While investigating the role of inflammation and its associations with stroke and delayed damage, I came across a couple of interesting articles that connect stroke and traumatic brain injury (TBI). By now we are all very familiar with the inflammatory response and various cytokines and cells associated with ischemic stroke. What may not be as clear, however, are the similarities between inflammation-mediated stroke reperfusion injury and other common causes of brain trauma.
TBI is commonly associated with high mortality and permanent neural deficits. In both the United States and Europe, TBI is the leading cause of death for individuals under the age of 45 and stroke is the second most common cause of death worldwide. Although traumatic tissue damage and ischemia have different causes, it has been shown that they are connected through the inflammatory pathway. Both TBI and stroke patients commonly suffer from delayed damage, mediated by the inflammatory response. Interestingly, in both cases, delayed damage often results in greater damage than that caused by the primary injury.
Besides direct mechanical injury, TBI leads to swelling of the brain due to local cellular edema. This increases the pressure on the cerebral microcirculatory vessels, which can cause ischemia (as seen with stroke). Often the blood-brain barrier is also broken down, which can lead to further swelling, hypoxia, and exacerbation of the problem. As with stroke, TBI causes up-regulation of cytokines, such as TNF, accumulation of leukocytes and macrophages, and increased expression of adhesion molecules.
This information clearly points out the need for further research regarding the inflammatory response in the brain. Whether it caused by transient ischemia or traumatic, mechanical force, the extent of many brain injuries has the potential to be greatly decreased through furthering our understanding of the delayed damage mechanism.
Finally, I think it is important to realize that post-insult inflammatory damage is not exclusive to stroke. The same inflammatory cells and mediators present in the ischemic brain can also be activated by other means and facilitate further tissue damage. I’m wondering if the connection between minor concussion (often seen in football) and any resulting inflammation related damage has been given much scrutiny. It would be interesting to determine exactly what portion of damage, resulting from minor concussion, is the result of delayed onset mechanisms.
References:
Andrews, Peter, and Rhodes, Jonathan. "The brain as a site of inflammation after acute injury". Blackwell, 2006. Pg: 275-276.
Feuerstein, Giora. “Inflammation and Stroke". Birkhauser, 2001. Pg: 181-186.
Subscribe to:
Post Comments (Atom)
2 comments:
thanks for posting this! It's easy to forget (at least for me)...that inflammation is an important part of healing and yet the "healing process" itself can lead to greater damage!
Last April my extremely healthy brother, only 32 years old, collapsed while playing soccer in California. He was unresponsive for hours and spent 3 days in the hospital. After many tests, doctors could not explain what happened to him. I think he either had a seizure or stroke. The week before he was accidentally hit in the head by another player. It was his 4th or 5th concussion to date. I think his past and present TBI led to this seizure or stroke. I'll ask him to read your blog! Thanks.
Post a Comment