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Effects of escitalopram on the sleep EEG power in patients with major depressive disorder

Xueqin Wang  Suxia Li  Yanping Bao  Jiajia Liu  Dequan Wang  Jiahui Deng  Jie Chen  Shaowei Wu  Hsuan-Nu Luk  Ling Yu  Wei Sun  Yong Yang  LU Lin  
【摘要】:Background Major Depressive Disorder(MDD) is easy to relapse after remission through the antidepressant treatment, mainly resulting from residual symptoms which are common in patients with MDD after treatment, especially sleep-wake rhythm disturbances. Previous studies mainly focused on the changes of sleep architecture, few on sleep EEG power analysis or related rhythmic abnormalities. Method Polysomnography(PSG) was detected overnight and blood samples were collected at 4 h intervals for 24 h from 13 male MDD patients and 13 male healthy controls before and after treatment with escitalopram for 8 weeks. The outcome measures included the levels of plasma melatonin, sleep architecture, and sleep EEG power ratio. Results Depressive symptoms significantly ameliorated after 8 weeks' treatment by escitalopram. Although patients were all well response to escitalopram, some of them did not reach complete remission in general. Subjective sleep quality and the severity of insomnia were also significantly improved, but not return to normal after 8 weeks of treatment by escitalopram. Different from subjective assessment, there was no significantly statistical changes in the sleep architecture in patients with MDD assessed with PSG. Residual sleep disturbances existed at the end of 8-week when most depressive symptoms had been ameliorated. Compared with healthy controls, MDD patients showed abnormality in the diurnal rhythm of the melatonin secretion with the peak phase delayed 3 h, accompanied with plasma levels of melatonin decrease at night and increase at daytime and sleep disturbances, even though most of the depressive symptoms had disappeared after 8 weeks of treatment. The sleep EEG power ratio of low frequency bands increased and high frequency bands decreased after treatment with escitalopram for 8 weeks. The theta power ratio in both hemispheres increased and changed from being lower on the left side than on the right side at baseline to being higher on the left side than on the right side, although still lower than that in the healthy control. The power ratios of delta2, theta, and alpha frequency band changed from being higher on the right hemisphere than that on the left or no statistical difference at baseline to being lower on the right hemisphere than that on the left after 8 weeks of treatment with escitalopram. While the power ratio of delta1 frequency band on the right hemisphere was higher than that on the left hemisphere after 8 weeks of treatment with escitalopram. The changes of power ratio of delta2 and theta frequency band were positively correlated with the changes of melatonin messor value, and the change of power ratio of delta1 frequency band was negatively correlated with the change of amplitude of melatonin rhythmic oscillation. Beyond that, we also found that the declines of the power ratio of gamma frequency band during sleep in general were positively correlated with the decrease of HAMA total scores and the improvement of disease severity of depression by CGI-S. Conclusions Depressive symptoms, subjective sleep quality and the severity of insomnia significantly ameliorated, but did not reach the complete remission level in general after 8 weeks' treatment of escitalopram. Escitalopram showed a potential effect on improving sleep quality, whereas it might also prolong sleep latency and REM latency. The 8-week treatment with escitalopram balanced and reconfigured the power ratio of each brain band in two hemispheres of patients with MDD, but the configuration of the delta1 frequency band is more abnormal. Escitalopram has no effects on the delayed peak phase of the melatonin secretion rhythm in patients with MDD. In conclusion, escitalopram, which is not specific to dysrhythmia, had limited effect on improving sleep, circadian rhythm and depressive symptoms. This suggests that further research on the pathogenesis of depression and the development of more targeted antidepressants are still needed.

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