![]() Their sleep quality was evaluated with Epworth Sleepiness Scale (ESS) and Pittsburgh Sleep Quality Index (PSQI), and their clinical performance was evaluated with HRSD and Clinical Globe Impression (CGI). The secondary endpoints were the changes of subjective sleep quality and clinical performance from baseline to the 56th Day. The primary endpoints were the changes of PSG variables from baseline to the 56th Day. The dosage of sertraline would be titrated during the 8-week treatment, and the maximum was lower than 200 mg/day. After 7-day wash-out period and 2 nights PSG (the first night as adaptive and the second night as baseline), 31 depressive patients were administered by sertraline as 50 mg in 8 am in the 1st day. Their Hamilton Rating Scale for Depression (HRSD) score was more than 18, and HRSD-sleep disturbance score was more than 3. Patients were diagnosed as major depressive disorder. Methods used: The study design was 8-week and open-label trial. Purpose of the study: To evaluate the effect of sertraline on polysomnographic (PSG) variables and clinical improvement in the treatment of depressive patients with insomnia. We hypothesized that sertraline could suppress the REM sleep, and have little damage to the sleep architecture of depressive patient. So it has chance to exhibit better effect on sleep architecture in depressive patients.įinally, it is difficult to be determined that the unique phenomenon of sertraline is its genuine characteristics or the tolerance after 12-week treatment, so it is crucial to assess the effect of sertraline on sleep architecture in acute treatment. Sertraline has a greater potency against 5-HT reuptake as well as better selectivity for 5-HT reuptake relative to NE reuptake than any other SSRIs, and the relative selectivity of sertraline for inhabiting 5-HT reuptake relative to DA reuptake is somewhat less than of any other SSRIs. However, this study compared the sleep architecture before and after 12 weeks of pharmacotherapy, so the tolerance to the disturbance of sleep architecture in antidepressants appears to develop over several weeks of treatment. One PSG study shown sertraline minimally increases sleep efficiency and reduces nocturnal wakefulness time, which may benefit depressive patients. SSRIs can suppress REM sleep and delay REM latency too, but they increase awakenings and reduce SWS at the same time. Many all-night PSG studies have shown tricyclic antidepressants can ameliorate the sleep architecture abnormality in depression by producing rapid suppression of REM sleep.Ĭompared to TCAs, SSRIs are generally less sedating because of its high selectivity for serotonin receptors. 5-HT also affects the regulation of the sleep-wake cycle and the sleep microarchitecture. It is well known that most of antidepressants treat depression through 5-hydroxytryptamine (5-HT) neurons. Many researchers have focused on the biological rhythm to investigate the etiological and pathophysiology of depression, and they think depression can be cured if its sleep abnormality is ameliorated. The first two patterns are common in other psychiatric disorders, while the REM pattern is very characteristic in depression, so the phase-advance theory was accepted by most of psychiatrists. ![]() Major depressive disorder is associated with several sleep Polysomnograph (PSG) findings: (1) impaired sleep continuity (2) non-REM (NREM) changes and (3) enhanced rapid eye movement (REM) sleep. Why Should I Register and Submit Results?.
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