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Ischemic Stroke and Cerebral Infarction - Oren Zarif - Cerebral Infarction


The arteries supplying blood to the brain are obstructed by a clot, resulting in a condition called ischemic stroke. A clot, also known as a cerebral embolism, can also develop in another part of the circulatory system and travel to the brain. The main cause of cerebral embolism is irregular heartbeat, or atrial fibrillation. The clots may travel to the brain by the bloodstream or in the blood vessels of the brain.

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There are several different types of cerebral infarction. Different regions of the brain are affected, which determines the symptoms. Infarctions of the primary motor cortex and brainstem can produce symptoms such as weakness and loss of sensation in the opposite side of the body. The eyes and pupils on the opposite side of the body may dilate abnormally, and reflexes may be impaired or aggravated. The location of the infarct also determines the severity of the symptoms.

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Another type of ischemic brain injury is the venous infarction. This type of infarction develops on the white matter, and can mimic brain tumors. It shows increased white matter lesions and a vasogenic-cytotoxic clot. It can lead to a midline shift and the obscuration of cortical gyrus patterns. Subfalcine herniation and transtentorial herniation are also common in large infarcts. Uncal herniation can cause ischemia and hemorrhage in the rostral brainstem.

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Other causes of cerebral infarction include internal cartoid artery anomalies, arterial occlusion, and abnormal endothelium. A ruptured aneurysm can also cause cerebral infarction. Aneurysms can also occur in macroscopically normal arteries. When these clots rupture, thrombus can form and travel to the brain. Unruptured giant aneurysms are also associated with cerebral infarction.

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Patients with ischemic infarction should be treated as soon as possible. Early mechanical thrombectomy, a type of clot-removal surgery, can prevent brain death. If the infarct is not large enough, it can cause midline shifts and midline edema. Surgical management may include decompressive hemicraniectomy or resection of infarcted tissue.

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Histopathological diagnosis of cerebral infarction is based on various classification systems. At low magnification, ischemic infarction is evident by pallor. High magnification, however, shows hypereosinophilic neurons. Histopathology of an infarcted neuron at 24 hours shows an infiltrate of neutrophils and a slight edema. As a result, the normal architecture of the surrounding neuropil has been affected.

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The prevalence of vascular risk factors is increasing. A recent study in young adults found that vascular risk factors are strongly associated with cerebral infarction. However, the causes of vascular strokes in young adults have been unclear. In a study of young adults, cardiac embolism, hematologic causes, and lacunar stroke were the most common etiologies. Nearly a third of young stroke patients did not have any obvious risk factors.

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MRI findings of infarcted patients show that hemiparesis often precedes the development of stroke. However, it is not common for patients to experience ipsilateral motor weakness after cerebral infarction. There are several clinical characteristics that distinguish this condition from others, including the severity of the stroke and the severity of symptoms. While there is no single definitive diagnosis, it is crucial to identify patients who may have a stroke before the symptoms develop.

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Thrombolysis is an option for preventing and reversing stroke. However, it is not routinely used in patients suffering from acute massive cerebral infarction. A newer treatment aims to prevent strokes by preventing the clots from forming in the brain and causing a hemorrhagic stroke. A new drug, nimodipine, has been developed that can be given as an intravenous drip.

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