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Symptoms and Treatment for Cerebral Ischemia - Oren Zarif - Cerebral Ischemia

Brain tissue can suffer from severe ischemia or mild ischemia. If you experience ischemia, your brain tissue can die within a matter of minutes. This condition is often called an ischemic stroke or cerebral infarction. Symptoms of brain ischemia may range from mild to severe, and the period of time in which symptoms occur varies greatly. Transient ischemic attack (TIA) is the most common type of ischemia.

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Ischemia can be due to a variety of causes, but is most commonly induced by a disruption in the blood supply to the brain. This disruption can occur due to cardiac arrest, carotid occlusion, hypotension, asphyxia, or anemia, while focal cerebral ischemia is related to vascular disease in the brain. In both cases, brain cells suffer death due to an abnormal rise in calcium ions that enter neurons through glutamate-activated channels. In turn, high calcium levels activate proteases and endonucleases, which can damage DNA and structural proteins.

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Symptoms of cerebral ischemia may be mild or even reversible. If left untreated, the condition can progress to a serious form of stroke, known as cerebral infarction. This form of cerebral ischemia can cause severe disability and even death. Depending on the severity of the case, cerebral ischemia may be reversible or progressive. Clinical deficits often occur in tandem with angiographic evidence of narrowing blood vessels.

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Acute ischemic stroke has been increasing in incidence in recent years. Currently, it accounts for 60 percent to 80% of all strokes. The insufficient blood flow to the brain tissue results in the death of brain cells and irreversible damage to tissue. Treatments for ischemic stroke include thrombolytic therapy, which has a limited window of effectiveness and a high recurrence rate. The most promising treatments will be those that have a clear link between the brain and the central nervous system.

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Cerebral ischemia occurs when the flow of blood cannot meet the metabolic demand of brain tissue. Without adequate oxygen, brain tissue is deprived of nutrients, leading to death. The condition is a subtype of stroke, but the symptoms and treatment for ischemic brain damage are similar. It can affect a large region of the brain in an arterial stroke, a venous stroke, or even the entire brain in a cardiac arrest. In addition, cerebral ischemia may contribute to secondary brain damage in mass lesions, hemorrhages, and traumatic brain injury.

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Strokes can occur for a variety of reasons, from heart attacks to blood clots in a peripheral artery. In the most severe cases, ischemia may be accompanied by a heart attack or carbon monoxide poisoning. People with a stroke history are more likely to develop global ischemia. Men are at a higher risk for ischemic stroke than women. It is also more common in black people than in whites. Age is a risk factor.

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Initial treatment of cerebral ischemia includes basic laboratory tests such as complete blood count, coagulation factors, and EKG. A stat non-contrast head CT is needed to rule out other causes of stroke. A large arterial occlusion may be visible, but if a smaller vessel is involved, this may be overlooked. MRI can be helpful in confirming ischemia. Acute large vessel occlusion may be obvious on the CT.

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MRI can be performed remotely, or directly within the MRI scanner. This is particularly useful for detecting early stages of cerebral ischemia. Because tMCAo is able to measure calcium concentration fluctuations, this technique can also help diagnose ischemia in patients who are otherwise unresponsive to treatments. It is important to note that MRI may not be as accurate as the MRI, so a tMCAo is an excellent tool to monitor cerebral ischemia.

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Neuropathology studies have identified several specific neuropathology characteristics of cerebral ischemia. Cerebral white matter lesions, neuronal cell death, calcium overload, and adenosine triphosphate level are all hallmarks of the disease. During ischemia, adenosine triphosphate level falls, thereby indicating that cerebral ischemia has a direct impact on the brain's function.

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The spatial matching between tissue classes was poor. HBV and IBV voxels showed similar reductions in CBF. HBV voxels had significantly lower CMRO2 values, and they showed less CBF and OEF than IBV. The HBV voxels were more likely to show physiologic signatures of irreversible injury than IBV voxels. Despite these limitations, the results of the study will be useful for improving diagnosis and treatment.

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