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Evidence for Cognitive Decline in Chronic Pain: A Systematic Review and Meta-Analysis.

ABSTRACT: Background: People with chronic pain (CP) sometimes report impaired cognitive function, including a deficit of attention, memory, executive planning, and information processing. However, the association between CP and cognitive decline was still not clear. Our study aimed to assess the association of CP as a risk factor with cognitive decline among adults. Methods: We included data from clinical studies. Publications were identified using a systematic search strategy from PubMed, Embase, and Cochrane Library databases from inception to October 10, 2020. We used the mean cognitive outcome data and the standard deviations from each group. The standardized mean difference (SMD) or odds ratio (OR), and 95% confidence intervals (CI) were performed for each cognitive decline outcome. I ²-values were assessed to quantify the heterogeneities. Results: We included 37 studies with a total of 52,373 patients with CP and 80,434 healthy control participants. Because these studies used different evaluative methods, we analyzed these studies. The results showed CP was associated with cognitive decline when the short-form 36 health survey questionnaire (SF-36) mental component summary (SMD = -1.50, 95% CI = -2.19 to -0.81), the Montreal cognitive assessment (SMD = -1.11, 95% CI = -1.60 to -0.61), performance validity testing (SMD = 3.05, 95% CI = 1.74 to 4.37), or operation span (SMD = -1.83, 95% CI = -2.98 to -0.68) were used. However, we got opposite results when the studies using International Classification of Diseases and Related Health Problems classification (OR = 1.58, 95% CI = 0.97 to 2.56), the Mini-Mental State Examination (SMD = -0.42, 95% CI = -0.94 to 0.10; OR = 1.14, 95% CI = 0.91 to 1.42), and Repeatable Battery for the Assessment of Neuropsychological Status memory component (SMD = -0.06, 95% CI = -0.37 to 0.25). Conclusion: There may be an association between CP and the incidence of cognitive decline when some cognitive, evaluative methods were used, such as short-form 36 health survey questionnaire, Montreal cognitive assessment, performance validity testing, and operation span.

SUBMITTER: Zhang X

PROVIDER: S-EPMC8492915 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ObjectivesThis review provides a broad overview of the effectiveness of interventions for subjective cognitive decline (SCD) in improving psychological well-being, metacognition and objective cognitive performance.MethodsDatabases including PubMed, Web of Science and Cochrane Systematic Reviews were searched up to August 2017 to identify randomised controlled trials evaluating interventions for SCD. Interventions were categorised as psychological, cognitive, lifestyle or pharmacological. Outcomes of interest included psychological well-being, metacognitive ability and objective cognitive performance. To assess the risk of bias, three authors independently rated study validity using criteria based on the Critical Appraisal Skills Programme. Random-effects meta-analyses were undertaken where three or more studies investigated similar interventions and reported comparable outcomes.ResultsTwenty studies met inclusion criteria and 16 had sufficient data for inclusion in the meta-analyses. Of these, only seven were rated as being high quality. Group psychological interventions significantly improved psychological well-being (g=0.40, 95% CI 0.03 to 0.76; p=0.03) but the improvement they conferred on metacognitive ability was not statistically significant (g=0.26, 95% CI -0.22 to 0.73; p=0.28). Overall, cognitive training interventions led to a small, statistically significant improvement in objective cognitive performance (g=0.13, 95% CI 0.01 to 0.25; p=0.03). However, the pooled effect sizes of studies using active control groups (g=0.02, 95% CI -0.19 to 0.22; p=0.85) or reporting global cognitive measures (g=0.06, 95% CI -0.19 to 0.31; p=0.66) were non-significant.ConclusionsThere is a lack of high-quality research in this field. Group psychological interventions improve psychological well-being and may also improve metacognition. A large, high-quality study is indicated to investigate this further. There is no evidence to suggest that cognitive interventions improve global cognitive performance and the clinical utility of small improvements in specific cognitive domains is questionable. There is a lack of research considering lifestyle interventions and poor quality evidence for pharmacological interventions.Prospero registration numberCRD42017079391.

Project description:At present, prevention is particularly important when there is no effective treatment for cognitive decline. Since the adverse events of pharmacological interventions counterbalance the benefits, nonpharmacological approaches seem desirable to prevent cognitive decline. To our knowledge, no meta-analyses have been published on nonpharmacological interventions preventing cognitive decline. To investigate whether nonpharmacological interventions play a role in preventing cognitive decline among older people, we searched related trials up to March 31, 2019, in MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials (CENTRAL), ClinicalTrials and the Cochrane library databases. Randomized controlled trials (RCTs) were included if they enrolled participants older than 60 years of age who had a risk of cognitive decline, and the interventions were nonpharmacological. Two reviewers independently extracted data and assessed study quality. The Grading of Recommendations Assessment Development and Evaluation (GRADE) approach was used to rate the quality of evidence. Heterogeneity was quantified with I2. Subgroup analysis and meta-regression were used to research the sources of heterogeneity. Influence analyses were used to detect and remove extreme effect sizes (outliers) in our meta-analysis. Publication bias was assessed with funnel plots and Egger test. Primary outcomes were the incidence of mild cognitive impairment (MCI) or dementia and Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) scores. Second outcomes were activities of daily living (ADL) and Mini-Mental State Examination (MMSE) scores. A total of 22 studies with 13,264 participants were identified for analysis. In terms of prevention, nonpharmacological interventions appeared to be more effective than control conditions, as assessed by the incidence of MCI or dementia (RR, 0.73; CI, 0.55-0.96; moderate-certainty evidence), while the results of ADAS-Cog suggested no significant differences between two groups (MD, -0.69; CI, -1.52-0.14; very low-certainty evidence). Second outcomes revealed a significant improvement from nonpharmacological interventions versus control in terms of the change in ADL (MD, 0.73; CI, 0.65-0.80) and MMSE scores (posttreatment scores: MD, 0.25; CI, 0.02-0.47; difference scores: MD, 0.59, CI, 0.29-0.88). Univariable meta-regression showed association between lower case of MCI or dementia and two subgroup factors (P = 0.013 for sample size; P = 0.037 for area). Multiple meta-regression suggested that these four subgroup factors were not associated with decreased incidence of MCI (P > 0.05 for interaction). The Naive RR estimate was calculated as 0.73. When the three studies that detected by outlier and influence analysis were left out, the Robust RR was 0.66. In conclusion, nonpharmacological therapy could have an indicative role in reducing the case of MCI or dementia. However, given the heterogeneity of the included RCTs, more preregistered trials are needed that explicitly examine the association between nonpharmacological therapy and cognitive decline prevention, and consider relevant moderators.

Project description:BACKGROUND:Development of cognitive decline represents substantial issues in today's society, steadily gaining importance with increasing life expectancy. One potential approach to preventing cognitive decline is to lower homocysteine by administering vitamin B. In this systematic review and meta-analysis, we address this topic and investigate whether oral supplementation of vitamin B can successfully prevent cognitive decline in cognitively unimpaired individuals. METHODS:A computerized systematic literature search was conducted using the electronic databases PubMed, Embase, and the Cochrane Library. Eligibility criteria included oral supplementation with vitamin B (B1, B6, folic acid, and B12) and the absence of cognitive impairment. A meta-analysis was conducted with "global cognition" as the primary outcome of this review. Secondary outcomes were changes in cognitive function in other cognitive domains reported in the included studies. Risk of bias was assessed according to the Cochrane Risk of Bias tool and the GRADE approach to establish the overall certainty of the evidence. RESULTS:The meta-analysis did not yield a significant overall effect of supplementation with vitamin B on cognitive function (Z = 0.87; p = 0.39; SMD, 0.02; 95% CI, -?0.034, 0.08). A sensitivity analysis focusing on specific risk factors did not alter this result. Some studies reported isolated significant effects of the intervention on secondary outcomes. However, these findings were outnumbered by the number of cognitive tests that did not yield significant effects. DISCUSSION:We found no overall evidence that oral vitamin B supplementation prevented cognitive decline. The isolated significant effects that were reported could be attributed to methodological issues. The results of this review do not provide evidence that population groups with certain risk factors would profit more from the intervention than others. Our findings do not apply to forms of administration other than oral supplementation nor do they offer information regarding the treatment of cognitively impaired individuals via the administration of vitamin B. SYSTEMATIC REVIEW REGISTRATION:PROSPERO CRD42017071692.

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Evidence for Cognitive Decline in Chronic Pain: A Systematic Review and Meta-Analysis.

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