Thresholds in cerebral ischemia-the ischemic penumbra.

J Astrup, BK Siesjö, L Symon - Stroke, 1981 - Am Heart Assoc
J Astrup, BK Siesjö, L Symon
Stroke, 1981Am Heart Assoc
COMPLETE ARREST of the cerebral circulation leads within seconds to cessation of
neuronal electrical activity and within a few minutes to deterioration of the energy state and
ion homeostasis. Depletion of high energy phosphates, membrane ion pump failure, efflux of
cellular potassium, influx of sodium, chloride and water, and membrane depolarization occur
swiftly. If such chaos persists for longer than 5-10 minutes, irreversible cell damage is likely.
Such is the inevitable sequence of events if blood flow to the brain is arrested. If, however …
COMPLETE ARREST of the cerebral circulation leads within seconds to cessation of neuronal electrical activity and within a few minutes to deterioration of the energy state and ion homeostasis. Depletion of high energy phosphates, membrane ion pump failure, efflux of cellular potassium, influx of sodium, chloride and water, and membrane depolarization occur swiftly. If such chaos persists for longer than 5-10 minutes, irreversible cell damage is likely. Such is the inevitable sequence of events if blood flow to the brain is arrested. If, however, the ischemia is incomplete the outcome is more difficult to predict and is largely dependent on residual perfusion and oxygen availability. It is in large measure the outcome of incomplete cerebral ischemia, which is of particular interest in cerebrovascular disease. With occlusion of a cerebral vessel and signs of acute stroke, ischemia is hardly ever total. Some residual perfusion persists in the ischemic area dependent on collateral vessels and local perfusion pressures.
Recent evidence indicates that immediate failure of basic functions such as synaptic transmission, ion pumping and energy metabolism in the ischemic brain, is critically dependent on residual blood flow, and that these functions fail at certain critical flow thresholds. It appears, further, that the development of infarction is critically correlated to residual perfusion, and there is a lethal threshold of residual blood flow below which tissue infarction develops after a certain time. Such knowledge provides the theoretical background for application of the instrumentation now being developed for repeated non-invasive 3-dimensional imaging of residual flow in the ischemic brain. By these means one hopes it will become possible to conduct treatment and to evaluate prognosis in the acute stroke patient by reproducible repeatable measurement in man.
Am Heart Assoc