Abstract
Bidirectional interactions between nocturnal hormone secretion and sleep regulation are well established. In particular, a link between PRL and rapid eye movement (REM) sleep has been hypothesized. Short-term administration of PRL and even long-term hyperprolactinemia in animals increases REM sleep. Furthermore, sleep disorders are frequent symptoms in patients with endocrine diseases. We compared the sleep electroencephalogram of seven drug-free patients with prolactinoma (mean PRL levels 1450 +/- 1810 ng/mL; range between 146 and 5106 ng/mL) with that of matched controls. The patients had secondary hypogonadism but no other endocrine abnormalities. They spent more time in slow wave sleep than the controls (79.4 +/- 54.4 min in patients vs. 36.6 +/- 23.5 min in controls, P < 0.05). REM sleep variables did not differ between the samples. Our data suggest that chronic excessive enhancement of PRL levels exerts influences on the sleep electroencephalogram in humans. Our result, which seems to be in contrast to the enhanced REM sleep under hyperprolactinemia in rats, leads to the hypothesis that both slow wave sleep and REM sleep can be stimulated by PRL. These findings are in accordance with reports of good sleep quality in patients with prolactinoma, which is in contrast to that of patients with other endocrine diseases.
Highlights
A VAST literature indicates that there are bidirectional interactions between the nocturnal secretion of different hormones and the sleep electroencephalogram (EEG)
The other two parameters tested, the amounts of sleep stages 2 and rapid eye movement (REM), did not differ significantly, but there was a trend towards a decrease in REM sleep in the patients’ group
The descriptive analysis showed that slow wave sleep (SWS) was somewhat increased in the first half of the night, with the increase in the second half of the night being about 2- to 3-fold
Summary
A VAST literature indicates that there are bidirectional interactions between the nocturnal secretion of different hormones and the sleep electroencephalogram (EEG) (for reviews see Refs. 1 and 2). Systemic short-term administration of PRL stimulated REM sleep in intact animals (for review see Ref. 13), as well as in pontine cats after hypophysectomy [14], but antiserum to PRL decreased REM sleep in rats [15] In all these studies non-REM sleep, including SWS, remained unchanged [14, 15]. In contrast to the latter study, in genetically hypoprolactinemic rats SWS enhancement and REM sleep suppression in sleep-waking registration has been reported [18] Taken together, these data support the hypothesis that there is an association between sleep parameters and PRL levels, either as a correlation between sleep-EEG parameters and nocturnal PRL secretion [11, 12], or as a direct promotion of sleep, of REM sleep, by administration of PRL [13, 17]. Because there are no studies examining longterm effects of increased PRL levels on sleep EEG in humans, the sleep-EEG investigation in patients with prolactinoma seemed to be a suitable instrument to study the relationship between excessively enhanced PRL levels and sleep in humans
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