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Postoperative cognitive dysfunction: advances based on pre-clinical studies
Anesth Pain Med 2018;13(2):113-21
Published online April 30, 2018
© 2018 The Korean Society of Anesthesiologists.

So Yeong Cheon1 and Bon-Nyeo Koo1,2
1Anesthesia and Pain Research Institute, 2Department of Anesthesiology and Pain Medicine, Yonsei University College of Medicine, Seoul, Korea
Correspondence to: Bon-Nyeo Koo, M.D., Ph.D.
Department of Anesthesiology and Pain Medicine, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, Korea
Tel: 82-2-2228-2420
Fax: 82-2-312-7185
Received February 8, 2018; Revised March 10, 2018; Accepted March 13, 2018.
cc This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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.
Key Words : Animal model, Cognitive dysfunction, Physiophathology, Surgery.

April 2018, 13 (2)
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