title: THE EFFECTS OF POSTTRAUMATIC HYPOTHERMIA ON DIFFUSE AXONAL INJURY FOLLOWING PARASAGGITAL FLUID PERCUSSION BRAIN INJURY IN RATS.
abstract: Previous investigations have demonstrated the beneficial effects of mild hypothermia following different types of traumatic brain injury (TBI). In some models, early cooling following TBI has been shown to reduce the frequency of axonal damage, a major consequence of head injury. The purpose of this study was to evaluate the effects of posttraumatic hypothermia in a model that has been shown to be sensitive to temperature manipulations in the early injury setting. Animals underwent moderate parasagittal fluid percussion (FP) brain injury and were then either randomized into normothermic or hypothermic groups. In the hypothermic groups, brain temperature was reduced to either 30 or 33°C 5 minutes after trauma and maintained for a three hour period. Normothermic or sham-operated animals were held under normal temperature conditions. At three days after TBI, animals were perfusion-fixed for quantitative assessment of β-APP immunohistochemistry and silver staining. Traumatic injury led to a significant increase in the frequency of β-APP immunoreactive profiles both within the corpus callosum, external capsule, as well as internal capsule. While early cooling revealed a trend for protection, no significant differences were shown between normothermic and hypothermic animals in terms of the frequency of injured axons at 3 days posttrauma. These results emphasize that axonal pathology is a major consequence of brain injury using this particular model. It is concluded that longer periods of posttraumatic hypothermia may be required to chronically protect axon populations undergoing progressive injury.
authors: The Miami Project to Cure Paralysis, The Department of Neurological Surgery University of Miami Miller School of Medicine Miami, Florida 33136.
authors: Helen M
authors: HM
authors: Bramlett
authors: W Dalton
authors: WD
authors: Dietrich
keywords: axonal damage; beta amyloid precursor protein; hypothermia; traumatic brain injury