What is the pathogenesis of MRI findings in acute stroke?

Updated: Dec 19, 2018
  • Author: Souvik Sen, MD, MPH, MS, FAHA; Chief Editor: Helmi L Lutsep, MD  more...
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Regardless of the cause, neuronal ischemia rapidly depletes intracellular adenosine triphosphate (ATP), which leads to failure of the membrane-bound, ATP-dependent ionic channels responsible for neuronal resting membrane potentials and the generation of action potentials. This metabolic aberration results in accumulation of intracellular ions (including calcium ions), creating an intracellular gradient responsible for intracellular accumulation of water (ie, cytotoxic edema).

Cerebral endothelial cells are more resistant to ischemia than are neurons and neuroglial cells. Approximately 3-4 hours after the onset of ischemia, the integrity of the blood-brain barrier becomes compromised, and plasma proteins are able to pass into the extracellular space. The intravascular water follows when reperfusion occurs (vasogenic edema); this process begins 6 hours after the onset of stroke and reaches a maximum 2-4 days after the onset of stroke. Reperfusion can also be accompanied by hemorrhagic transformation of the infarct, which is usually related to the volume and site of the infarct, being more common in large cortical infarcts.

Changes in MRI scans due to ischemic stroke follow the vascular territory of the occluded blood vessel, which is characteristic of cerebrovascular disease and helps in differentiating it from other disease entities.

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