Depression and Sleep Steiger, Axel; Pawlowski, Marcel
International journal of molecular sciences,
01/2019, Letnik:
20, Številka:
3
Journal Article
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Impaired sleep is both a risk factor and a symptom of depression. Objective sleep is assessed using the sleep electroencephalogram (EEG). Characteristic sleep-EEG changes in patients with depression ...include disinhibition of rapid eye movement (REM) sleep, changes of sleep continuity, and impaired non-REM sleep. Most antidepressants suppress REM sleep both in healthy volunteers and depressed patients. Various sleep-EEG variables may be suitable as biomarkers for diagnosis, prognosis, and prediction of therapy response in depression. In family studies of depression, enhanced REM density, a measure for frequency of rapid eye movements, is characteristic for an endophenotype. Cordance is an EEG measure distinctly correlated with regional brain perfusion. Prefrontal theta cordance, derived from REM sleep, appears to be a biomarker of antidepressant treatment response. Some predictive sleep-EEG markers of depression appear to be related to hypothalamo-pituitary-adrenocortical system activity.
Features of sleep were shown to reflect aging, typical sex differences and cognitive abilities of humans. However, these measures are characterized by redundancy and arbitrariness. Our present ...approach relies on the assumptions that the spontaneous human brain activity as reflected by the scalp-derived electroencephalogram (EEG) during non-rapid eye movement (NREM) sleep is characterized by arrhythmic, scale-free properties and is based on the power law scaling of the Fourier spectra with the additional consideration of the rhythmic, oscillatory waves at specific frequencies, including sleep spindles. Measures derived are the spectral intercept and slope, as well as the maximal spectral peak amplitude and frequency in the sleep spindle range, effectively reducing 191 spectral measures to 4, which were efficient in characterizing known age-effects, sex-differences and cognitive correlates of sleep EEG. Future clinical and basic studies are supposed to be significantly empowered by the efficient data reduction provided by our approach.
The intention of this review is to summarize the current knowledge on the bidirectional interaction between sleep EEG and the secretion of corticotropin (ACTH) and cortisol. The administration of ...various hypothalamic–pituitary– adrenocortical (HPA) hormones and their antagonists exerts specific sleep-EEG changes in several species including humans. It is well documented that corticotropin releasing hormone (CRH) impairs sleep and enhances vigilance. In addition, it may promote REM sleep. Changes in the growth hormone-releasing hormone (GHRH):CRH ratio in favour of CRH appear to contribute to shallow sleep, elevated cortisol levels and blunted GH in depression and ageing. On the other hand, in women GHRH appears to exert CRH-like effects on sleep. Acute cortisol administration increases slow-wave sleep (SWS) and GH, probably due to feedback inhibition of CRH, and inhibits REM sleep. With the mixed glucocorticoid and progesterone receptor antagonist mifepriston sleep is disrupted. Subchronic administration of the glucocorticoid agonist methylprednisolone desinhibited REM sleep. A synergism of elevated CRH and cortisol activity may contribute to REM disinhibition during depression. Also ACTH and vasopressin modulate sleep specifically but their physiological role remains unclear. For example acute icv vasopressin enhances wakefulness in rats, whereas its long-term administration increases SWS in the elderly. In various studies the interaction of sleep EEG and HPA hormones has been investigated at the baseline, after manipulation of sleep–wake behaviour and after environmental changes. Most studies agree that the circadian pattern of cortisol is relatively independent from sleep and environmental influences. Some data suggest a major effect of light on cortisol secretion. Sleeping is widely associated with blunting and awakenings are linked with increases of HPA hormones. 2002 Harcourt Publishers Ltd
Abstract Background Overnight memory consolidation is disturbed in both depression and schizophrenia, creating an ideal situation to investigate the mechanisms underlying sleep-related consolidation ...and to distinguish disease-specific processes from common elements in their pathophysiology. Methods We investigated patients with depression and schizophrenia, as well as healthy control subjects (each n = 16), under a motor memory consolidation protocol with functional magnetic resonance imaging and polysomnography. Results In a sequential finger-tapping task associated with the degree of hippocampal-prefrontal cortex functional connectivity during the task, significantly less overnight improvement was identified as a common deficit in both patient groups. A task-related overnight decrease in activation of the basal ganglia was observed in control subjects and schizophrenia patients; in contrast, patients with depression showed an increase. During the task, schizophrenia patients, in comparison with control subjects, additionally recruited adjacent cortical areas, which showed a decrease in functional magnetic resonance imaging activation overnight and were related to disease severity. Effective connectivity analyses revealed that the hippocampus was functionally connected to the motor task network, and the cerebellum decoupled from this network overnight. Conclusions While both patient groups showed similar deficits in consolidation associated with hippocampal-prefrontal cortex connectivity, other activity patterns more specific for disease pathology differed.
Summary The benefit of sleep in general for memory consolidation is well known. The relevance of sleep characteristics and the influence of hormones are not well studied. We explored the effects of a ...nap on memory consolidation of motor (finger-tapping-task) and verbal (associated-word-pairs) tasks in following settings: A: young, healthy males and females during early-follicular phase ( n = 40) and B: females during mid-luteal and early-follicular phase in the menstrual cycle ( n = 15). We found a sex and in women a menstrual cycle effect on memory performance following a nap. Men performed significantly better after a nap and women did so only in the mid-luteal phase of their menstrual cycle. Only the men and the women in their mid-luteal phase experienced a significant increase in spindle activity after learning. Furthermore, in women estrogen correlated significantly with the offline change in declarative learning and progesterone with motor learning. The ratio of the 2nd and 4th digit, which has been associated to fetal sex hormones and cognitive sex differences, significantly predicted the average performance of the female subjects in the learning tasks. Our results demonstrate that sleep-related memory consolidation has a higher complexity and more influencing factors than previously assumed. There is a sex and menstrual cycle effect, which seems to be mediated by female hormones and sleep spindles. Further, contrary to previous reports, consolidation of a simple motor task can be induced by a 45 min NREM sleep nap, thus not dependent on REM sleep.
Abstract This review summarizes recent developments in the field of sleep regulation, particularly in the role of hormones, and of synthetic GABAA receptor agonists. Certain hormones play a specific ...role in sleep regulation. A reciprocal interaction of the neuropeptides growth hormone (GH)-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) plays a key role in sleep regulation. At least in males GHRH is a common stimulus of non-rapid-eye-movement sleep (NREMS) and GH and inhibits the hypothalamo-pituitary adrenocortical (HPA) hormones, whereas CRH exerts opposite effects. Furthermore CRH may enhance rapid-eye-movement sleep (REMS). Changes in the GHRH:CRH ratio in favor of CRH appear to contribute to sleep EEG and endocrine changes during depression and normal ageing. In women, however, CRH-like effects of GHRH were found. Besides CRH somatostatin impairs sleep, whereas ghrelin, galanin and neuropeptide Y promote sleep. Vasoactive intestinal polypeptide appears to be involved in the temporal organization of human sleep. Beside of peptides, steroids participate in sleep regulation. Cortisol appears to promote REMS. Various neuroactive steroids exert specific effects on sleep. The beneficial effect of estrogen replacement therapy in menopausal women suggests a role of estrogen in sleep regulation. The GABAA receptor or GABAergic neurons are involved in the action of many of these hormones. Recently synthetic GABAA agonists, particularly gaboxadol and the GABA reuptake inhibitor tiagabine were shown to differ distinctly in their action from allosteric modulators of the GABAA receptor like benzodiazepines as they promote slow-wave sleep, decrease wakefulness and do not affect REMS.
Mounting evidence for the role of sleep spindles in neuroplasticity has led to an increased interest in these non-rapid eye movement (NREM) sleep oscillations. It has been hypothesized that fast and ...slow spindles might play a different role in memory processing. Here, we present a new sleep spindle detection algorithm utilizing a continuous wavelet transform (CWT) and individual adjustment of slow and fast spindle frequency ranges. Eighteen nap recordings of ten subjects were used for algorithm validation. Our method was compared with both a human scorer and a commercially available SIESTA spindle detector. For the validation set, mean agreement between our detector and human scorer measured during sleep stage 2 using kappa coefficient was 0.45, whereas mean agreement between our detector and SIESTA algorithm was 0.62. Our algorithm was also applied to sleep-related memory consolidation data previously analyzed with a SIESTA detector and confirmed previous findings of significant correlation between spindle density and declarative memory consolidation. We then applied our method to a study in monozygotic (MZ) and dizygotic (DZ) twins, examining the genetic component of slow and fast sleep spindle parameters. Our analysis revealed strong genetic influence on variance of all slow spindle parameters, weaker genetic effect on fast spindles, and no effects on fast spindle density and number during stage 2 sleep.
Abstract Both wake and sleep electroencephalogram (EEG) provide biomarkers of depression and antidepressive therapy, respectively. For a long time it is known that EEG activity is altered by drugs. ...Quantitative EEG analysis helps to delineate effects of antidepressants on brain activity. Cordance is an EEG measure with a superior correlation with regional brain perfusion. Prefrontal quantitative EEG cordance appears to be a predictor of the response to antidepressants. Sleep EEG shows characteristic changes in depression as impaired sleep continuity, desinhibition of REM sleep and changes of nonREM sleep. Elevated REM density (a measure for frequency of rapid eye movements) characterizes an endophenotype in family studies of depression. REM-sleep changes including a more distinct REM rebound after sleep deprivation are found in animal models of depression. Most antidepressants suppress REM sleep in depressed patients, normal controls and laboratory animals. REM suppression appears to be a distinct, but not an absolute requirement for antidepressive effects of a compound. Sleep-EEG variables like REM latency or certain clusters of variables were shown to predict the response to the treatment with a certain antidepressant or even the course of the disorder for several years. Some of these predictive sleep-EEG markers of the longterm course of depression appear to be closely related to hypothalamo-pituitary-adrenocortical system activity.
•Exploratory study: no systematically altered sleep macrostructure in MDD patients.•Non-REM fast sleep spindle amplitudes higher in unmedicated patients.•Antidepressants altered slow-wave activity ...and coupling to fast sleep spindles.•Long-term, not short-term medication linked to lower spindle density in patients.•Medicated patients had impaired procedural memory consolidation.
Disturbed sleep is a key symptom in major depressive disorder (MDD). REM sleep alterations are well described in the current literature, but little is known about non-REM sleep alterations. Additionally, sleep disturbances relate to a variety of cognitive symptoms in MDD, but which features of non-REM sleep EEG contribute to this, remains unknown. We comprehensively analyzed non-REM sleep EEG features in two central channels in three independently collected datasets (N = 284 recordings of 216 participants). This exploratory and descriptive study included MDD patients with a broad age range, varying duration and severity of depression, unmedicated or medicated, age- and gender-matched to healthy controls. We explored changes in sleep architecture including sleep stages and cycles, spectral power, sleep spindles, slow waves (SW), and SW-spindle coupling. Next, we analyzed the association of these sleep features with acute measures of depression severity and overnight consolidation of procedural memory. Overall, no major systematic alterations in non-REM sleep architecture were found in patients compared to controls. For the microstructure of non-REM sleep, we observed a higher spindle amplitude in unmedicated patients compared to controls, and after the start of antidepressant medication longer SWs with lower amplitude and a more dispersed SW-spindle coupling. In addition, long-term, but not short-term medication seemed to lower spindle density. Overnight procedural memory consolidation was impaired in medicated patients and associated with lower sleep spindle density. Our results suggest that alterations of non-REM sleep EEG in MDD might be more subtle than previously reported. We discuss these findings in the context of antidepressant medication intake and age.
Abstract Sleep is critically involved in the consolidation of procedural memory. In major depression (MD) and during antidepressant pharmacotherapy, changes in sleep EEG are well documented. Here, we ...test if off-line motor memory consolidation is impaired in MD. 50 medicated patients with an acute episode of MD, 50 normal controls and 12 patients with a remitted episode of MD were assessed using a sequential finger tapping task before and after a night of sleep. Although depressed patients and control subjects did not differ in practice-dependent learning, healthy subjects showed markedly overnight improvements in tapping performance of 18% while patients failed to show any improvement. This pattern became even more striking when the subjects were divided by an age threshold of 30 years: In the 30+ yrs group the healthy subjects showed 16% overnight increase in motor performance, whereas the patients showed − 10% overnight decrease. In contrast, patients and controls in the ≤ 30 yrs group showed virtually the same motor performance, as well as remitted patients and controls in the 30+ yrs group. In addition, the younger controls showed stronger overnight improvements than the older controls. This pattern might be interpreted as a synergistic interaction between age and depression: Off-line motor memory consolidation is not affected in young patients, but severely impaired in older patients with an acute episode of MD. This impairment seems to recover after remission from depression.
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