PURPOSE OF REVIEW: Inflammation is now considered to be a critically important determinant of outcome following acute injury to the CNS, potentially contributing to the development of secondary injury. The current review summarizes the most recent advances in the understanding of inflammatory mechanisms following both ischemic and hemorrhagic stroke, and highlights areas of therapeutic promise. RECENT FINDINGS: A prominent inflammatory response occurs following both ischemic and hemorrhagic stroke, thereby exacerbating secondary injury. Recent efforts have been directed toward understanding the mechanisms by which immediate triggers of poststroke inflammation mediate their effects. Inflammatory stimuli administered acutely prestroke are deleterious, but subacute stimuli can be either deleterious or protective; toll-like receptor signaling has been implicated as a regulatory factor. There is growing evidence that systemic inflammation, whether prestroke or stroke-induced, influences stroke outcome and that therapies may need to also attenuate systemic inflammation to be effective. The beneficial effects of stem cell therapy may be mediated, at least in part, by its systemic anti-inflammatory effects. SUMMARY: Inhibiting inflammation following both ischemic and hemorrhagic stroke remains a promising approach. More sophisticated therapies, with pleiotropic beneficial effects, and more sophisticated targeting of potential recipients, will increase the likelihood of successful clinical translation.
PURPOSE OF REVIEW: Inflammation is now considered to be a critically important determinant of outcome following acute injury to the CNS, potentially contributing to the development of secondary injury. The current review summarizes the most recent advances in the understanding of inflammatory mechanisms following both ischemic and hemorrhagic stroke, and highlights areas of therapeutic promise. RECENT FINDINGS: A prominent inflammatory response occurs following both ischemic and hemorrhagic stroke, thereby exacerbating secondary injury. Recent efforts have been directed toward understanding the mechanisms by which immediate triggers of poststroke inflammation mediate their effects. Inflammatory stimuli administered acutely prestroke are deleterious, but subacute stimuli can be either deleterious or protective; toll-like receptor signaling has been implicated as a regulatory factor. There is growing evidence that systemic inflammation, whether prestroke or stroke-induced, influences stroke outcome and that therapies may need to also attenuate systemic inflammation to be effective. The beneficial effects of stem cell therapy may be mediated, at least in part, by its systemic anti-inflammatory effects. SUMMARY: Inhibiting inflammation following both ischemic and hemorrhagic stroke remains a promising approach. More sophisticated therapies, with pleiotropic beneficial effects, and more sophisticated targeting of potential recipients, will increase the likelihood of successful clinical translation.