What is Cerebral Infarction? - Oren Zarif - Cerebral Infarction
What is cerebral infarction? It is an ischemic disorder of the brain and is characterized by a focal neurologic deficit. Pulmonary infarction, in contrast, is a localized necrosis of lung tissue caused by a pulmonary embolism. Both disorders can cause a wide range of clinical manifestations, including subclinical chest pain, tachycardia, and hemoptysis.
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Cerebral infarction can be caused by various conditions, including internal cartoid artery anomalies, arterial occlusion, and abnormal endothelium. It can also result from embolism in a branch of the middle cerebral artery. Remote hemorrhage may result from aneurysm that has not ruptured. A small meningioma can also cause cerebral infarction.
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There are different classification systems for cerebral infarction. The most common type is arterial-to-artery embolism. Emboli often lodge in superficial vessels, which can lead to a wedge-shaped infarct. The most common location of cerebral embolism is in the middle cerebral artery territory. Emboli in this region tend to lodge in the distal branches of the superficial artery. However, infarcts can also be caused by a hemorrhage.
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While cerebral infarction is mostly a disease of aging, it can also occur in younger age groups. Researchers have found that an increased risk of a stroke is associated with certain vascular risk factors. A recent study of young adults found a correlation between cerebral infarction and the presence of hematologic disorders. The authors also concluded that the etiology of the first stroke was not determined. A study of vascular risk factors in young adults suggests that the occurrence of this disease has a racial/ethnic component.
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In patients with atrial fibrillation, an enlarged left atrium may be responsible for the thrombosis of the cerebral artery. However, a large number of these patients are still asymptomatic, and the symptoms of cerebral infarction are not apparent. Although the cause of cerebral infarction is not known, the condition does increase the risk of stroke. The severity of the disease is largely determined by the location and time of the clot in the brain.
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In chronic meningitis, cerebral infarction can result in a reduced supply of blood to the brain. A fatty plaque within the blood vessel is responsible for this condition. If this plaque develops, the clot can break off and travel to the brain. This is called a cerebral embolism. This condition affects 87 percent of strokes. However, there is no specific cure for cerebral infarction, so it is important to receive regular care in this case.
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Although most strokes are sudden and progress rapidly, some may occur with rapid changes in focal neurological status. Among the causes of sudden change in focal neurological status, seizure, postepileptic paralysis, hemorrhage into a tumor, and migraine are common. Neuroimaging may help differentiate between these causes. Although this may be the case, the precise classification of stroke evades the best of clinical skills.
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The initial workup for cerebral ischemia should include basic lab tests, including complete blood count, chemistry, coagulation factors, and EKG. A stat non-contrast head CT should be ordered to rule out any mass lesion. Vascular imaging is particularly useful in acute stroke etiology. An acute large vessel occlusion may be present and symptoms of syncope are relieved by lowering the head.
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In the case of acute ischemic stroke, the infarcted parenchyma continues to show a high DWI signal and low ADC signal. In addition, the infarcted cortex is often hyperintense on T2 and FLAIR. In acute ischemic stroke, cortical intrinsic high T1 signal may be present at as early as three days after the infarction. After day five, the cortex will typically show contrast enhancement on T1 C+. Arterial enhancement is encountered in half of stroke cases; meningeal enhancement is rare and typically occurs between two and six days after the stroke.
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