Abstract
Primary brain injury is caused by disease, injury and infection. All too frequently, the damage is irreversible and leads to death or disability with significant consequences for the patient, the family and society. It is very important, therefore, to protect the brain from secondary damage. In clinical medicine, methods for providing cerebral protection are depressingly few in number and relatively crude. Animal experiments, however, offer the promise that in the future, targeted cerebral protection will be possible. This chapter describes the pathophysiological features of cerebral damage, defines the meaning of the term protection, reviews animal models of protection and discusses cerebral protection in clinical anaesthesia.
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References
Wheeler DW, Menon DK (2002) Secondary Neuronal injury mechanisms. Anaesth Intensive Care Med 3: 120–123
Wright DW, Bauer ME, Hoffman SW et al (2001) Serum progesterone levels correlate with decreased cerebral edema after traumatic brain injury in rats. J Neurotrauma 18: 901–909
Mesenge C, Margailli I, Verrecchia C et al (1998) Protective effect of melatonin in a model of traumatic brain injury in mice. J Pineal Res 25: 41–46
Sullivan PG, Thompson M, Scheff SW (2000) Continuous infusion of cyclosporin A postinjury significantly ameliorates cortical damage following traumatic brain injury. Exp Neurol 161: 631–637
Kapinya KJ, Lowl D, Futterer C et al (2002) Tolerance against ischemic neuronal injury can be induced by volatile anesthetics and is inducible NO synthase dependent. Stroke 33: 1889–1898
Teasdale GM, Bannan PE (1997) Neuroprotection in head injury. In: Reilly P, Bullock R (eds) Head injury. Chapman and Hall, London, pp 423–438
Chesnut RM (1997) Guidelines for the management of severe head injury: what we know and what we think we know. J Trauma 42: S19–22
Gregson B, Todd NV, Crawford D et al (1999) CRASH trial is based on problematic meta-analysis. BMJ 319: 578
Muizelaar JP, Marmarou A, Young HF et al (1993) Improving the outcome of severe head injury with the oxygen radical scavenger polyethylene glycol-conjugated superoxide dismutase: a phase 2 trial. J Neurosurg 78: 375–82
Marshall LE, Marshall SB (1986) Pitfalls and advances from international tirilazad trial in moderate and severe head injury. J Neurotrauma 12: 929–932.
Pickard JD, Murray GD, Illingworth R et al (1989) Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ 298: 636–642
Harders A, Kakarieka A, Braakman R (1996) Traumatic subarachnoid haemorrhage and its treatment with nimodipine. German tSAH study group. J Neurosurg 85: 82–89
Chesnut RM, Marshall SB, Piek Jet al (1993) Early and late systemic hypotension as a frequent and fundamental source of cerebral ischemia following severe brain injury in the Traumatic Coma Data Bank. Acta Neurochir (Wien) 59: 121–125
Walia S, Sutcliffe AJ (2002) The relationship between blood glucose, mean arterial pressure and outcome after severe head injury: an observational study. Injury 33: 339–344
Reinstrup P, Stahl N, Mellergard P et al (2000) Intracerebral microdialysis in clinical practice: baseline values to chemical markers during wakefulness, anesthesia, and neurosurgery. Neurosurgery 47: 701–709
Eker C, Asgeirsson B, Grande P-O et al (1998) Improved outcome after severe head injury with a new therapy based on principles for brain volume regulation and preserved microcirculation. Crit Care Med 26: 1881–1886
Sato K, Sato K, Yashimoto T (2000) Systemic and cerebral haemodynamics during craniotomy under mild hypothermia in patients with acute subarachnoid haemorrhage. Acta Neurochir (Wien) 142: 1013–1019
Marion DW, Penrod LE, Kelsey SF et al (1997) Treatment of traumatic brain injury with moderate hypothermia. N Engl J Med 336: 540–546
Clifton GL, Miller ER, Choi SC et al (2001) Lack of effect of induction of hypothermia after acute brain injury. N Engl J Med 344: 556–563
Harper CM, McNicholas T, Gowrie-Mohan S (2003) Maintaining perioperative normothermia. BMJ 326: 271–272
Danielisova V, Marsala M, Chavko M et al (1990) Postischemic hypoxia improves metabolic and functional recovery of the spinal cord. Neurology 40: 1125–1129
Sutcliffe AJ (2003) Neuroanaesthesia: key points during the perioperative period. Minerva Anestesiol (in press)
Yundt KD, Grubb RL, Diringer MN et al (1997) Cerebral hemodynamic and metabolic changes caused by brain retraction after aneurysmal subarachnoid hemorrhage. Neurosurgery 40: 442–450
Sato K, Karibe H, Yoshimoto T (1999) Advantage of intravenous anaesthesia for acute stage surgery for aneurysmal subarachnoid haemorrhage. Acta Neurochir (Wien) 141: 161–163
Engelhard K, Werner C, Reeker W et al (1999) Desflurane and isoflurane improve neurological outcome after incomplete cerebral ischaemia in rats. Br J Anaesth 83: 415–421
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Sutcliffe, A.J. (2004). Cerebral protection during anaesthesia. In: Gullo, A. (eds) Anaesthesia, Pain, Intensive Care and Emergency Medicine — A.P.I.C.E.. Springer, Milano. https://doi.org/10.1007/978-88-470-2189-1_4
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DOI: https://doi.org/10.1007/978-88-470-2189-1_4
Publisher Name: Springer, Milano
Print ISBN: 978-88-470-0235-7
Online ISBN: 978-88-470-2189-1
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