Post-Ischemic Dementia - Causes and Symptoms of Cerebral Ischemia - Oren Zarif - Cerebral Ischemia

There are several causes of cerebral ischemia. One of the most common is an untreated heart attack, which can slow the blood flow and form a clot that prevents the brain from receiving adequate blood flow. Other causes include congenital heart defects and sickle-cell anemia, a condition in which hemoglobin, the part of red blood cells that carry oxygen, is not produced in sufficient quantities. Patients with sickle-cell anemia have a reduced number of red blood cells and the irregular shape of sickle-cell anemia tends to clot more easily.

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The initial workup for cerebral ischemia should include basic lab tests, including a complete blood count, coagulation factors, EKG, and cardiac enzymes. If hemorrhage or a mass lesion are suspected, a stat non-contrast head CT is recommended to rule out other conditions. Vascular imaging is also very helpful in determining the cause of the stroke, as acute large vessel occlusion is often obvious.

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In addition to studying the causes of cerebral ischemia, patients with post-ischemic dementia should also learn the latest research on a wide range of treatments. Currently, there are two main types of treatment. First-line therapy is intended for patients with newly diagnosed DCI, characterized by neurological decline and characteristic imaging findings of ischemia. Second-line "rescue therapy" is intended for patients with refractory cerebral ischemia or DCI despite initial treatment.

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Ischemic brain tissue ceases to function and eventually dies. Severe damage can occur when brain cells are deprived of oxygen for several minutes. Often, this happens with brain tissue death, and it is then known as cerebral infarction or ischemic stroke. Symptoms of cerebral ischemia vary, and can last from a few seconds to several minutes. It is also sometimes referred to as a transient ischemic attack.

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The NINDS tPA trial provides detailed information on the neurological changes that occur within 24 hours of stroke. Although only 8% of patients recovered completely, the chances of subsequent neurological deterioration were much greater. The odds of deterioration increased with the severity of the acute recovery. And those with more advanced acute neurologic dysfunction had greater odds of developing a stroke within the first 90 days of treatment. So, while the NINDS tPA trial provides useful data for those with ischemic stroke, it is important to know how to recognize this potentially life-threatening condition.

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In addition to using oxygen 15-labeled fluoromisonidazole positron emission tomography to assess brain injury, researchers have been able to create a cellular model that induces an ischemic stroke in vivo. By analyzing calcium concentration fluctuations, the researchers were able to identify the onset of cerebral ischemia and assess its consequences. Using this new technology, scientists hope to develop more effective treatments for this condition.

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Brain injury in this condition leads to an imbalance in proteostasis. Inflammation signals are released by damaged brain tissue and recruit inflammatory cells. Some of these cytokines include TNFa, which is responsible for mediating inflammatory and apoptotic signals via NF-khB and FADD. Autophagy is another important pathway to understand the pathophysiology of cerebral ischemia. It is involved in neuroprotection, promoting neuronal survival and differentiation after cerebral ischemia.

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Treatment of ischemic stroke varies depending on the part of the body affected by the stroke. The first goal of treatment is to restore breathing and blood pressure, and then the next step is to reduce the pressure on the brain. Antiplatelet drugs, anticoagulants, and surgery may be used to open the blood vessels. The effectiveness of these treatments largely depends on which part of the brain is affected and how much brain tissue is affected.

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Imaging techniques are important for diagnosis of cerebral ischemia. Conventional techniques like computed tomography and ultrasonography may not detect ischemia in its early stages. Recent developments include the development of 18F-based positron emission tomography (PET) probes that can detect neuronal death. Magnetic resonance imaging has a higher sensitivity than the other neuroimaging techniques and allows the differentiation of damaged regions even at early stages of ischemia. Moreover, these procedures do not require radioactive tracers.

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The inflammatory response to cerebral ischemia triggers two different mechanisms in the brain. Both autophagy and the UPR are activated when the brain suffers from cerebral ischemia. These two processes should be studied together. The role of autophagy in cerebral ischemia is not clear, but they are essential for stroke recovery. These studies have been conducted on mice models and humans. The findings indicate that both pathways contribute to the process of brain cell death.