Journal of neurotrauma
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Journal of neurotrauma · Aug 2000
Prolonged cyclooxygenase-2 induction in neurons and glia following traumatic brain injury in the rat.
Cyclooxygenase-2 (COX2) is a primary inflammatory mediator that converts arachidonic acid into precursors of vasoactive prostaglandins, producing reactive oxygen species in the process. Under normal conditions COX2 is not detectable, except at low abundance in the brain. This study demonstrates a distinctive pattern of COX2 increases in the brain over time following traumatic brain injury (TBI). ⋯ These increases are distinct from those observed following inflammatory challenge, and correspond to brain areas previously identified with the neurological and cognitive deficits associated with TBI. While COX2 induction following TBI may result in selective beneficial responses, chronic COX2 production may contribute to free radical mediated cellular damage, vascular dysfunction, and alterations in cellular metabolism. These may cause secondary injuries to the brain that promote neuropathology and worsen behavioral outcome.
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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 · 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. Use of mannitol.
There are two "class 1" studies, and one "class 2" study, and a large body of "Class 3" data, which can be used to support mannitol. The evidence supporting use of mannitol for ICP control is sufficiently strong to warrant guideline status. ⋯ Serum osmolalities >320 mOsm and hypovolemia should be avoided. There is some data to suggest that bolus administration is preferable to continuous infusion.
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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. Glasgow coma scale score.
When considering the use of the initial GCS for prognosis, the two most important problems are the reliability of the initial measurement, and its lack of precision for prediction of a good outcome if the initial GCS is low. If the initial GCS is reliably obtained and not tainted by prehospital medications or intubation, approximately 20% of the patients with the worst initial GCS will survive and 8-10% will have a functional survival (GOS 4-5).