The long term goal of this proposal is to establish whether sleep and waking EEG activity in depressed patients has pathological characteristics. Such an endeavor must be based on a solid understanding of temporal regulation of EEG activity in normal control subjects and must include a full assessment of EEG activity in both cerebral hemispheres. This project evaluates quantitative sleep EEG in symptomatic and remitted depressed outpatients and normal controls at several electrode sites.
The specific aims of the proposed project are: 1) Using a central and parietal EEG montage, to determine the microarchitectural sleep EEG parameters (such as coherence and phase of period-analyzed EEG) that differentiate 40 symptomatic and 40 remitted depressed outpatients from age- and gender-matched normal controls over two consecutive nights in the sleep laboratory. 2) To identify the interhemispheric EEG frequency and amplitude characteristics of sleep in outpatient depressed and control samples, comparing two EEG quantification strategies, FFTs and DPA. 3) To explore temperature variations and ultradian EEG rhythms in sleep in the three groups. 4) To evaluate the relationship between microarchitecture parameters and standard polysomnographic sleep macroarchitectural variables (REM latency, total sleep time, %NREM, etc.), contrasting the normal controls to the symptomatic and remitted groups. This project has clinical, theoretical and methodological significance. From the clinical perspective, refinement of available laboratory methods may improve diagnosis, prognostication, or early case identification. In particular, by studying remitted depressed patients, we will be able to determine whether certain laboratory measures are more """"""""trait-like"""""""", thereby rendering them potential candidates for true antecedents of the first episode of the illness. Careful quantification of the sleep EEG together with temperature regulation in both symptomatic and remitted depressed may elucidate some underlying CNS abnormalities and perhaps also the contribution of chronophysiological dysregulation in etiology of depression. Future directions of this work include comparisons of cerebral blood flow, hypothalamic regulation of temperature and sleep microarchitecture in depression.
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