After resuscitation, patients with cardiac arrest often experience varying degrees of neurological dysfunction, and a significant number of neuronal deaths in the brain contribute to post-resuscitation brain injury. Traditional studies have indicated that necrosis and apoptosis are the primary mechanisms of neuronal death following resuscitation. However, as research on cell death mechanisms advances, it has been discovered that resuscitated neurons can also undergo Ferroptosis, Pyroptosis, Necroptosis and Autophagy. This paper provides an overview of potential pathways leading to neuronal death after cardiac arrest and resuscitation. A comprehensive understanding of these pathways will facilitate intervention at different stages within specific cascade reactions to delay cell death or rescue dysfunctional neurons. This is crucial for reducing the incidence of neurological sequelae. Furthermore, this paper discusses the potential application prospects of various inhibitors related to neuronal death in order to provide theoretical references for brain protection after resuscitation.