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Postoperative Cognitive Dysfunction (postoperative + cognitive_dysfunction)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Cognitive dysfunction 1,2 years after non-cardiac surgery in the elderly

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2000
H. Abildstrom
Background: Postoperative cognitive dysfunction (POCD) is a well-recognised complication of cardiac surgery, but evidence of POCD after general surgery has been lacking. We recently showed that POCD was present in 9.9% of elderly patients 3 months after major non-cardiac surgery. The aim of the present study was to investigate whether POCD persists for 1,2 years after operation. Methods: A total of 336 elderly patients (median age 69 years, range 60,86) was studied after major surgery under general anesthesia. Psychometric testing was performed before surgery and at a median of 7, 98 and 532 days postoperatively using a neuropsychological test battery with 7 subtests. A control group of 47 non-hospitalised volunteers of similar age were tested with the test battery at the same intervals. Results: 1,2 years after surgery, 35 out of 336 patients (10.4%, CI: 7.2,13.7%) had cognitive dysfunction. Three patients had POCD at all three postoperative test sessions (0.9%). From our definition of POCD, there is only a 1:64 000 likelihood that a single subject would have POCD at all three test points by chance. Logistic regression analysis identified age, early POCD, and infection within the first three postoperative months as significant risk factors for long-term cognitive dysfunction. Five of 47 normal controls fulfilled the criteria for cognitive dysfunction 1,2 years after initial testing (10.6%, CI: 1.8,19.4%), i.e. a similar incidence of age-related cognitive impairment as among patients. Conclusion: POCD is a reversible condition in the majority of cases but may persist in approximately 1% of patients. [source]

Protective effects of lithium treatment for spatial memory deficits induced by tau hyperphosphorylation in splenectomized rats

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2010
Wen-Fei Tan
Summary 1. Postoperative cognitive dysfunction has become more prevalent in recent years. We used a splenectomized rat model with postoperative spatial learning and memory deficits to investigate the role of tau hyperphosphorylation and glycogen synthase kinase-3, (GSK-3,) within the hippocampus. 2. Cognitive function was assessed in a Y-maze 1 day before and 1, 3 and 7 days after surgery. We measured site-specific phosphorylation of hippocampal tau (Thr-205 and Ser-396), GSK-3, activity and expression of interleukin-1, (IL-1,), tumour necrosis factor-, (TNF-,) mRNA and protein as markers of inflammation. We also tested the effects of treatment with lithium chloride (LiCl), a GSK-3, inhibitor. 3. Splenectomy was associated with learning and memory impairment 3 days later, as well as a rapid and massive hyperphosphorylation of hippocampal tau at Thr-205 and Ser-396, activated GSK-3,, and increased IL-1, and TNF-, expression. LiCl completely restored tau hyperphosphorylation to control levels. 4. These data from the splenectomized rat model suggest that inflammatory factors affect tau pathology through the GSK-3, signalling pathway and that LiCl is a promising treatment for postoperative cognitive deficits. [source]

New insights into the pathophysiology of postoperative cognitive dysfunction

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2010
L. KRENK
There is evidence that postoperative cognitive dysfunction (POCD) is a significant problem after major surgery, but the pathophysiology has not been fully elucidated. The interpretation of available studies is difficult due to differences in neuropsychological test batteries as well as the lack of appropriate controls. Furthermore, there are no internationally accepted criteria for defining POCD. This article aims to provide an update of current knowledge of the pathogenesis of POCD with a focus on perioperative pathophysiology and possible benefits achieved from an enhanced postoperative recovery using a fast-track methodology. It is concluded that the pathogenesis of POCD is multifactorial and future studies should focus on evaluating the role of postoperative sleep disturbances, inflammatory stress responses, pain and environmental factors. Potential prophylactic intervention may include minimal invasive surgery, multi-modal non-opioid pain management and pharmacological manipulation of the inflammatory response and sleep architecture. [source]

Anaesthetics and postoperative cognitive dysfunction: a pathological mechanism mimicking Alzheimer's disease

ANAESTHESIA, Issue 4 2010
V. Fodale
Summary With longevity, postoperative cognitive decline in the elderly has emerged as a major health concern for which several factors have been implicated, one of the most recent being the role of anaesthetics. Interactions of anaesthetic agents and different targets have been studied at the molecular, cellular and structural anatomical levels. Recent in vitro nuclear magnetic resonance spectroscopy studies have shown that several anaesthetics act on the oligomerisation of amyloid , peptide. Uncontrolled production, oligomerisation and deposition of amyloid , peptide, with subsequent development of amyloid plaques, are fundamental steps in the generation of Alzheimer's disease. Amyloid , peptide is naturally present in the central nervous system, and is found at higher tissue concentrations in the elderly. We argue that administering certain general anaesthetics to elderly patients may worsen amyloid , peptide oligomerisation and deposition and thus increase the risk of developing postoperative cognitive dysfunction. The aim of this review is to highlight the clinical aspects of postoperative cognitive dysfunction and to find plausible links between possible anaesthetic effects and the molecular pathological mechanism of Alzheimer's disease. It is hoped that our hypothesis will stimulate further enquiry, especially triggering research into elucidating those anaesthetics that may be more suitable when cognitive dysfunction is a particular concern. [source]

Role of interleukin-1, in postoperative cognitive dysfunction

ANNALS OF NEUROLOGY, Issue 3 2010
Mario Cibelli MD
Objective: Although postoperative cognitive dysfunction (POCD) often complicates recovery from major surgery, the pathogenic mechanisms remain unknown. We explored whether systemic inflammation, in response to surgical trauma, triggers hippocampal inflammation and subsequent memory impairment, in a mouse model of orthopedic surgery. Methods: C57BL/6J, knock out (lacking interleukin [IL]-1 receptor, IL-1R,/,) and wild type mice underwent surgery of the tibia under general anesthesia. Separate cohorts of animals were tested for memory function with fear conditioning tests, or euthanized at different times to assess levels of systemic and hippocampal cytokines and microglial activation; the effects of interventions, designed to interrupt inflammation (specifically and nonspecifically), were also assessed. Results: Surgery caused hippocampal-dependent memory impairment that was associated with increased plasma cytokines, as well as reactive microgliosis and IL-1, transcription and expression in the hippocampus. Nonspecific attenuation of innate immunity with minocycline prevented surgery-induced changes. Functional inhibition of IL-1,, both in mice pretreated with IL-1 receptor antagonist and in IL-1R,/, mice, mitigated the neuroinflammatory effects of surgery and memory dysfunction. Interpretation: A peripheral surgery-induced innate immune response triggers an IL-1,-mediated inflammatory process in the hippocampus that underlies memory impairment. This may represent a viable target to interrupt the pathogenesis of postoperative cognitive dysfunction. ANN NEUROL 2010;68:360,368 [source]