Ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, and traumatic brain injury-all have in common early brain injury due to brain tissue destruction, reduced cerebral blood flow and oxygen delivery, and overall substantial morbidity and mortality. The pathophysiology of brain tissue damage likely includes common cellular mechanisms. Neuroprotection has seldom, if ever, been shown to reduce early brain injury. Secondary brain injury develops after these conditions due to macroscopic events such as increased intracranial pressure and reduced cerebral blood flow, as well as cellular processes including vascular damage, inflammation, and apoptotic/necrotic cell death. Preclinical as well as some human studies show successful neuroprotection with, for example, hypothermia for cardiac arrest. Nevertheless, there remains much room for improvement that will require randomized clinical trials of emerging neuroprotective strategies.
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