SYMPOSIA

Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Abstracts of the Invited Speakers
of the majority of antidepressants is the observed strong and sustained suppression of REM sleep, without overlooking other factors
involved in the mechanisms underlying treatment response. Moreover, tryptophan depletion and studies of selective serotonin reutake
inhibitors (SSRIs) in sleep have shown that increases in serotonin levels could mediate the effect on REM sleep, which is often observed
during antidepressant treatment. However, changes in non-REM sleep and sleep maintenance may be mediated through the action of
other neurotransmitter systems.
Although each antidepressant drug affects sleep architecture differently, there are some common features that characterize the various
types of antidepressants. Thus, the majority of antidepressant drugs suppress REM sleep. Some, however, with little or no noradrenergic
or serotoninergic reuptake inhibition, such as amineptine, tianeptine, nefazodone, trazodone, bupropion, and trimipramine, do not
have clear-cut REM suppressant effects. Sleep continuity and total sleep time are improved with sedative medications, such as most
tricyclic antidepressants (TCAs) and several antidepressants with 5-HT2c receptor antagonist properties, such as mianserin, mirtazapine,
nefazodone, and trazodone. On the other hand, most (SSRIs) and clomipramine, show evidence early in treatment of stimulating effects,
thereby reducing total sleep time and sleep efficiency, and promote wakefulness. However, these effects are fairly short-lived and there
are few significant differences among drugs after a few weeks of treatment.
In conclusion, the majority of antidepressant drugs suppress REM sleep and increase REM latency, although this is not always the case. As
far as sleep efficiency and total sleep time are concerned, antidepressants can be distinguished as either sedative or energizing agents.
This individualized profiling of antidepressants provides a diversity of therapeutic options in terms of the management of concomitant
sleep disturbances in depression.
Key words: Depression, antidepressants, medication, sleep
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S42-3
Insomnia and the effects of hypnotics on sleep
Constantin R. Soldatos, Thomas Paparrigopoulos
Athens University Medical School
E-mail: egslelabath@hol.gr
Insomnia is conceived as the subjective complaint of reduced sleep quantity and/or quality and affects a significant proportion of
the general population. Approximately 10% of the population worldwide meet the full ICD-10 criteria for chronic insomnia. Insomnia
is the outcome of the interplay of many environmental, biological, and psychological factors; consequently, its treatment should not
only focus on ameliorating sleeplessness but should also address all those predisposing, precipitating and perpetuating factors that
cause and maintain insomnia. Insomniacs need an integrative individualized management, which includes sleep hygiene measures,
psychotherapeutic techniques, and the utilization of sleep-promoting drugs. The focus of treatment should be nighttime symptoms, the
feeling of non-restorative sleep, and impaired daytime functioning as well.
Benzodiazepine or benzodiazepine-like hypnotics (z-drugs) are still considered as the drugs of choice for the treatment of insomnia.
However, due to their abuse potential, their pharmacological properties, and their widespread use (there are estimates that one of
every four adults in developed countries takes sleeping aids at some time point during the year), it is highly recommended that the
use of hypnotic drugs is restricted to the initial period of treatment mostly as adjuncts to other psychotherapeutic measures. Both
types of hypnotics focus primarily on the inhibitory neurotransmitter GABA through binding to GABAA receptors; however, other
neurotransmitter systems, such as the serotoninergic and histaminergic, are also involved in the regulation of sleep-wakefulness and
may be targeted by other compounds. The non-benzodiazepine drugs are generally preferred as a result of their improved binding
selectivity and pharmacokinetic profile. However, their potential adverse effects, such as amnestic symptoms, next day residual
sedation, and abuse potential, indicate the need for novel pharmacotherapies. In this line, agents acting on the melatonergic system
and circadian mechanisms have been developed and approved for the treatment of insomnia (melatonin and the melatonin receptor
agonist, ramelteon). Furthermore, a variety of other compounds targeting several neuroreceptors (i.e., GABAA agonism, melatonergic
MT1/MT2 agonism, 5-HT2A antagonism, orexin receptor OX1/OX2 antagonism) are under investigation and may be added in the
psychopharmacological armamentarium in the near future.
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S43
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