Sleep Patterns in Growth Hormone Deficient Children and Age-Matched Controls: Developmental Considerations

Orr, William C.; Vogel, Gerald W.; Ståhl, M; Griffiths, William J.; Seely, J. Rodman

doi:10.1159/000122721

Cited by 20 publications

(12 citation statements)

References 3 publications

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“…Our data confirm in part the first report on GHD children before GH therapy [17] that showed only an increase in sleep stage 1 compared to age-matched normative data (9.7 vs. 2.3%); unfortunately no other parameters of sleep fragmentation were reported in that study. Our results are in agreement with Van Cauter et al [16] who showed, in adults with GHD of pituitary origin, an increased sleep fragmentation (indicated by an increase in WASO and arousal index and by a decrease in sleep efficiency and sleep maintenance index), while no differences were evident in sleep stage distribution.…”

Section: Discussionsupporting

confidence: 88%

“…The different studies on the effects of GH replacement in GHD patients showed that it minimally affects sleep architecture, night sleep and daytime sleep propensity [6,17,20,21]. …”

Section: Discussionmentioning

confidence: 99%

“…The studies in children reported different results: a paper comparing GHD children and controls showed no significant differences in SWS, negating the hypothesis of a monotonic relationship between SWS and GH secretion[17]. In contrast, a more recent study reported that GHD subjects had more non-rapid eye movement (NREM) sleep stages 1 and 3 and less rapid eye movement (REM) sleep as compared with age-matched normal children: in these children GH replacement was followed by a decrease in NREM sleep stage 3, while the other sleep parameters were not affected [18].…”

Section: Introductionmentioning

confidence: 99%

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Sleep Characteristics in Children with Growth Hormone Deficiency

et al. 2011

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Background/Aims: Growth hormone (GH) is preferentially secreted during slow wave sleep and the interactions between human sleep and the somatotropic system are well documented, although only few studies have investigated the sleep EEG in children with GH deficiency (GHD). The aim of this study was to evaluate the sleep structure of children with dysregulation of the GH/insulin-like growth factor axis. Methods: Laboratory polysomnographic sleep recordings were obtained from 10 GHD children and 20 normal healthy age-matched children. The classical sleep parameters were evaluated together with sleep microstructure, by means of the cyclic alternating pattern (CAP), in GHD patients and compared to the control group. Results: GHD children showed a significant decrease in total sleep time, sleep efficiency, movement time and in non-rapid eye movement sleep stage 2. Although some indicators of sleep fragmentation were increased in GHD children, we found a general decrease in EEG arousability represented by a significant global decrease in the CAP rate, involving all CAP A phase subtypes. Conclusions: The analysis of sleep microstructure by means of CAP, in children with GHD, showed a reduction of transient EEG amplitude oscillations. Further studies are needed in order to better clarify whether GH therapy is able to modify sleep microstructure in GHD children, and the relationships between sleep microstructure, hormonal secretion and neurocognitive function in these patients.

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Section: Discussionsupporting

confidence: 88%

“…The different studies on the effects of GH replacement in GHD patients showed that it minimally affects sleep architecture, night sleep and daytime sleep propensity [6,17,20,21]. …”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Sleep Characteristics in Children with Growth Hormone Deficiency

et al. 2011

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“…GH is, in fact, capable of promoting REMS; increases in REMS are reported after acute administration of GH in rats (Drucker-Colin et al, 1975), cats (Stern et al, 1975), and humans (Mendelson et al, 1980), whereas immunoneutralization of GH is followed by decreases in REMS in rats (Obál et al, 1997). GH deficiency is often associated with decreases in REMS in children, but REMS might be normal in GH-deficient young adults (Orr et al, 1977;Hayashi et al, 1992). We suggest that the decreases in REMS result from the GH deficiency in the dw/dw rat, whereas the intracerebral hGH compensates for the loss of pituitary GH and maintains normal REMS in the TH-hGH transgenic mouse.…”

Section: Discussionmentioning

confidence: 78%

Deficiency of Growth Hormone-Releasing Hormone Signaling Is Associated with Sleep Alterations in the Dwarf Rat

et al. 2001

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The somatotropic axis, and particularly growth hormonereleasing hormone (GHRH), is implicated in the regulation of sleep-wake activity. To evaluate sleep in chronic somatotropic deficiency, sleep-wake activity was studied in dwarf (dw/dw) rats that are known to have a defective GHRH signaling mechanism in the pituitary and in normal Lewis rats, the parental strain of the dw/dw rats. In addition, expression of GHRH receptor (GHRH-R) mRNA in the hypothalamus/preoptic region and in the pituitary was also determined by means of reverse transcription-PCR, and GHRH content of the hypothalamus was measured. Hypothalamic/preoptic and pituitary GHRH-R mRNA levels were decreased in the dw/dw rats, indicating deficits in the central GHRHergic transmission. Hypothalamic GHRH content in dw/dw rats was also less than that found in Lewis rats. The dw/dw rats had less spontaneous nonrapid eye movement sleep (NREMS) (light and dark period) and rapid eye movement sleep (REMS) (light period) than did the control Lewis rats. After 4 hr of sleep deprivation, rebound increases in NREMS and REMS were normal in the dw/dw rat. As determined by fast Fourier analysis of the electroencephalogram (EEG), the sleep deprivation-induced enhancements in EEG slow-wave activity in the dw/dw rats were only one-half of the response in the Lewis rats. The results are compared with sleep findings previously obtained in GHRH-deficient transgenic mice. The alterations in NREMS are attributed to the defect in GHRH signaling, whereas the decreases in REMS might result from the growth hormone deficiency in the dw/dw rat.

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“…But, from reports of several other studies, such a SWS-hGH link has to be qualified. For example, SWS deprivation results in smaller, but still significant, amounts of hGH release during the remaining sleep (Karacan, Rosenbloom, Will iams, Finley, & Hursch, 1971;Sassin, Parker, Johnson, Rossman, Mace, & Gotlin, 1969); hGH-inhibiting factor (somatostatin) or an elevation in plasma-free fatty acids will suppress the sleep hGH release but not SWS (Lipman, Taylor, Schenk, & Mintz, 1972;Lucke, Hoffken, & von zur Muhlen, 1976); sleep hGH can be elevated without there being any significant quantitative effect upon SWS (Adamson, Hunter, Ogunremi, Oswald, & Percy-Robb, 1974); finally, hGH-deficient children have normal SWS levels but no sleep-hGH release (Orr, Vogel, Stahl, Griffiths, & Seely, 1977).…”

mentioning

confidence: 99%

Restitution and human sleep: A critical review

Horne

1979

Psychobiology

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It is often assumed that human non-REM sleep, especially its apparently more intense form of slow-wave sleep (SWS), is associated with large increases in body restitutional processes, for example, protein synthesis. However, findings from total sleep deprivation appear only to support a brain restitutional role for human sleep and not one of body restitution. Although rises in human growth hormone (hGH) release during SWS might support a body restitutional role, the variety of complex actions of hGH indicate that other effects, particularly the redistribution of energy substrates, are likely. Sleep hGH release may be a misleading factor in the understanding of SWS function. Increases in protein synthesis during human sleep are unlikely for several reasons. The elevation of mitosis which can occur in sleep is probably a concomitant phenomenon. While relaxed wakefulness should provide for man's body restitutional need, the lack of such a relaxed state in certain mammals may necessitate that sleep fulfills this need for these animals. Although REM sleep, alone, is generally considered to be for cerebral restitution, evidence in support of this viewpoint needs qualification. It is argued that non-REM sleep, especially SWS, is of equal benefit to the human brain.Among sleep researchers, the opinion is generally held that sleep is a state of enforced rest and energy conservation, wherein both body and brain can recover from the wear and tear of wakefulness. Ostensibly, non-REM (nondreaming) sleep is considered to be oriented towards promotion of the synthetic processes of growth and repair in the body, and REM (dreaming) sleep is believed to be directed towards increases in synthetic processes within the brain, including the consolidation of memory. The purpose of this review is to appraise these assumptions for the functions of sleep, with particular regard to man.

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Sleep Patterns in Growth Hormone Deficient Children and Age-Matched Controls: Developmental Considerations

Cited by 20 publications

References 3 publications

Sleep Characteristics in Children with Growth Hormone Deficiency

Sleep Characteristics in Children with Growth Hormone Deficiency

Deficiency of Growth Hormone-Releasing Hormone Signaling Is Associated with Sleep Alterations in the Dwarf Rat

Restitution and human sleep: A critical review

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