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Le sommeil de sujets dépressifs endogenes avant, pendant et apres un décalage des horaires de sommeil

Published online by Cambridge University Press:  28 April 2020

E. Souêtre
Affiliation:
Clinique de Psychiatrie et de Psychologie Médicale de la Faculté de Médecine de Nice, Hôpital Pasteur. B.P. N°69 - 06002, NICE CÉDEX
E. Salvati
Affiliation:
Clinique de Psychiatrie et de Psychologie Médicale de la Faculté de Médecine de Nice, Hôpital Pasteur. B.P. N°69 - 06002, NICE CÉDEX
D. Pringuey
Affiliation:
Clinique de Psychiatrie et de Psychologie Médicale de la Faculté de Médecine de Nice, Hôpital Pasteur. B.P. N°69 - 06002, NICE CÉDEX
G. Darcourt*
Affiliation:
Clinique de Psychiatrie et de Psychologie Médicale de la Faculté de Médecine de Nice, Hôpital Pasteur. B.P. N°69 - 06002, NICE CÉDEX
*
Correspondance à adresser à: G. Darcourt Corresponding author
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Résumé

Cette étude décrit la structure et l'organisation temporelle du sommeil de 5 sujets dépressifs endogènes qui participèrent à un processus de décalage en avance de 5 heures des horaires de sommeil maintenu pendant deux semaines.

Comparée à ces témoins du même âage, I'architecture du sommeil est, chez les dépressifs avant décalage, très perturbée avec, notamment, fragmentation et inefficacité du sommeil, réduction du taux de sommeil lent et raccourcissement de la latence du sommeil paradoxal. L'organisation temporelle semble traduire, elle, une lutte entre tendance au sommeil lent et tendance au sommeil paradoxal.

Le sommeil des mêmes sujets s'est pratiquement normalisé pendant et surtout après le decalage des horaires de sommeil, exceptée la persistance de la réduction importante de la latence du sommeil paradoxal.

Il serait ainsi possible d'associer la dépression à une désynchronisation entre rythmicités contrôlant sommeil lent, sommeil paradoxal et d'autres rythmes circadiens. Une resynchronisation forcée par décalage des horaires de sommeil pourrait alors rendre compte des améliorations cliniques et biologiques qui ont été observées.

Summary

Summary

This study describes the structure and the temporal organization of the sleep of 5 depressed patients placed on a phase shift protocol, and of 6 controls (age range 30-52).

The same depressed patients (Bipolar, D.S.M. Ill) (age range 33-57) (1 male, 4 females) were observed :

- after a drug-free period of at least 10 days;

- on the 3rd and 4th days of a 5-hour phase advance process (advancing by 5 hours the major synchronizers: the sleep/wake cycle, the light/dark cycle, meals, and social activities). This phase advance was maintained for 14 days;

- on the 2nd and 3rd days after a 5-hour phase delay process (return to normal).

At each session, sleep was continuously recorded by means of a 4-channel Medilog recorder for at least 3 nights. Daily clinical evaluations were performed using the Hamilton rating scale. Other circadian parameters such as temperature, and plasma Cortisol, T.S.H. and norepinephrine were also recorded (results described elsewhere).

Compared to controls, the sleep continuity of depressed patients was altered; there was an increased percentage of wakefulness, an increased sleep latency, and a reduced sleep efficiency. The main disruption of the sleep architecture was the reduced rate of S.W.S.*. The REM sleep latency was dramatically lower in depressed patients. Concerning the temporal organization, even though the REM sleep propensity was advanced (2 hours) in depression, the S. W.S. propensity appeared to be delayed, involving a reduced and abnormal margin between the two propensities.

During the phase advance process, despite a significant clinical improvement, the sleep of the patients remained altered, showing reduced T.S.T.* and sleep efficiency. The S.W.S. duration was normal but the REM sleep latency remained reduced. The process seemed to have entrained the S. W.S. and the REM sleep rhythms since the two propensities were shifted in advance by 5 to 7 hours with a very short margin.

Under a normal schedule, the sleep of the patients appeared improved. Although the REM sleep latency remained reduced, the temporal organization was then close to that of the controls with a normalization of the S.W.S. propensity. However, the REM sleep propensity remained advanced (2 hours).

These results, especially the temporal organization analysis, support the hypothesis of a chronobiological disruption in depression. Depression could be linked to a temporal desynchronization between the S.W.S., REM sleep propensities and other circadian rhythms. The clinical and biological improvement observed after the phase advance process may thus be understood as a re-entrainment effect of this process. Tliis desynchronization could be explained by a failure of the entrainment process of the external synchronizers; the internal clocks could then oscillate on their own period, leading to an unsteady internal desynchronization.

Type
Research Article
Copyright
Copyright © European Psychiatric Association 1986

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Footnotes

*S.W.S.: Slow Waves Sleep

T.S.T: Total Sleep Time

References

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