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  • Writer's pictureOren Zarif

Imaging in Acute Stroke - Oren Zarif - Cerebral Ischemia

Imaging has become an integral part of the treatment of acute cerebral ischemia. In the past, the role of neuroradiology in acute stroke was peripheral. However, the development of thrombolysis techniques has transformed the role of neuroradiologists in the stroke process. Accurate and timely imaging is critical for the success of interventions. State-of-the-art reviews of imaging in acute stroke explain the role of computed tomography (CT) in diagnosis and treatment.

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Depending on the location of ischemia, the condition can occur in two ways: focal or global. Focal ischemia affects a specific part of the brain, such as a particular artery. Global ischemia, on the other hand, affects a wider area of the brain and is caused when the blood supply to the brain is severely reduced or stopped entirely. Surgical treatment is an option only in the most severe cases.

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The goal of treatment in acute ischemic stroke is to restore breathing, heart rate, and blood pressure. The next goal of treatment is to reduce the pressure on the brain. tPA is used to temporarily relieve pressure in the brain. This drug may not be suitable for people taking anticoagulants. Surgical procedures and mechanical clot removal may be necessary. Long-term treatments include taking anticoagulants and aspirin. However, these treatments can't reverse the effects of cerebral ischemia.

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Using a previously described model of focal cerebral ischemia, scientists were able to investigate the effects of a common type of ischemic injury. The ischemic event induced neuropathologies including neuronal cell death, calcium overload, and excitotoxicity, as well as cytotoxic oedema. In addition, the blood-brain barrier is compromised. These findings indicate a need for novel neuroprotective strategies.

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A number of cellular mechanisms are required for a thorough understanding of the underlying causes of cerebral ischemia. Initially, the brain is damaged, releasing inflammatory cells and cytokines, which recruit inflammatory cells to the area. Apoptosis signals are mediated by TNFa, while NF-khB promotes neuronal survival. A protein called p62, which regulates the activity of NF-kb, plays a critical role in regulating inflammatory responses and neuronal survival. Furthermore, autophagy may potentiate UPR, resulting in a cellular response reminiscent of brain damage.

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While cerebrovascular ischemia is generally asymptomatic, it can still lead to dementia. The cause of cerebral ischemia is not known, but pathological changes in the CA1 area are believed to be the primary culprit. The earliest clinical symptom of post-ischemic dementia is episodic memory impairment. The 13 chapters of this book present a new picture of ischemic brain disease, synthesizing recent findings on the cause, diagnosis, treatment, and potential therapeutic targets. The chapters present clinical characteristics and risk factors from infancy through adulthood.

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Another potential cause of cerebral ischemia is a heart attack. When the blood pressure falls extremely low, the brain receives very little oxygen. This results in a reduced blood flow that slows the heartbeat and prevents blood flow to major organs. Other factors can result in cerebral ischemia, such as congenital heart disease and blood clots. Those who suffer from this condition are at greater risk of developing cerebral ischemia than people without such conditions.

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If an embolic stroke occurs, blood clots travel through the bloodstream to the brain. A stroke of this type may be temporary or chronic. Symptoms range from mild to severe and last seconds to minutes. It is also known as a transient ischemic attack (TIA).

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MRI imaging has also been proven to be helpful for diagnosing and monitoring ischemic stroke. Using calcium-chelating molecules, researchers are able to monitor cerebral ischemia in vivo. Calcium concentration fluctuations, a common indicator of ischemia, are triggered by tMCAo. This technology can help detect ischemia early enough for effective treatment. So, while MRI may not be a foolproof method, it is an important first step in assessing the risk of stroke.

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In patients with acute focal neurologic deficits, reperfusion therapies are critical. These therapies include intravenous thrombolysis with tissue plasminogen activator (TPA), endovascular therapy, and mechanical thrombectomy. These treatments are most effective when administered as quickly as possible. The faster the treatment, the better the chance of neurologic recovery. The key is not to wait until symptoms appear to be more severe to decide whether reperfusion therapy is the best option.

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Despite the challenges that come with neuroimaging, a few techniques have proved useful for diagnosis and monitoring. In addition to using a variety of imaging techniques, a specialized team can assess the presence of cerebral ischemia using a combination of methods. The most common neuroimaging methods are computed tomography and ultrasound. However, these two imaging methods lack the sensitivity required to identify early ischemia. They use 18F-based positron emission tomography probes and the mitochondrial complex I activity, which is a marker of neuronal death. This technique is considered more reliable than any other neuroimaging method because it allows differentiation of damaged regions at earlier stages of the ischemia process without the use of radioactive tracers.

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