Longitudinal measurements of sleep EEG in adolescence

青春期睡眠脑电图的纵向测量

• 批准号: 7567607
• 负责人: IRWIN FEINBERG
• 金额: $ 43.73万
• 依托单位: UNIVERSITY OF CALIFORNIA AT DAVIS
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-04-17 至 2012-02-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7567607
• 关键词: 15 year old; 18 year old; 6 year old; Adolescence; Adolescent; Age; Area; Beds; Behavior; Benchmarking; Biological; Brain; Child; Childhood; Cohort Studies; Collaborations; Computer Analysis; Data; Data Collection; Deceleration; Development; Electroencephalography; Electrophysiology (science); Employee Strikes; Endocrine; Enrollment; Event; Fourier Transform; Frequencies; Goals; Homeostasis; Human; Incidence; Individual; Longitudinal Studies; Magnetic Resonance Imaging; Measurement; Measures; Mental disorders; Methods; Modeling; Neurosciences; Patients; Pattern; Performance; Physiology; Polysomnography; Process; Public Health; REM Sleep; Research; Research Personnel; Schedule; Schizophrenia; Schools; Sex Characteristics; Sleep; Slow-Wave Sleep; Staging; Suggestion; Synapses; Task Performances; Testing; Thick; Time; United States National Institutes of Health; Visual; Work; aged; boys; brain metabolism; cohort; data sharing; density; depression; girls; gray matter; high risk; indexing; interest; neurophysiology; non rapid eye movement; programs; sex; vigilance

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.

描述（由申请人提供）：青春期现在被认为是重大脑重组以及快速内分泌和身体发育的时期。最突出的大脑变化是NREM睡眠的增量（<4 Hz）脑电图大幅下降。我们正在进行的研究使用光谱和周期振幅分析来检查睡眠，并在两个队列中半年度的4晚录音中纵向检查：C9（n = 30）年龄9-13和C12（n = 38）年龄12-16年龄12-16。最初两年的数据提出了重要问题的答案，但提出了新的问题，这些问题需要扩展这些队列的研究并添加了年轻的队列，C6（n = 30）年龄在6-10岁。与横截面发现相反，我们来自C9的纵向结果显示，受试者内部的三角洲在9到11年之间的下降很少。相比之下，C12数据表明，在12 - 14年间的增量下降强劲，女孩的水平明显降低，这表明她们较早地开始了成熟过程。与以前的建议相矛盾的一个惊人结果是，随着年龄的控制，三角洲的下降与青春期（坦纳）的地位无关。三角洲下降也与睡眠时间表的同时变化无关。在C12中，白天嗜睡的增加与三角洲的下降有关，但与睡眠时间表的变化无关。扩展当前的研究将使我们能够确定三角洲在青春期结束时从开始下降到下降的个体内部模式。我们还将在更广泛的年龄范围内确定这种下降是否与以下年龄有关：青春期发展，白天嗜睡的出现，白天精神运动警惕任务的表现以及扩展睡眠的能力。我们已经与Jay Giedd博士启动了数据共享合作，后者在同一年龄范围内具有皮质厚度的纵向MRI测量。新的6年旧队列将为整个儿童期在年龄范围内提供定量的基准，以增加皮质灰质的年龄范围。这些数据是跨青春期增量功率下降的S内测量值。我们假设这种下降是人类青春期期间普遍成熟重组的组成部分。这种重组是由突触修剪驱动的，包括醒来的脑代谢的明显下降。我们还假设，此过程中的错误可能导致精神疾病，尤其是精神分裂症。阐明整个青春期的三角洲变化的规范轨迹可以提供相关的成熟大脑事件的指标，这可以为精神分裂症高危患者最终研究提供必要的平台。此外，这些数据对睡眠体内平衡以及对青少年睡眠时间表的公共卫生影响具有影响。