Impact of insomnia on pain in postmenopausal women.

BACKGROUND: Sleep disturbances and pain are assumed to be reciprocally linked. Insomnia and pain are central symptoms of the postmenopausal period and are closely related. Insomnia affects quality of life, increases pain sensitivity, the risk of pain-related disability, and other health problems. OBJECTIVE: To investigate whether insomnia influences aspects of pain (pain intensity and the effect of pain on daily function) in postmenopausal women, and to evaluate the objective sleep pattern of insomniacs with pain. METHODS: Fifty-seven women completed questionnaires about insomnia, climacteric symptoms, and pain. Polysomnography data were collected as well as their medical history. Patients were allocated into three groups: control, subthreshold insomnia, and insomnia. Pain intensity, climacteric symptoms and objective sleep pattern were compared between groups. RESULTS: Postmenopausal women with insomnia had statistically significant higher pain interference in their activities (e.g. relationships with other people, enjoyment of life and sleep) than controls, and had more severe climacteric symptoms. There were no statistically significant differences in pain intensity and objective sleep pattern between groups. CONCLUSIONS: Insomnia status affected climacteric symptoms and pain interference, but not pain intensity in postmenopausal women. Women with insomnia had higher rates of climacteric symptoms than those without insomnia or those with subthreshold insomnia. No changes in objective sleep pattern were found.

Hormone treatment facilitates penile erection in castrated rats after sleep deprivation and cocaine.

Sleep deprivation is associated with cocaine-enhanced genital reflexes in male rats, and castration of the male rat causes a decline in sexual behaviour, which can be reversed by hormone administration. We conducted two experiments to determine whether sleep deprivation and cocaine administration could also induce spontaneous penile erection in castrated rats after hormonal treatment (testosterone, progesterone and oestradiol). Different doses of hormones or vehicle were administered to rats during the 4-day period of sleep deprivation, and in home-cage control rats. Testosterone did not restore penile erection in castrated sleep-deprived rats. Progesterone triggered penile erection, and 100 mg/day of progesterone induced the highest proportion of rats displaying penile erection, and restored the frequency of penile erection observed in noncastrated sleep deprived rats. Penile erection was absent in vehicle as well as oestradiol-treated sleep-deprived castrated rats. Whereas sleep deprivation increased progesterone concentrations in noncastrated rats, sleep deprivation decreased progesterone concentrations in castrated rats. Corticosterone concentrations were lower in the castrated sleep-deprived rats than in respective control group. These data show that progesterone treatment facilitates penile erection in sleep deprived-cocaine castrated rats.