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Caspase-8 and caspase-3 also contribute by cleaving gasdermin E (GSDME), resulting in additional pore formation and cytokine release ( As previously discussed, disturbances in iron metabolism play a critical role the pathophysiology following aSAH, with abnormal increases in intracellular ferrous iron serving as a key initiating factor of ferroptosis ( Pathophysiology of delayed cerebral ischemia DCI is defined as the occurrence of a focal neurological impairment (e.g., hemiparesis, aphasia, apraxia, neglect), or a decrease of at least 2 points on the Glasgow Coma Scale (total scale or one of the components) lasting for at least one hour which was not apparent immediately after aneurysm occlusion and which cannot be attributed to other causes (clinical assessment, radiographic findings of the brain, appropriate laboratory studies) ( DCI following aSAH is a major contributor to poor neurological outcome and typically will affect 20-30% of aSAH survivors ( Beyond vasospasm For decades, DCI was attributed primarily to cerebral vasospasm
