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|Title:||DISSOCIATING THE HYPNOTIC AND HYPOTHERMIC EFFECTS OF MELATONIN: RESULTS FROM A SLEEP STUDY IN WOMEN WITH PREMENSTRUAL DYSPHORIC DISORDER|
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|Authors/Affiliations:||1 Ari Shechter*; 2 Paul Lespérance; 1 Diane Boivin; |
1 Centre for Study and Treatment of Circadian Rhythms, Douglas Mental Health University Institute, McGill University; 2 Department of Psychiatry, Centre Hospitalier de l’Université de Montréal, Université de Montréal, QC, Canada
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|Content:||Objectives: Women with premenstrual dysphoric disorder (PMDD) experience disturbed mood, altered circadian rhythms of core body temperature (CBT) and melatonin and frequent sleep/wake disruptions during the luteal phase (LP) of their menstrual cycle. The aim of this study was to investigate the interaction between nocturnal sleep and CBT following administration of exogenous melatonin in PMDD women. |
Methods: Participants included five women diagnosed with PMDD based on DSM-IV criteria, who also indicated insomnia symptoms. During the baseline condition, participants entered the laboratory every third night for a complete menstrual cycle to undergo recordings of polysomnographic sleep and CBT. At two times (i.e. during the follicular phase and the luteal phase) participants were studied under constant posture conditions for 24 hours to investigate the circadian variation of CBT. In the intervention condition, participants ingested a 2-mg slow-release melatonin capsule 60 minutes prior to bedtime throughout the LP for three consecutive menstrual cycles. During the third cycle, participants returned to the lab for a repeat of baseline procedures, including the two 24-hour visits.
Results: The circadian curve of CBT was significantly altered across the menstrual cycle, with elevated 24-hour values and decreased amplitude observed during the LP compared to the follicular phase (FP) in both conditions. Melatonin administration during the LP had no effect on nocturnal CBT when comparing between baseline and intervention conditions. Compared to baseline, exogenous melatonin during the LP reduced sleep onset latency (SOL) and slow wave sleep (SWS), while it increased stage 2 sleep. A menstrual cycle modulation of electroencephalographic activity in the spindle frequency range (SFA; 12-16 Hz in non-rapid eye movement sleep) was also observed, with significantly elevated values throughout the LP compared to the FP, though no between-condition differences were detected.
Conclusions: The changes in sleep induced by exogenous melatonin in PMDD women during the LP are similar to what has been previously reported for melatonin and hypnotics including benzodiazepines. The effects of melatonin on sleep occurred without concomitant reductions in CBT, indicating a mechanism of action independent of the thermoregulatory system. These results may also support the hypothesis of a resistance to melatonin’s hypothermic effects during the LP. Finally, increased SFA during the LP is emerging as the most characteristic menstrual cycle associated sleep alteration.
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