Postoperative cognitive dysfunction in geriatric patients

Hartholt, Klaas A.; Cammen, Tischa J. M. van der; Klimek, Markus

doi:10.1007/s00391-012-0326-2

Cited by 46 publications

(27 citation statements)

References 41 publications

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“…Some studies also find that lower educational level is associated with increased risk of POCD [51,52]. However, we did not find these associations in the present study.…”

Section: Discussioncontrasting

confidence: 98%

High Postoperative Serum Cortisol Level Is Associated with Increased Risk of Cognitive Dysfunction Early after Coronary Artery Bypass Graft Surgery: A Prospective Cohort Study

Wang

et al. 2013

PLoS ONE

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ContextStress response induced by surgery is proposed to play an important role in the pathogenesis of postoperative cognitive dysfunction.ObjectiveTo investigate the association between postoperative serum cortisol level and occurrence of cognitive dysfunction early after coronary artery bypass graft surgery.DesignProspective cohort study.SettingTwo teaching hospitals.PatientsOne hundred and sixth-six adult patients who were referred to elective coronary artery bypass graft surgery from March 2008 to December 2009.InterventionNone.Main Outcome MeasuresNeuropsychological tests were completed one day before and seven days after surgery. Cognitive dysfunction was defined using the same definition as used in the ISPOCD1-study. Blood samples were obtained in the first postoperative morning for measurement of serum cortisol concentration. Multivariate Logistic regression analyses were performed to assess the relationship between serum cortisol level and occurrence of postoperative cognitive dysfunction.ResultsCognitive dysfunction occurred in 39.8% (66 of 166) of patients seven days after surgery. Multivariate Logistic regression analysis showed that high serum cortisol level was significantly associated with the occurrence of postoperative cognitive dysfunction (odds ratio [OR] 2.603, 95% confidence interval [CI] 1.371-4.944, P = 0.003). Other independent predictors of early postoperative cognitive dysfunction included high preoperative New York Heart Association functional class (OR 0.402, 95% CI 0.207-0.782, P = 0.007), poor preoperative Grooved Pegboard test score of nondominant hand (OR 1.022, 95% CI 1.003-1.040, P = 0.020), use of penehyclidine as premedication (OR 2.565, 95% CI 1.109-5.933, P = 0.028), and occurrence of complications within seven days after surgery (OR 2.677, 95% CI 1.201-5.963, P = 0.016).ConclusionsHigh serum cortisol level in the first postoperative morning was associated with increased risk of cognitive dysfunction seven days after coronary artery bypass graft surgery.

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“…Some studies also find that lower educational level is associated with increased risk of POCD [51,52]. However, we did not find these associations in the present study.…”

Section: Discussioncontrasting

confidence: 98%

High Postoperative Serum Cortisol Level Is Associated with Increased Risk of Cognitive Dysfunction Early after Coronary Artery Bypass Graft Surgery: A Prospective Cohort Study

Wang

et al. 2013

PLoS ONE

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“…POCD, a decline in cognitive function following surgery, is commonly observed in elderly patients (11). It has been demonstrated that extracts from Polygala tenuifolia root are able to promote memory in healthy individuals and enhance cognitive functions in elderly patients (12,13).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of senegenin on splenectomy-induced postoperative cognitive dysfunction in elderly rats

Sun²,

Su-li

2014

Experimental and Therapeutic Medicine

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Postoperative cognitive dysfunction (POCD) is common in elderly patients. Senegenin, an active component of extracts from Polygala tenuifolia root, a traditional Chinese medicine, has neuroprotective and neuroregenerative effects. However, the mechanism underlying the effects of senegenin against postoperative cognitive impairment in elderly individuals has yet to be elucidated. The aim of this study was to investigate the protective effects of senegenin on the cognitive functions of elderly rats with splenectomy-induced POCD. Results from a Morris water maze test suggested that splenectomy induced a transient cognitive deficiency in the elderly rats; however, when the rats were treated with senegenin, the cognitive impairment was notably attenuated. Further experiments showed that senegenin significantly inhibited the mRNA and protein expression of several key pro-inflammatory cytokines, specifically, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and IL-8, in the hippocampal tissues of elderly rats following splenectomy. In order to investigate the molecular mechanism involved, the expression and activity of the Toll-like receptor 4 (TLR4) signaling pathway was assessed. On day 1 postoperatively, it was observed that senegenin markedly suppressed the mRNA and protein expression of TLR4, myeloid differentiation factor 88 (MyD88) and TIR domain-containing adaptor-inducing interferon-β (TRIF). Furthermore, the phosphorylation levels of nuclear factor-κB (NF-κB) p65 and inhibitor of NF-κB (IκBα) were also decreased following senegenin treatment on the first day subsequent to surgery. These results suggest that senegenin suppressed splenectomy-induced transient cognitive impairment in elderly rats, possibly by downregulating two signaling pathways involved in inflammation, TLR4/MyD88/NF-κB and TLR4/TRIF/NF-κB, to further inhibit the expression of key pro-inflammatory cytokines, specifically, TNF-α, IL-1β, IL-6 and IL-8, and ultimately the neuroinflammation in the hippocampal tissues. In conclusion, the present study revealed that senegenin exhibited neuroprotective effects against splenectomy-induced transient cognitive impairment in elderly rats, which indicated that senegenin may be a promising agent for the treatment of POCD.

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“…Surgical procedures and administration of anesthesia are associated with a transient or permanent decline in cognitive function, termed postoperative cognitive dysfunction (POCD). POCD delays rehabilitation and increases morbidity and early mortality [5] , and also has emerged as a major health concern, especially in the geriatric population [6] .…”

Section: Introductionmentioning

confidence: 99%

Duration-dependent regulation of autophagy by isoflurane exposure in aged rats

et al. 2015

Neurosci. Bull.

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Current evidence suggests a central role for autophagy in many inflammatory brain disorders, including Alzheimer's disease (AD). Furthermore, it is also well accepted that some i nhalation anesthetics, such as isoflurane, may cause ADlike neuropathogenesis and resultant postoperative cognitive dysfunction, especially in the elderly population. However, the impact of inhalation anesthetics on autophagic components in the brain remains to be documented. Hence, our objective was to investigate the effects of different durations of isoflurane exposure on hippocampus-dependent learning and hippocampal autophagy in aged rats. Aged Sprague-Dawley rats (20 months old) were randomly exposed to 1.5% isoflurane or 100% oxygen for 1 or 4 h. Animals were then trained in the Morris water maze (4 trials/day for 5 consecutive days). Hippocampal phagophore formation markers, beclin 1 and protein microtubule-associated protein 1 light chain-3B (LC3B), as well as p62, an indicator of autophagic fl ux, were quantifi ed by western blotting. There was no significant difference in the escape latencies and time spent in the target quadrant, as well as hippocampal expression of beclin 1, LC3B-II, and p62 at 24 h post-anesthesia between the 1-h isoflurane-exposed rats and their controls (P >0.05). Four-hour exposure to isofl urane resulted in spatial learning and memory deficits, as evidenced by prolonged escape latencies on days 4 and 5 postanesthesia and less time spent in the target quadrant than sham-exposed animals (P <0.05). These events were accompanied by a decline in hippocampal expression of LC3B-I, LC3B-II, and beclin 1 24 h after isofl urane (P <0.01 and P <0.05). Nevertheless, no significant change in p62 expression was found. Further kinetics study of autophagic changes induced by 4 h of isofl urane showed a transient upregulation of LC3B-I, LC3B-II, and beclin 1 at the end of exposure and a subsequent striking decrease w ithin 12-24 h post-anesthesia (P <0.05). Hippocampal p62 p eaked at 6 h but subsequently resolved. These results from our pilot in vivo study support a durationdependent relationship between 1.5% isoflurane exposure, and s patial cognitive function as well as hippocampal phagophore formation.

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Postoperative cognitive dysfunction in geriatric patients

Cited by 46 publications

References 41 publications

High Postoperative Serum Cortisol Level Is Associated with Increased Risk of Cognitive Dysfunction Early after Coronary Artery Bypass Graft Surgery: A Prospective Cohort Study

High Postoperative Serum Cortisol Level Is Associated with Increased Risk of Cognitive Dysfunction Early after Coronary Artery Bypass Graft Surgery: A Prospective Cohort Study

Protective effect of senegenin on splenectomy-induced postoperative cognitive dysfunction in elderly rats

Duration-dependent regulation of autophagy by isoflurane exposure in aged rats

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