Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04
  • 2024-05

    • br Alterations in sleep architecture in patients with MD A

    2018-11-13


    Alterations in sleep architecture in patients with MD A significant proportion of patients with MD exhibit alterations in sleep architecture, in comparison with good sleepers. These alterations include a decrease of the slow wave sleep, reduction of latency after the first episode of REM sleep, as well as an increase in the percentage and density of REM (in other words, increase in eye movements per minute during REM sleep) [36], the latter being associated with nightmares and vivid dreams. They also present a decrease in sleep efficiency, which is related with an increase in sleep latency and with awakenings after the beginning of sleep (WASO) [37]. Some studies with patients with history of MD demonstrated that the alterations in sleep architecture will persist during the remission even with the posterior withdrawal of the antidepressant [38]. In general, relapses and the improvement of depressive symptoms are frequently preceded by alterations in sleep architecture [39].
    Antidepressant effect and electroencephalogram Electroencephalogram (EEG) shows major alpha wave activity with the eyes closed in patients with MD, which is interpreted as a decrease in cortical activity. Besides, EEG has also been utilized to point out that patients with MD who respond to fluoxetine, imipramine and amytriptilin, have major alpha power, especially at the occipital level [40]. In another study, depressed patients who responded to fluoxetine differed from nonresponders in the asymmetry of the alpha rhythm, which indicated a major activation of the right Caspase-6 Colorimetric Assay Kit hemisphere in comparison with the left [15]. Tarn et al. found a significant decrease in beta activity at 4 weeks of treatment with amytriptilin [41]. Considering the effects of antidepressants upon sleep, the potency of these drugs in suppressing the REM sleep differ, for example, clomipramine and fenelzine do completely suppress REM sleep. It has been considered that since the majority of antidepressants suppress REM sleep, this suppression could be due to the antidepressants; however, trimipramine, mirtazapine and bupropione increase REM sleep [15]. The polysomnographic abnormalities that are characteristic of MD improve with antidepressant therapy, although fluoxetine does not restore the normal sleep pattern in patients with remitted depression [42].
    Treatment of MD and sleep alterations Considering the pharmacological one, Franzen et al. studied depressed patients with persistent insomnia treated with selective inhibitors of serotonin reuptake, which were assigned to a placebo or Zolpidem (agonist of the benzodiazepine receptors). Compared with the placebo group, patients treated with Zolpidem improved their diurnal function and their quality of sleep [43]. Sedative antidepressants such as mirtazapine, trimipramine and Amytriptilin are frequently prescribed in clinical practice for MD and insomnia, concomitantly, although little evidence supports its long-term usage [44]. On the other hand, Trazodone is an antidepressant with a mechanism of action that involves the inhibition of the serotonin transporter and antagonism to the 5HT2A and 5HT2C receptors, besides having antihistaminergic properties and, in a small proportion, some anticholinergic property. It is effective upon the reduction of sleep alterations in depressed patients due to its sedative effects [45]. A novel antidepressant is Agomelatine, which is an agonist of the MT1 and MT2 receptors and an antagonist of the 5HT2C receptors. From its effects upon sleep, we can point out the increase in sleep efficiency, improvement in terms of quality and quantity of sleep, increase in slow wave sleep and normalization of REM sleep in MD [46,47]. From the non-pharmacological treatment, we include behavioral interventions such as the instructions for the control of stimuli and sleep restrictions. The Behavioral Cognitive Therapy for insomnia encompasses cognitive components to correct dysfunctional beliefs towards sleep. These interventions have been demonstrated as effective in improving sleep [43].