Conclusion

Although specific antagonists of mediators of cerebral damage are unlikely to be clinically available for some years, there is still much which can be done to minimize ischemic cerebral damage in the neurosurgical patient. Balance of cerebral substrate supply with demand and prevention of hyperglycemia and hyperthermia will provide optimal conditions for cerebral recovery and are measures which can easily be undertaken in the ICU. Bibliography

Illievich, U.M. and Spiss, C.K. (1994). Hypothermic therapy for the injured brain. Current Opinion in Anaesthesiology, 7, 394-400.

Lam, A., Winn, H., Cullen, B., and Sundling, N. (1991). Hyperglycemia and neurological outcome in patients with head injury. Journal of Neurosurgery, 75, 545-51. Siesjo, B.K. (1992). Pathophysiology and treatment of focal cerebral ischemia I. Pathophysiology. Journal of Neurosurgery, 77, 169-84.

Verhaegen, M. and Warner, D.S. (1995). Brain protection and brain death. In Neuroanaestheticpractice (ed. H. Van Aken), pp. 267-93. BMJ Publishing, London. Warner, D.S. (1994). Perioperative neuroprotection. Current Opinion in Anaesthesiology, 7, 416-20.

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