Association of Delirium With Cognitive Decline in Late Life: A Neuropathologic Study of 3 Population-Based Cohort Studies.
Association of Delirium With Cognitive Decline in Late Life: A Neuropathologic Study of 3 Population-Based Cohort Studies.
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DOI：
10.1001/jamapsychiatry.2016.3423
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发表时间：
2017-03-01
期刊：
影响因子：
25.8
通讯作者：
Epidemiological Clinicopathological Studies in Europe (EClipSE) Collaborative Members
中科院分区：
文献类型：
--
作者：
Davis DH;Muniz-Terrera G;Keage HA;Stephan BC;Fleming J;Ince PG;Matthews FE;Cunningham C;Ely EW;MacLullich AM;Brayne C;Epidemiological Clinicopathological Studies in Europe (EClipSE) Collaborative Members
谵妄与认知能力加速下降有关。这种关联的病理基础尚不清楚，也就是说，它们是否与痴呆相关的病理基础相同，是独立的，还是相互关联的。探讨谵妄后认知能力加速下降是否独立于典型痴呆的病理过程。本研究使用了从1985年1月1日至2011年12月31日进行的3项基于人群抽样的观察性队列研究（Vantaa 85+，剑桥市75岁以上队列，认知功能和衰老研究）的987名个体脑供体的统一数据，中位随访时间为5.2年，直至死亡。神经病理学评估是在不了解临床数据的情况下进行的。数据分析时间为2012年1月1日至2013年12月31日。脑供体的临床特征与其他队列没有什么不同。考虑到参与者是脑供体，结果确定是完整的。谵妄（从未vs从未）和神经原纤维缠结、淀粉样斑块、血管病变和路易小体的病理负担。使用随机效应线性回归模型和谵妄与病理负担之间的相互作用进行评估。死亡前6年简易精神状态检查（MMSE）分数的变化。有神经病理学数据的987名参与者（290名来自Vantaa 85岁以上，241名来自剑桥市75岁以上队列，456名来自认知功能和衰老研究）；平均（SD）死亡年龄为90（6.4）岁，包括682名女性（69%）。死亡前6年MMSE平均得分为24.7分。279例谵妄患者（75%为女性）的初始评分较差（- 2.8分；95% CI, - 4.5至- 1.0;P < .001）。谵妄导致的认知能力下降每年为- 0.37 MMSE点（95% CI, - 0.60至- 0.13;P < 0.001）。痴呆病理过程导致的下降每年为- 0.39 MMSE点（95% CI, - 0.57至- 0.22;P < .001）。然而，谵妄和痴呆病理过程的结合导致最大的下降，其中相互作用每年贡献额外的- 0.16 MMSE点（95% CI, - 0.29至- 0.03;P = 0.01）。这些变量的乘法性质导致谵妄和痴呆病理过程的个体比年龄、性别和教育水平匹配的对照组每年下降0.72 MMSE点。痴呆病理过程中出现的谵妄与认知能力的加速下降有关，超出了谵妄或病理过程本身的预期。这些发现表明额外的未测量的病理过程与谵妄特别相关。与年龄相关的认知能力下降有许多因素，这些在人群水平上的发现支持谵妄在典型痴呆的病理过程中独立和倍增的作用。
Delirium is associated with accelerated cognitive decline. The pathologic substrates of this association are not yet known, that is, whether they are the same as those associated with dementia, are independent, or are interrelated. To examine whether the accelerated cognitive decline observed after delirium is independent of the pathologic processes of classic dementia. Harmonized data from 987 individual brain donors from 3 observational cohort studies with population-based sampling (Vantaa 85+, Cambridge City Over-75s Cohort, Cognitive Function and Ageing Study) performed from January 1, 1985, through December 31, 2011, with a median follow-up of 5.2 years until death, were used in this study. Neuropathologic assessments were performed with investigators masked to clinical data. Data analysis was performed from January 1, 2012, through December 31, 2013. Clinical characteristics of brain donors were not different from the rest of the cohort. Outcome ascertainment was complete given that the participants were brain donors. Delirium (never vs ever) and pathologic burden of neurofibrillary tangles, amyloid plaques, vascular lesions, and Lewy bodies. Effects modeled using random-effects linear regression and interactions between delirium and pathologic burden were assessed. Change in Mini-Mental State Examination (MMSE) scores during the 6 years before death. There were 987 participants (290 from Vantaa 85+, 241 from the Cambridge City Over-75s Cohort, and 456 from the Cognitive Function and Ageing Study) with neuropathologic data; mean (SD) age at death was 90 (6.4) years, including 682 women (69%). The mean MMSE score 6 years before death was 24.7 points. The 279 individuals with delirium (75% women) had worse initial scores (−2.8 points; 95% CI, −4.5 to −1.0; P < .001). Cognitive decline attributable to delirium was −0.37 MMSE points per year (95% CI, −0.60 to −0.13; P < .001). Decline attributable to the pathologic processes of dementia was −0.39 MMSE points per year (95% CI, −0.57 to −0.22; P < .001). However, the combination of delirium and the pathologic processes of dementia resulted in the greatest decline, in which the interaction contributed an additional −0.16 MMSE points per year (95% CI, −0.29 to −0.03; P = .01). The multiplicative nature of these variables resulted in individuals with delirium and the pathologic processes of dementia declining 0.72 MMSE points per year faster than age-, sex-, and educational level–matched controls. Delirium in the presence of the pathologic processes of dementia is associated with accelerated cognitive decline beyond that expected for delirium or the pathologic process itself. These findings suggest that additional unmeasured pathologic processes specifically relate to delirium. Age-related cognitive decline has many contributors, and these findings at the population level support a role for delirium acting independently and multiplicatively to the pathologic processes of classic dementia.
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