What is Cerebral Ischemia? - Oren Zarif - Cerebral Ischemia
Cerebral ischemia is a life-threatening condition that occurs when blood vessels are blocked. It reduces the amount of oxygen and glucose that reach brain tissue, causing brain injury and impairing the energetics required to maintain ionic gradients. The process also results in a complex series of pathophysiological events. High calcium ions that enter neurons through glutamate-activated channels trigger cell death by activating proteases and endonucleases that damage DNA and structural proteins.
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Animal models of cerebral ischemia are often used to dissect the mechanisms of injury and to identify potential targets for neuroprotection. A review of the different ischemic injury cascades is provided by Dirnagl et al. (1999), a leading authority on animal models of ischemic damage. The review also highlights some potential limitations of animal models. This is a critical step for finding new treatments and developing new strategies to protect brain tissue.
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Other conditions that cause a lack of blood supply to the brain include trauma, severe infections, and ruptured blood vessels. If the blood pressure is low, cerebral blood flow will be reduced and a stroke can result. The problem may be localized to a particular area of the brain, a condition known as focal ischemia. Some other causes of cerebral ischemia include a blood clot or a splinter of a clot, called an embolism.
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Acute MCAO in rats has been used to study the brain's response to incomplete ischemia. This model involves occlusion of the bilateral common carotid artery. The infarcted regions are the cortex and caudoputamen. The authors of these studies used the two-vessel model to assess cerebral blood flow. The resulting infarcted areas are reversible.
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The duration of ischemia affects neurological recovery. When cerebral blood flow is impaired for more than a few minutes, severe damage can occur. If the brain tissue has lost a significant amount of brain tissue, this is known as an ischemic stroke or cerebral infarction. Although the symptoms of brain ischemia are mild to severe, they can last for several minutes. In such cases, the condition is known as transient ischemic attack or TISA.
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In acute ischemic stroke, the initial workup should include a complete blood count, coagulation factors, EKG, and cardiac enzymes. CT scans should rule out hemorrhage and a mass lesion. Vascular imaging is also valuable in acute stroke etiology. Acute large vessel occlusion may be obvious, whereas a smaller ischemia may be hard to detect.
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Although cerebral ischemia is associated with heart attacks, it can also occur due to other causes. Untreated heart attacks can result in extremely low blood pressure and can block the flow of blood to major organs. Other events may result in cerebral ischemia, such as the onset of congenital heart disease. Patients with heart defects are prone to developing blood clots. However, if the condition occurs untreated, the consequences are devastating.
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After ischemic stroke, the goal of treatment is to restore the patient's breathing, heart rate, and blood pressure. Next, treatment for the underlying condition will help reduce pressure in the brain. Oftentimes, patients will require rehabilitation. Physical therapy and occupational therapy will help them regain lost motor skills and coordination. Patients may need long-term treatments like aspirin or anticoagulants. They may also need to undergo surgery to remove the clot.
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MRI imaging has shown that Gd2L1 shows clear separation from Gd2L2 when tMCAo is induced. The T1-weighted MRI signal during cerebral ischemia decreases by approximately 5% and recovers after reperfusion. In vivo, Gd2L1 responds to calcium fluctuations while Gd2L2 does not show much change during cerebral ischemia.
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Experimental models of global ischemia have also been used to study the effects of cerebral ischemia in rodents. This is because gerbils have a unique vascular anatomy and lack a posterior communicating artery between the vertebrobasilar arterial system and carotid artery. Therefore, in gerbils, bilateral common carotid artery occlusion is enough to induce global cerebral ischemia. In other animals, this can lead to a CBF reduction to almost zero.
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In addition, RBC transfusion has been shown to improve the oxygen tension of brain tissue in patients with poor-grade SAH. In this way, RBC transfusion is considered an important tool in optimizing cerebral oxygen delivery. However, it should be noted that many studies report negative outcomes and higher mortality in patients with SAH. However, despite these results, there are still no definitive studies that support the practice of RBC transfusion in the acute care setting.
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