Journal of neurotrauma
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Journal of neurotrauma · Aug 2000
Impaired autoregulation of cerebral blood flow in an experimental model of traumatic brain injury.
In order to study the pathophysiology and the intracranial hemodynamics of traumatic brain injury, we have developed a modified closed-head injury model of impact-acceleration that expresses several features of severe head injury in humans, including acute and long-lasting intracranial hypertension, diffuse axonal injury, neuronal necrosis, bleeding, and edema. In view of the clinical relevance of impaired autoregulation of cerebral blood flow after traumatic brain injury, and aiming at further characterization of the model, we investigated the autoregulation efficiency 24 h after experimental closed-head injury. Cortical blood flow was continuously monitored with a laser-Doppler flowmeter, and the mean arterial blood pressure was progressively decreased by controlled hemorrhage. ⋯ The break point tended towards higher values in the closed head injury group (62.2 +/- 20.8 mm Hg versus 46.9 +/- 12.7 mm Hg; mean +/- SD, p = 0.198). It is concluded that cerebral autoregulation in this modified closed head injury model is impaired 24 h after traumatic brain injury. This finding, in addition to other characteristic features of severe head injury established earlier in this model, significantly contributes to its clinical relevance.
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Journal of neurotrauma · Aug 2000
Cerebral metabolic response to traumatic brain injury sustained early in development: a 2-deoxy-D-glucose autoradiographic study.
Following fluid percussion (FP) traumatic brain injury (TBI), adult rats exhibit dynamic regional changes in cerebral glucose metabolism characterized by an acute (hours) increase and subsequent chronic (weeks) decrease in metabolic rates. The injury-induced hyperglycolysis is the result of ionic fluxes across cell membranes and the degree and extent of metabolic depression is predictive of neurobehavioral deficits. Given that younger animals appear to exhibit similar physiological responses to injury yet show an improved rate of recovery compared to adults, we wanted to determine if this injury-induced dynamic metabolic response to TBI is different if the injury is sustained early in life. ⋯ This hyperglycolytic state subsided within 30 min, and by 1 day all cerebral structures, except the ipsilateral cerebellar cortex, showed lower rates of glucose metabolism (ranging from 5.7% to 63.0% below controls). This period of posttraumatic metabolic depression resolved within 3 days for all structures measured. Compared to previous adult studies these results suggest that the young rat pup, although exhibiting acute hyperglycolysis, is not subjected to a prolonged period of metabolic depression, which supports the findings that at this level of injury severity, these young animals show remarkable neurological sparing following TBI.
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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. Role of steroids.
The majority of available evidence indicates that steroids do not improve outcome or lower ICP in severely head-injured patients. The routine use of steroids is not recommended for these purposes.
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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. Intracranial pressure treatment threshold.
An absolute ICP threshold that is uniformly applicable is unlikely to exist. Current data, however, support 20-25 mm Hg as an upper threshold above which treatment to lower ICP should generally be initiated.