The relationship between inflammation and stroke seems to be multi-layered. First, it is important to look at inflammation as a risk factor for stroke. Secondly, it is important to investigate the role of inflammation in the severity and spread of infarct and damage during and after stroke. And thirdly, it is important to look at the role of inflammation in the recovery process after stroke.
1. According to the National Stroke Association, certain controllable and non-controllable risk factors increase the chances of a person having a stroke. Non-controllable risk factors include: age, gender and race. Controllable risk factors include: hypertension, hypercholesterolemia, diabetes, atherosclerosis, circulation problems, physical inactivity, and obesity. Chronic low-levels of inflammation have been linked to these controllable risk factors, and therefore can be linked to stroke as well. It seems to me that these risk factors and chronic inflammation should be linked more to thrombotic stroke than to hemorrhagic stroke, with the possible exception of hypertension. What are your thoughts on this? Has anyone seen any data to support or discount this?
2. In patients with ischemic stroke, increased levels of proinflammatory cytokines are related to larger cerebral infact and poorer clinical outcome (Vila et al. 'Levels of anti-inflammatory cytokines and neurological worsening in acute ischemic stroke'. Stroke (2003) pp. 671-675). Furthermore, administration of IL-10, an anti-inflammatory molecule, has been shown to reduce infarct size (Vila et al.) and SCID mice have reduced lesion size with middle cerebral artery occlusion compared to wild-type mice (Hurn, et al. 'T- and B-cell-deficient mice with experimental stroke have reduced lesion size and inflammation'. Journal of Cerebral Blood Flow and Metabolism (2007) 27, pp. 1798-1805). However, both of these studies have focused on the short term effect of inflammation during ischemic stroke. What about the long term?
3. What are the long term effects of inflammation during ischemic stroke? Even though inflammation has been shown to increase infart size, isn't inflammation critical during the healing processes? It is very difficult to analyze the role of inflammation during and after stroke. More research needs to be done to evaluate the full spatial and temporal relationship between the two.
As a side note to this post... Worried about having a stroke? Use this scorecard to evaluate your risk! http://www.stroke.org/site/DocServer/scorecard_risk.pdf?docID=601
I agree a lot of those risk factors are for thrombotic stroke and that hypertension is more relevant to hemorrhagic stroke. However, most of the risk factors can contribute to hypertension, including inflammation, atherosclerosis, and diabetes, which could lead to a hemorrhagic stroke.
ReplyDeleteIn respect to the SCID study, I also thought it would be interesting to address the long term effects. Would inflammation decrease? Would IFN gamma be suppressed without T and B cell regulation? However, the data would conflict with the fact that stroke induced SCID mice after 22 hours of testing will most likely develop problems extraneous to the study. Unfortunate.
You can't discount hypertension's role in thrombotic stroke either though. Hypertension is known to cause micro-tears in systemic blood vessels which require an inflammatory response to repair. This leads to scar tissue within vessicular lumens that plaques can develop on, break off, travel to the brain and result in a thrombotic stroke.
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