I thought this would be a nice play by play of the cascade of things that occur in the event of a stroke. First, a little background of the types of strokes again:
There are two types of stroke, ischemic and hemorrhagic. 80 percent of strokes are ischemic in nature where "decreased or absent circulating blood deprives neurons of necessary substrates," whereas hemorrhagic stroke (15-20 percent) causes "disrupting of connective pathways" leading to "localized pressure injury." Ischemia can affect the brain rapidly because the brain does not have an independent supply of glucose and does not anaerobically metabolize. In the case of a hemorrhage, this becomes a much slower process because the effect on the brain is prolonged. However, both types induce a release of factors that in turn play major roles in the destruction of brain tissue.
In class I presented that there were two subtypes of ischemic stroke, either focal or global, which led into one of the reasons why the model for the study done by Leslie Ritter was highly valuable. Global ischemia is just caused by "profound reduction in systemic blood pressure due to any reason," also known as hypotension (found on page 7 where hypotensive stroke is discussed) Focal ischemia normally happens as a result of a thrombus or an embolus. A thrombus is a "solid mass of platelets and/or fibrin (and other components of blood) that forms locally in a vessel" and an embolus is "often a piece of a thrombus that has broken free and is carried toward the brain by the bloodstream" (refer to #2 in references for more info). whether it be caused by a thrombus or embolus, injury to the brain is determined by parameters such as rate of onset and duration, collateral circulation, health of systemic circulation, hematologic factors, temperature, and glucose metabolism. For further understanding of these parameters look to page 2 of the article under Focal Ischemic Injury. No matter the source of the stroke (ischemic, hemorrhagic, focal, or global), the following changes happen in attempt to reach homeostasis:
The reduction in cerebral blood flow causes vasodilatation of the surrounding vessels as a compensatory mechanism, but if the rate of flow is too low (less than 20 ml/100g/min) then electrical output is skewed to save energy. This leads to neuronal injury, which can be initiated through several excitotoxic mechanisms that the paper highlights in detail ranging from prolonged opening of calcium channels to the inflammatory response. There was great emphasis on the endothelial response at all levels of organization in regards to its promotion of inflammation. This reminded me of the necessity to know timing of post-ischemic events for optimization of treatment talked about in both mine and Carl's articles.
We briefly covered what a penumbral region was with Dr. Cohen in class, but the section called Ischemic Penumbra (IP) elaborates upon what constitutes this region. It is generalized by ineffective autoregulation, meaning there are no compensatory measures in this area. This is due to the reduction in cerebral blood flow that falls to a quarter or half of what is physiologically normal.
The IP is the primary region that experiences cell death by one of two known processes in regards to stroke. The first is Coagulation Necrosis (described on the bottom of page 4 in the article) where the cells are severely damaged and basically condense to nothing. The second, we all should be familiar with- Apoptosis in which the cells are programmed for death by the inflammatory response. Apoptosis by inflammatory targeting was shown to occur within the hour after ischemia, whereas coagulation necrosis did not begin until six hours after. Once I read this, the importance of understanding the relationships between inflammation and stroke became apparent to me. If the cell programming could be rewired to hinder or slow the inflammatory response by modification or inhibitory measures, then neuronal injury could be greatly reduced or at best case avoided.
Sid Shah created an outstanding schematic of the pathophysiology of stroke by the collaborative knowledge he obtained from 50 scholarly articles. This was such a great help at grasping the concepts and mechanisms behind how stroke is initiated, what happens during, and terminal effects post-ischemia. If you happen to read it, or even just my blog, please let me know your thoughts.
References:
1) Shah, Sid. "Stroke Pathophysiology." Foundation
for education and research in neurological emergencies [FERNE]: 1-14. web.
13 october 2013. http://tigger.uic.edu/com/ferne/pdf2/saem_0501/shah_stroke_saem_0501.pdf
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