Postoperative cognitive dysfunction: advances based on pre-clinical studies.
10.17085/apm.2018.13.2.113
- Author:
So Yeong CHEON
1
;
Bon Nyeo KOO
Author Information
1. Anesthesia and Pain Research Institute, Yonsei University College of Medicine, Seoul, Korea. koobn@yuhs.ac
- Publication Type:Review
- Keywords:
Animal model;
Cognitive dysfunction;
Physiophathology;
Surgery
- MeSH:
Anesthesia;
Blood-Brain Barrier;
Cognition;
Critical Care;
Erythropoietin;
Hepatectomy;
Humans;
Length of Stay;
Memory;
Models, Animal;
Mortality;
NADP;
NF-kappa B;
Oxidoreductases;
Phosphorylation;
Plaque, Amyloid;
Tibial Fractures;
Tumor Necrosis Factor-alpha;
Water
- From:Anesthesia and Pain Medicine
2018;13(2):113-121
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Postoperative cognitive dysfunction (POCD) occurs immediately after surgery and is characterized by impairment of memory and changes in cognition. POCD can last for several months or years and have adverse effects including delayed hospital stays, diminished function in daily life, and increased complications and mortality. Despite improvements in surgical technique, anesthesia management, and intensive care, many patients suffer from POCD. POCD is one of the important clinical issues in surgical management and understanding its pathophysiology is necessary. In this review, therefore, we have focused on animal models of POCD and measurements of cognitive ability in preclinical studies, and we have suggested novel approaches for prevention/treatment of POCD. In preclinical studies, major abdominal surgery (laparotomy, hepatectomy, and splenectomy), minor abdominal surgery (laparotomy, probe exploration), and tibial fracture surgery, are used as POCD models. In addition, cognitive function is assessed by Morris water maze, passive avoidance task, elevated plus maze, and T maze test. Neuroinflammation, blood-brain barrier dysfunction, beta amyloid deposition, and tau phosphorylation are suggested as pathological mechanisms of POCD in preclinical studies. Based on several studies of these, we suggest erythropoietin, nuclear factor kappa B, interleukin17A, tumor necrosis factor alpha, and nicotinamide adenine dinucleotide phosphate oxidase 2 as candidates for prevention/treatment of POCD. In the preclinical stage, drug development/exploration and research is being carried out to solve cognitive dysfunction after surgery. Ultimately, based on the results of preclinical studies, we expect to overcome POCD.
