Hypothermia traumatic brain injury

Hypothermia improves imbalances of TXA2 and PGI2 after traumatic brain injury in humans (Aibiki et al., 2000). 

Palmer A. M., Marion D. W., BotschellerM. L., and Redd E. E. (1993) Therapeutic hypothermia is cytoprotective without attenuating the traumatic brain injury-induced elevations in interstitial concentrations of aspartate and glutamate. J. Neurotrauma 10, 363-372. 

Matsushita Y., BramlettH. M., Alonso O., and Dietrich W. D. (2001) Posttraumatic hypothermia is neuroprotective in amodel of traumatic brain injury complicated by a secondary hypoxic insult. Crit. Care Med. 29, 2060-2066. 

Clifton G. L., Jiang J. Y., Lyeth B. G., Jenkins L. W., Hamm R. J., and Hayes R. L. (1991) Marked protection by moderate hypothermia after experimental traumatic brain injury../. Cereb. Blood Flow Metab. 11, 114—121. 

Goss J. R., Styren S. D., Miller P. D., et al. (1995) Hypothermia attenuates the normal increase in interleukin 1 beta RNA and nerve growth factor following traumatic brain injury in the rat. J. Neurotrauma 12, 159-167. 

Taft W. C Yang K Dixon C. E Clifton G. L and Hayes R. L. (1993) Hypothermia attenuates the loss of hippocampal microtubule-associated protein 2 (MAP2) following traumatic brain injury. J. Cereb. Blood Flow Metab. 13, 796-802. 

Chatzipanteli K., Wada K., Busto R., and Dietrich W. D. (1999) Effects of moderate hypothermia on constitutive and inducible nitric oxide synthase activities after traumatic brain injury in the rat. J. Neurochem. 72, 2047-2052. 

Kline A. E., Bolinger B. D., Kochanek P. M., et al. (2002) Acute systemic administration of interleukin-10 suppresses the beneficial effects of moderate hypothermia following traumatic brain injury in rats. Brain Res. 937, 22-31. 

Kahveci et al. (13) compared the cerebral protective effects of two known protective anesthetics, isoflurane and propofol, in combination with hypothermia (33-34°C) after traumatic brain injury (TBI). In that study, the authors found that propofol anesthesia plus hypothermia following TBI was better than the isoflurane-hypothermia combination because it reduced intracranial pressure and increased cerebral perfusion pressure under those conditions. 

Management of Traumatic Brain Injury With Moderate Hypothermia... 

Early reports of therapeutic hypothermia for severe traumatic brain injury can be traced back to the first half of the 20th century. It is only within the last two decades that clinical studies have demonstrated that therapeutic moderate hypothermia for brief durations can improve patient outcomes following brain injury. The historical background, recent clinical experience, and mechanisms of action of moderate hypothermia are reviewed. 

Several animal models suggest that the time to initiate cooling following TBI is brief. Some rat models suggest that the therapeutic window for treatment with hypothermia is approx 25 min (41,42). These data would seem quite discouraging, as most traumatic brain injury patients do not arrive at the hospital and receive complete evaluation until significantly more time has elapsed. Even with rapid transporta-... 

Therapeutic Moderate Hypothermia in Experimental Traumatic Brain Injury Models... 

Jiang J.,YuM., and Zhu C. (2000) Effect of long-term mild hypothermia therapy in patients with severe traumatic brain injury 1 -year follow-up review of 87 cases. J. Neurosurg. 93,546-549. 

Marion D. W. (1997) Therapeutic moderate hypothermia for severe traumatic brain injury. J. Intern. Care Med. 12, 239-248. 

It is known from animal models with global ischemia and traumatic brain injury that moderate hypothermia attenuates secondary brain damage by reducing cerebral ischemia and postischemic brain edema and preserving the blood-brainbarrier. Even though hypothermia has potent cerebroprotective effects after experimental focal ischemia, clinical studies on hypothermic therapy after MCA infarction were not available until recently. We performed a pilot study investigating the efficacy, feasibility, and safety of induced moderate hypothermia in the therapy of patients with acute, severe MCA infarction and increased ICP. 

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