Cardioembolic stroke and Pathophysiology of Cerebral Infarction

• Another important cause of acute brain infarction is an embolus. Most embolic disease is caused by thrombus formation in the heart (cardioembolic) or extracranial vessels (aorta or carotid). The thrombus then travels distally into one of the cerebral vessels, most commonly the middle cerebral artery. Frequently, a second stroke follows because the underlying cause of the embolus remains.

• Cardioembolic stroke is commonly associated with atrial fibrillation, myocardial infarction, and valvular heart disease. Individuals with these cardiovascular disorders are usually placed on a regimen of anticoagulation therapy to prevent this dreaded complication.

• There are two other types of brain infarction: lacunar stroke and global hypoperfusion (or watershed) stroke.

Lacunar Stroke

Lacunar stroke refers to small infarcts (less than 1 cm) that occur deep in the brain because of obstruction of very small intracerebral vessels. Lacunar stems from the Latin word “lacuna,” which means “little lake.” It refers to the small areas of infarcted brain tissue surrounded by normal brain. These strokes occur most commonly in individuals with diabetes and hypertension and can result in very localized and unpredictable neurologic deficits.



Global Hypotension Stroke

• Global hypotension (or watershed) strokes occur when total brain perfusion falls because of cardiovascular collapse like that seen in severe myocardial infarction, major dysrhythmias, overwhelming systemic hemorrhage, or massive pulmonary emboli.

• The parts of the brain first affected by this type of stroke are near the surface of the cortex. They are in areas where the appearance of the cerebrovascular vessels is reminiscent of the small streams that feed a large river or lake, thus the name watershed. This type of stroke results in global cognitive dysfunction, irreversible coma, and death.

Hemorrhagic stroke is most often associated with :

• hypertension and weakening of the walls of intracerebral vessels.

• congenital aneurysms or vascular malformations.

• condition that is associated with an increased risk for bleeding, including thrombocytopenia (e.g., caused by drugs or bone marrow disease)

• coagulopathies such as liver disease, hemophilia, and iatrogenic anticoagulation.

• Blood is ejected through the damaged wall of the vessel into the surrounding brain tissue and can leak into the ventricles.

• The expanding collection of intracerebral blood (hematoma) compresses surrounding tissues, resulting in ischemia and increasing intracranial pressure.

• In many cases, bleeding will cease spontaneously, and the blood eventually will be reabsorbed, leaving a cavity.

• In other cases, rebleeding with expansion of the hematoma leads to worsening neurologic function and death.


Pathophysiology of Cerebral Infarction

• Infarction of brain tissue (also called cerebral infarction) occurs within minutes of complete cessation of cerebral blood flow. Because the brain is fed by an extensive system of collateral arterial flow, some of the brain surrounding the area of infarction may be ischemic but can survive up to 90 minutes without restoration of perfusion. This area of the brain is called the penumbra.

• Infarcted brain tissue undergoes a series of changes, including:

• Inflammation

• Breakdown of cell membrane pump function

• Cellular edema

• Necrosis

• In addition, ischemic neurons release excitotoxins, which are amino acids released in large amounts at the synapse and contribute to neuronal injury and death.

• Excitotoxin and inflammatory cytokine release can cause hyperpolarization of neurons, which increases tissue demand for oxygen, worsens ischemia, and may lead to seizures.


• Acute brain infarction, one type of cerebrovascular accident (CVA), is typically characterized by the abrupt painless loss of neurologic function. The location and extent of neurologic deficit depends upon the vessel that is obstructed. Because the middle cerebral artery is most commonly affected by atherothrombotic and embolic disease, common manifestations of acute brain infarction are:
Hemiparesis—Decreased motor ability on the affected side

• Hemisensory loss—Decreased sensation on the affected side

• Aphasia—Loss of speech ability

• Subsequent development of cerebral edema can lead to:

• Decreased levels of consciousness

• Possible brain herniation and death

• Intracerebral hemorrhage is most often associated with the sudden onset of severe headache and loss of consciousness. The extent of focal neurologic deficits depends upon the location and extent of the bleeding. The clinical status of the individual may deteriorate rapidly despite intervention.

• Markedly increased intracranial pressure is common in hemorrhage.

• In general, hemorrhagic strokes are considered more catastrophic than ischemic strokes.

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