Citation

Powers WJ. Stroke 2010; 41(10 Suppl): S107-10.

Affiliation

Department of Neurology, University of North Carolina, Chapel Hill, NC 27599-7025, USA. powersw@neurology.unc.edu

Copyright

(Copyright © 2010, American Heart Association, Publisher Lippincott Williams and Wilkins)

DOI

10.1161/STROKEAHA.110.595058

PMID

20876480

PMCID

PMC2953718

Abstract

Nontraumatic intracerebral hemorrhage (ICH) remains a devastating condition with 30-day mortality rates of 35% to 52%. Until the pathophysiology of this condition is better understood, it will not be possible to develop effective therapies. Studies of cerebral blood flow and metabolism in patients with acute ICH show similar abnormalities to those that occur in patients with traumatic brain injury, thus raising the question of whether there are common mechanisms of injury shared by the 2 conditions. In both ICH and traumatic brain injury, there is an early reduction in the cerebral metabolic rate of oxygen without ischemia, mitochondrial dysfunction, and transient focal increases in regional glucose metabolism that occur after a few days. ICH and traumatic brain injury share barotrauma from pressure waves that propagate through the intracranial contents as a common mechanism of brain injury. Recent data demonstrating contralateral hemispheric damage in patients with acute ICH provide further support for this theory of common injury mechanisms.

Language: en