2024-11-0920121019-514910.5137/1019-5149.JTN.5731-12.12-s2.0-84870211252http://dx.doi.org/10.5137/1019-5149.JTN.5731-12.1https://hdl.handle.net/20.500.14288/14025Subarachnoid hemorrhage (SAH) due to intracranial aneurysm rupture is a complex clinical disease with high mortality and morbidity. Recent studies suggest that early brain injury (EBI) rather than vasospasm might be responsible for morbidity and mortality within 24-72 hours after SAH. The rise in intracranial pressure following SAH causes a significant drop in cerebral perfusion press re that leads to global cerebral ischemia and initiates the acute injury cascade. Various molecular mechanisms have been shown to involve in the pathophysiology of EBI including cellular apoptosis. In this review, we summarize apoptotic molecular mechanisms involved in the etiology of EBI and its potential as a target for future therapeutic intervention.Clinical neuropsychologySurgeryReview3101186000019796