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Rythmes endocriniens en période de dépression et de rémission

Published online by Cambridge University Press:  28 April 2020

E. Souêtre
Affiliation:
Clinique de psychiatrie et de psychologie médicale, Hôpital Pasteur, BP69, 06002, Nice Cedex, France National Institute of Health, Psychobiology Branch, Bldg 10, Bethesda, MD20817, USA
E. Salvati
Affiliation:
Clinique de psychiatrie et de psychologie médicale, Hôpital Pasteur, BP69, 06002, Nice Cedex, France
M. Savelli
Affiliation:
Clinique de psychiatrie et de psychologie médicale, Hôpital Pasteur, BP69, 06002, Nice Cedex, France
B. Krebs
Affiliation:
Laboratoire de radioimmunologie, Centre A.-Lacassagne, voie Romaine, 06000Nice, France
A. Jorlet
Affiliation:
Laboratoire de radioimmunologie, Centre A.-Lacassagne, voie Romaine, 06000Nice, France
J.L. Ardisson
Affiliation:
Laboratoire de physiologie, Faculté de Médecine, av. de Vallombrose, 06000Nice, France
G. Darcourt
Affiliation:
Clinique de psychiatrie et de psychologie médicale, Hôpital Pasteur, BP69, 06002, Nice Cedex, France
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Résumé

La participation des rythmes biologiques circadiens à la pathogénie de la dépression repose sur une série d’arguments cliniques, thérapeutiques et biologiques. La recrudescence matinale des symptômes dépressifs oriente vers une anomalie de l’organisation temporelle. Les aspects épidémiologiques de la dépression ou des suicides évoquent, quant à eux, l’existence de recrudescence saisonnière dans laquelle les facteurs naturels de synchronisation pourraient jouer un role. De plus, les thérapeutiques de la dépression agissent directement sur les horloges biologiques, qu’il s’agisse des manipulations du cycle veille/sommeil, de la photothérapie ou des antidépresseurs.

Notre étude longitudinale a permis de comparer les rythmes circadiens de cortisol, de TSH et de mélatonine plasmatique chez des sujets déprimés (n = 16), chez des sujets en rémission clinique (n = 15) ainsi que chez des sujets sains (n = 16). Nos résultats montrent de profondes perturbations du système circadien endocrinien en période dépressive. L’anomalie essentielle semble porter sur l’amplitude des rythmes, les sécrétions nocturnes de TSH et de mélatonine étant effondrées chez les sujets dépressifs. Ces perturbations disparaissent avec l’amélioration clinique des sujets.

Nos résultats confirment, dans une certaine mesure, les interrelations temporelles et fonctionnelles qui existent entre les sécrétions de cortisol, de TSH et de mélatonine. Par ailleurs, l’absence de décalage horaire de la position des rythmes étudiés incite à nuancer l’hypothèse d’une désynchronisation biologique dans la dépression pour privilégier une défaillance des mécanismes de couplage entre les facteurs synchronisants de l’environnement et les oscillateurs centraux. Dans cette perspective, les traitements de la dépression tels que les manipulations du cycle veille/sommeil, la photothérapie ainsi que les tricycliques semblent agir sur ces mécanismes de transmission de l’information temporelle soit en augmentant artificiellement leur intensité, soit en abaissant le seuil de perception. Cette hypothèse pourrait aboutir à concevoir de nouveaux outils thérapeutiques des troubles de l’humeur.

Summary

Summary

The chronobiological hypotheses of depression are based on epidemiological, biological as well as therapeutic pieces of evidence. The seasonal pattern of depression and suicide rates tend to link affective disorders and the daylight duration. In addition, treatments of depression, such as manipulations of the sleep/wake cycle, phototherapy or tricyclics, may involve chronobiological mechanisms or endogenous pacemakers.

In our longitudinal experiment, we compared the circadian rhythms of plasma cortisol, TSH and melatonin in depressed (n = 16) and recovered (n = 15) patients and in normal control (n = 16) subjects. Our findings pointed out clear abnormalities of the circadian system in depression, consisting mainly in amplitude reduction of the rhythms. The nocturnal secretions of both TSH and melatonin were dramatically blunted in depression. Endocrine circadian rhythms were normalized under recovery.

To some extent, our findings support the hypothesis of temporal and functional relationships between cortisol, TSH and melatonin secretions. We failed to detect any phase abnormalities of the rhythms in depression which tend to rule out the «desynchronization» hypothesis for depression. On the other hand, the reduction of amplitude may be linked to a failure of the entrainment and coupling processes between external synchronizing factors and biological clocks. In this respect, treatments of depression such as manipulations of the sleep/wake cycle, phototherapy and tricyclics have been shown to act either on the level of these external factors, or at the perception threshold. According to this hypothesis, it is possible to concieve new therapeutic strategies for affective disorders.

Type
Article original
Copyright
Copyright © European Psychiatric Association 1988

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