The Effects of Posttraumatic Hypothermia on Diffuse Axonal Injury Following Parasagittal Fluid Percussion Brain Injury in Rats

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 post-traumatic 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 degrees C or 33 degrees C 5 minutes after trauma and maintained for a 3-hour period. Normothermic or sham-operated animals were held under normal temperature conditions. At 3 days after TBI, animals were perfusion-fixed for a quantitative assessment of beta amyloid precursor protein (beta-APP) immunohistochemistry and silver staining. Traumatic injury led to a significant increase in the frequency of beta-APP immunoreactive profiles within both the corpus callosum, external capsule, and the 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 post-trauma. These results emphasize that axonal pathology is a major consequence of brain injury using this particular model. It is concluded that longer periods of post-traumatic hypothermia may be required to chronically protect axon populations undergoing a progressive injury.