Guy L. Clifton

TL;DR: Hypothermia-treated rats had significantly less beam-walking beam-balance, and body weight loss deficits compared to normothermic (38°C) rats, and the greatest protection was observed in the 30°C hypothermia group.

TL;DR: It is concluded that even mild mechanical injury can potentiate selective ischemic hippocampal neuronal necrosis in the absence of overt axonal injury, and this potentiation also occurs in conjunction with more generalized electrophysiological disturbances such as EEG evidence of postischemic neuronal hyperactivity suggesting that mild concussion may also decrease the threshold for post-ischemics neuronal excitation.

TL;DR: Data suggest that NMDA agonist-receptor interactions contribute to the pathophysiology of brain injury, and neural mechanisms that mediate transient unconsciousness following moderate levels of head injury may differ from mechanisms that Mediate more persistent neurologic deficits.

TL;DR: External monitoring of temporalis muscle temperature can provide a reliable indirect measure of brain temperature in the course of experimental brain injury and indicated that brain injury itself does not influence brain temperature, anesthesia alone decreases brain temperature to levels producing cerebral protection in this model.

TL;DR: The result suggests that muscarinic and/or NMDA receptor-mediated events confined to TBI and the early posttraumatic period are in part responsible for the phenomenon of increased posttraumatic ischemic vulnerability.