Kay Daniel B, Karim Helmet T, Soehner Adriane M, Hasler Brant P, James Jeffrey A, Germain Anne, Hall Martica H, Franzen Peter L, Price Julie C, Nofzinger Eric A, Buysse Daniel J
Department of Psychology, Brigham Young University, Provo, UT.
Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA.
Sleep. 2017 Nov 1;40(11). doi: 10.1093/sleep/zsx155.
Sleep discrepancies are common in primary insomnia (PI) and include reports of longer sleep onset latency (SOL) than measured by polysomnography (PSG) or "negative SOL discrepancy." We hypothesized that negative SOL discrepancy in PI would be associated with higher relative glucose metabolism during nonrapid eye movement (NREM) sleep in brain networks involved in conscious awareness, including the salience, left executive control, and default mode networks.
PI (n = 32) and good sleeper controls (GS; n = 30) completed [18F]fluorodeoxyglucose positron emission tomography (FDG-PET) scans during NREM sleep, and relative regional cerebral metabolic rate for glucose (rCMRglc) was measured. Sleep discrepancy was calculated by subtracting PSG-measured SOL on the PET night from corresponding self-report values the following morning. We tested for interactions between group (PI vs. GS) and SOL discrepancy for rCMRglc during NREM sleep using both a region of interest mask and exploratory whole-brain analyses.
Significant group by SOL discrepancy interactions for rCMRglc were observed in several brain regions (pcorrected < .05 for all clusters). In the PI group, more negative SOL discrepancy (self-reported > PSG-measured SOL) was associated with significantly higher relative rCMRglc in the right anterior insula and middle/posterior cingulate during NREM sleep. In GS, more positive SOL discrepancy (self-reported < PSG-measured SOL) was associated with significantly higher relative rCMRglc in the right anterior insula, left anterior cingulate cortex, and middle/posterior cingulate cortex.
Although preliminary, these findings suggest regions of the brain previously shown to be involved in conscious awareness, and the perception of PSG-defined states may also be involved in the phenomena of SOL discrepancy.
睡眠差异在原发性失眠(PI)中很常见,包括报告的睡眠起始潜伏期(SOL)比多导睡眠图(PSG)测量的更长,即“负SOL差异”。我们假设,PI中的负SOL差异与非快速眼动(NREM)睡眠期间参与意识的脑网络(包括突显网络、左执行控制网络和默认模式网络)中较高的相对葡萄糖代谢有关。
PI组(n = 32)和良好睡眠者对照组(GS;n = 30)在NREM睡眠期间完成了[18F]氟脱氧葡萄糖正电子发射断层扫描(FDG-PET),并测量了相对局部脑葡萄糖代谢率(rCMRglc)。通过用第二天早晨相应的自我报告值减去PET当晚PSG测量的SOL来计算睡眠差异。我们使用感兴趣区域掩码和探索性全脑分析,测试了NREM睡眠期间组(PI与GS)和rCMRglc的SOL差异之间的相互作用。
在几个脑区观察到rCMRglc的显著组间与SOL差异相互作用(所有簇的校正p <.05)。在PI组中,更多的负SOL差异(自我报告的>SOL的PSG测量值)与NREM睡眠期间右侧前脑岛和中/后扣带回中显著更高的相对rCMRglc相关。在GS组中,更多的正SOL差异(自我报告的<PSG测量的SOL)与右侧前脑岛、左侧前扣带回皮质和中/后扣带回皮质中显著更高的相对rCMRglc相关。
尽管这些发现是初步的,但它们表明,先前显示参与意识的脑区以及PSG定义状态的感知可能也参与了SOL差异现象。