The Role of Inflammation in Postoperative Cognitive Dysfunction

Abstract

Aim of review:Postoperative cognitive dysfunction (POCD) is a common complication following surgery, especially in the elderly population. Surgery exposes patients to extensive trauma, blood loss, and tissue injury, all of which contribute to an inflammatory response. In recent years, inflammation has been shown to be a key contributor to the pathogenesis of cognitive decline and neuroinflammatory processes, both in animal models and initial clinical observations. Method: We review the recent literatures on the proposed mechanisms whereby peripheral trauma leads to cognitive impairments and some of the new neuroprotective strategies that may be implemented to prevent neuroinflammation and POCD. Recent findings: Changes in pro-inflammatory cytokines, alarmins, macrophage activation and blood-brain barrier (BBB) dysfunction have been proven to be related to the pathogenesis of cognitive decline using a variety of models, reagents, and technologies. Strategies to harness these pathways through anti-inflammatory and pro-resolving strategies show remarkable effects in modulating neuronal function, synaptic plasticity, glia activity and memory processes. Summary: Further studies are needed to better identify the patients at higher risk for cognitive decline in the postoperative period and which interventions may be suitable for translation and new clinical trials.

Pyrrolidine Dithiocarbamate Prevents Neuroinflammation and Cognitive Dysfunction after Endotoxemia in Rats

“…Its effects on behavior have been well documented (Dantzer et al, 1998 ), but the mechanisms underlying cognitive impairments after endotoxemia are not fully understood. Inflammatory molecules can access the CNS through different immune-to-brain mechanisms, both blood-borne and neuronal (Capuron and Miller, 2011 ; Xu et al, 2014 ). After LPS exposure, we found a significant increase in systemic pro-inflammatory cytokines, including TNF-α and IL-1β, which initiate a pro-inflammatory response that affects long-term CNS function.…”

Single Intraperitoneal Injection of Low-Dose Ketamine Pretreatment Alleviates Mechanical Hyperalgesia and Downregulates the Expression of Inflammatory Cytokines in Spinal Dorsal Horn of Rats

“…In addition, the timing of administration may be another factor. Synaptic long-term potentiation (LTP) is the cell model of central sensitization, and is associated with the degree of pain (45) and postoperative cognitive decline (46). Low dose of ketamine could prevent the development of long-term potentiation, but couldn't influence its maintenance (47).…”