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Reperfusion injury plays a major part in the biochemistry of hypoxic brain injury in stroke. Similar failure processes are involved in brain failure following reversal of cardiac arrest; [3] control of these processes is the subject of ongoing research.
Cerebral hyperperfusion syndrome, also known as reperfusion syndrome, is a dysregulated state of cerebral blood flow following the restoration of arterial blood flow to the brain, usually following treatment of carotid artery stenosis. [1]
Brain ischemia has been linked to a variety of diseases or abnormalities. Individuals with sickle cell anemia, compressed blood vessels, ventricular tachycardia, plaque buildup in the arteries, blood clots, extremely low blood pressure as a result of heart attack, and congenital heart defects have a higher predisposition to brain ischemia in comparison to the average population.
Woman experiencing mini stroke symptoms. Every year, nearly 800,000 people will have a stroke, according to the CDC. Most of these strokes will be what's called "ischemic," which happens when ...
[2] [3] Signs and symptoms often appear soon after the stroke has occurred. [3] If symptoms last less than 24 hours, the stroke is a transient ischemic attack (TIA), also called a mini-stroke. [3] Hemorrhagic stroke may also be associated with a severe headache. [3] The symptoms of stroke can be permanent. [5]
Other symptoms can include numbness in the face, arm, or leg, particularly if it’s one side of the body, confusion, trouble seeing, trouble walking, and a severe headache with no known cause.
A transient ischemic attack (TIA), commonly known as a mini-stroke, is a temporary (transient) stroke with noticeable symptoms that end within 24 hours. A TIA causes the same symptoms associated with a stroke, such as weakness or numbness on one side of the body, sudden dimming or loss of vision, difficulty speaking or understanding language or slurred speech.
This reperfusion results in inflammatory injury through three overlapping mechanisms. Some complimentary combination of, first, mitochondrial damage and, second, endothelial activation , causes a release of reactive oxygen species (ROS), which initiates and/or exacerbates a pathophysiological inflammatory response.