Résumé
In pathology and anatomy the penumbra is the area surrounding an ischemic event such as thrombotic or embolic stroke. Immediately following the event, blood flow and therefore oxygen transport is reduced locally, leading to hypoxia of the cells near the location of the original insult. This can lead to hypoxic cell death (infarction) and amplify the original damage from the ischemia; however, the penumbra area may remain viable for several hours after an ischemic event due to the collateral arteries that supply the penumbral zone. As time elapses after the onset of stroke, the extent of the penumbra tends to decrease; therefore, in the emergency department a major concern is to protect the penumbra by increasing oxygen transport and delivery to cells in the danger zone, thereby limiting cell death. The existence of a penumbra implies that salvage of the cells is possible. There is a high correlation between the extent of spontaneous neurological recovery and the volume of penumbra that escapes infarction; therefore, saving the penumbra should improve the clinical outcome. One widely accepted definition for penumbra describes the area as "ischemic tissue potentially destined for infarction but it isn't irreversibly injured and [is therefore] the target of any acute therapies." The original definition of the penumbra referred to areas of the brain that were damaged but not yet dead, and offered promise to rescue the brain tissue with the appropriate therapies. The penumbra region typically occurs when blood flow drops below 20 mL/100 g/min. At this point electrical communication between neurons fails to exist. Cells in this region are alive but metabolic pumps are inhibited, oxidative metabolism is reduced but neurons may begin to depolarize again. Areas of the brain generally do not become infarcted until blood flow to the region drops below 10 to 12 mL/100 g/min. At this point, glutamate release becomes unregulated, ion pumps are inhibited and adenosine triphosphate (ATP) synthesis also stops which ultimately leads to the disruption of intracellular processes and neuronal death.
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