Longitudinal measurements of sleep EEG in adolescence

描述（由申请人提供）：青春期现在被认为是一个主要的大脑重组以及快速内分泌和身体发育的时期。其中最突出的大脑变化是NREM睡眠的δ（<4 Hz）EEG的大幅下降。我们正在进行的研究使用频谱和周期振幅分析，以检查睡眠和EEG纵向在两个队列：C9（N=30）9-13岁和C12（N=38）12-16岁，每半年4晚记录。前两年的数据为重要问题提供了答案，但提出了新的问题，需要扩展这些队列的研究，并增加一个更年轻的队列，C6（N=30）6-10岁。与横断面研究结果相反，我们从C9的纵向结果显示，受试者内δ在9至11岁之间几乎没有下降。相比之下，C12数据显示，12-14岁之间的δ下降幅度很大，女孩的水平明显较低，这表明她们的成熟过程开始得更早。一个与以前的建议相矛盾的惊人结果是，在控制年龄的情况下，三角洲下降与青春期（坦纳）状态无关。δ下降也与睡眠时间表的同时变化无关。在C12中，白天嗜睡的增加与δ的下降有关，但与睡眠时间表的变化无关。扩展目前的研究将使我们能够确定从青春期开始到青春期结束时减速的三角洲下降的个体内模式。我们还将在更广泛的年龄范围内确定这种下降是否与青春期发育，白天嗜睡的出现，白天精神警觉任务的表现以及延长睡眠的能力有关。我们已经与Jay Giedd博士发起了一项数据共享合作，他在相同年龄范围内对皮质厚度进行了纵向MRI测量。新的6岁年龄组将提供在皮质灰质增加的年龄范围内儿童期睡眠EEG的定量基准。这些数据是第一个S内测量整个青春期的三角洲力量下降。我们假设这种下降是人类青春期普遍成熟重组的一个组成部分。这种重组是由突触修剪驱动的，包括清醒时大脑代谢的显著下降。我们还假设，这个过程中的错误可能会导致精神疾病，特别是精神分裂症。阐明整个青春期的三角洲变化的规范轨迹可以提供一个相关的成熟大脑事件的指数，这可以提供必要的平台，为精神分裂症高危患者的最终研究。此外，这些数据对睡眠稳态和青少年睡眠时间表的公共卫生影响有影响。

DESCRIPTION (provided by applicant): Adolescence is now recognized as a period of major brain reorganization as well as rapid endocrine and physical development. Among the most prominent brain changes is a huge decline in the delta (<4 Hz) EEG of NREM sleep. Our ongoing study uses spectral and period-amplitude analyses to examine sleep and EEG longitudinally in semiannual 4-night recordings in two cohorts: C9 (N=30) ages 9-13 and C12 (N=38) ages 12-16. Data from the first two years yielded answers to important questions but raised new questions that require extending the study of these cohorts and adding a younger cohort, C6 (N=30) ages 6-10. Contrary to cross-sectional findings, our longitudinal results from C9 show little within-subject delta decline between 9 and 11 years. In contrast, C12 data show a strong delta decline across 12-14 years and levels were significantly lower in girls suggesting that they initiated the maturation process earlier. A striking result that contradicts previous suggestions is that, with age controlled, the delta decline was unrelated to pubertal (Tanner) status. The delta decline was also unrelated to the concurrent changes in sleep schedule. In C12 the increase in daytime sleepiness was related to the decline in delta but was not related to changes in sleep schedule. Extending the current study will enable us to determine within-individual patterns of delta decline from its start through its deceleration at the end of adolescence. We will also determine over a wider age range whether this decline is related to: pubertal development, the emergence of daytime sleepiness, performance on a daytime psychomotor vigilance task, and the ability to extend sleep. We have initiated a data sharing collaboration with Dr. Jay Giedd who has longitudinal MRI measures of cortical thickness over the same age ranges. The new 6 yr old cohort will provide quantitative benchmarks for sleep EEG across childhood over an age range where cortical grey matter is increasing. These data are the first within-S measurements of the decline in delta power across adolescence. We hypothesize that this decline is one component of a pervasive maturational reorganization during human adolescence. This reorganization is driven by synaptic pruning and includes a marked decline in waking brain metabolism. We have also hypothesized that errors in this process can give rise to mental illness, notably schizophrenia. Elucidating the normative trajectory of the delta changes across adolescence could provide an index of the related maturational brain events which could provide the platform necessary for the eventual study of patients at high-risk for schizophrenia. In addition, these data have implications for sleep homeostasis and for the public health implications for adolescent sleep schedules.