The pharmacology of disordered sleep. A laboratory approach.
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Fluoxetine is an efficacious, nonsedative antidepressant, but its selective efficacy on symptoms of insomnia has not been thoroughly explored. In this analysis, the effects of fluoxetine versus placebo on symptoms of insomnia were evaluated in three clinical subgroups: patients with baseline sleep disturbance, melancholia, or reduced rapid eye movement (REM) latency. Eighty-nine outpatients with major depression completed 2 nights of polysomnography (PSG) and were randomized to fluoxetine or placebo. Within each subgroup of patients, fluoxetine was statistically significantly more effective than placebo in improving non-sleep Hamilton Rating Scale for Depression (HAM-D) items (HAM-D-17 total minus scores from Items 4, 5, and 6). Numerical improvement in HAM-D sleep total (sum of HAM-D Items 4, 5, and 6) was also seen for fluoxetine versus placebo. Fluoxetine did not exacerbate sleep disturbance either at Week 1 or at endpoint. These findings suggest that fluoxetine is an effective antidepressant in patients with baseline sleep disturbance, melancholia, and reduced REM latency.
There is a general tendency to restrict the notion of sleep disorders to insomnia and consequently to limit treatment to the prescription of hypnotics. However, it is very often of benefit to prescribe psychotropic agents, in particular antidepressants, not only in insomnia but also in certain cases of hypersomnia, parasomnia and dysomnia associated with organic diseases. In some conditions, however, antidepressants may either induce or aggravate sleep disorders. This is the case with a number of psychostimulants that occasionally induce insomnia. It is also true of the tricyclic antidepressants, which may worsen or even induce a restlessleg syndrome that is often associated with periodic movement syndrome. On the other hand, the antidepressants may play a therapeutic role in certain sleep disorders : - depression-related insomnia is of course the << primary >> indication for antidepressants. Furthermore, certain antidepressants exhibit a sedative action resulting in a hypnogenic-type effect which appears well before the antidepressant effect; - the other types of insomnia may also often be treated with antidepressants : not acute reactional insomnia, against which hypnotics are remarkably effective, but chronic insomnia. In addition, all antidepressants may eventually correct depressive hypersomnia, but in these cases, it is evidently preferable to prescribe non-sedative drugs. Although some tricyclic antidepressants have been proposed for use in hypersomnia due to sleep apnea, their therapeutic interest is minor compared with mechanical and surgical treatment. In contrast, antidepressants play an important role in the treatment of narcolepsy, particularly for the correction of attacks of cataplexy. Antidepressants have also been used for some time in the treatment of parasomnia related to slow deep sleep (night terrors and sleepwalking), but the antidepressants may also be used in enuresis and in parasomnia related to REM sleep : nightmares, sleep paralysis, behavioral problems associated with REM sleep. Antidepressant (mainly serotoninergic drugs) are often used in the treatment of fibrolitis syndrome. Finally, antidepressants (particularly the serotoninergic antidepressants) play an important role in the drug treatment of fibromyalgia.
PURPOSE OF REVIEW: Sleep-wake problems such as night wakings, excessive crying, or difficulties in falling asleep are frequent behavioral issues during childhood. Maturational changes in sleep and circadian regulation likely contribute to the development and maintenance of such problems. This review highlights the recent research examining bioregulatory sleep mechanisms during development and provides a model for predicting sleep-wake behavior in young humans. RECENT FINDINGS: Findings demonstrate that circadian and sleep homeostatic processes exhibit maturational changes during the first two decades of life. The developing interaction of both processes may be a key determinant of sleep-wake and crying behavior in infancy. Evidence shows that the dynamics of sleep homeostatic processes slow down in the course of childhood (i.e., sleep pressure accumulates more slowly with increasing age) enabling children to be awake for consolidated periods during the day. Another current topic is the adolescent sleep phase delay, which appears to be driven primarily by maturational changes in sleep homeostatic and circadian processes. SUMMARY: The two-process model of sleep regulation is a valuable framework for understanding and predicting sleep-wake behavior in young humans. Such knowledge is important for improving anticipatory guidance, parental education, and patient care, as well as for developing appropriate social policies.
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In this study, two females, siblings who exhibited a non-24 h sleep-wake rhythm (non-24 h) at home were observed. However, they showed a delayed sleep phase syndrome (DSPS) immediately after admission to Kurume University Hospital. Melatonin (3 mg) was commenced following chronotherapy and this improved their sleep-wake rhythm. Polysomnography (PSG) showed decreased sleep latency and increased sleep stage. In these cases, the involvement of environmental factors was strongly suggested for the sleep-wake rhythm abnormalities as well as familial factors.
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