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The Munich vulnerability study on affective disorders: microstructure of sleep in high-risk subjects

Vulnerability markers for affective disorders have focused on stress hormone regulation and sleep. Among rapid eye movement (REM) sleep, increased REM pressure and elevated REM density are promising candidates for vulnerability markers. Regarding nonREM sleep, a deficit in amount of and latency unti...

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Autores principales: Friess, Elisabeth, Modell, Sieglinde, Brunner, Hans, Tagaya, Hirokuni, Lauer, Christoph J., Holsboer, Florian, Ising, Marcus
Formato: Texto
Lenguaje:English
Publicado: D. Steinkopff-Verlag 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755744/
https://www.ncbi.nlm.nih.gov/pubmed/18504636
http://dx.doi.org/10.1007/s00406-007-0795-2
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author Friess, Elisabeth
Modell, Sieglinde
Brunner, Hans
Tagaya, Hirokuni
Lauer, Christoph J.
Holsboer, Florian
Ising, Marcus
author_facet Friess, Elisabeth
Modell, Sieglinde
Brunner, Hans
Tagaya, Hirokuni
Lauer, Christoph J.
Holsboer, Florian
Ising, Marcus
author_sort Friess, Elisabeth
collection PubMed
description Vulnerability markers for affective disorders have focused on stress hormone regulation and sleep. Among rapid eye movement (REM) sleep, increased REM pressure and elevated REM density are promising candidates for vulnerability markers. Regarding nonREM sleep, a deficit in amount of and latency until slow wave sleep during the first half of the night is a characteristic for depression. To further elucidate whether changes in the microstructure of sleep may serve as vulnerability markers we investigated the premorbid sleep composition in 21 healthy high-risk proband (HRPs) with a positive family history for affective disorders and compared HRPs with a control group of healthy subjects (HCs) without personal and family history for psychiatric disorders. The sleep electroencephalogram (EEG) was conventionally scored and submitted to a quantitative EEG analysis. The main difference in sleep characteristics between HRPs and HCs was an abnormally increased REM density. Differences in the spectral composition of sleep EEG were restricted to an increased power in the sigma frequency range. Since the HRP group comprised six unrelated and 15 related subjects we controlled for sibling effects. We could replicate the increased REM density in the group of HRPs whereas elevated power in the low sigma frequencies persisted only with approaching significance. The present study further supports elevated REM density as putative vulnerability marker for affective disorders. However, sleep EEG in our group of HRPs did not show slow wave sleep abnormalities. Ongoing follow up investigations of HRPs will clarify whether the observed increase in sigma EEG activity during nonREM sleep is of clinical relevance with respect to the likelihood to develop an affective disorder.
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spelling pubmed-27557442009-10-07 The Munich vulnerability study on affective disorders: microstructure of sleep in high-risk subjects Friess, Elisabeth Modell, Sieglinde Brunner, Hans Tagaya, Hirokuni Lauer, Christoph J. Holsboer, Florian Ising, Marcus Eur Arch Psychiatry Clin Neurosci Original Paper Vulnerability markers for affective disorders have focused on stress hormone regulation and sleep. Among rapid eye movement (REM) sleep, increased REM pressure and elevated REM density are promising candidates for vulnerability markers. Regarding nonREM sleep, a deficit in amount of and latency until slow wave sleep during the first half of the night is a characteristic for depression. To further elucidate whether changes in the microstructure of sleep may serve as vulnerability markers we investigated the premorbid sleep composition in 21 healthy high-risk proband (HRPs) with a positive family history for affective disorders and compared HRPs with a control group of healthy subjects (HCs) without personal and family history for psychiatric disorders. The sleep electroencephalogram (EEG) was conventionally scored and submitted to a quantitative EEG analysis. The main difference in sleep characteristics between HRPs and HCs was an abnormally increased REM density. Differences in the spectral composition of sleep EEG were restricted to an increased power in the sigma frequency range. Since the HRP group comprised six unrelated and 15 related subjects we controlled for sibling effects. We could replicate the increased REM density in the group of HRPs whereas elevated power in the low sigma frequencies persisted only with approaching significance. The present study further supports elevated REM density as putative vulnerability marker for affective disorders. However, sleep EEG in our group of HRPs did not show slow wave sleep abnormalities. Ongoing follow up investigations of HRPs will clarify whether the observed increase in sigma EEG activity during nonREM sleep is of clinical relevance with respect to the likelihood to develop an affective disorder. D. Steinkopff-Verlag 2008-05-26 2008-08 /pmc/articles/PMC2755744/ /pubmed/18504636 http://dx.doi.org/10.1007/s00406-007-0795-2 Text en © Springer 2008
spellingShingle Original Paper
Friess, Elisabeth
Modell, Sieglinde
Brunner, Hans
Tagaya, Hirokuni
Lauer, Christoph J.
Holsboer, Florian
Ising, Marcus
The Munich vulnerability study on affective disorders: microstructure of sleep in high-risk subjects
title The Munich vulnerability study on affective disorders: microstructure of sleep in high-risk subjects
title_full The Munich vulnerability study on affective disorders: microstructure of sleep in high-risk subjects
title_fullStr The Munich vulnerability study on affective disorders: microstructure of sleep in high-risk subjects
title_full_unstemmed The Munich vulnerability study on affective disorders: microstructure of sleep in high-risk subjects
title_short The Munich vulnerability study on affective disorders: microstructure of sleep in high-risk subjects
title_sort munich vulnerability study on affective disorders: microstructure of sleep in high-risk subjects
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755744/
https://www.ncbi.nlm.nih.gov/pubmed/18504636
http://dx.doi.org/10.1007/s00406-007-0795-2
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