Stroke Week

Every week our class holds a rhetoric discussing, debating, and clarifying the role of inflammation in disease. During these discussions and accompanying readings on ischemic strokes I realized that it is largely accepted inflammation contributes to the tissue damage of stroke beyond the initial ischemic event; Inflammation causes more damage than necessary. However the mechanism of exactly how inflammation causes more damage than necessary is lacking.

Apparently hypoxia causes neurons to release excess glutamate which opens Ca2+ channels. The excess Ca2+ results in apoptosis of neighboring cells. This also results in free radical production which roams around causing more injury. Where does inflammation come in and cause extra damage? As far as I can tell inflammation is being activated properly in response to damaged tissue. For example damaged cells activate damage associated molecular pattern toll like receptors and the ensuing inflammation. It appears to me that inflammation is activated in response to damage. There does not seem to be any evidence that inflammation causes gratuitous damage.

I have questions for the experts. To what extent is the extra damage beyond the ischemic damage? How does inflammation cause extra damage after stroke? What evidence shows that inflammation causes extra damage and how is it possible to distinguish between ischemic damage and inflammatory damage?