Cognitive-behavioral therapy for insomnia in knee osteoarthritis: a randomized, double-blind, active placebo-controlled clinical trial.

Cognitive-behavioral therapy for insomnia in knee osteoarthritis: a randomized, double-blind, active placebo-controlled clinical trial.
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DOI:
10.1002/art.39048
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发表时间:
2015-05
期刊:
Arthritis & rheumatology (Hoboken, N.J.)
影响因子:
--
通讯作者:
Haythornthwaite JA
Haythornthwaite JA
中科院分区:
其他
文献类型:
--
作者:
Smith MT;Finan PH;Buenaver LF;Robinson M;Haque U;Quain A;McInrue E;Han D;Leoutsakis J;Haythornthwaite JA

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失眠在膝骨关节炎(KOA)中很常见。研究表明,睡眠中断可能会通过改变中枢疼痛调节来放大临床疼痛,这表明治疗失眠可能会改善疼痛。我们试图:1)评估认知行为治疗失眠(CBT-I)在KOA中的疗效,2)确定睡眠的改善是否预示着疼痛的减轻,3)确定疼痛调节的改变是否介导临床疼痛的改善。我们在100例KOA失眠患者中进行了一项双盲、随机、主动安慰剂对照的CBT-I临床试验[平均年龄= 59.5(9.5)]。患者被随机分配到8个疗程的CBT-I或行为脱敏-安慰剂。我们在基线、治疗后、3个月和6个月时进行了家庭多导睡眠图、日记评估和疼痛调节的感觉测试。意向治疗分析表明,两组患者在睡眠方面都有显著改善。通过日记和活动记录仪测量,CBT-I显示睡眠开始时间(WASO)明显减少[PSG趋势,(p= 0.075)]。两组患者在6个月内均报告疼痛显著减轻,其中第三组患者疼痛严重程度减轻≥30%。基线至治疗后日记和PSG WASO的减少预示着随后临床疼痛的减少。与BD相比,CBT-I的效果明显更大。我们发现疼痛调节的实验室测量没有显著变化。与有效安慰剂相比,CBT-I在减少睡眠维持性失眠方面有效。治疗减少了临床疼痛,但没有疼痛调节,这表明CBT-I有可能增强KOA的疼痛管理。未来的工作需要确定改善睡眠减少临床疼痛的机制。
Insomnia is prevalent in knee osteoarthritis (KOA). Research indicates that sleep disruption may amplify clinical pain by altering central pain modulation, suggesting that treating insomnia may improve pain. We sought to: 1) evaluate the efficacy of Cognitive-Behavioral Therapy for Insomnia (CBT-I) in KOA, 2) determine whether improvements in sleep predict reduced pain, and 3) determine whether alterations in pain modulation mediate improvements in clinical pain. We conducted a double-blinded, randomized, active placebo-controlled clinical trial of CBT-I in 100 KOA patients with insomnia [Mean Age = 59.5(9.5)]. Patients were randomized to 8-sessions of CBT-I or Behavioral Desensitization-Placebo. We conducted in-home polysomnograms, diary assessment, and sensory tests of pain modulation at baseline, posttreatment, 3-and 6-months. Intent-to-treat analyses demonstrated that both groups yielded substantial improvements in sleep. CBT-I demonstrated significantly greater reductions in wake after sleep onset time (WASO), measured via diary and actigraphy [PSG trended, (p=.075)]. Both groups reported significant and comparable reductions in pain over 6 months with a third demonstrating ≥ 30% reduction in pain severity. Baseline-to-posttreatment reductions in Diary and PSG WASO predicted subsequent decreases in clinical pain. This effect was significantly greater for CBT-I compared to BD. We found no significant changes in laboratory measures of pain modulation. Compared to active placebo, CBT-I was efficacious in reducing sleep maintenance insomnia. Treatment decreased clinical pain, but not pain modulation, suggesting that CBT-I has potential to augment pain management in KOA. Future work is needed to identify the mechanisms by which improved sleep reduces clinical pain.
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