1,721,049 research outputs found
Sunrise and sunset changes in relation to permanent daylight saving time and continuous standard time in four metropolitan areas in Germany
No full textNeuroendocrine dysregulation in primary insomnia
No full textRecent research has pointed to a functional link between stress, disturbed sleep, psychiatric disorders, ageing, and neuroendocrine dysfunctions. In particular, increased activation of the hypothalamic-pituitary adrenal (HPA) axis - expressed as elevated plasma cortisol levels - was shown in physiological ageing and patients with psychiatric disorders. We found increased evening and nocturnal plasma cortisol concentrations in patients with primary insomnia. Considering that both ageing and psychiatric disorders are commonly associated with sleep disturbances, our results implicate that elevated cortisol concentrations are a rather unspecific feature of disturbed sleep. Furthermore, our data revealed a strong positive correlation between evening cortisol secretion and the number of nocturnal awakenings in both insomniac patients and controls. Since nocturnal exposure to increased HPA activity promotes sleep fragmentation even in healthy controls, increased evening cortisol levels may be a crucial factor in inducing and maintaining sleep disturbances. We therefore propose a model of HPA dysregulation in insomnia. This model is based on the arousal theory of insomnia and the strong correlation between evening cortisol secretion and sleep fragmentation as a pathophysiological mechanism of a vicious cycle of Insomnia. In patients with long-lasting insomniac complaints we found decreased nocturnal plasma melatonin levels thereby indicating a labilisation of circadian rhythm functions. Taken together, the neuroendocrine dysregulation seems to be more expressed in chronic insomnia than in acute insomnia and may be a contributing factor in maintaining disturbed sleep
Neuroendocrine dysregulation in primary insomnia
No full textRecent research has pointed to a functional link between stress, disturbed sleep, psychiatric disorders, ageing, and neuroendocrine dysfunctions. In particular, increased activation of the hypothalamic-pituitary adrenal (HPA) axis - expressed as elevated plasma cortisol levels - was shown in physiological ageing and patients with psychiatric disorders. We found increased evening and nocturnal plasma cortisol concentrations in patients with primary insomnia. Considering that both ageing and psychiatric disorders are commonly associated with sleep disturbances, our results implicate that elevated cortisol concentrations are a rather unspecific feature of disturbed sleep. Furthermore, our data revealed a strong positive correlation between evening cortisol secretion and the number of nocturnal awakenings in both insomniac patients and controls. Since nocturnal exposure to increased HPA activity promotes sleep fragmentation even in healthy controls, increased evening cortisol levels may be a crucial factor in inducing and maintaining sleep disturbances. We therefore propose a model of HPA dysregulation in insomnia. This model is based on the arousal theory of insomnia and the strong correlation between evening cortisol secretion and sleep fragmentation as a pathophysiological mechanism of a vicious cycle of Insomnia. In patients with long-lasting insomniac complaints we found decreased nocturnal plasma melatonin levels thereby indicating a labilisation of circadian rhythm functions. Taken together, the neuroendocrine dysregulation seems to be more expressed in chronic insomnia than in acute insomnia and may be a contributing factor in maintaining disturbed sleep
Aktuelle Entwicklungen in der Schlafforschung und Schlafmedizin – eine Einschätzung der AG „Chronobiologie“
No full textInteractions between evening and nocturnal cortisol secretion and sleep parameters in patients with severe chronic primary insomnia
No full textRecent research provides evidence for an interaction between sleep and the activation of the hypothalamic-pituitary-adrenal (HPA)-axis, but detailed studies in patients are still missing. We investigated hourly evening and nocturnal plasma cortisol secretion and sleep in seven male patients with severe chronic primary insomnia and age- and gender-matched controls. Evening and nocturnal cortisol levels were significantly increased in patients. Evening cortisol correlated with the number of nocturnal awakenings in patients and controls. Additionally, patients showed significant correlations between sleep parameters and the first 4 h of nocturnal cortisol secretion. These results are indicative of changes in the HPA system in insomnia and may reflect a path of physiological mechanism of chronic insomnia resulting in a vicious cycle of both disturbed HPA functions and chronic insomnia according to the arousal hypothesis of insomnia. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved
Polysomnographic findings in five adult patients with pituitary insufficiency before and after cessation of human growth hormone replacement therapy
No full textOBJECTIVE We observed the new onset of severe obstructive sleep apnoea syndrome (OSAS) in an adult male patient during human growth hormone (hGH) replacement therapy. This prompted us to evaluate the potential influence of hGH substitution therapy on sleep in middle-aged men. DESIGN A longitudinal study. SUBJECTS Five male patients (aged 44-56 years, median age 54 years) with postoperative pituitary insufficiency given hGH replacement therapy for 12 years (median dose 2.0 U/day; median IGF-I serum concentration 351 mug/l) and 6 months after cessation of hGH treatment (median IGF-I level 77 mug/l - 1 mug/l = 0.131 nmol/l). MEASUREMENTS Polysomnographic studies were performed, and the following parameters were determined: time in bed (TIB), sleep period time (SPT), total sleep time (TST), sleep efficiency (SE = TST/TIB), sleep stage I onset latency (SL), different sleep stages [W (wake), S1, S2, SWS (slow wave sleep = S3 + S4) and REM; % of SPT], stage shifts per hour of SPT (SS[h), stage shifts to W/h of SPT [A/h (awakening)], index of apnoea and hypopnoea events per hour of TST (AH/h), arousals from apnoea and hypopnoea per hour of TST (Ar/h), index of obstructive (OAH/h), central (CAH/h) and mixed (MAH/h) events of apnoea and hypopnoea per hour of TST and minimal desaturation (MD). RESULTS Median baseline results were: TIB, 479 min; SPT, 465 min; TST, 405 min; SE, 77%; SL, 8.5 min; W, 18.9%; S1, 8.2%; S2, 52.7%; REM, 13.5%; SS/h, 17.7; A/h, 2.8; AH/h, 11.9; Ar/h, 4.4; MD, 80%. These parameters did not change significantly after cessation of hGH treatment. In contrast, median SWS decreased significantly from 33 min (7.1%) to 7.5 min (1.8%; P= 0.03). Median OAH/h decreased significantly from 4.4 to 0.1 (P = 0.03) whereas CAH/h increased from 6.3 to 14.6 (P = 0.03) after cessation of hGH. Correspondingly, one patient with OSAS improved markedly whereas another patient developed new and asymptomatic central SAS after cessation of hGH. CONCLUSION This study showed that hGH replacement therapy influenced sleep reaction in a complex way in middle-aged men; cessation of treatment was associated with a significant decrease in slow wave sleep and a shift from obstructive to central apnoea and hypopnoea
Elevated cortisol secretion in patients suffering from both depression and sleep-related breathing disorders
No full textThe Influence of the Tricyclic Antidepressant Amitriptyline on Periodic Limb Movements during Sleep
No full textIntroduction: Many antidepressants are associated with periodic limb movements (PLM) during sleep. Although some tricyclic antidepressants, such as amitriptyline, promote sleep and are thus often prescribed as a treatment for sleep disturbances that can accompany depression, it remains unclear whether amitriptyline is associated with PLM. Methods: 32 healthy males (18-39 years) spent 2 consecutive nights in the sleep lab for polysomnographic recording. During the second night, they received either 75 mg amitriptyline or placebo in a randomized, double-blind, placebo-controlled manner. Results: In subjects receiving amitriptyline but not in subjects receiving placebo, the number of periodic leg movements per h was significantly increased from baseline to intervention night. However, objective polysomnographic sleep parameters (such. as the number of awakenings, wake after sleep onset, and sleep efficiency) and subjective sleep perception were not significantly associated with any PLM indices. Discussion: Our findings indicate that amitriptyline can induce or even increase the number of PLM during sleep in healthy subjects. When treating sleep disturbances with amitriptyline, PLM should be considered as a possible cause of insufficient improvement
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