The use of erythtropoietin in cerebral diseases.

Global and focal cerebral ischemia is followed by a secondary damage characterized by oxidative stress, excitotoxicity, inflammation and apoptosis. Erythropoietin (EPO) exerts antiapoptotic, anti-inflammatory, antioxidative, angiogenetic and neurotrophic properties. Its potential therapeutic role has been demonstrated in several animal models of cerebral ischemia and also in a clinical trial of ischemic stroke, so it could be considered an ideal compound for neuroprotection in ischemic stroke and in cardiac arrest. Intracerebral hemorrhage (ICH) is the least treatable form of stroke; the mechanisms involved in the secondary brain injury include hematoma mass effect, neuronal apoptosis and necrosis, inflammation. It has been demonstrated in an experimental ICH that EPO intervenes in the inflammatory process, reduces brain water content, hemorrhage volume and hemispheric atrophy, promotes cell survival, preserves cerebral blood flow, has antiapoptotic protective function against oxidative stress and excitotoxic damage. EPO can attenuate acute vasoconstriction and prevent brain ischemic damage in subarachnoid hemorrhage. The neuroprotective function of EPO has been studied also in traumatic brain injury: it reduces the inflammation and improves cognitive and motor deficits. The authors review some of the physiological actions of EPO in the physiopathology of ischemic and hemorrhagic stroke, subarachnoid hemorrhage and brain trauma, and its potential usefulness in the brain injured patient management.