What is the pathophysiology of ischemic stroke?

Updated: Nov 30, 2018
  • Author: Andrew Danziger; Chief Editor: L Gill Naul, MD  more...
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Acute ischemic strokes are the result of vascular occlusion secondary to thromboembolic disease. Ischemia results in cell hypoxia and depletion of cellular adenosine triphosphate (ATP). Without ATP, energy failure results in an inability to maintain ionic gradients across the cell membrane and cell depolarization. Influx of sodium and calcium ions and passive inflow of water into the cell ensues, resulting in cytotoxic edema. Further, cell depolarization leads to the release of glutamate and free radicals, mitochondrial membrane disruption, and a cascade that ultimately leads to apoptotic cell death. [5, 10]

Ischemia also directly results in dysfunction of the cerebral vasculature, with breakdown of the blood-brain barrier occurring within 4-6 hours after infarction. Following breakdown of the blood-brain barrier, proteins and water flood into the extracellular space, leading to vasogenic edema. Vasogenic edema produces greater levels of brain swelling and mass effect that peak at 3-5 days and resolves over the next several weeks with resorption of water and proteins. [11, 12]

Infarction results in the death of astrocytes as well as the supporting oligodendroglia and microglia cells. The infarcted tissue eventually undergoes liquefaction necrosis and is removed by macrophages with the development of parenchymal volume loss. A well-circumscribed region of cerebrospinal-fluidlike low density is eventually seen, consisting of encephalomalacia and cystic change. The evolution of these chronic changes may be seen in the weeks to months following the infarction.

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