An Update on Postoperative Cognitive Dysfunction

Department of Anesthesia & Perioperative Care, University of California, San Francisco, 94143-0648 (Tsai & Leung), and School of Nursing, Purdue University, West Lafayette, IN 47907-2069 (Sands).
Advances in Anesthesia 12/2010; 28(1):269-284. DOI: 10.1016/j.aan.2010.09.003
Source: PubMed
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Available from: Laura Sands, Oct 07, 2015
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    • "Comparisons between studies are difficult because of the differences in the tests selected. This variability in choices of tests may be due to the absence of a clear, theoretically derived and empirically tested model, which describes the causes and outcomes of postoperative cognitive changes [5]. Preliminary recommendations were given by the " Statement of Consensus on Assessment of Neurobehavioral Outcomes after Cardiac Surgery " in 1995 [54]. "
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    ABSTRACT: Postoperative cognitive dysfunction (POCD) is a mild form of perioperative ischemic brain injury, which emerges as memory decline, decreased attention, and decreased concentration during several months, or even years, after surgery. Here we present results of our three neuropsychological studies, which overall included 145 patients after on-pump operations. We found that the auditory memory span test (digit span) was more effective as a tool for registration of POCD, in comparison with the word-list learning and story-learning tests. Nonverbal memory or visuoconstruction tests were sensitive to POCD in patients after intraoperative opening of cardiac chambers with increased cerebral air embolism. Psychomotor speed tests (digit symbol, or TMT A) registered POCD, which was characteristic for elderly atherosclerotic patients. Finally, we observed that there were significant effects of the order of position of a test on the performance on this test. For example, the postoperative performance on the core tests (digit span and digit symbol) showed minimal impairment when either of these tests was administered at the beginning of testing. Overall, our data shows that the selection of tests, and the order of which these tests are administered, may considerably influence the results of studies of POCD.
    Stroke Research and Treatment 04/2014; 2014:302824. DOI:10.1155/2014/302824
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    • "A recent retrospective population-based study has found that general anesthesia is a risk factor of AD with an adjusted odds ratio of 3.22 [41]. Moreover, cognitive dysfunction or decline occurs after anesthesia and surgery [[42-52], reviewed in 53], which is associated with impairments in daily functioning [54], dependency on government economic assistance [52], and increased morbidity and mortality [[42,55], reviewed in [56]]. However, opposing findings also exist [57-59]. "
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    ABSTRACT: β-Amyloid protein (Aβ) has been shown to potentiate the caspase-3 activation induced by the commonly used inhalation anesthetic isoflurane. However, it is unknown whether reduction in Aβ levels can attenuate the isoflurane-induced caspase-3 activation. We therefore set out to determine the effects of RNA interference-mediated silencing of amyloid precursor protein (APP) and β-site APP-cleaving enzyme (BACE) on the levels of Aβ and the isoflurane-induced caspase-3 activation. H4 human neuroglioma cells stably transfected to express full-length human APP (H4-APP cells) were treated with small interference RNAs (siRNAs) targeted at silencing BACE and APP for 48 hours. The cells were then treated with 2% isoflurane for six hours. The levels of BACE, APP, and caspase-3 were determined using Western blot analysis. Sandwich Enzyme-linked immunosorbent assay (ELISA) was used to determine the extracellular Aβ levels in the conditioned cell culture media. Here we show for the first time that treatment with BACE and APP siRNAs can decrease levels of BACE, full-length APP, and APP c-terminal fragments. Moreover, the treatment attenuates the Aβ levels and the isoflurane-induced caspase-3 activation. These results further suggest a potential role of Aβ in the isoflurane-induced caspase-3 activation such that the reduction in Aβ levels attenuates the isoflurane-induced caspase-3 activation. These findings will lead to more studies which aim at illustrating the underlying mechanism by which isoflurane and other anesthetics may affect Alzheimer's disease neuropathogenesis.
    04/2011; 1(1):5. DOI:10.1186/2045-9912-1-5
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