Bresser Tom, Leerssen Jeanne, Hölsken Stefanie, Groote Inge, Foster-Dingley Jessica C, van den Heuvel Martijn P, Van Someren Eus J W
Department of Sleep and Cognition, Netherlands Institute for Neuroscience, 1105 BA, Amsterdam, The Netherlands.
Department of Integrative Neurophysiology, Center for Neurogenomics and Cognitive Research (CNCR), Amsterdam Neuroscience, Vrije Universtiteit Amsterdam, 1081 HV, Amsterdam, The Netherlands.
Brain Commun. 2023 Aug 2;5(4):fcad210. doi: 10.1093/braincomms/fcad210. eCollection 2023.
Insomnia poses a high risk for depression. Brain mechanisms of sleep and mood improvement following cognitive behavioural therapy for insomnia remain elusive. This longitudinal study evaluated whether (i) individual differences in baseline brain white matter microstructure predict improvements and (ii) intervention affects brain white matter microstructure. People meeting the Diagnostic and Statistical Manual of Mental Disorders-5 criteria for Insomnia Disorder ( = 117) participated in a randomized controlled trial comparing 6 weeks of no treatment with therapist-guided digital cognitive behavioural therapy for insomnia, circadian rhythm support or their combination (cognitive behavioural therapy for insomnia + circadian rhythm support). Insomnia Severity Index and Inventory of Depressive Symptomatology-Self Report were assessed at baseline and followed up at Weeks 7, 26, 39 and 52. Diffusion-weighted magnetic resonance images were acquired at baseline and Week 7. Skeletonized white matter tracts, fractional anisotropy and mean diffusivity were quantified both tract-wise and voxel-wise using tract-based spatial statistics. Analyses used linear and mixed effect models while correcting for multiple testing using false discovery rate and Bonferroni for correlated endpoint measures. Our results show the following: (i) tract-wise lower fractional anisotropy in the left retrolenticular part of the internal capsule at baseline predicted both worse progression of depressive symptoms in untreated participants and more improvement in treated participants (fractional anisotropy × any intervention, = 0.053, = 0.045). (ii) Only the cognitive behavioural therapy for insomnia + circadian rhythm support intervention induced a trend-level mean diffusivity decrease in the right superior corona radiata ( = 0.128, = 0.108), and individuals with a stronger mean diffusivity decrease showed a stronger alleviation of insomnia ( = 0.20, = 0.035). In summary, individual differences in risk and treatment-supported resilience of depression involve white matter microstructure. Future studies could target the role of the left retrolenticular part of the internal capsule and right superior corona radiata and the brain areas they connect.
失眠会带来较高的抑郁风险。认知行为疗法治疗失眠后睡眠和情绪改善的脑机制仍不清楚。这项纵向研究评估了：（i）基线脑白质微观结构的个体差异是否能预测改善情况；（ii）干预是否会影响脑白质微观结构。符合《精神疾病诊断与统计手册》第5版失眠症标准的人群（n = 117）参与了一项随机对照试验，该试验比较了6周不治疗、治疗师指导的数字认知行为疗法治疗失眠、昼夜节律支持或它们的组合（认知行为疗法治疗失眠 + 昼夜节律支持）。在基线时评估失眠严重程度指数和抑郁症状自评量表，并在第7、26、39和52周进行随访。在基线和第7周采集扩散加权磁共振图像。使用基于束的空间统计学方法，在束层面和体素层面量化了骨骼化白质束、分数各向异性和平均扩散率。分析使用线性和混合效应模型，同时使用错误发现率和Bonferroni方法对相关终点测量进行多重检验校正。我们的结果如下：（i）基线时内囊左后晶状体部束层面分数各向异性较低，既预示着未治疗参与者抑郁症状的进展更差，也预示着治疗参与者的改善更大（分数各向异性×任何干预，p = 0.053，β = 0.045）。（ii）只有认知行为疗法治疗失眠 + 昼夜节律支持干预导致右侧放射冠上部平均扩散率有趋势性降低（p = 0.128，β = 0.108），平均扩散率降低越强的个体失眠缓解越明显（p = 0.20，β = 0.035）。总之，抑郁风险和治疗支持的恢复力方面的个体差异涉及白质微观结构。未来的研究可以针对内囊左后晶状体部和右侧放射冠上部及其连接的脑区的作用。
