Oxidative stress during the chronic phase after stroke.

Stroke is a complex disease originating and developing on the background of genetic predisposition and interaction between different risk factors that chronically damage blood vessels. The search for an effective treatment of stroke patients is the main priority of basic and clinical sciences. The chronic phase of stroke provides possibilities for therapy directed toward stimulation of recovery processes as well as prophylaxis, which reduces the probability of subsequent cerebrovascular events. Oxidative stress is a potential contributor to the pathophysiological consequences of stroke. The aim of the present review is to summarize the current knowledge of the role of oxidative stress during the chronic phase after stroke and its contribution to the initiation of subsequent stroke. The relationship among inflammation, hemostatic abnormalities, and platelet activation in chronic stroke patients is discussed in the context of ongoing free radical processes and oxidative damage. Free radical-mediated effects of increased plasma level of homocysteine and its possible contribution to the processes leading to recurrent stroke are discussed as well. The status of the antioxidant defense system and the degree of oxidative damage in the circulation of stroke survivors are examined. The results are interpreted in view of the effects of the vascular risk factors for stroke that include additional activation of inflammatory and free radical mechanisms. Also, the possibilities for combined therapy including antioxidants in the acute and convalescent stages of stroke are considered. Future investigations are expected to elucidate the role of free radical processes in the chronic phase after stroke and to evaluate the prophylactic and therapeutic potential of anti-radical agents.