Department of Epidemiology, Erasmus MC University Medical Center, Rotterdam, The Netherlands.
Department of Child and Adolescent Psychiatry, Erasmus MC University Medical Center, Rotterdam, The Netherlands.
Sleep. 2019 Oct 9;42(10). doi: 10.1093/sleep/zsz140.
Poor sleep may destabilize axonal integrity and deteriorate cerebral white matter. In middle-aged and older adults sleep problems increase alongside structural brain changes, but the temporal relation between these processes is poorly understood. We studied longitudinal associations between sleep and cerebral white matter microstructure.
One thousand one persons (59.3 ± 7.9 years, 55% women) were followed across 5.8 years (3.9-10.8). Total sleep time (TST, hours), sleep efficiency (SE, percentage), sleep onset latency (SOL, minutes), and wake after sleep onset (WASO, minutes) were measured at baseline using a wrist-worn actigraph. White matter microstructure (global and tract-specific fractional anisotropy [FA] and mean diffusivity [MD]) was measured twice with diffusion tensor imaging (DTI).
Poor sleep was associated with worse white matter microstructure up to 7 years later but did not predict trajectories of DTI over time. Longer TST was associated with higher global FA (β = 0.06, 95% CI: 0.01 to 0.12), but not with MD. Persons with higher SE had higher global FA (β = 0.01, 95% CI: 0.002 to 0.01) and lower MD (β = -0.01, 95% CI: -0.01 to -0.0004). Consistently, those with more WASO had lower global FA (β = -0.003, 95% CI: -0.005 to -0.001) and higher MD (β = 0.002, 95% CI: 0.0004 to 0.004). Global findings seemed to be driven by microstructural alterations in the cingulum, anterior forceps of corpus callosum, projection and association tracts.
Middle-aged and older persons with more WASO, lower SE and shorter TST have worse microstructure of cerebral white matter. Microstructural alterations are most pronounced projection and association tracts, in the cingulum, and in the anterior forceps of corpus callosum.
较差的睡眠可能会破坏轴突完整性并使脑白质恶化。在中年及以上成年人中,随着大脑结构的变化,睡眠问题也会增加,但这些过程之间的时间关系尚不清楚。我们研究了睡眠与脑白质微观结构之间的纵向关联。
共有 1100 人(59.3±7.9 岁,55%为女性)参与了为期 5.8 年(3.9-10.8 年)的随访。使用腕戴式活动记录仪在基线时测量总睡眠时间(TST,小时)、睡眠效率(SE,百分比)、入睡潜伏期(SOL,分钟)和睡眠后觉醒时间(WASO,分钟)。使用弥散张量成像(DTI)两次测量白质微观结构(整体和特定束的各向异性分数[FA]和平均弥散度[MD])。
较差的睡眠与 7 年后更差的白质微观结构有关,但不能预测 DTI 随时间的轨迹。TST 较长与更高的全脑 FA 相关(β=0.06,95%CI:0.01-0.12),但与 MD 无关。SE 较高的人全脑 FA 较高(β=0.01,95%CI:0.002-0.01),MD 较低(β=-0.01,95%CI:-0.01 至-0.0004)。同样,WASO 较多的人全脑 FA 较低(β=-0.003,95%CI:-0.005 至-0.001),MD 较高(β=0.002,95%CI:0.0004 至 0.004)。总体发现似乎是由胼胝体前连合的扣带回、联合纤维、投射和联合束的微观结构改变引起的。
WASO 较多、SE 较低和 TST 较短的中年及以上成年人脑白质微观结构较差。结构改变最明显的是扣带回、胼胝体前连合的投射和联合束。