![]() 10 Phenelzine is more typically sedating and is less frequently associated with complaints of insomnia. In polysomnographic studies, tranylcypromine has been demonstrated to prolong sleep onset latency and increase awakenings and arousals during sleep. Tranylcypromine is structurally related to amphetamine and tends to be activating and associated with insomnia. 8While the MAOIs have demonstrated efficacy in the treatment of depression in general, they especially have been associated with efficacy in the treatment of atypical depression characterized by hypersomnolence as well as by apathy and low energy. These agents increase concentrations of norepinephrine, dopamine, and serotonin by decreasing their metabolism. Pulmonary specialists sometimes advocate use of an activating TCA such as protriptyline because it may help suppress REM sleep-when sleep apnea episodes may be accentuated-and also provide benefit for the daytime somnolence that many patients with sleep apnea experience. 1,6 A clinical consequence of REM suppression can be a change in frequency and intensity of dreaming, as well as a pronounced exacerbation of intense, disturbing dreams related to “REM rebound” on discontinuation. The majority of TCAs markedly suppress REM sleep, except for trimipramine, trazodone, nefazodone, bupropion, and mirtazapine. 5 These findings underscore the important lesson that treatment with an antidepressant does not automatically result in improvement in sleep in depressed patients. 3 In polysomnographic studies of patients with depression, administration of the activating TCA desipramine has been reported to produce an increase in sleep onset latency, a decrease in sleep efficiency, and a heightened number of awakenings. Examples of TCAs in this category include desipramine and protriptyline, agents that are characterized by the selective blockade of norepinephrine presynaptic uptake sites. Some TCAs are more activating and have been used to treat a subset of depressed patients who experience hypersomnolence and daytime lethargy. 4 Doxepin is now marketed in the US as Silenor, in 3- and 6-mg dose strengths for primary insomnia.Īntidepressants and their effects on sleep physiology ![]() The studies demonstrate the efficacy of low-dosage doxepin therapy (3 and 6 mg qhs) for alleviating symptoms of insomnia. 3 Doxepin has been studied at very low dosages in patients with primary insomnia. Pharmacologically, the TCAs noted for their sleep-enhancing effects are more potent in blocking the serotonin transporter than the norepinephrine transporter, in addition to exerting prominent blockade of histamine H 1 receptors. In recent years, clinicians have scaled down the dosages of these antidepressants to well below established ranges to treat insomnia symptoms. TCAs such as amitriptyline and doxepin are used in depressed patients who have prominent insomnia. Pharmacological differences among TCAs translate into clinically differentiating features. 2 A number of antidepressants affect other neurotransmitter receptors, such as muscarinic ACh, α 1-adrenergic, and histamine H 1receptors, that are implicated in sleep regulation. 1 In particular, norepinephrine and serotonin play prominent roles in suppressing REM sleep, while acetylcholine (ACh) plays a key role in the initiation of REM sleep. It is thought that all approved antidepressants work through modulation of monoamine neurotransmitters, including norepinephrine, dopamine, and serotonin, all of which have been shown to exert prominent effects in regulating sleep-wakefulness and sleep architecture ( Table). The antidepressants are a prototypical example of the potentially complex interactions between psychiatric medications and sleep. In addition to resolving sleep-related symptoms through their primary therapeutic effects, many psychiatric medications have secondary effects on sleep that can contribute to their overall therapeutic benefit or sometimes counter them through adverse effects. ![]() Many psychiatric disorders are accompanied by disturbance of sleep.
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