Longitudinal measurements of sleep EEG in adolescence

描述(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内分泌和身体快速发展的时期。在最显著的大脑变化中，NREM睡眠的增量(&lt；4赫兹)脑电大幅下降。我们正在进行的研究使用频谱和周期幅度分析来纵向检查两个队列中每半年一次的4夜记录中的睡眠和脑电：9-13岁的C9(N=30)和12-16岁的C12(N=38)。头两年的数据为重要问题提供了答案，但也提出了新的问题，需要扩大对这些队列的研究，并增加一个更年轻的队列，C6(N=30)，年龄6-10岁。与横断面研究结果相反，我们从C9得到的纵向结果显示，在9到11年间，受试者内部的三角洲几乎没有下降。相比之下，C12的数据显示，在12-14岁期间，三角洲显著下降，女孩的水平明显较低，这表明她们更早开始成熟过程。一个与以前的建议相矛盾的显著结果是，在控制了年龄后，三角洲下降与青春期(晒黑)状态无关。增量的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Delta值的下降有关，但与睡眠时间表的变化无关。延长目前的研究将使我们能够确定个体内部的三角洲下降模式，从开始到青春期结束时减速。我们还将在更广泛的年龄范围内确定这种下降是否与以下因素有关：青春期发育，白天嗜睡的出现，白天精神运动警惕任务的表现，以及延长睡眠的能力。我们已经启动了与Jay Giedd博士的数据共享合作，他拥有相同年龄范围内皮质厚度的纵向MRI测量。新的6岁队列将为皮质灰质增加的年龄范围内儿童时期的睡眠脑电提供量化基准。这些数据是S对青少年德尔塔力量衰退的第一次内部测量。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推动的，包括清醒的大脑新陈代谢明显下降。我们还假设，这一过程中的错误可能会导致精神疾病，特别是精神分裂症。阐明青春期期间Delta变化的标准轨迹可以提供相关成熟脑事件的指数，这可能为最终研究精神分裂症高危患者提供必要的平台。此外，这些数据对睡眠动态平衡和青少年睡眠时间表的公共健康影响也有影响。

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.