The Effect of Fluvoxamine on Polysonogram in Depressed Patients With Insomnia
Status:
Unknown status
Trial end date:
2016-12-01
Target enrollment:
Participant gender:
Summary
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. 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. 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.
It is well known that most of antidepressants treat depression through 5-hydroxytryptamine
(5-HT) neurons. 5-HT also affects the regulation of the sleep-wake cycle and the sleep
microarchitecture. Many all-night PSG studies have shown tricyclic antidepressants can
ameliorate the sleep architecture abnormality in depression by producing rapid suppression of
REM sleep.
Compared to TCAs, SSRIs are generally less sedating because of its high selectivity for
serotonin receptors. On the other hand, it is known that, although all of SSRIs mainly
increase the extracellular serotonin level by inhibiting serotonin transport in the
presynaptic neuron, each SSRI has its unique pharmacological characteristics. For example, it
was reported by accumulating researches that the serum melatonin level increased markedly
after ingestion of fluvoxamine. The mechanism behind this effect is unknown, but one
possibility is increased melatonin synthesis, caused by effects on serotonin, which is a
melatonin precursor. Another possibility is that fluvoxamine inhibits the metabolism of
melatonin in the liver.
Thus, the property of fluvoxamine to increase serum melatonin level, or even recover the
circadian rhythm of melatonin in depressed patients, might improve the clinical outcome by
improving the sleep quality and quantity. By now, the changes of sleep architecture in
fluvoxamine treatment were assessed by only three clinical trials, and their results were
contradictive. This discrepancy might be due to the small sample size and different study
design, such as clinical trial duration. Moreover, two of three researches applied home-based
PSG assessment, which might have distorted the results of sleep architecture to some extent.
Thus, the effects of fluvoxamine on sleep architecture need to be clarified by more clinical
trials with standard PSG assessment.