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Sleep architecture in seasonal affective disorder: the effects of light therapy and changing seasons
... A number of studies have investigated sleep structure and sleep electroencephalogram (EEG) in depressed SAD patients before and after LT (Rosenthal et al 1989;Endo 1993;Partonen et al 1993;Anderson et al 1994;Kohsaka et al 1994;Palchikov et al 1996). None found the typical pattem of EEG changes characterizing sleep in major depression, nor did they report consistent or large effects of bright LT on sleep structure. ...
... Taken together, there is no strong evidence that polysomnographic sleep of SAD patients differs from that of healthy controls. In agreement with this notion, none of the sleep EEG studies in SAD (Rosenthal et al 1989;Endo 1993;Partonen et al 1993;Anderson et al 1994;Kohsaka et al 1994;Palchikov et al 1996) has found the pattern of sleep EEG changes that characterizes melancholic depression. This notion is further supported by a direct comparison of polysomnographic sleep in seasonal and nonseasonal depressed patients (Thase 1989). ...
The role of sleep regulation in Seasonal Affective Disorder (SAD) was studied in 11 female SAD patients and eight controls in winter before and after light treatment (LT, 6000 lux, 10-14h, 5 days). The sleep electroencephalogram (EEG) was recorded at baseline and after the total sleep deprivation (TSD) of a 40-h constant routine. The well-known effects of TSD on sleep parameters and on EEG power spectra were replicated, indicating normal homeostatic sleep regulation in SAD. Sleep improved after LT in both groups. Since the condition following LT was the second session, these improvements may be an order effect and/or an effect of LT itself. After LT, sleep EEG spectra of SAD patients, but not of controls, showed modifications resembling those of recovery sleep. Since only SAD patients curtailed their sleep while remitting during the LT period, these EEG modifications can be explained by normal sleep regulation alone. We conclude that the robust antidepressant effect of LT in SAD is unlikely to be mediated by changes in sleep, and that sleep regulatory mechanisms are not a crucial factor in the pathogenesis of winter depression.
... In several studies polysomnographically recorded sleep in SAD has been examined . Recordings of SAD patients in winter were compared with those in summer (Anderson et al. 1994; Endo et al. 1992; Palchikov et al. 1997; Rosenthal et al. 1984, 1985, 1989) and with those in control subjects in winter (Anderson et al. 1994; Rosenthal et al. 1989; Schwartz et al. 2000). Furthermore, comparisons have been made between recordings of SAD patients in winter before and after light treatment (Anderson et al. 1994; Brunner et al. 1996; Endo 1993; Kohsaka et al. 1994; Palchikov et al. 1997; Partonen et al. 1993; Rosenthal et al. 1989). ...
... Recordings of SAD patients in winter were compared with those in summer (Anderson et al. 1994; Endo et al. 1992; Palchikov et al. 1997; Rosenthal et al. 1984, 1985, 1989) and with those in control subjects in winter (Anderson et al. 1994; Rosenthal et al. 1989; Schwartz et al. 2000). Furthermore, comparisons have been made between recordings of SAD patients in winter before and after light treatment (Anderson et al. 1994; Brunner et al. 1996; Endo 1993; Kohsaka et al. 1994; Palchikov et al. 1997; Partonen et al. 1993; Rosenthal et al. 1989). Sleep in SAD patients in winter was found to differ from sleep in matched controls, but the sleep pattern which is characteristic for non-seasonal depression has not been observed. ...
The majority of winter-type seasonal affective disorder (SAD) patients complain of hypersomnia and daytime drowsiness. As human sleep is regulated by the interaction of circadian, ultradian and homeostatic processes, sleep disturbances may be caused by either one of these factors. The present study focuses on homeostatic and ultradian aspects of sleep regulation in SAD. Sleep was recorded polysomnographically in seven SAD patients and matched controls subjected to a 120-h forced desynchrony protocol. In time isolation, subjects were exposed to six 20-h days, each comprising a 6.5-h period for sleep. Patients participated while being depressed, while remitted after light therapy and in summer. Controls were studied in winter and in summer. In each condition, the data of each subject were averaged across all recordings. Thus, the influence of the effects of the circadian pacemaker on sleep was excluded mathematically. The comparison of patients with controls and with themselves in the various conditions revealed no abnormalities in homeostatic parameters: sleep stage variables, relative power spectra and time courses of power in various frequency bands across the first three non-rapid eye movement-rapid eye movement (NREM-REM) cycles showed no differences. The data suggest that homeostatic processes are not involved in the disturbance of sleep in SAD.
... Some investigations described more pronounced abnormalities in REM sleep in adolescent and adult patients with psychotic depression (Kupfer and Foster, 1972; Kupfer et al., 1986; Naylor et al., 1990), whereas other studies did not detect such differences (Ivanenko et al., 2005; Kerkhofs et al., 1988; Riemann et al., 2001). Several studies examined EEG sleep profiles in adult patients with seasonal affective disorder, and none of them found the typical sleep patterns observed in major depression (Anderson et al., 1994; (Brunner et al., 1993 (Brunner et al., , 1996 Partonen et al., 1993; Rosenthal et al., 1989). In conclusion, there is substantial evidence for developmental differences in sleep regulation. ...
Depressive illness beginning early in life can have serious developmental and functional consequences. Therefore, understanding its etiology and pathophysiology during this developmental stage is critical for developing effective prevention and intervention strategies. There is considerable evidence of sleep alterations in adult major depressive disorder. However, studies in children and adolescents have not found consistent changes in sleep architecture paralleling adult depression. This review article summarizes sleep polysomnography research in early-onset depression, highlighting the factors associated with variable findings across studies. In addition, potential avenues for future research will be suggested in order to develop more comprehensive theoretical models and interventions for pediatric depression.
Sowohl die Pathophysiologic der Winterdepression (engl, seasonal affective disorder, SAD) -wie auch die Mechanismen, die den Wirkungen der Lichttherapie unterliegen, sind noch weitgehend unklar. Untersuchungen zur Schlaf-Wach-Regulation sowie zur Erfassung des cirkadianen Temperaturrhythmus können jedoch Informationen liefern, die zur Entwicklung und Überprüfung der Hypothesen zu diesen Fragen wesentlich beitragen.
One of the major functions of the circadian timing system is to generate robust rhythms of wakefulness and sleep, whether the dominant pattern is one of short sleep bouts during a portion of the 24-hour day (as in many nocturnal rodents) or one of sustained and consolidated sleep (as in humans). Dysfunction of the circadian system, or a mismatch between demands of the circadian system and volitional behavior, can lead to sleep disruption. Indeed, models of human sleep regulation and laboratory studies predict that sleep attempts at unfavorable circadian times will result in difficulty falling asleep or maintaining sleep (Dijk & Czeisler, 1995). The sleep/wake problems of jet lag and shift work verify this prediction. Numerous other factors besides circadian regulation can also produce sleep problems, including “primary” disturbances of sleep mechanisms, psychiatric and medical problems, and sleep-related breathing disorders. Even among these common “noncircadian” sleep disorders, disturbances in biological rhythms may play a role in symptom patterns and pathophysiology. For instance, the sleep onset difficulties of some patients with chronic insomnia may be related to a phase delay of circadian rhythms, and the daytime sleepiness of patients with narcolepsy may indicate reduced amplitude of circadian rhythms
The present study was designed to investigate the clinical efficacy of trimipramine with adjunct sleep deprivation (SD) or bright light (BL) and to evaluate psychometric and neurobiological variables that might be of predictive value for treatment response. We used (1) the combined dexamethasone-corticotropin releasing hormone test (DEX-CRH test) to characterize alterations of the hypothalamic-pituitary-adrenal (HPA) system; (2) polysomnography to evaluate sleep disturbances; and (3) a standardized test battery to assess cognitive psychomotor functions after study initiation and after 5 weeks of treatment. The overall response rate (> or = 50% decrease in score on Hamilton Rating Scale for Depression [HRS]) was 55% (N = 42). The response rate in the group with trimipramine monotherapy (N = 14) was 79%, whereas in the groups with adjunct SD (N = 14) and BL (N = 14), respectively, it was only 43%. All three groups showed significant improvement at the end of the third week of treatment. Neither of the adjunct treatments hastened the onset of antidepressant action as measured by HRS. A significantly higher proportion of nonresponders than responders (p < .05) had HPA dysregulation, disturbed rapid eye movement (REM) sleep (REM latency, REM% first third of night) and decreased non-REM sleep (% stage 2). The non-responders showed significantly more corticotropin (ACTH) secretion after CRH stimulation in the DEX-CRH test than the responders and a less rapid normalization of the neuroendocrine dysregulation (cortisol secretion) (p < .01). In addition, REM latency was significantly shorter in the BL group than in the monotherapy group and estimated duration of illness significantly longer in the SD group than in the monotherapy group. REM latency, percentage of REM sleep during the first third of the total sleep period, percentage of non-REM sleep stage 2 and ACTH release after a DEX-CRH challenge predicted response across all three treatment groups. The neurobiological symptoms were unevenly distributed, among the three groups, thus creating heterogeneity in these measures. This heterogeneity may have contributed to the different treatment response rates as defined by psychopathology (HRS). In contrast, the neuropsychological tests and some of the sleep-EEG investigations revealed different response patterns for different groups: The onset of improvement in simple cognitive functions and in sleep continuity was earlier in the adjunct treatment groups. This study underlines the need for a multidimensional approach including use of neurobiological and neuropsychological measures to identify the therapeutic profiles of different treatment strategies and predictors of outcome.
Disturbances of sleep are typical for most depressed patients and belong to the core symptoms of the disorder. Polysomnographic sleep research has demonstrated that besides disturbances of sleep continuity, in depression sleep is characterized by a reduction of slow wave sleep and a disinhibition of REM sleep, with a shortening of REM latency, a prolongation of the first REM period and increased REM density. These findings have stimulated many sleep studies in depressive patients and patients with other psychiatric disorders. In the meantime, several theoretical models, originating from basic research, have been developed to explain sleep abnormalities of depression, like the two-process-model of sleep and sleep regulation, the GRF/CRF imbalance model and the reciprocal interaction model of non-REM and REM sleep regulation. Interestingly, most of the effective antidepressant agents suppress REM sleep. Furthermore, manipulations of the sleep-wake cycle, like sleep deprivation or a phase advance of the sleep period, alleviate depressive symptoms. These data indicate a strong bi-directional relationship between sleep, sleep alterations and depression.
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