Cerebral metabolism [Neurosurgery Wiki]

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====== Cerebral metabolism ======

Animal [[behavior]] and [[metabolism]] are tightly coordinated with sleep-wake cycles governed by the [[brain]] in harmony with environmental light: dark cycles.

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Changes in [[metabolism]] are known to contribute to [[tumor]] [[phenotype]]s. If and how metabolic alterations in brain tumours contribute to patient outcome is still poorly understood. Epigenetics impact metabolism and mitochondrial function.

Disturbed [[brain]] metabolism is a signature of primary [[damage]] and/or precipitates secondary [[injury]] processes after [[severe brain injury]]. [[Sedative]]s and analgesics target electrophysiological functioning and are as such well-known modulators of brain energy metabolism. Still unclear, however, is how sedatives impact glucose metabolism and whether they differentially influence brain metabolism in normally active, healthy brain and critically impaired, injured brain. 
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An intricate relationship normally exists between cerebral [[metabolism]] and energy substrate supply because of the brain's high substrate demand and limited storage capacity. In head-injured patients, this balance can be disrupted. The brain parenchyma directly involved by the injury is hypometabolic in respect to glucose and oxygen, whereas peri-injury tissue may have an elevated metabolic rate
((Ritter AM, Robertson CS. Cerebral metabolism. Neurosurg Clin N Am. 1994
Oct;5(4):633-45. Review. PubMed PMID: 7827475.
)).