NAVIGATING THE AFTERMATH OF HYPOXIC -I SCHEMIC ENCEPHALOPATHY (HIE): A REVIEW ON PATHOPHYSIOLOGICAL CASCADES, METABOLIC DYSFUNCTION, AND EMERGING NEUROPROTECTIVE STRATEGIES

Abstract

Hypoxic-ischemic encephalopathy (HIE) is a neonatal brain injury caused by a lack of oxygen during the prenatal, intrapartum, or postnatal period. It is a major cause of long-term neurological disorders in children. The clinical manifestations range from mild behavioral abnormalities to severe seizures, motor dysfunction, cerebral palsy, and permanent brain damage. Despite recent advances in antenatal diagnosis and improvements in hospital-based neonatal care, the incidence of perinatal asphyxia remains high. The underlying pathophysiological mechanisms are not yet fully understood, and effective therapeutic options remain limited. Therefore, the present review summarizes the established pathophysiological mechanisms of perinatal asphyxia and discusses current therapeutic strategies aimed at reducing disease severity and preventing disease progression at an early stage. Furthermore, it highlights the mechanisms of action of existing drugs and identifies emerging molecular targets that may facilitate the development of more effective therapeutic interventions.