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Neonatal MRI Detects Cerebral Infarction - Oren Zarif - Cerebral Infarction


Approximately one third of all stroke patients have some kind of vascular risk factor. The study looked at young adults in a region with racial and ethnic diversity. The most common causes of cerebral infarction were cardiac embolism, hematologic disorders, and lacunar stroke. However, nearly a third of first strokes were not due to any known risk factor. Several vascular risk factors are associated with the risk of stroke, including alcohol consumption and tobacco use.

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Some of the complications of cerebral infarction are very different from each other. Cerebral edema is a complication of cerebral infarction. It is a cytotoxic and vasogenic complication and usually reaches its peak four to five days after cerebral infarction. This complication may lead to midline shift or obscuration of cortical gyral pattern. Other complications of cerebral infarction include subfalcine herniation, transtentorial herniation, and uncal herniation.

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Neonatal MRI allows physicians to detect infarction of major arteries and branching arteries. In this way, they can differentiate acute strokes from chronic ones. In a newborn, the diagnosis is more likely to be correct with neonatal MRI. With increased access to this procedure, neonatal MRI has become the standard of care for identifying brain damage. The resulting images of cerebral infarction show a wide spectrum of signs and symptoms, ranging from ischemic penumbra to frank infarction.

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The symptoms of cerebral infarction depend on the part of the brain affected. In the primary motor cortex, infarction results in weakness of the opposite side of the body. Eye movements are impaired and pupil dilation abnormal. Speech infarction on the left side of the brain causes slurred speech. Reflexes are also affected. So, if the symptoms of cerebral infarction are similar to those of stroke, it is likely that a hemorrhage has occurred.

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The initial workup for cerebral ischemia involves basic labs, including complete blood count, coagulation factors, and cardiac enzymes. If there are signs of a mass lesion or hemorrhage, a stat non-contrast head CT should be performed. In some instances, vascular imaging may be necessary to protect the brain tissue from further damage. If the underlying cause is unclear, reperfusion may result in reperfusion injury, a type of damage that is worse than the ischemia itself.

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In a recent study, an underlying cause of silent cerebral infarction was found to be thrombotic occlusion of a cerebral artery. A stroke caused by a blood clot is often classified as hemorrhagic. The CTA can help determine the exact cause of silent cerebral infarction. By determining the underlying cause, a treatment plan can be developed to minimize the risk of a silent cerebral infarction.

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A massive cerebral infarction may cause a coma and a midline shift in the brain. These symptoms can cause permanent brain damage and even death. If caught early, surgery is the best way to restore blood flow to the cerebrum. This procedure is often performed during an outpatient stay, but non-ambulatory patients may require hospitalization. If no medical treatment is possible, thrombolytic agents are frequently used.

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The imaging findings of ischemic stroke vary from case to case. On DWI, an ill-defined mass or region with parenchymal enhancement is indicative of acute ischemic stroke. Similarly, the appearance of hemorrhagic infarction varies, and can be difficult to differentiate from the signs of a tumor or vascular disease. Nonetheless, the T2*GRE sequence is ideal for identifying hemorrhage and ischemic stroke. In contrast, air and mineralization of the brain are hypointense and can be indicative of hemorrhage.

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Moreover, cerebral infarction can mimic brain tumors. Most commonly, this condition causes less extensive white matter lesions, and the appearance of hemorrhagic changes and irregular contrast enhancement is suggestive of a tumor. MR venography and T2-weighted imaging can help differentiate cerebral infarction from venous infarction. These imaging studies may also help differentiate patients with symptoms of both conditions. If the clinical presentation is unusual or the patient's history is unreliable, cerebral infarction should be diagnosed and treated.

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Cerebrovascular strokes may be associated with an elevated risk of death or severe disability. Although there is no clear link between aPL and risk of MI, there are numerous other risk factors for cerebrovascular disease. It is thought that antiphospholipid antibodies, which are specifically directed against phospholipids, may increase the risk of cerebral ischemia. APL may increase the risk of stroke and venous thrombosis, but the association is controversial.

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