that the previously observed acute alterations in brain metabolism persist for at least 48 h posttrauma. Further, the measured parameters from the contralateral side can be used as controls since they did not differ from the sham group. Combining microdialysis with a fluid percussion trauma model may be a tool to explore secondary brain injury mechanisms and evaluate new therapies for the treatment of traumatic brain injury.