Long-Term Pain Treatment Did Not Improve Sleep in Nursing Home Patients with Comorbid Dementia and Depression: A 13-Week Randomized Placebo-Controlled Trial

Long-Term Pain Treatment Did Not Improve Sleep in Nursing Home Patients with Comorbid Dementia and Depression: A 13-Week Randomized Placebo-Controlled Trial
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DOI:
10.3389/fpsyg.2018.00134
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发表时间:
2018-02-13
影响因子:
3.8
通讯作者:
Bjorvatn, Bjorn
Bjorvatn, Bjorn
中科院分区:
心理学3区
文献类型:
--
作者:
Blytt, Kjersti M.;Husebo, Bettina;Bjorvatn, Bjorn

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目的:以往的研究表明,疼痛治疗可以改善护理之家患者的睡眠。我们的目的是调查疼痛治疗对抑郁症和痴呆症共病患者24小时睡眠模式的长期影响。设计:一项为期13周的多中心、平行组、双盲、安慰剂对照随机临床试验,于2014年8月至2016年9月进行。设置:来自挪威47家疗养院的长期患者。参与者:我们纳入了106例根据简易精神状态检查(MMSE)和康奈尔痴呆抑郁量表(CSDD)诊断的痴呆和抑郁共病患者。干预:未使用镇痛药的患者随机接受扑热息痛(3 g/天)或安慰剂片剂。那些已经接受疼痛治疗的人被随机分配到丁丙诺啡透皮系统(最大10毫克/小时/7天)或安慰剂透皮patchs.Measurements:睡眠连续7天进行评估,在基线和第13周的活动。评估总睡眠时间(TST)、睡眠效率(SE)、入睡潜伏期(SOL)、入睡后觉醒(WASO)、清晨觉醒(EMA)和觉醒次数(NoW)。此外,还估计了日间总睡眠时间(days total sleep time,dos)。结果:TST、SE、SOL、WASO、EMA、NoW、ADL的线性混合模型分析显示,主动疼痛治疗组与安慰剂组之间的TST、SE、SOL、WASO、EMA、NoW、ADL的差异无统计学意义。事后亚组分析显示,在基线时疼痛(MOBID-2 >= 3)的患者或基线时睡眠不佳(定义为SE < 85%)的患者中,活性药物治疗组和安慰剂组从基线至第13周无统计学显著差异。谁收到积极丁丙诺啡的患者表现出增加TST和SE相比,那些谁收到积极paracetamol.Conclusion:的主要分析表明,长期疼痛治疗并没有改善睡眠与腕动计测量。与扑热息痛相比,接受丁丙诺啡治疗的患者的TST和SE增加。这可能表明,一些患者从最有效的疼痛治疗中获益。然而,根据目前的研究结果,不建议将长期疼痛治疗作为改善睡眠的策略。临床试验https://clinicaltrials.gov/ct2/show/NCT02267057。
Objective: Previous research indicates that pain treatment may improve sleep among nursing home patients. We aimed to investigate the long-term effect of pain treatment on 24-h sleep patterns in patients with comorbid depression and dementia.Design: A 13-week, multicenter, parallel-group, double-blind, placebo-controlled randomized clinical trial conducted between August 2014 and September 2016.Setting: Long-term patients from 47 nursing homes in Norway.Participants: We included 106 patients with comorbid dementia and depression according to the Mini Mental Status Examination (MMSE) and the Cornell Scale for Depression in Dementia (CSDD).Intervention: Patients who were not using analgesics were randomized to receive either paracetamol (3 g/day) or placebo tablets. Those who already received pain treatment were randomized to buprenorphine transdermal system (maximum 10 m g/h/7 days) or placebo transdermal patches.Measurements: Sleep was assessed continuously for 7 days by actigraphy, at baseline and in week 13. Total sleep time (TST), sleep efficiency (SE), sleep onset latency (SOL), wake after sleep onset (WASO), early morning awakening (EMA), and number of wake bouts (NoW) were evaluated. In addition, daytime total sleep time (DTS) was estimated. Pain was assessed with Mobilization-Observation-Behavior-Intensity-Dementia-2 Pain Scale (MOBID-2).Results: The linear mixed model analyses for TST, SE, SOL, WASO, EMA, NoW and DTS showed no statistically significant differences between patients who received active pain treatment and those who received placebo. Post hoc subgroup analyses showed that there were no statistically significant differences between active treatment and placebo from baseline to week 13 in patients who were in pain (MOBID-2 >= 3) at baseline, or in patients who had poor sleep (defined as SE < 85%) at baseline. Patients who received active buprenorphine showed an increase in TST and SE compared to those who received active paracetamol.Conclusion: The main analyses showed that long-term pain treatment did not improve sleep as measured with actigraphy. Compared to paracetamol, TST and SE increased among patients who received buprenorphine. This could indicate that some patients had beneficial effects from the most potent pain treatment. However, based on the present findings, long-term pain treatment is not recommended as a strategy to improve sleep. Clinical Trial https://clinicaltrials.gov/ct2/show/NCT02267057.