While the cause of depression is not fully understood, trazodone affects the brain's neurotransmitters by inhibiting the uptake of serotonin by nerves and stimulating other nerves. Patients who take the drug for a sleep disorder can experience the sedative effects within 30 minutes, depending on the type used.

Patients who take the drug as an antidepressant may not notice symptom relief for one to two weeks, and it may take up to four weeks to experience the full benefits. Like all medications, trazodone can cause side effects in some people. Ask your physician to discuss all potential side effects as well as drug interactions and potential withdrawal symptoms associated with the medication.

While all antidepressant medications are designed to affect brain chemistry, various pharmaceutical formulations of the drugs have different targets and paths. The most commonly prescribed antidepressants are reuptake inhibitors.

Reuptake, as described by WebMD, is "the process in which neurotransmitters are naturally reabsorbed back into nerve cells in the brain after they are released to send messages between nerve cells.

There are three different types: selective serotonin reuptake inhibitors SSRIs , serotonin and norepinephrine reuptake inhibitors SNRIs , and norepinephrine and dopamine reuptake inhibitors NDRIs. Common SSRIs are Prozac, Zoloft, Paxil, Lexapro, Celexa and Luvox; common SNRIs include Cymbalta and Effexor; and NDRIs are found in only one drug: Wellbutrin.

Although trazodone was designed to treat depression and anxiety disorders, the medication is now widely prescribed as a nighttime sleep aid for patients who suffer from acute insomnia.

Trazodone differs from Ambien, Sonata, Lunesta and other "sleeping pill" medications in a few ways:. There are heightened risks for patients under age 24, particularly with regard to mental health.

According to Medline Plus, the following side effects and symptoms can occur among patients under age "new or worsening depression; thinking about harming or killing yourself, or planning or trying to do so; extreme worry; agitation; panic attacks; difficulty falling asleep or staying asleep; aggressive behavior; irritability; acting without thinking; severe restlessness; and frenzied abnormal excitement.

It's also imperative that patients know what to avoid while taking SSRIs, SNRIs or other antidepressants.

Whether a person has a cold, is having trouble sleeping or is searching for allergy relief, they should talk to their doctor before self-treating with an over-the-counter medication. According to Psychiatry Advisor, one patient who was taking melatonin for insomnia while also prescribed an SSRI woke up with a "headache, dizziness and feeling like his face was on fire"—signs of elevated blood pressure that could have been severe had he taken higher doses.

Taking an antidepressant medication in combination with supplements, such as St. To avoid adverse drug reactions, experts advise making a list of all medications, supplements and other OTC drugs, and sharing it with your physician prior to taking trazodone. Absolutely not. Since both alcohol and trazodone affect the central nervous system, the consequences of mixing the two can be deadly.

And mixing the medication with drugs of abuse can result in the onset of serotonin syndrome, a potentially lethal adverse drug reaction. While the potential for trazodone abuse is fairly low, any amount over mg.

in 24 hours is an overdose. Serotonin syndrome occurs when, according to Mayo Clinic, "high levels of serotonin accumulate in the body. According to the journal U. Pharmacist , "Serotonin syndrome SS is caused most often when certain antidepressant agents are taken concurrently with other drugs that modulate synaptic serotonin levels.

When patients take two or more antidepressants from different pharmacologic classes, drug-drug interactions may occur; these interactions may lead to potentially severe serotonin toxicity, or serotonin syndrome.

Trazodone usage can cause a decrease in sodium levels in the body, a disruption of the nervous system or serotonin syndrome. The most common side effects include:. The drug can stay in a person's system for 42 hours after the final dose.

Higher doses can produce more severe side effects. While the drug is considered non-addictive and non-habit-forming, it should only be taken as prescribed and under a physician's care in order to avoid misuse. This is especially important for individuals who have a history of substance abuse or other drug addiction.

According to the National Center for Biotechnology Information, "The trazodone metabolite meta-Chlorophenylpiperazine [m-CPP] can cause false-positive urine amphetamine immunoassay results.

Although technically a non-addictive substance, regular use of the medication can result in mild physical dependence. For this reason, trazodone withdrawal is a concern.

Rather than discontinuing use "cold-turkey," physicians typically recommend a gradual tapering. Trazodone is an antidepressant medicine. It's used to treat depression , anxiety , or a combination of depression and anxiety. Trazodone works by increasing your levels of serotonin and noradrenaline so you feel better.

It can help if you're having problems like low mood, not sleeping insomnia and poor concentration. Trazodone comes as tablets, capsules and liquid that you swallow.

It's only available on prescription. Page last reviewed: 9 March Next review due: 9 March

The dose-effect relationships curves between somnolence or insomnia and dose included linear shape, inverted U-shape, and other shapes.

There was no significant heterogeneity among individual studies. The quality of evidence for results in network meta-analyses was rated as very low to moderate by Grading of Recommendations Assessment, Development, and Evaluation.

Most antidepressants had higher risks for insomnia or somnolence than placebo. The diverse relationship curves between somnolence or insomnia and dose of antidepressants can guide clinicians to adjust the doses.

These findings suggest clinicians pay more attention to sleep-related adverse effects during acute treatment with antidepressants. Sleep-related adverse effects reduce efficacy and acceptability of antidepressants for the acute treatment of patients with major depressive disorder, but are underreported in many clinical trials.

We addressed the odd ratios of treatment-emergent somnolence and insomnia of antidepressants and depicted the relationship between dose and sleep-related adverse events.

We found that most antidepressants had higher risks for insomnia or somnolence compared to placebo, among which fluvoxamine, trazodone, and mirtazapine ranked top three for somnolence and reboxetine, vilazodone, and desvenlafaxine ranked top three for insomnia.

The dose-effect relationships curves between risks of somnolence or insomnia and doses of antidepressants not only appeared linear, but also appeared inverted U-shapes and other shapes. This complex dose-effect relationship requires more attention.

Antidepressants are usually prescribed for MDD patients and are recommended as a first-line treatment for moderate and severe depression [ 2 ].

At present, more than 30 antidepressants are generally used in treatment of MDD, including selective serotonin reuptake inhibitors, serotonin and norepinephrine reuptake inhibitors, and others. Although most of these are effective, it is necessary for clinicians to balance their efficacy and acceptability [ 3 ].

There are many adverse effects commonly associated with antidepressants, including disordered sleep, sexual dysfunction, and gastrointestinal side effects, and these may result in discontinuation during the acute-phase treatment [ 2 ].

Reviews and meta-analyses on sexual dysfunction [ 4 ] and gastrointestinal side effects [ 5 ] were reported recently. Sleep-related adverse effects during short-term treatment with antidepressants not only undermine patient adherence but are also associated with an impediment to achieve remission, greater functional impairment, and higher risk of recurrence [ 6 ].

But meta-analysis on the sleep-related adverse effects is still scarce and the prevalence of treatment-emergent sleep disturbance in patients with MDD taking antidepressants is ambiguous. Some systematic reviews have reported the influence of antidepressants on sleep architecture and physiology [ 7 , 8 ], providing evidence that different antidepressants with different action mechanisms and pharmacokinetics may have different adverse effects on sleep [ 9 ].

Insomnia and somnolence have a significant influence on patients who require alertness in their work, which may include driving or operating heavy machinery, resulting in severe adverse events.

A post-marketing adverse drug reaction study [ 10 ] assessed and ranked the odds ratios ORs of somnolence among 30 antidepressants under a wide array of clinical indications circumstances not limited to MDD. Some meta-analyses [ 11 , 12 ] qualified and compared the rates of insomnia and somnolence associated with second-generation antidepressants during acute-phase treatment of MDD.

Thus, it is important to clarify the association between antidepressants and adverse effects on sleep [ 7 , 9 ]. A comprehensive comparative analysis that ranks the odds of adverse effects of common antidepressants on sleep during short-term treatment for MDD is an unmet clinical need. Network meta-analyses of datasets from high-quality double-blinded randomized controlled trials RCTs make it possible to measure the rates and risks of sleep-related adverse events and provide essential evidence for clinicians to conduct optimal treatment [ 3 ].

Dose-effect relationships of antidepressants have been reported in several studies [ 14—16 ], which show that efficacy is not always dose-dependent. The debate on whether higher doses are more efficacious or not is still ongoing, and the same happens with dose and sleep-related adverse effects.

For instance, different dosages of trazodone have different effects on sleep architecture [ 8 ]. Low doses of mirtazapine are often prescribed off-label for insomnia clinically.

And its sedation effect might be attenuated at higher doses, probably due to increased serotonin and norepinephrine release [ 17 ]. It is essential for clinicians to identify the relationship between dosage and sleep-related adverse effects to make better use of antidepressants, but few studies focus on this aspect.

Our study was specifically designed to address the different subtypes of sleep-related adverse effects during acute treatment with antidepressants for patients living with MDD and depict the relationship between dose and these adverse events.

To this end, we conducted a systematic review and dose-effect network meta-analysis. We reported this study according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses PRISMA [ 18 ]. The protocol was registered on PROSPERO, the International prospective register of systematic reviews CRD We systematically searched multiple databases, including PubMed, Embase, the Cochrane Central Register of Controlled Trials CENTRAL , and Web of Science, for articles published before April 30th, We also searched clinicaltrials.

gov for unpublished trials. The reference lists of previous systematic reviews were screened to supplement study inclusion.

The detailed search strategy is described in Supplementary Table S1. Studies reporting sleep-related adverse effects that occurred during the trial period were included.

For the screened studies, we went through their method section and protocol, if applicable, to confirm all the investigated outcomes. If any sleep-related adverse effect was mentioned in the method section or protocol but not reported in the result, we consider zero events occurred for this outcome.

According to the previous large-scale reviews [ 3 , 4 ] and clinical practice, we included 21 antidepressants in the analysis of odds risks of sleep-related adverse effects and dose-effect network meta-analysis see Table 1 and Table 2. Toludesvenlafaxine, a new triple reuptake inhibitor with a good effect profile [ 19 , 20 ], was only included in the analysis of the risk of somnolence because of the limited study data, which were a revision from original protocol.

Only monotherapy was considered. We extracted the name and the dosage per day of the antidepressants, as well as the feature of the study populations, including sample size, baseline severity, percentage of females, and mean age. Basic information was also extracted, such as year of publication, first author, and study region.

We summarized information on study design and result reporting to assess the risk of bias within each individual study.

The main outcomes that we focused on were somnolence and insomnia. Both self-reported and clinically confirmed treatment-emergent somnolence and insomnia were extracted. In addition, we also extracted the numbers of participants that experienced other subtypes of sleep-related adverse effects, including nightmares, restless leg syndrome, rapid eye movement sleep behavior disorder, and sleepwalking.

The risk of bias in each included study was assessed using the Cochrane risk of bias tool RoB2. The quality of evidence for results in network meta-analyses was rated through the Grading of Recommendations Assessment, Development, and Evaluation GRADE process from five aspects, including risk of bias, imprecision, inconsistency, indirectness, and publication bias [ 22 ].

Two groups of reviewers selected the studies, extracted information, and conducted the quality assessment independently. Every group consisted of three reviews, who were master or PhD candidates PL, JWZ, YMT and XFL, MZ, and FQL.

We did not use any automation tool in this process. Data were double-checked across two groups who worked independently. Discrepancies were resolved by discussion or consultation with senior investigators FS and XZL , both were associate professors and specialists.

We conducted network meta-analyses using the frequentist method, where different doses of the same antidepressant were treated as a single treatment.

We calculated the surface under the cumulative ranking curve SUCRA to rank different treatments. This alternative analysis method was a modification of the original protocol which had been amended in PROSPERO.

In the Bayesian models, the number of the chain was three and the number of total interactions per chain was 50 Global inconsistency was evaluated using a generalized Q test, while local inconsistencies were detected using a node split approach [ 23 ].

Funnel plots were drawn to check for publication bias. The transitivity assumption was assessed by comparing the baseline characteristics of populations with different treatment comparisons, and box plots were used to display the similarity of the baseline characteristics.

Sensitivity analysis was carried out by excluding studies that were assessed to feature high risk of bias. Using a Bayesian approach, we implemented model-based network meta-analyses to explore the dose-effect relationship between dose and the risks for sleep-related adverse effects [ 24 ].

Only fixed-dose arms were included in the dose-effect modeling. We performed the statistical analyses with R 4. In all, 38 records were identified from the databases, and studies were retrieved from the reference lists of published reviews.

After screening the titles and abstracts, the full texts of studies were reviewed. Following this, studies were included in our systematic review, of which were included in the meta-analyses for somnolence and were included in the meta-analyses for insomnia Figure 1.

Other subtypes of sleep-related adverse effects were reported sparsely and could not be synthesized quantitively. In total, 64 participants were enrolled in the included studies, of whom Of the included studies, In addition, 85 Because we only included double-blinded RCTs, there was a low risk of deviation from the intended interventions in the majority of the studies.

Notably, 51 In all, studies were included to construct a network for comparing the associations between different antidepressants and somnolence Figure 3A. The prevalence of somnolence for placebo was approximately 4. The estimated prevalence of somnolence for every antidepressant was calculated based on the OR of relative effect and the prevalence for placebo, such as agomelatine 6.

The network of evidence for main outcomes: A Somnolence; B Insomnia. The size of the nodes represents the sample size of each treatment group, and the width of the lines connecting different nodes is proportional to the number of RCTs comparing every pair of treatments.

Forest plot displaying the result of network meta-analysis for main outcomes. A Somnolence; B Insomnia. The studies that compared different antidepressants with respect to insomnia outcomes were included in a network Figure 3B. The prevalence of insomnia for placebo was approximately 5.

The prevalence of insomnia for every antidepressant was calculated based on the OR of relative effect and the prevalence for placebo, such as agomelatine 5.

In the meta-regression, there was no significant interaction between baseline characteristics mean age, percentage of females, and baseline severity and antidepressants in terms of the risk for both main outcomes, except for gender, and baseline severity had an effect on toludesvenlafaxine Supplementary Tables S4—S9.

However, a significant global inconsistency was detected in the networks of both outcomes. The local inconsistency was explored using the node split approach Supplementary Table S No publication bias was detected from the funnel plot Supplementary Figures S3 and S4.

Baseline characteristics, including the percentage of females, mean age, and baseline severity, were similar across different designs Supplementary Figure S5. When studies with high risk of bias were excluded from the network, the results were consistent with the main analyses Supplementary Figures S6 and S7.

Information on other subtypes of sleep-related adverse effects was presented in Supplementary Table S Sleep disorders, abnormal dreams, and yawning were the most commonly reported secondary outcomes, although the rates were very low. The quality of evidence for results in network meta-analyses was rated as very low to moderate.

The results of GRADE assessment are displayed in Table 1 and Table 2. Dose-effect relationships of antidepressants between dose and sleep-related adverse events were presented in Figure 5.

As for fluoxetine, milnacipran, nefazodone, and sertraline, the risks of somnolence increased linearly along with the dose increasing within conventional therapeutic doses. When it comes to amitriptyline, desvenlafaxine, duloxetine, escitalopram, paroxetine, toludesvenlafaxine, trazodone, and venlafaxine the risks of somnolence gradually increased from low doses to moderate doses and then showed a decreasing trend through the high doses.

In regard to fluvoxamine and mirtazapine, the risks of somnolence were shown as an inverted U-shape, increasing steeply up to maximum effect and then decreasing. Dose-effect relationship of each drug between dose and sleep-related adverse events.

A somnolence; B insomnia; Y -axis represents the absolute risk for somnolence or insomnia of different doses of antidepressants. X -axis represents doses of antidepressants, 0 represents placebo.

Meanwhile, the risks of insomnia stayed flat from low doses to moderate doses and then increased through high doses of bupropion, citalopram, escitalopram, paroxetine, sertraline, and vortioxetine. With respect to desvenlafaxine, duloxetine, fluoxetine, venlafaxine, and vilazodone, the risks of insomnia increased gently and then presented a flat trend.

Regarding to maximum effects of insomnia, 11 antidepressants were estimated to have significantly higher risks of insomnia compared to placebo, which was consistent with the results of network meta-analysis.

The dose-effect models were fitted with the estimated effect size of the specific dose of antidepressants. The Odds Ratios of Somnolence and Insomnia of Antidepressants Compared to Placebo in Dose-Effect Models.

Our study investigated double-blinded RCTs including 64 depressed patients to identify the ORs of insomnia and somnolence induced by different antidepressants. We found that fluvoxamine, trazodone, mirtazapine, amitriptyline, duloxetine, escitalopram, paroxetine, nefazodone, sertraline, fluoxetine, venlafaxine, desvenlafaxine, milnacipran, and agomelatine had higher ORs for somnolence and bupropion had a lower OR than placebo.

For insomnia, reboxetine, vilazodone, desvenlafaxine, duloxetine, bupropion, venlafaxine, sertraline, citalopram, fluoxetine, paroxetine, and escitalopram had higher ORs and amitriptyline had a lower OR than placebo. But the risks of somnolence and insomnia were not always increased linearly along with the dose increase for 21 antidepressants.

With the exception of fluvoxamine, selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors had higher risks for somnolence and insomnia than placebo. This finding is consistent with previous studies [ 2 , 9 ] that reported that patients taking an SSRI or SNRI had similar likelihood of presenting with somnolence or insomnia.

If patients complained of lethargy after taking an SSRI or SNRI in the morning, it was appropriate to administer it closer to bedtime. However, for fluvoxamine which had significantly higher risks for hypersomnia but not for insomnia than placebo, patients would benefit more by taking it at night.

This might be related to the well-characterized ability of fluvoxamine to increase nocturnal serum levels of melatonin by 2- to 3-fold [ 26 ], with probable mechanism of inhibiting hepatic metabolism of melatonin by cytochrome P enzymes. Agomelatine, mirtazapine, and trazodone are usually used to improve insomnia in depressed patients by changing their polysomnographic sleep architecture [ 8 , 16 ].

Our results are consistent with the findings of previous studies. But these three antidepressants have different properties due to their different mechanisms. Agomelatine was given top acceptability in a previous network meta-analysis [ 3 ].

As a melatonin receptor agonist MT1 and MT2 , agomelatine can increase total sleep time, improve sleep efficiency [ 16 ], and restore circadian rhythm.

Compared to mirtazapine, agomelatine has a lower frequency of oversedation or tiredness within 90 days of treatment [ 27 ]. Mirtazapine is a noradrenaline and specific serotonergic antidepressant that shows antagonism against the alpha-2 autoreceptor and heteroreceptors and strong antagonism against the 5-HT2, 5-HT3, and H1 receptors.

In one study, mirtazapine was the most frequently associated with akathisia and restless leg syndrome, which can lead to difficulty falling asleep [ 28 ]. Mirtazapine might show optimal acceptability at 30 mg instead of 45 mg [ 29 ].

In a previous study, compared to the control group, somnolence, and dizziness occurred with greater frequency in the trazodone group [ 8 ], and a particularly complex action of antagonist on H1 histamine receptor, alpha 1, and alpha 2 adrenergic receptors of trazodone resulted in these unwanted side effects [ 30 ].

Whether trazodone should be first-line therapy for insomnia is still under discussion [ 31 ]. Vortioxetine, vilazodone, and levomilnacipran have been approved for the treatment of MDD in recent years.

Among all studies considered in our analysis, there were no significantly higher risk of vortioxetine for somnolence and insomnia comparing placebo [ 33 ].

Bupropion is a norepinephrine-dopamine disinhibitor. Insomnia is among the most commonly reported side effects associated with higher erythrohydrobupropion concentrations, and vivid dreams have also been reported [ 34 ].

Toludesvenlafaxine [ 19 ] is a new chemical compound that inhibits the reuptake of serotonin, norepinephrine, and dopamine, a triple reuptake inhibitor.

Antidepressant management of insomnia disorder in the absence of a mood disorder Pargol K. Nazarian, PharmD, BCPP ; Pargol K.

Nazarian, PharmD, BCPP. This Site. Google Scholar. Susie H. Park, PharmD, BCPP, FCSHP Susie H. Park, PharmD, BCPP, FCSHP. Mental Health Clinician 4 2 : 41— Get Permissions. Cite Icon Cite. toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest. insomnia , antidepressant , sleep disorder.

Table 1. Antidepressants used in the treatment of insomnia. View large. View Large. National Institutes of Health. National Institutes of Health State of the Science Conference statement on Manifestations and Management of Chronic Insomnia in Adults, June 13—15, Search ADS.

Drugs used to treat insomnia in regulatory-based rather than evidence-based medicine. Clinical guideline for the evaluation and management of chronic insomnia in adults. Trazodone product information.

Prevalence and factors associated with off-label antidepressant prescriptions for insomnia. Subjective hypnotic efficacy of trazodone and zolpidem in DSMIII-R primary insomnia.

DOI: Effects on sleep stages and microarchitecture of caffeine and its combination with zolpidem or trazodone in healthy volunteers. PubMed PMID: The effectiveness of treatment with trazodone in patients with primary insomnia without and with prior history of hypnotics use. Patients with insomnia and subthreshold depression show marked worsening of insomnia after discontinuation of sleep promoting medication.

Cognitive, psychomotor and polysomnographic effects of trazodone in primary insomniacs. PubMed PMID: ; PubMed Central PMCID: PMC What is the role of sedating antidepressants, antipsychotics, and anticonvulsants in the management of insomnia? Acute behavioral effects and abuse potential of trazodone, zolpidem and triazolam in humans.

A Review of the evidence for the efficacy and safety of trazodone in insomnia. Remeron mirtazapine product information. The effects of mirtazapine on sleep: a placebo controlled, double-blind study in young healthy volunteers. Acute effects of mirtazapine on sleep continuity and sleep architecture in depressed patients: a pilot study.

Comparative effects of mirtazapine and fluoxetine on sleep physiology measures in patients with major depression and insomnia. Real-world, open-label study to evaluate the effectiveness of mirtazapine on sleep quality in outpatients with major depressive disorder.

Mirtazapine effects on alertness and sleep in patients as recorded by interactive telecommunication during treatment with different dosing regimens.

Actual driving performance and psychomotor function in healthy subjects after acute and subchronic treatment with escitalopram, mirtazapine, and placebo.

Effects of nocturnal doses of mirtazapine and mianserin on sleep and on daytime psychomotor and driving performance in young, healthy volunteers.

Effects on sleep: a double-blind study comparing trimipramine to imipramine in depressed insomniac patients. Selective histamine H1 antagonism: novel hypnotic and pharmacologic actions challenge classical notions of antihistamines.

Comparison of effects of desipramine and amitriptyline on EEG sleep of depressed patients. Silenor doxepin product information.

Efficacy and safety of doxepin 1 mg, 3 mg, and 6 mg in adults with primary insomnia. Efficacy and safety of doxepin 3 and 6 mg in a day sleep laboratory trial in adults with chronic primary insomnia.

Efficacy and safety of doxepin 1 mg, 3 mg, and 6 mg in elderly patients with primary insomnia: a randomized, double-blind, placebo-controlled crossover study. Efficacy and safety of doxepin 1 mg and 3 mg in a week sleep laboratory and outpatient trial of elderly subjects with chronic primary insomnia.

Efficacy and safety of doxepin 6 mg in a four-week outpatient trial of elderly adults with chronic primary insomnia. Doxepin in the treatment of primary insomnia: a placebo-controlled, double-blind, polysomnographic study. EULAR evidence-based recommendations for the management of fibromyalgia syndrome.

Comparative efficacy and acceptability of amitriptyline, duloxetine and milnacipran in fibromyalgia syndrome: a systematic review with meta-analysis. lorazepam in the treatment of opiate-withdrawal insomnia: a randomized double-blind study.

Acta Psychiatr Scand. Trimipramine in primary insomnia: results of a polysomnographic double-blind controlled study. Paroxetine in the treatment of primary insomnia: preliminary clinical and electroencephalogram sleep data.

Accessed October 17, Food and Drug Administration. FDA proposes new warnings about suicidal thinking, behavior in young adults who take antidepressant medications. Accessed October 18, Send Email Recipient s will receive an email with a link to 'Antidepressant management of insomnia disorder in the absence of a mood disorder' and will not need an account to access the content.

Recipient Bupropion and restless legs syndrome: a randomized controlled trial. J Am Board Fam Med. Rottach KG, Schaner BM, Kirch MH, et al.

Restless legs syndrome as side effect of second generation antidepressants. J Psychiatri Res. Aiken CB. Pramipexole in psychiatry: a systematic review of the literature. J Clin Psychiatry. Hanzel DA, Proia NG, Hudgel DW. Response of obstructive sleep apnea to fluoxetine and protriptyline.

Kraiczi H, Hedner J, Dahlof P, et al. Effect of serotonin uptake inhibition on breathing during sleep and daytime symptoms in obstructive sleep apnea.

Marshall NS, Yee BJ, Desai AV, et al. Two randomized placebo-controlled trials to evaluate the efficacy and tolerability of mirtazapine for the treatment of obstructive sleep apnea.

Williams SG, Collen J, Orr N, et al. Sleep disorders in combat-related PTSD. Sleep Breath. Issa FG. Effect of clonidine in obstructive sleep apnea. Am Rev Respir Dis. Alao A, Selvarajah J, Razi S.

The use of clonidine in the treatment of nightmares among patients with co-morbid PTSD and traumatic brain injury. Int J Psychiatry Med. Positive Data on Oral Orexin Receptor 2 Agonist for Patients with Narcolepsy Type 1.

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