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Abstract
Ten=hour sleep monitoring was carried out in 34 patients suffering from a vital depressive illness as well as in a group of 16 healthy volunteers; 18 of the depressed patients were deprived of treatment. The EEG was evaluated visually for data concerning the REM cycle and the REM latency. Spectral analysis of the all-night recordings yielded interval histograms for a group comparison of background activity. Fourier spectrograms and digital filtering were used to analyze ultradian patterns within the long-term frequency distribution. The result showed a trend in depression toward prolongation of the REM cycle and shortening of REM latencies. More significant, however, was the activation of 16- to 8-Hz waves together with a decreased occurrence of delta activity in depressed subjects without treatment. Depressed patients had significantly slower ultradian periodicities with 102-min cycles compared to 86-min cycles in healthy subjects. This disturbance could be temporally located in the early morning hours.
... Of the 24 included studies, 21 could differentiate between melancholic depression, non-melancholic depression, and/or HC. By subgroup, four (22)(23)(24)(25) out of five (22)(23)(24)(25)(26) resting state studies identified one or several EEG parameters that could distinguish groups; among the ERP studies, seven (27)(28)(29)(30)(31)(32)(33) out of nine (27)(28)(29)(30)(31)(32)(33)(34)(35) could separate melancholic depression from the other groups (27)(28)(29)(30)(31)(32)(33), while this was the case in all 10 sleep EEG studies (36)(37)(38)(39)(40)(41)(42)(43)(44)(45). Although sharing study design, the choice of EEG methods, analyses and outcome variables differed considerably within each subgroup, preventing any meaningful pooling of data to meta-analyses or any other statistical aggregation. ...
... Regarding the quality of individual studies, 10 studies were classified as of low quality (22,25,28,30,31,34,(36)(37)(38)42), eight studies as of high quality (23,24,27,29,32,33,35,40), and six studies of moderate quality (26,39,41,(43)(44)(45). ...
... Ten of the included studies performed sleep EEG (36)(37)(38)(39)(40)(41)(42)(43)(44)(45). Key characteristics are presented in Table 1C. ...
Introduction: The objective of this systematic review was to investigate whether electroencephalographic parameters can serve as a tool to distinguish between melancholic depression, non-melancholic depression, and healthy controls in adults.
Methods: A systematic review comprising an extensive literature search conducted in PubMed, Embase, Google Scholar, and PsycINFO in August 2020 with monthly updates until November 1st, 2020. In addition, we performed a citation search and scanned reference lists. Clinical trials that performed an EEG-based examination on an adult patient group diagnosed with melancholic unipolar depression and compared with a control group of non-melancholic unipolar depression and/or healthy controls were eligible. Risk of bias was assessed by the Strengthening of Reporting of Observational Studies in Epidemiology (STROBE) checklist.
Results: A total of 24 studies, all case-control design, met the inclusion criteria and could be divided into three subgroups: Resting state studies (n = 5), sleep EEG studies (n = 10), and event-related potentials (ERP) studies (n = 9). Within each subgroup, studies were characterized by marked variability on almost all levels, preventing pooling of data, and many studies were subject to weighty methodological problems. However, the main part of the studies identified one or several EEG parameters that differentiated the groups.
Conclusions: Multiple EEG modalities showed an ability to distinguish melancholic patients from non-melancholic patients and/or healthy controls. The considerable heterogeneity across studies and the frequent methodological difficulties at the individual study level were the main limitations to this work. Also, the underlying premise of shifting diagnostic paradigms may have resulted in an inhomogeneous patient population.
Systematic Review Registration: Registered in the PROSPERO registry on August 8th, 2020, registration number CRD42020197472.
... To the best of our knowledge, there is no primary study investigating the sleep EEG spectral analysis in remitted depressed patients. On the other hand, previous work has investigated and showed various modifications on the sleep EEG spectral analysis characteristics in acutely depressed patients (Lange, 1982;Borbély et al., 1984;Toussaint et al., 2000;Coutin-Churchman et al., 2003). ...
... They are no significant differences between the controls and the remitted depressed patients in each of the frequency bands we have investigated. Therefore, in regard to the studies performed on the acutely depressed patients (Lange, 1982;Borbély et al., 1984;Toussaint et al., 2000;Coutin-Churchman et al., 2003), we may think that our results show a tendency for sleep EEG spectral analysis characteristics to normalize with the status of remission. ...
The aim of the present study is to investigate the scaling properties of the sleep electroencephalogram (EEG) in remitted depressed men, and to evaluate if a past history of major depressive disorder (MDD) could modify significantly and definitively, as a "scar marker," the dynamics of the sleep EEG time series.
Whole night sleep electroencephalogram signals were recorded in 24 men: 10 untreated depressed men in full to partial remission (42.43+/-5.62 years) and 14 healthy subjects (42.8+/-8.55 years). Scaling properties in these time series were investigated with detrended fluctuation analysis (DFA) (time range: 0.16-2.00 s). The scaling exponent alpha was determined in stage 2, in slow wave sleep (stages 3 and 4), and during rapid eye movement (REM) sleep. Forty-five epochs of 20 s were chosen randomly in each of these stages for each subject in both groups.
We did not observe a significant difference and deviation of the scaling exponents between the two groups during the three sleep stages of interest.
In this study, we do not observe any functional sequelae of a past history of one or more unipolar major depressive episode on the fluctuation properties of the sleep EEG. This finding is a sign of similar underlying neuronal dynamics in healthy controls and patients with a lifetime history of MDD. This study gives an additional argument to the theory that depression does not modify definitively the dynamics of the neuronal networks and is therefore against the "depressive scar hypothesis," in which permanent residual deficit is created by the acute state of the depressive disease.
... Oscillations in the ratio again suggest that antidepressants enhance cyclic interdependent features in the relationship between 5HT and DA turnover rates. The periodic features appear to coincide with circadian and also ultradian rhythms of basic rest-activity and REM cycles (e.g., see Lange, 1982). ...
Oscillations in brain activities with periods of minutes to hours may be critical for normal mood behaviors. Ultradian (faster than circadian) rhythms of mood behaviors and associated central nervous system activities are altered in depression. Recent data suggest that ultradian rhythms in serotonin (5HT) function also change in depression. In two separate studies, 5HT metabolites in cerebrospinal fluid (CSF) were measured every 10 m for 24 h before and after chronic antidepressant treatment. Antidepressant treatments were associated with enhanced ultradian amplitudes of CSF metabolite levels. Another study used resting-state functional magnetic resonance imaging (fMRI) to measure amplitudes of dorsal raphé activation cycles following sham or active dietary depletions of the 5HT precursor (tryptophan). During depletion, amplitudes of dorsal raphé activation cycles increased with rapid 6 s periods (about 0.18 Hz) while functional connectivity weakened between dorsal raphé and thalamus at slower periods of 20 s (0.05 Hz). A third approach studied MDMA (ecstasy) users because of their chronically diminished 5HT function compared to non-MDMA polysubstance users (Karageorgiou et al., 2009). Compared to a non-MDMA using cohort, MDMA users showed diminished fMRI intra-regional coherence in motor regions along with altered functional connectivity, again suggesting effects of altered 5HT oscillatory function. These data support a hypothesis that qualities of ultradian oscillations in 5HT function may critically influence moods and behaviors. Dysfunctional 5HT rhythms in depression may be a common endpoint and biomarker for depression, linking dysfunction of slow brain network oscillators to 5HT mechanisms affected by commonly available treatments. 5HT oscillatory dysfunction may define illness subtypes and predict responses to serotonergic agents. Further studies of 5HT oscillations in depression are indicated. Synapse, 2013. © 2013 Wiley Periodicals, Inc.
The study examined the effect of sustained-release bupropion on sleep microarchitecture in unipolar depression, and evaluated the relationship between the observed sleep changes in response to a single-dose bupropion administration and clinical response to the drug during short-term treatment. Twenty adult patients with major depressive disorder were studied in the sleep laboratory twice for two consecutive nights. On the morning of second night during each session, either placebo or sustained-release bupropion (Wellbutrin SR7; 150 mg, PO) was administered. The participants then received open-label treatment with Wellbutrin-SR for eight weeks. Bupropion produced several effects on sleep microarchitecture. Overall, the frequency distribution of EEG was shifted towards faster frequencies, suggesting greater desynchronization. Bupropion also increased mean wave amplitude during REM sleep and exacerbated inter-hemispheric differences in the number of wave peaks. Neither sleep microarchitecture measures at baseline, nor those following bupropion administration, were related to treatment response. The lack of a predictive microarchitecture measure for response to bupropion treatment may be due to the modest sample size or due to its pharmacological profile of having minimal serotonergic activity. A simultaneous study of bupropion and serotonergic agents would be helpful in clarifying this issue.
Objective:
Although poor sleep accompanies depression, it is unknown which specific sleep abnormalities precede depression. This is similarly the case for depression developing during interferon-α (IFN-α) therapy. Because vulnerability becomes evident in those who slept poorly before IFN-α, we prospectively determined which specific aspect of sleep could predict subsequent depression.
Methods:
Two nights of polysomnography with quantitative electroencephalogram (EEG) were obtained in 24 adult, euthymic subjects--all subsequently treated with IFN-α for hepatitis C. Every 2 weeks, a Beck Depression Inventory-II (BDI-II) score was obtained, and the maximal increase in BDI-II from pre-treatment baseline--excluding the sleep question--was determined.
Results:
The delta sleep ratio (DSR; an index of early-night restorative delta power) was inversely associated with BDI-II increases (p<0.01), as was elevated alpha power (8-12 Hz; p<0.001). Both delta (0.5-4 Hz) and alpha power exhibited high between-night correlations (r=0.83 and 0.92, respectively). In mixed-effect repeated-measure analyses, there was an interaction between alpha power and DSR (p<0.001)--subjects with low alpha power and elevated DSR were resilient to developing depression. Most other sleep parameters--including total sleep time and percentage of time in slow wave sleep--were not associated with subsequent changes in depression.
Conclusions:
Both high DSR and low alpha power may be specific indices of resilience. As most other aspects of sleep were not associated with resilience or vulnerability, sleep interventions to prevent depression may need to specifically target these specific sleep parameters.
Developing rats, studied in environmental isolation, display prominent fluctuations in locomotor activity with a periodicity of about 1–3 hr. This ultradian rhythmic pattern is most marked at 2 weeks of age, and appears to be endogenously mediated. (+)Amphetamine (1 mg/kg) was administered to 2 week old rat pups, and their locomotor activity levels were recorded continuously and stored in 5 min intervals using a sensitive computer-interfaced vibrational activity monitor. Activity was recorded for 12 hr after treatment and resulting time-series data were analyzed by harmonic spectral techniques. During the first 6 hr of testing, amphetamine induced a prominent low frequency perturbation in baseline activity levels corresponding to the expected period of acute drug action. During this time, normally prominent ultradian activity rhythms in the range of 8–12 cycles per day (cpd) were diminished in amplitude, even following low frequency smoothing to remove the changes in baseline. Correspondingly, there was also an increase in ultradian rhythm amplitude in amphetamine-treated pups at higher frequencies (32–40 cpd). During the final 6 hr of testing there was a marked suppression of typical ultradian rhythms in amphetamine-treated pups but not in controls. These results suggest that amphetamine treatment both accelerates and attenuates ultradian activity rhythms in developing rats during the acute period of drug action, and produces a prominent diminution in these rhythms during subsequent rebound and recovery periods.
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