When therapeutically effective, decompressive craniectomy typically reduces intracerebral pressure, improves cerebral blood flow and tissue oxygenation, and increases aerobic cerebral energy metabolism. The efficacy of craniectomy following traumatic brain injury may at times be limited by damage to mitochondrial oxidative phosphorylation proteins that occurs prior to surgery. Moreover, when the craniectomy stimulates reperfusion following even partial ischemia, secondary mechanisms of injury to metabolism and other activities may be activated, thereby defeating the purpose. This chapter reviews the evidence for a causative role of mitochondrial and metabolic dysfunction in poor outcomes following traumatic brain injury. An appraisal of the literature devoted to decompressive craniectomy reveals a scarcity of studies that assess the role of cerebral energy metabolism in the success or failure of craniectomies. A case is made for much more research testing combinations of decompressive craniectomy with other neuroprotective interventions, particularly those that improve brain energy metabolism and are effective in animal models of cerebral ischemia/reperfusion.
|Original language||English (US)|
|Title of host publication||Decompressive Craniectomy|
|Publisher||Nova Science Publishers, Inc.|
|Number of pages||22|
|Publication status||Published - Jan 1 2018|
- Oxidative stress
ASJC Scopus subject areas