11 October 2010

Ischemic Stroke and Immunodepression: The Downside.

Since we have looked at some of the many classified correlations between post-stroke immunosuppression and increased recovery from an ischemic brain attack, I thought a post that put immunodeficiency in a different light was warranted. Post-stroke infection is a very crippling problem as about 85% of all stroke patients have some sort of infectious complications. Infection is also the most relevant complication during recovery from stroke, and it is the number one cause of death day 1 post-stroke. (Dirnagl et al.) It has been relatively controversial whether stroke caused immunosuppression or if it simply was a correlation. Recently, it has been realized that CNS injury is likely responsible for induced immunodepression.

One study looked into this controversy:

"Infection After Acute Ischemic Stroke" Angel Chamorro, et al. Stroke: 2007.

They observed that stroke patients would usually develop infections shortly after acute stroke regardless of the quality of care and treatment received. Furthermore, the mortality risk from infection increases with the severity of the stroke. It is recently discovered that the brain and immune system are linked through neural and humoral mechanisms, and so this is one of many experiments seeking a mechanistic answer. They found that in experimental brain ischemia (in mice), infections were associated with the activation of the ANS (autonomic nervous system) and neuroendocrine pathways, which ultimately increased the strength of anti-inflammatory signals. Also observed was a cytokine-mediated anti-inflammatory response in stroke patients with high infection risk.

This study gives some insight on what is causing the high infection rate in stroke patients. However, the authors admit that although a connection exists between an anti-inflammatory response and bran ischemia, more needs to be understood about the cross-talk between brain and the immune system. It is also still unclear whether infection is independently detrimental in stroke patients' recovery of brain tissue.

Fortunately, more has been done on this subject. From this same journal that the above study was found in, a review article did a wonderful job of organizing recently studies into assembled hypotheses:

"Stroke-Induced Immunodepression. Experimental Evidence and Clinical Relevance" Dirnagl et al. Stroke: 2007.

Not only does the review article describe how the immunodepression is acquired, it also explains what causes it. They show that it is known that the SNS and HPA axis are key players in the progression to immunodepression in brain ischemia. They also propose a few mechanism for what stimulates these systems after ischemia. This review was very useful for understanding the current knowledge of post-stoke immunodepression.

There is much research being done to attempt to understand the complicated workings of the immune system post-ischemia, but unfortunately the mechanisms are still not clearly understood. Moreover, the results from studies are really only relevant in mice! Nonetheless, progress is still happening and someday we will be more competent.

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