Peri-infarct depolarization (PID)

Peri-infarct depolarizations are recurring, spreading waves of sustained neuronal and glial depolarization that occur in regions surrounding a focal cerebral infarct (the penumbra) or traumatized cortex. They are triggered by anoxic release of potassium and excitatory amino acids from infarcted tissue and propagate across the cortex at a rate of approximately 3 mm/min. These events induce metabolic stress, expression of immediate early genes and stress proteins, and can result in hypoxic injury and stepwise expansion of the infarct core if perfusion is inadequate[1][2][5]. Suppression of peri-infarct depolarizations using NMDA/non-NMDA receptor antagonists or sodium channel blockers has been shown to minimize infarct size and improve outcomes in preclinical models, making the process a therapeutic target for neuroprotection in stroke and related brain injuries[1][3].

Other names

Peri-infarct depolarizationsPIDsspreading depression (in post-stroke context)SD-like depolarizations

Suppression of glutamate-mediated excitotoxic depolarizations; Prevention of electrical propagation of depolarizations; Reduction in expression of stress response proteins and infarct size[1][3]