This review highlights the pivotal role of peripheral pro-inflammatory cytokines in compromising blood-brain barrier integrity and initiating neuroinflammation in perioperative neurocognitive disorders.
This review outlines the pathophysiological mechanisms by which surgical trauma and subsequent cytokine-mediated neuroinflammation contribute to perioperative neurocognitive disorders in older patients.
Perioperative neurocognitive disorders (PNDs), including postoperative delirium, delayed neurocognitive recovery, and long-term postoperative neurocognitive disorders, present significant challenges for older patients undergoing surgery. Inflammation is a protective mechanism triggered in response to external pathogens or cellular damage. Historically, the central nervous system (CNS) was considered immunoprivileged due to the presence of the blood-brain barrier (BBB), which serves as a physical barrier preventing systemic inflammatory changes from influencing the CNS. However, aseptic surgical trauma is now recognized to induce localized inflammation at the surgical site, further exacerbated by the release of peripheral pro-inflammatory cytokines, which can compromise BBB integrity. This breakdown of the BBB facilitates the activation of microglia, initiating a cascade of neuroinflammatory responses that may contribute to the onset of PNDs. This review explores the mechanisms underlying neuroinflammation, with a particular focus on the pivotal role of cytokines in the pathogenesis of PNDs.
Koh et al. (Tue,) conducted a review in Perioperative neurocognitive disorders. This review highlights the pivotal role of peripheral pro-inflammatory cytokines in compromising blood-brain barrier integrity and initiating neuroinflammation in perioperative neurocognitive disorders.