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  • 1
    ISSN: 1433-8491
    Keywords: Eating disorder ; Cranial computed tomography ; Cortisol ; Triiodothyronine ; REM sleep
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Neuroendocrine disturbances [low plasma levels of triiodothyronine (T3), high plasma concentrations of cortisol], morphological brain alterations [enlarged external cerebrospinal fluid (CSF) spaces, dilatation of the ventricles] and altered sleep patterns [fragmented sleep continuity, a reduction of slow wave sleep (SWS) or REM sleep] have been described in patients with anorexia nervosa and bulimia nervosa. The present study investigates to what degree these disturbances interact with each other. In ten anorexic and five bulimic patients cranial computed tomography (CT) to estimate the size of the CSF spaces, blood sampling to measure cortisol and T3 plasma concentrations, and all-night polysomnography were performed. In comparison with patients with normal CT scans, the patients displaying enlarged CSF spaces spent more time in SWS, and the duration of REM sleep was reduced. In the whole sample, a negative correlation was found between the amount of REM sleep and cortisol, whereas a positive association was found between the amount of REM sleep and the T3 level. In addition, the degree of brain shrinkage correlated positively with cortisol and negatively with T3. On the basis of these results, it can be assumed that in patients with eating disorders the disease process with its neuroendocrine alterations affects brain morphology as well as EEG sleep.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European archives of psychiatry and clinical neuroscience 242 (1992), S. 53-56 
    ISSN: 1433-8491
    Keywords: Cytokines ; Interleukin-1β ; Interleukin-6 ; Tumor-necrosis-factor ; Sleep
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Nocturnal cytokine levels were measured serially in 12 healthy male volunteers for 12 h, including 8 h of polygraphically monitored nocturnal sleep. Plasma concentrations of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were determined in 30-min intervals by enzyme-linked immunoadsorbant assays. In some subjects cytokines were not detectable at all. In the remaining volunteers (27% for IL-1β, 58% for IL-6 and TNF-α, respectively) occasional values near to the detection limits (DL) of the assays could be measured. With respect to IL-1β and IL-6, plasma levels above the DL were significantly more frequent during sleep than during the preceding time of wakefulness. No temporal association with NREM or REM episodes could be shown. TNF-α values above the DL were randomly distributed across the 12-h period investigated. It is concluded that in a considerable percentage of healthy subjects small amounts of cytokines are released at night. Release of IL-1β and IL-6 is temporally associated with sleep, whereas the release of TNF-α is not. It remains to be established whether nocturnal cytokine release reflects either an interaction between sleep and host defense mechanisms or a sleep-independent circadian rhythmicity.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1433-8491
    Keywords: Mifepriston ; RU 486 ; Cortisol ; ACTH ; sleep ; antiglucocorticoids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mifepriston (RU 486) is a steroid antagonist which binds with high affinity to glucocorticoid receptors (GR), and also to progesterone receptors. The antiglucocorticoid action of Mifepriston in man has been demonstrated by blockade of the negative feedback action of endogenous cortisol and by antagonism of the effects of exogenously aministered dexamethasone. In the present study Mifepriston was administered to a normal male volunteer at 14.00 h and its effects on pituitary-adrenal activity and nocturnal sleep pattern were recorded. Mifepriston caused a large rise in plasma ACTH levels during the morning hours in comparison to untreated male control subjects. Plasma ACTH levels in the Mifepriston treated subject at 7.00 h were threefold greater than in the control subjects (104.4 pg/ml vs. 37.6±13.9 pg/ml; $$\bar x$$ ±SD). Subsequently the cortisol secretion was enhanced and the rise was advanced by about 60 minutes compared to controls. The main effects of Mifepriston on EEG sleep pattern were a dramatic disruption of sleep quality with a prolonged sleep onset latency, increased nocturnal awakenings and a considerable reduction of both slow wave sleep (SWS) and REM sleep. After Mifepriston, SWS was reduced by about 80% in comparison to placebo, and REM sleep was reduced by more than 50%. While the present data were collected from only a single subject the effects observed were so pronounced that tentative conclusions seem to be justified: The well-established pharmacological properties of Mifepriston as a glucocorticoid antagonist are reflected by its action on sleep physiology since it influences sleep in a direction opposite to that produced by cortisol. This observation further substantiates the view that changes in SWS and REM sleep may be mediated by GR effects.
    Type of Medium: Electronic Resource
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