DISRUPTION OF ENDOCRINE RHYTHMS IN SLEEPING SICKNESS WITH PRESERVED RELATIONSHIP BETWEEN HORMONAL PULSATILITY AND THE REM-NREM SLEEP CYCLES

Citation
G. Brandenberger et al., DISRUPTION OF ENDOCRINE RHYTHMS IN SLEEPING SICKNESS WITH PRESERVED RELATIONSHIP BETWEEN HORMONAL PULSATILITY AND THE REM-NREM SLEEP CYCLES, Journal of biological rhythms, 11(3), 1996, pp. 258-267
Citations number
32
Categorie Soggetti
Behavioral Sciences",Biology
ISSN journal
07487304
Volume
11
Issue
3
Year of publication
1996
Pages
258 - 267
Database
ISI
SICI code
0748-7304(1996)11:3<258:DOERIS>2.0.ZU;2-Q
Abstract
In human African trypanosomiasis (sleeping sickness), sleep and wake e pisodes are sporadically distributed throughout the day and the night. To determine whether these sleep disturbances affect the 24-h hormone profiles and the normal relationships between hormone pulsatility and sleep stages, polygraphic sleep recordings and concomitant hormone pr ofiles were obtained in 6 African patients with sleeping sickness and in 5 healthy African subjects selected from Abidjan on the Ivory Coast . Polysomnographic recordings were continuous, and blood was taken eve ry 10 min throughout the 24-h period. Plasma was analyzed for cortisol , prolactin, and plasma renin activity (PRA). The 24-h rhythm of corti sol, considered to be an endogenous circadian rhythm, was attenuated i n all of the patients except one. However, as in normal subjects, slow wave sleep (SWS) remained associated with the declining phases of the cortisol secretory episodes. Prolactin and PRA profiles, which are st rongly influenced by the sleep-wake cycle, did not manifest the noctur nal increase normally associated with the sleep period; instead, they reflected a sporadic distribution of the sleep and wake episodes throu ghout the 24-h period. In patients with sleeping sickness as in normal subjects, rapid eye movement (REM) sleep began during the descending phases of prolactin pulses. In both groups, PRA reflected the sleep st age distribution with non REM (NREM) sleep occurring during the ascend ing phases and REM sleep during the descending phases of the PRA oscil lations. However, in sleeping sickness patients, the marked sleep frag mentation often did not allow sufficient time for PRA to increase sign ificantly, as is normally the case in subjects with regular NREM-REM s leep cycles. These results demonstrate that, together with the disrupt ion of the sleep-wake cycle, there are profound differences in the tem poral organization of the 24-h hormone profiles in humans with African trypanosomiasis. However, the relationship between hormonal pulses an d specific sleep stages persists, indicating the existence of a robust link between hormonal release and the internal sleep structure.