Antidepressants have been consistently reported to be useful in
treatment of ethanol withdrawal and dependence (Cheaha et al.
2014; Uzbay et al. 2004). However, their most common effect is a reduction of REM sleep (Thase 1998). Consistent findings indicate
that antidepressant drugs including tricyclics, tetracyclics,
monoamine oxidase inhibitors or selective serotonin reuptake inhibitors
(SSRIs) produce substantial effects on REM sleep. In general,
they prolong REM sleep latency and suppress REM sleep time
in healthy subjects (Thase 1998; Rijnbeek et al. 2003) as well as laboratory
animals (Ivarsson et al. 2005). A decrease in cholinergic activity
and an increase in aminergic activity are two main factors in the
REM sleep suppression mechanism of antidepressant drugs (Costa e
Silva 2006). In terms of etiology, sleep disturbance is positively correlated
with psychiatric illness (Costa e Silva 2006). In particular, REM
disturbance was related to neurodegenerative disease such as Parkinson’s
(Naismith et al. 2010). REM analysis also showed high predictive
power for Parkinson’s symptoms (Mahale et al. 2014). Any enhancement
of REM disturbance is likely to aggravate neurodegeneration.
Thus, antidepressants that do not disturb REM are being sought to
avoid undesirable effects. Until recently, only a few antidepressants
have been demonstrated with no apparent REM sleep inhibition, such
as trimipramine (Riemann et al. 2002).