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.
[1] 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.
[4] 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.
[3] In the penumbra, microglia are thought to exert neuroprotective effects via specialized contacts with neuronal somata, termed somatic junctions.
[8] Understanding and supporting these microglial actions could broaden the therapeutic window and lead to higher amount of preserved nervous tissue.
[citation needed] The concept of the ischemic penumbra was developed in Lindsay Symons laboratory, The National Hospital, Queens Square, London, in 1976 by combined focal measurements of neurofunction, blood flow and extracellular K+ in the baboon brain following a MCA occlusion.
The first decade of research focused on physiologic profile of the penumbra tissue after stroke, mapping the cerebral blood flow, and quantifying oxygen and glucose consumption to define these areas.