Introduction: Inflammation may play an important role in acute ischemic stroke. Experimental and clinical data suggest that post-stroke inflammatory responses are complex cascade phenomena, which may have detrimental or beneficial effects on outcome. This review focuses on the current understanding of inflammation effector pathways in focal cerebral ischemia and on therapeutic perspectives.
State of arts/perspectives: Somatic markers, such as admission body temperature or C-reactive protein, seem to be correlated with outcome, but data are heterogeous and contradictory, perhaps because their kinetics are complex during the first hours of a stroke. The most studied effectors of inflammation are cellular adhesion molecules--CAM (including integrins, selectins and members of the immunoglobulin superfamily), leucocytes, microglia, and blood brain barrier permeability. Evidence from animal data has lead to some clinical trials investigating anti adhesion molecules and hypothermia. However, current results remain disappointing. Recent experimental data also suggest a possible beneficial role of insulin and statins, which may be mediated by their effects on the inflammatory response.
Conclusion: Inflammation is an important avenue of therapeutic research in acute stroke. A better understanding of the inflammatory pathophysiology may help to a better design of clinical trials.