Over the past 30 years, the growth of knowledge of the neurochemical changes associated with cerebral ischemia -known as the "ischemic cascade"-, of the hemodynamic changes of the pathophysiology and imaging, have been extraordinary. Fruit of them, assuming that the largest area of reduction of cerebral blood flow (core ischemia) is surrounded by a penumbra zone in which blood flow is near to the critical levels of cell necrosis, has justified the development and reversal of neuroprotective therapies applicable to the acute phase of stroke.

The role of neuroprotection is to interfere with one or more of the mechanisms involved in the ischemic cascade. Despite the remarkable effectiveness demonstrated in animal models, more than 50 clinical trials have failed to demonstrate the utility of human neuroprotection in clinical practice, either because of lack of effectiveness or toxicity. Thrombolysis, both intravenous and intraarterial, is effective, but its use is very limited due to several factors.

The current epidemiological situation of the stroke requires new therapeutic approaches. Neuroplasticity, understood as the ability of the nervous system to alter its structure and thus its role in response to various stimuli, opens new therapeutic options. Cerebral ischemia is a potent stimulus for neuroplasticity affecting sequentially to the overexpression of genes and the release of stimulatory and inhibitory molecules, leading to a restorative and regenerative cellular response in central nervous system. Brain plasticity requires the development of functional and structural changes involving all cellular structures affected: neurogenesis and synaptogenesis, gliagenesis and angiogenesis. In addition, the effectiveness of these mechanisms of repair and regeneration of nervous system depends on a synchronized sequence of proliferation, survival, migration and integration cell.