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Circadian rhythms and sleep regulation in seasonal affective disorder

Wirz-Justice, A. ; Kräuchi, K. ; Brunner, D.P. ; Graw, P. ; Haug, H.-J ; Leonhardt, G. ; Sarrafzadeh, A. ; English, J. ; Arendt, J.

In: Acta Neuropsychiatrica, 1995, vol. 7, no. 2, p. 41-43

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    Titel
    • Circadian rhythms and sleep regulation in seasonal affective disorder
    Autor
    • Wirz-Justice, A.. Psychiatric University Clinic, Wilhelm-Klein-Strasse 27, CH 4025 Basel, Switzerland
    • Kräuchi, K.. * Dept. of Biological Sciences, University of Surrey, UK
    • Brunner, D.P.. * Dept. of Biological Sciences, University of Surrey, UK
    • Graw, P.. * Dept. of Biological Sciences, University of Surrey, UK
    • Haug, H.-J. * Dept. of Biological Sciences, University of Surrey, UK
    • Leonhardt, G.. * Dept. of Biological Sciences, University of Surrey, UK
    • Sarrafzadeh, A.. * Dept. of Biological Sciences, University of Surrey, UK
    • English, J.. Dept. of Biological Sciences, University of Surrey, UK
    • Arendt, J.. Dept. of Biological Sciences, University of Surrey, UK
    Dokumententyp
    • Postprint
    Sprache
    • Englisch
    Veröffentlicht in
    • Acta Neuropsychiatrica, 1995, vol. 7, no. 2, p. 41-43. Cambridge University Press
    Andere elektronische Ausgabe
    OAI-PMH-ID
    • oai:doc.rero.ch:295719
    Summary
    Seasonal affective disorder (SAD) is characterised by recurrent episodes in autumn and winter of depression, hypersomnia, augmented appetite with carbohydrate craving, and weight gain, and can be successfully treated with bright light. Circadian rhythm hypotheses (summarized in) have stimulated research into the pathophysiology of SAD, postulating that: 1.The illness is a consequence of delayed phase position, 2.It is correlated with diminished circadian amplitude, or 3.It results from changes in the nocturnal duration between dusk and dawn e.g. of low core body temperature or melatonin secretion. Light is considered to act directly on the circadian pacemaker (‘Process C') and not on sleep dependent processes (‘Process S'). Thus successful treatment of SAD must act via mechanisms within known retinohypothalamic pathways. Conversely, emergence of SAD symptoms may reflect inappropriate neurobiological response to decreasing daylength