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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.
Post-resuscitation disease: Symptoms: Brain injury, myocardial injury, systemic ischemia/reperfusion response: Usual onset: After resuscitation from a cardiac arrest: Duration: Weeks: Causes: Global ischemia-reperfusion injury: Risk factors: Prolonged cardiac arrest: Differential diagnosis: Systemic inflammatory response syndrome: Management
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.
Without special treatment after circulation is restarted, full recovery of the brain after more than 3 minutes of clinical death at normal body temperature is rare. [6] [7] Usually brain damage or later brain death results after longer intervals of clinical death even if the heart is restarted and blood circulation is successfully restored ...
The onset of this disease is typically between 54 – 66 years of age and the first symptoms are usually mental deterioration or stroke. [4] The vessels that supply the subcortical white matter come from the vessels that support basal ganglia, internal capsule, and thalamus. It is described as its own zone by and susceptible to injury.
Life expectancy in the United States has started to rebound after historic drops earlier in the Covid-19 pandemic, but it has far from recovered.
Functional no reflow phenomenon occurs when the microvasculature is anatomically intact, but has been temporarily compromised due to spasm, microembolization, or reperfusion injury, ultimately leading to MVO. Functional no reflow phenomenon is largely reversible due to the fact that the microvasculature is still intact.