The DOI matches its Crossref record; 50 of the 50 references it cites were found in a registry or an index; 14 of the 83 sources its claims cite were checked for support.
Effects of Antidepressants on Sleep
Open accessAbstract
PURPOSE OF REVIEW: The aim of this review article was to summarize recent publications on effects of antidepressants on sleep and to show that these effects not only depend on the kind of antidepressant drugs but are also related to the dose, the time of drug administration, and the duration of the treatment. RECENT FINDINGS: Complaints of disrupted sleep are very common in patients suffering from depression, and they are listed among diagnostic criteria for this disorder. Moreover, midnocturnal insomnia is the most frequent residual symptom of depression. Thus, all antidepressants should normalize sleep. However, at least in short-term treatment, many antidepressants with so-called activating effects (e.g. fluoxetine, venlafaxine) may disrupt sleep, while others with sedative properties (e.g., doxepin, mirtazapine, trazodone) rapidly improve sleep, but may cause problems in long-term treatment due to oversedation.For sleep-promoting action, the best effects can frequently be achieved with a very low dose, administered early enough before bedtime and importantly, always as a part of more complex interventions based on the cognitive-behavioral protocol to treat insomnia (CBT-I). For successful treatment of depression, it is necessary to understand the effects of antidepressants on sleep. Each physician should also be aware that some antidepressants may worsen or induce primary sleep disorders like restless legs syndrome, sleep bruxism, REM sleep behavior disorder, nightmares, and sleep apnea, which may result from an antidepressant-induced weight gain.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
This narrative review summarizes how antidepressants affect sleep, emphasizing that effects depend on drug class, dose, timing of administration, and treatment duration. Activating antidepressants may disrupt sleep short-term, sedating antidepressants can promote sleep but risk oversedation, and low-dose sedative antidepressants plus CBT-I may help insomnia.
Key findings
- Sleep disturbance is common in depression: insomnia complaints are present in 60–90% of patients with major depression; in bipolar depressive episodes, 60% have insomnia and 20–30% have hypersomnia. In STAR*D, midnocturnal insomnia remained the most common residual symptom, present in 79% of patients who responded but did not remit after up to 12 weeks of citalopram.
- Antidepressant classes differ in acute sleep effects: SSRI, SNRI, NRI, MAOI, and activating TCA tend to increase REM latency, suppress REM sleep, and may impair sleep continuity; sedating antidepressants such as mirtazapine, trazodone, and sedating TCA decrease sleep latency, improve sleep efficiency, increase slow wave sleep, and usually have little or no effect on REM sleep.
- From FDA study-register data, average treatment-emergent insomnia with SSRI was 17% vs 9% placebo, and somnolence was 16% vs 8% placebo; with SNRI, insomnia was 13% vs 7% and somnolence 10% vs 5%. With sedating antidepressants, treatment-emergent insomnia was below 2%, but somnolence was 54% for mirtazapine vs 18% placebo and 46% for trazodone vs 19% placebo.
- For insomnia treatment, only doxepin is FDA-approved among antidepressants for sleep maintenance insomnia; suggested low doses are doxepin 3–6 mg or trazodone 25–50 mg, taken at least 2 hours before sleep and combined with CBT-I. Agomelatine improved sleep latency after 2 and 24 weeks compared with escitalopram, and vortioxetine at 20 and 40 mg suppressed REM sleep similarly to paroxetine 20 mg in healthy male volunteers.
Methods
- Narrative review summarizing recent literature on antidepressant effects on sleep, intended as an addition to prior reviews and including the authors’ personal view on antidepressant use for insomnia.
- Evidence synthesized includes polysomnographic studies, FDA study-register data, clinical trials, meta-analyses, and treatment guidelines; the article states it contains no studies with human or animal subjects performed by the authors.
- Main analysis is qualitative, organized by drug class and sleep parameters such as sleep continuity, slow wave sleep, REM latency, and REM sleep, with summary tables.
Limitations
- The paper does not state a formal limitations section; it reports that no human or animal studies were performed by the authors and discloses that Adam Wichniak received speaker honoraria and congress travel grants from Angelini, Janssen-Cilag, Lundbeck, Sanofi, and Servier.
- Evident from the text: this is a narrative review without a described systematic search strategy, risk-of-bias assessment, or meta-analytic pooling.
- Evident from the text: several recommendations and observations rely on the authors’ clinical experience, published case reports, or personal opinion rather than randomized trial evidence, such as the low risk of phase shift with low-dose sedative antidepressants and morning low-dose citalopram for insomnia.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
14 of 83 cited sources checked · 6 supported · 0 flagged · accuracy not yet measured
- Premisecitation
Midnocturnal insomnia is the most frequent residual symptom of depression.
“midnocturnal insomnia is the most frequent residual symptom of depression.”
- Also stated in: § Polysomnographic Sleep Studies in Depression · p. 2 · plain
“found that midnocturnal insomnia was the most commonly observed residual symptom of depression, as it was still present in 79% patients [13].”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [13] McClintock SM, Husain MM, Wisniewski SR, Nierenberg AA, Stewart JW, Trivedi MH, et al. Residual symptoms in depressed outpatients who respond by 50% but do not remit to antidepressant medication. J Clin Psychopharmacol. 2011;31:180–6. source
The Abstract (page not supplied) identifies midnocturnal insomnia as the most common individual residual symptom, at 79.0%. But the study concerns outpatients who responded to citalopram without remitting; it does not establish that this is the most frequent residual symptom of depression generally. (LLM, conf=0.85)
Experimental — accuracy not yet measured
- Also stated in: § Polysomnographic Sleep Studies in Depression · p. 2 · plain
- Premisecitation
In the STAR*D study, midnocturnal insomnia was still present in 79% of patients who responded without remitting after up to 12 weeks of citalopram.
“The Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study, which included a large sample of outpatients with non-psychotic MDD who responded without remitting after up to 12 weeks treatment with citalopram, found that midnocturnal insomnia was the most commonly observed residual symptom of depression, as it was still present in 79% patients [13].”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [13] McClintock SM, Husain MM, Wisniewski SR, Nierenberg AA, Stewart JW, Trivedi MH, et al. Residual symptoms in depressed outpatients who respond by 50% but do not remit to antidepressant medication. J Clin Psychopharmacol. 2011;31:180–6. source
- Premisecitation
Insomnia complaints are present in 60-90% of patients with major depression, depending on episode severity.
“The complaints of insomnia are present in 60 -90%ofpatients with major depression, depending on the episode ' s severity.”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites [11] Abad VC, Guilleminault C. Sleep and psychiatry. Dialogues Clin Neurosci. 2005;7:291–303. source
The Mood (affective) disorders section says approximately two-thirds of depressed patients complain of insomnia, supporting the general prevalence claim. It does not give a 60–90% range or link complaint rates to episode severity. The 90% figure in the Major depressive disorder section refers instead to polysomnographic abnormalities in inpatients. (LLM, conf=0.87)
Experimental — accuracy not yet measured - cites [12] Kaplan KA, Harvey AG. Hypersomnia across mood disorders: a review and synthesis. Sleep Med Rev. 2009;13:275–85. source
- Premisecitation
In bipolar disorder, insomnia is present during a depressive episode in 60% of patients.
“When it comes to bipolar disorder, insomnia is present during a depressive episode in 60% of patients”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites [11] Abad VC, Guilleminault C. Sleep and psychiatry. Dialogues Clin Neurosci. 2005;7:291–303. source
The Mood (affective) disorders section says approximately two-thirds of depressed patients complain of insomnia. The Bipolar disorder subsection says sleep-study findings in bipolar depression resemble those in major depressive disorder, but it gives no insomnia prevalence for bipolar depressive episodes; the claimed 60% is not established. (LLM, conf=0.84)
Experimental — accuracy not yet measured - cites [12] Kaplan KA, Harvey AG. Hypersomnia across mood disorders: a review and synthesis. Sleep Med Rev. 2009;13:275–85. source
- Premisecitation
The negative effects of vortioxetine on sleep continuity are significant only for the higher dose.
“These negative effects of vortioxetine on sleep continuity are significant only for the higher dose [28 · ].”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [28] • Wilson S, Hojer AM, Buchberg J, Areberg J, Nutt DJ. Differentiated effects of the multimodal antidepressant vortioxetine on sleep architecture: part 1, a pharmacokinetic/pharmacodynamic comparison with paroxetine in healthy men. J Psychopharmacol. 2015;29:1085–91. This is the first polysomnographic study presenting effects of vortioxetine on sleep architecture in comparison to placebo and paroxetine. source
The Results (Sleep architecture, Table 1; page not specified in our copy) show that reduced total sleep time and increased wake after sleep onset were significant only at the higher, 40 mg dose. But increased stage 1 sleep—a sleep-continuity effect discussed by the authors—was significant at both 20 mg and 40 mg, so the claim is too broad. (LLM, conf=0.90)
Experimental — accuracy not yet measured
- Premisecitation
In a study of 24 healthy male volunteers, vortioxetine at doses of 20 and 40 mg and paroxetine at 20 mg suppress REM sleep by increasing REM sleep latency and diminishing duration of REM sleep.
“In a study which has compared the effects of vortioxetine and paroxetine to the placebo in a group of 24 healthy male volunteers, it has been shown that the vortioxetine dose of 20 and 40 mg similarly to the paroxetine dose of 20 mg suppresses REM sleep by increasing REM sleep latency and diminishing duration of REM sleep.”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [28] • Wilson S, Hojer AM, Buchberg J, Areberg J, Nutt DJ. Differentiated effects of the multimodal antidepressant vortioxetine on sleep architecture: part 1, a pharmacokinetic/pharmacodynamic comparison with paroxetine in healthy men. J Psychopharmacol. 2015;29:1085–91. This is the first polysomnographic study presenting effects of vortioxetine on sleep architecture in comparison to placebo and paroxetine. source
- Premisecitation
Treatment-emergent restless legs syndrome has also been described for SSRI and venlafaxine.
“Treatment-emergent RLS has also been described for SSRI and venlafaxine [30].”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [30] Narowska D, Bozek M, Krysiak K, Antczak J, Holka-Pokorska J, Jernajczyk W, et al. Frequent difficulties in the treatment of restless legs syndrome—case report and literature review. Psychiatr Pol. 2015;49:921–30. source
The available case-description passage says that some antidepressants, specifically mirtazapine, mianserin, and tricyclic antidepressants, can increase the severity of existing RLS. Searches for SSRIs, venlafaxine, and treatment-emergent RLS found no passage in our copy addressing the claimed drugs or new-onset RLS. The indexed passages have no section or page labels. (LLM, conf=0.72)
Experimental — accuracy not yet measured
- Premisecitation
Persistent insomnia symptoms may result in unfavorable clinical outcome, e.g., increased suicide risk.
“Persistent insomnia symptoms may also result in unfavorable clinical outcome, e.g., increased suicide risk [14].”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [14] Kay DB, Dombrovski AY, Buysse DJ, Reynolds CF, Begley A, Szanto K. Insomnia is associated with suicide attempt in middle-aged and older adults with depression. Int Psychogeriatr. 2016;28:613–9. source
The Discussion reports an association between insomnia severity and suicide attempts in middle-aged and older adults with depression. However, it says chronicity was not assessed and the cross-sectional study cannot establish whether insomnia precedes or causes suicidal behavior. The source therefore supports increased risk as a possibility, but not the claim specifically about persistent symptoms resulting in that outcome. (LLM, conf=0.88)
Experimental — accuracy not yet measured
- Premisecitation
In bipolar disorder, 20-30% of patients suffer from prolonged sleep (hypersomnia) and increased daytime sleepiness.
“while 20 -30% suffer from prolonged sleep (hypersomnia) and increased daytime sleepiness [11, 12].”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites [11] Abad VC, Guilleminault C. Sleep and psychiatry. Dialogues Clin Neurosci. 2005;7:291–303. source
The Bipolar disorder section describes reduced need for sleep during mania and sleep findings in bipolar depression, but gives no prevalence of hypersomnia or daytime sleepiness. A separate Mood (affective) disorders passage says 15% of depressed patients report hypersomnia; it does not establish the claimed 20–30% figure for bipolar disorder. Searches for that figure and for prolonged sleep with daytime sleepiness found no supporting passage in our copy. (LLM, conf=0.75)
Experimental — accuracy not yet measured - cites [12] Kaplan KA, Harvey AG. Hypersomnia across mood disorders: a review and synthesis. Sleep Med Rev. 2009;13:275–85. source
- Premisenone given
In many patients, difficulties with sleep persist.
“However in many patients, difficulties with sleep persist.”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [13] McClintock SM, Husain MM, Wisniewski SR, Nierenberg AA, Stewart JW, Trivedi MH, et al. Residual symptoms in depressed outpatients who respond by 50% but do not remit to antidepressant medication. J Clin Psychopharmacol. 2011;31:180–6. source
- Interpretationcitation
Based on clinical experience and review of published case reports, the use of sedative antidepressants in a low dose is not related to increased risk of phase shift in bipolar disorder.
“Based on our clinical experience and review of published case reports, we believe that the use of sedative antidepressants in a low dose is not related to the increased risk of phase shift in bipolar disorder [45].”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [45] Wichniak A, Jarkiewicz M, Okruszek L, Wierzbicka A, Holka-Pokorska J, Rybakowski JK. Low risk for switch to mania during treatment with sleep promoting antidepressants. Pharmacopsychiatry. 2015;48:83–8. source
- Findingcitation
Low doses (5-10 mg) of citalopram administered in the morning can be an alternative to sedative antidepressants for treatment of insomnia with good treatment effects.
“Moreover, we have observed that for the treatment of insomnia low doses (5 -10 mg) of citalopram administered in the morning can be an alternative to sedative antidepressants with good treatment effects [46].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [46] Jernajczyk W, Sobańska A, Wierzbicka A, Wichniak A, Szatkowska E. The therapy of primary insomnia with citalopram. J Sleep Res. 2006;15(Suppl. 1):154.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
Disturbed sleep is a core symptom of depression.
“Complaints of disrupted sleep are very common in patients suffering from depression, and they are listed among diagnostic criteria for this disorder.”
- Also stated in: § Polysomnographic Sleep Studies in Depression · p. 2 · boosted
“The recent meta-analysis summarizing the current evidence from studies using PSG about sleep architecture in mental disorders has confirmed that disturbed sleep is a core symptom of depression.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [10 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Also stated in: § Polysomnographic Sleep Studies in Depression · p. 2 · boosted
- Premisecitation
Many antidepressants with activating effects (e.g., fluoxetine, venlafaxine) may disrupt sleep at least in short-term treatment.
“at least in short-term treatment, many antidepressants with so-called activating effects (e.g. fluoxetine, venlafaxine) may disrupt sleep”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [3, 6, 7, 17 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisenone given
Antidepressants with sedative properties (e.g., doxepin, mirtazapine, trazodone) rapidly improve sleep.
“others with sedative properties (e.g., doxepin, mirtazapine, trazodone) rapidly improve sleep”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [3, 6, 7, 17 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
There is a risk that a patient with depression and insomnia will not be able to stop combination treatment with benzodiazepines and SSRI/SNRI after 14-28 days and will develop dependence.
“However, there is a related risk that the patient suffering from depression and insomnia will not be able to stop such treatment after 14 -28 days of therapy and will develop a dependence [21, 22].”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [21] Jindal RD, Friedman ES, Berman SR, Fasiczka AL, Howland RH, Thase ME. Effects of sertraline on sleep architecture in patients with depression. J Clin Psychopharmacol. 2003;23:540–8. source
- cites [22] Furukawa TA, Streiner DL, Young LT. Antidepressant and benzodiazepine for major depression. Cochrane Database Syst Rev. 2002; CD001026. source
- Premisereasoning
Antidepressants with antihistaminergic action (sedating TCA, mirtazapine, mianserine) or strong antagonistic action at serotonergic 5-HT2 receptors (trazodone, nefazodone) quickly improve sleep.
“On the contrary, antidepressants with antihistaminergic action, like sedating TCA, mirtazapine, mianserine, or strong antagonistic action at serotonergic 5-HT2 receptors, like trazodone and nefazodone quickly improve sleep.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Table 2
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
Trazodone is very often used as a sleep-promoting drug.
“This is especially true for trazodone that is very often used as a sleep-promoting drug [3, 39 -42].”
Quote in the paperNot a substantial claim0 of 5 sources checked- cites [3] Wichniak A, Wierzbicka A, Jernajczyk W. Sleep and antidepressant treatment. Curr Pharm Des. 2012;18:5802–17. source
- cites [39] Riemann D, Spiegelhalder K, Feige B, Voderholzer U, Berger M, Perlis M, et al. The hyperarousal model of insomnia: a review of the concept and its evidence. Sleep Med Rev. 2010;14:19–31. source
- cites [40] Mendelson WB, Roth T, Cassella J, Roehrs T, Walsh JK, Woods JH, et al. The treatment of chronic insomnia: drug indications, chronic use and abuse liability. Summary of a 2001 new clinical drug evaluation unit meeting symposium. Sleep Med Rev. 2004;8:7–17. source
- cites [41] Wiegand MH. Antidepressants for the treatment of insomnia : a suitable approach? Drugs. 2008;68:2411–7. source
- cites [42] Wilson SJ, Nutt DJ, Alford C, Argyropoulos SV, Baldwin DS, Bateson A, et al. British Association for Psychopharmacology consensus statement on evidence-based treatment of insomnia, parasomnias and circadian rhythm disorders. J Psychopharmacol. 2010;24:1577–601. source
- Premisecitation
Depression is associated with alterations in most sleep variables compared to healthy controls.
“It was found that affective disorders and major depression were associated with alterations in most variables compared to healthy controls [10 ·· ].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [10 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
In clinical trials with SNRI, treatment-emergent insomnia was reported on average in 13% of SNRI-treated patients vs 7% placebo.
“In clinical trials with SNRI, treatment-emergent insomnia was reported on average in 13% out of SNRI-treated patients as compared to 7% out of the placebo arm”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [17 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
Treatment-emergent somnolence in SNRI trials was 10% vs 5% placebo.
“and treatment-emergent somnolence in 10% of SNRI-treated patients in comparison to 5% out of patients receiving placebo.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [17 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationcitation
REM sleep without atonia may induce or worsen REM Sleep Behavior Disorder.
“SSRI, SNRI, and TCA are known to induce or exacerbate sleep bruxism and disturb regulation of muscle tone during REM sleep, causing REM sleep without atonia, which may induce or worsen REM Sleep Behavior Disorder [3, 6].”
Quote in the paperSubstantial claim0 of 2 sources checked - Premisecitation
In many insomnia patients, physiological parameters such as hormone secretion, whole body metabolic rate, and brain metabolic rate are altered similarly to depressed patients, a state called hyperarousal.
“Moreover, in many insomnia patients, physiological parameters, e.g., hormone secretion, whole body, and brain metabolic rate, are altered in a similar fashion to the depressed ones what is called a hyperarousal [38, 39], supporting the use of sedative antidepressants to treat such patients.”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [38] Bonnet MH, Arand DL. Hyperarousal and insomnia: state of the science. Sleep Med Rev. 2010;14:9–15. source
- cites [39] Riemann D, Spiegelhalder K, Feige B, Voderholzer U, Berger M, Perlis M, et al. The hyperarousal model of insomnia: a review of the concept and its evidence. Sleep Med Rev. 2010;14:19–31. source
- Premisecitation
Agomelatine leads to improvement of daytime alertness.
“Moreover, treatment with agomelatine is not related to the suppression of REM sleep: it restores cyclical sleep profile, may increase the amount of SWS, and most importantly leads to the improvement of daytime alertness [26].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [26] Quera-Salva MA, Lemoine P, Guilleminault C. Impact of the novel antidepressant agomelatine on disturbed sleep-wake cycles in depressed patients. Hum Psychopharmacol. 2010;25:222–9. source
- Interpretationreasoning
In most patients, sleep disturbances diminish with improvement of depressive symptoms.
“Fortunately, in most patients, sleep disturbances diminish with the improvement of depressive symptoms”
Quote in the paperNot a substantial claim - Premisecitation
According to the FDA clinical trial register, the rate of treatment-emergent insomnia complaints or somnolence during vortioxetine therapy is lower than with SSRI and SNRI drugs.
“According to the FDA clinical trial register, the rate of treatment-emergent insomnia complaints or somnolence during the therapy with vortioxetine is lower when compared to SSRI and SNRI drugs [17 ·· ].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [17] •• Doghramji K, Jangro WC. Adverse effects of psychotropic medications on sleep. Psychiatr Clin North Am. 2016;39:487–502. This study presents effects of psychotropic medications such as antidepressants, antipsychotics, stimulants, and benzodiazepines on sleep based on analysis of data from US Food and Drug Administration (FDA) study register. It shows that that medication has significant impact on sleep, resulting in both beneficial and adverse effects on sleep. source
- Premisecitation
Some patients show improvement of sleep quality already after the first drug dose.
“Some patients show improvement of sleep quality already after the first drug dose [15]”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [15] Schmid DA, Wichniak A, Uhr M, Ising M, Brunner H, Held K, et al. Changes of sleep architecture, spectral composition of sleep EEG, the nocturnal secretion of cortisol, ACTH, GH, prolactin, melatonin, ghrelin, and leptin, and the DEX-CRH test in depressed patients during treatment with mirtazapine. Neuropsychopharmacology. 2006;31:832–44. source
- Premisecitation
Average rate of treatment-emergent somnolence in SSRI-treated patients was 16% vs 8% placebo.
“The average rate of treatment emergent somnolence in patients being treated with SSRI amounted to 16%ascompared to 8% out of patients receiving placebo.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [16] Thompson C. Onset of action of antidepressants: results of different analyses. Hum Psychopharmacol. 2002;17(Suppl 1):S27–32. source
- Premisecitation
Vortioxetine's clinical action is mediated mainly by selective blockade of serotonin reuptake and direct modulation of serotonergic receptor activity, including 5-HT3, 5-HT7, 5-HT1D, and 5-HT1B.
“Effects on sleep has recently been also reported for a vortioxetine, with clinical action mediated mainly by selective blockade of serotonin reuptake and direct modulation of serotonergic receptors activity (such as 5-HT3, 5-HT7, 5-HT1D, and 5-HT1B) [27].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [27] Sowa-Kucma M, Panczyszyn-Trzewik P, Misztak P, Jaeschke RR, Sendek K, Styczen K, et al. Vortioxetine: a review of the pharmacology and clinical profile of the novel antidepressant. Pharmacol Rep. 2017;69:595–601. source
- Premisecitation
None of the sleep parameters is specific to depression.
“Although none of the sleep parameters was specific to depression”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [10 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
Treatment with a sedative antidepressant significantly reduces the need to use benzodiazepines in patients with MDD.
“It was recently shown that such treatment significantly reduces the need to use benzodiazepines in patients with MDD [20 · ].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [20 · ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
Based on FDA study register, average prevalence of treatment-emergent insomnia in clinical trials with SSRI was 17% vs 9% placebo.
“Based on data from the US Food and Drug Administration (FDA) study register [16], the average prevalence of treatment-emergent insomnia in clinical trials with SSRI was 17% as compared to 9% out of patients randomized to the placebo arm.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [16] Thompson C. Onset of action of antidepressants: results of different analyses. Hum Psychopharmacol. 2002;17(Suppl 1):S27–32. source
- Premisecitation
In clinical studies with sedating antidepressants (mirtazapine and trazodone), reported prevalence of treatment-emergent insomnia complaints in MDD was very low (below 2%).
“On the contrary to the treatment with SSRI and SNRI, in clinical studies with sedating antidepressants, e.g., mirtazapine and trazodone, the reported prevalence of treatment-emergent insomnia complaints in patients with major depressive disorder (MDD) was very low (below 2%).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [17 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
Antidepressants can induce nightmares.
“Moreover, although antidepressants are recommended for the treatment of post-traumatic sleep disorder, they can induce nightmares.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [31] Buschkamp JA, Frohn C, Juckel G. Mirtazapine induces nightmares in depressed patients. Pharmacopsychiatry. 2017. source
- Premisecitation
Both treatment-emergent insomnia and somnolence were most frequent (both 24%) in patients with generalized anxiety disorder treated with venlafaxine.
“Both treatment-emergent insomnia and somnolence were the most frequent (both equal to 24%) in patients with generalized anxiety disorders treated with venlafaxine.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [17 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationreasoning
Due to the lack of methodologically sound randomized clinical trials in insomnia, only doxepin is approved by the FDA for the treatment of sleep maintenance insomnia.
“However, due to the lack of methodologically sound randomized clinical trials in insomnia, only one of them, doxepin, is approved by FDA for the treatment of sleep maintenance insomnia.”
Quote in the paperSubstantial claim - Premisecitation
Mirtazapine most frequently induces nightmares.
“We observe this side effect most frequently during the treatment with mirtazapine, just as it was recently reported [31].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [31] Buschkamp JA, Frohn C, Juckel G. Mirtazapine induces nightmares in depressed patients. Pharmacopsychiatry. 2017. source
- Premisecitation
Subjective complaints of insomnia or daytime somnolence are frequent in patients with depression or anxiety disorders treated with SSRI and SNRI.
“In a recent review article on the prevalence of treatment emergent insomnia and somnolence in depressed patients, it was shown that subjective complaints of insomnia or daytime somnolence were frequent in patients suffering from depression or anxiety disorders treated with SSRI and SNRI [16].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [16] Thompson C. Onset of action of antidepressants: results of different analyses. Hum Psychopharmacol. 2002;17(Suppl 1):S27–32. source
- Premisecitation
In the second week, escitalopram worsens sleep continuity.
“In the second week, agomelatine slightly improves sleep continuity (increased total sleep time and sleep efficiency) and escitalopram worsens it [25].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [25] Quera-Salva MA, Hajak G, Philip P, Montplaisir J, Keufer-Le GS, Laredo J, et al. Comparison of agomelatine and escitalopram on nighttime sleep and daytime condition and efficacy in major depressive disorder patients. Int Clin Psychopharmacol. 2011;26:252–62. source
- Premisecitation
Agomelatine and escitalopram differ significantly in their effect on sleep continuity.
“Moreover, both drugs differ significantly in their effect on sleep continuity.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [25] Quera-Salva MA, Hajak G, Philip P, Montplaisir J, Keufer-Le GS, Laredo J, et al. Comparison of agomelatine and escitalopram on nighttime sleep and daytime condition and efficacy in major depressive disorder patients. Int Clin Psychopharmacol. 2011;26:252–62. source
- Premisecitation
For mirtazapine, improvement of sleep quality after first dose is related to faster onset of antidepressant action.
“which was specially discussed for mirtazapine as related to the faster onset of antidepressant action [16].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [16] Thompson C. Onset of action of antidepressants: results of different analyses. Hum Psychopharmacol. 2002;17(Suppl 1):S27–32. source
- Premisenone given
Antidepressant drugs substantially differ in their acute effects on sleep.
“Antidepressant drugs substantially differ in their acute effects on sleep.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [3, 6, 7, 17 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
Agomelatine restores cyclical sleep profile.
“Moreover, treatment with agomelatine is not related to the suppression of REM sleep: it restores cyclical sleep profile, may increase the amount of SWS, and most importantly leads to the improvement of daytime alertness [26].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [26] Quera-Salva MA, Lemoine P, Guilleminault C. Impact of the novel antidepressant agomelatine on disturbed sleep-wake cycles in depressed patients. Hum Psychopharmacol. 2010;25:222–9. source
- Premisecitation
Lowest rate of treatment-emergent insomnia and somnolence (both below 2%) was reported for levomilnacipran.
“The lowest rate of treatment emergent insomnia and somnolence (both below 2%) was reported for levomilnacipran.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [17 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
Rate of treatment-emergent somnolence was 46% for trazodone vs 19% placebo.
“and 46% in patients being treated with trazodone as compared to 19% out of patients receiving placebo.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [17 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationnone given
Disruption of sleep by antidepressants is related to poor treatment compliance.
“which is related to poor treatment compliance.”
Quote in the paperSubstantial claim - Premisecitation
SSRI, SNRI, and TCA disturb regulation of muscle tone during REM sleep, causing REM sleep without atonia.
“SSRI, SNRI, and TCA are known to induce or exacerbate sleep bruxism and disturb regulation of muscle tone during REM sleep, causing REM sleep without atonia, which may induce or worsen REM Sleep Behavior Disorder [3, 6].”
Quote in the paperSubstantial claim0 of 2 sources checked - Premisecitation
SSRI, SNRI, and TCA are known to induce or exacerbate sleep bruxism.
“SSRI, SNRI, and TCA are known to induce or exacerbate sleep bruxism and disturb regulation of muscle tone during REM sleep, causing REM sleep without atonia, which may induce or worsen REM Sleep Behavior Disorder [3, 6].”
Quote in the paperNot a substantial claim0 of 2 sources checked - Interpretationcitation
The use of antidepressants, including those with sedative properties, may impair sleep by inducing sleep disorders or worsening already existing ones.
“The use of antidepressants, also those with sedative properties, may impair sleep due to the induction of sleep disorders or worsening already existing ones.”
Quote in the paperSubstantial claim - Premisereasoning
The most prominent sleep-deteriorating antidepressants are SNRI, NRI, MAOI, SSRI, and activating TCA.
“Among them, most prominent are serotonin and norepinephrine reuptake inhibitors (SNRI), norepinephrine reuptake inhibitors (NRI), monoamine oxidase inhibitors (MAOI), selective serotonin reuptake inhibitors (SSRI), and activating tricyclic antidepressants (TCA).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Table 2
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
Treatment with agomelatine is not related to suppression of REM sleep.
“Moreover, treatment with agomelatine is not related to the suppression of REM sleep: it restores cyclical sleep profile, may increase the amount of SWS, and most importantly leads to the improvement of daytime alertness [26].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [26] Quera-Salva MA, Lemoine P, Guilleminault C. Impact of the novel antidepressant agomelatine on disturbed sleep-wake cycles in depressed patients. Hum Psychopharmacol. 2010;25:222–9. source
- Premisecitation
Mianserin and mirtazapine may induce restless legs syndrome in as many as 28% of patients.
“Mianserin and mirtazapine may induce restless legs syndrome in as many as 28% of patients [29].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [29] Rottach KG, Schaner BM, Kirch MH, Zivotofsky AZ, Teufel LM, Gallwitz T, et al. Restless legs syndrome as side effect of second generation antidepressants. J Psychiatr Res. 2008;43:70–5. source
- Premisecitation
Compared with escitalopram, agomelatine improves sleep latency after short (2 weeks) and long (24 weeks) treatment.
“In comparison to escitalopram, agomelatine is knowntoimprove sleep latency after both short (after 2 weeks) and long (after 24 weeks) treatment.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [25] Quera-Salva MA, Hajak G, Philip P, Montplaisir J, Keufer-Le GS, Laredo J, et al. Comparison of agomelatine and escitalopram on nighttime sleep and daytime condition and efficacy in major depressive disorder patients. Int Clin Psychopharmacol. 2011;26:252–62. source
- Premisecitation
Both sleep-disrupting and sleep-promoting effects of antidepressants are strongest only in the first few weeks of treatment.
“Although both the sleep-disrupting and sleep-promoting effects of the antidepressants are the strongest only in the first few weeks of treatment”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [18] Fava M. Daytime sleepiness and insomnia as correlates of depression. J Clin Psychiatry. 2004;65(Suppl 16):27–32.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationreasoning
Reduction of sedative antidepressant dose may substantially diminish the efficacy of maintenance treatment.
“It may substantially diminish the efficacy of the maintenance treatment.”
Quote in the paperSubstantial claim- Rests on an assumption: The sedating effect of sedative antidepressants becomes an increasing problem in long-term maintenance treatment, frequently requiring dose reduction.
- Premisecitation
Some classes of antidepressant drugs may deteriorate sleep quality mainly due to activation of serotonergic 5-HT2 receptors and increased noradrenergic and dopaminergic neurotransmission.
“It is well known that some classes of antidepressant drugs may deteriorate sleep quality mainly due to activation of serotonergic 5-HT2 receptors and increased noradrenergic and dopaminergic neurotransmission (Table 2).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Table 2
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
Rate of treatment-emergent somnolence was 54% for mirtazapine vs 18% placebo.
“the rate of treatment-emergent somnolence was very high, 54% in patients being treated with mirtazapine as compared to 18% out of patients in the placebo arm”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [17 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
Agomelatine may increase the amount of slow-wave sleep.
“Moreover, treatment with agomelatine is not related to the suppression of REM sleep: it restores cyclical sleep profile, may increase the amount of SWS, and most importantly leads to the improvement of daytime alertness [26].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [26] Quera-Salva MA, Lemoine P, Guilleminault C. Impact of the novel antidepressant agomelatine on disturbed sleep-wake cycles in depressed patients. Hum Psychopharmacol. 2010;25:222–9. source
- Premisecitation
There is evidence for efficacy of sedative antidepressants to promote sleep, for example for TCA in a recent meta-analytic study.
“Indeed, although there is evidence for efficacy of sedative antidepressants to promote sleep, for example for TCA in a form of a recent meta-analytic study [43 · ], it is important to remember that these drugs should be used in insomnia patients only in a very low dose, e.g., for doxepin as low as 3 to 6 mg or 25 -50 mg for trazodone.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [43] • Liu Y, Xu X, Dong M, Jia S, Wei Y. Treatment of insomnia with tricyclic antidepressants: a meta-analysis of polysomnographic randomized controlled trials. Sleep Med. 2017;34:126–33. This meta-analysis summarizes the evidence on effects of tricyclic antidepressants on sleep in insomnia patients. TCAs has been found as an effective pharmacological treatment for insomnia, but may cause dangerous side effects. source
- Interpretationnone given
In the long term, all antidepressants that show clinical efficacy improve sleep secondary to improvement of mood and daytime activity.
“In the long term, all antidepressants which show clinical efficacy improve sleep secondary to improvement of mood and daytime activity.”
Quote in the paperNot a substantial claim - Interpretationreasoning
Sleep-promoting action may be problematic during maintenance treatment after recovery from depression due to oversedation.
“Although sleep-promoting action is desired in depressed patients with coexisting anxiety or insomnia, it may be problematic during the maintenance treatment after recovery from depression due to oversedation.”
Quote in the paperSubstantial claim
- It may state two separate claims as one. 19
- Probably not a substantial claim. 5
It may state two separate claims as one.
PremisecitationBoth vortioxetine and paroxetine decrease total sleep time and increase duration of sleep stage N1.
“Both drugs also decrease total sleep time and increase duration of sleep stage N1.”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [28] • Wilson S, Hojer AM, Buchberg J, Areberg J, Nutt DJ. Differentiated effects of the multimodal antidepressant vortioxetine on sleep architecture: part 1, a pharmacokinetic/pharmacodynamic comparison with paroxetine in healthy men. J Psychopharmacol. 2015;29:1085–91. This is the first polysomnographic study presenting effects of vortioxetine on sleep architecture in comparison to placebo and paroxetine. source
Probably not a substantial claim.
PremisecitationRecent recommendations discourage the use of drugs from the sedative antidepressant class other than doxepin for insomnia treatment.
“Furthermore, recent recommendations discourage the use of other drugs from this class than doxepin for the insomnia treatment [37 ·· ].”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [37] •• Sateia MJ, Buysse DJ, Krystal AD, Neubauer DN, Heald JL. Clinical practice guideline for the pharmacologic treatment of chronic insomnia in adults: an American Academy of sleep medicine clinical practice guideline. J Clin Sleep Med. 2017;13:307–49. This publication contains recent recommendations for clinicians in choosing a specific pharmacological agent for treatment of chronic insomnia in adults. source
The Clinical Practice Recommendations suggest using low-dose doxepin for sleep-maintenance insomnia and suggest not using trazodone for sleep-onset or sleep-maintenance insomnia (page not provided). They do not discourage every other sedating antidepressant, so the claim extends the trazodone recommendation to the class as a whole. (LLM, conf=0.86)
Experimental — accuracy not yet measured
It may state two separate claims as one.
PremisecitationSleep apnea is an overlooked but frequent sleep disorder in people suffering from mental illness.
“Finally, antidepressants inducing weight gain are contraindicated in patients with sleep apnea, that is an overlooked but frequent sleep disorder in people suffering from mental illness [32].”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [32] Szaulińska K, Pływaczewski R, Sikorska O, Holka-Pokorska J, Wierzbicka A, Wichniak A, et al. Obstructive sleep apnea in severe mental disorders. Psychiatr Pol. 2015;49:883–95. source
Probably not a substantial claim. It may state two separate claims as one.
PremisecitationCurrent treatment guidelines strongly recommend CBT-I as the initial treatment for chronic insomnia disorder and only short-term use of sleep-promoting drugs in patients with insufficient response to CBT-I.
“Current treatment guidelines [36 ·· ] strongly recommend the use of cognitive-behavioral therapy (CBT-I) as the initial treatment for chronic insomnia disorder and only short-term use of the sleep-promoting drugs in patients with insufficient response to CBI-I.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [36] •• Qaseem A, Kansagara D, Forciea MA, Cooke M, Denberg TD. Management of chronic insomnia disorder in adults: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2016;165:125–33. This publication presents guidelines for chronic insomnia treatment indicating that cognitive-behavioral therapy should be used as a first line treatment. source
It may state two separate claims as one.
PremisecitationAcute effects of antidepressants on sleep are reflected in subjective complaints and can also be demonstrated in PSG studies.
“It is important to note that acute effects of antidepressants on sleep are reflected not only in the patients ' subjective complaints but they can also be demonstrated in studies with PSG (Table 2).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Table 2
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
It may state two separate claims as one.
Premiseown dataMAOI may decrease or have no effect on sleep continuity, have unknown effect on SWS, increase REM latency, and decrease REM sleep.
“MAOI (e.g., tranylcypromine, moclobemide) | ↓ /0 | ? | ↑ | ↓ | inhibition of monoamine oxidase enzyme”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Table 2
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
It may state two separate claims as one.
PremisecitationIn the second week, agomelatine slightly improves sleep continuity, with increased total sleep time and sleep efficiency.
“In the second week, agomelatine slightly improves sleep continuity (increased total sleep time and sleep efficiency) and escitalopram worsens it [25].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [25] Quera-Salva MA, Hajak G, Philip P, Montplaisir J, Keufer-Le GS, Laredo J, et al. Comparison of agomelatine and escitalopram on nighttime sleep and daytime condition and efficacy in major depressive disorder patients. Int Clin Psychopharmacol. 2011;26:252–62. source
It may state two separate claims as one.
InterpretationreasoningAgomelatine's pharmacodynamic profile is related to sleep-promoting action without the risk of sedation and weight gain.
“Such pharmacodynamic profile is related to sleep-promoting action without the risk of sedation and weight gain.”
Quote in the paperSubstantial claimIt may state two separate claims as one.
PremisecitationAgomelatine is a non-sedative antidepressant that acts as an agonist at melatonergic M1 and M2 receptors and an antagonist at serotonergic 5-HT2C receptors.
“Agomelatine is a non-sedative antidepressant drug exerting agonistic action at melatonergic M1 and M2 receptors, and antagonistic action at serotonergic 5HT2creceptors [24].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [24] Hickie IB, Rogers NL. Novel melatonin-based therapies: potential advances in the treatment of major depression. Lancet. 2011;378:621–31. source
It may state two separate claims as one.
PremisereasoningSome antidepressants alleviate sleep disturbances, while others may disrupt sleep.
“Some of them alleviate sleep disturbances, but other may disrupt sleep”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [3, 6, 7, 17 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
It may state two separate claims as one.
PremisereasoningSedative TCA increase sleep continuity, SWS, REM latency, and decrease REM sleep.
“Sedative TCA (e.g., amitriptyline, doxepin, trimipramine) | ↑ | ↑ | ↑ | ↓ | antihistaminergic effect, inhibition of serotonin, and norepinephrine reuptake”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Table 2
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
It may state two separate claims as one.
PremisecitationSedative antidepressants may induce weight gain, particularly shown for mirtazapine but not trazodone.
“The sedative antidepressants may also induce a weight gain, what is particularly shown for mirtazapine but not for trazodone [23].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [23] Serretti A, Mandelli L. Antidepressants and body weight: a comprehensive review and meta-analysis. J Clin Psychiatry. 2010;71:1259–72. source
It may state two separate claims as one.
Premiseown dataActivating TCA decrease sleep continuity, SWS, increase REM latency, and decrease REM sleep.
“Activating TCA (e.g., imipramine, desipramine) | ↓ | ↓ | ↑ | ↓ | inhibition of serotonin and norepinephrine reuptake”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Table 2
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
It may state two separate claims as one.
Premiseown dataSSRI may decrease or have no effect on sleep continuity, have no effect or increase SWS, increase REM latency, and decrease REM sleep.
“SSRI (e.g., fluoxetine, escitalopram, | ↓ /0 | 0/ ↑ | ↑ | ↓ | selective inhibition of serotonin reuptake”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Table 2
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
It may state two separate claims as one.
PremisecitationSSRI, SNRI, and activating TCA increase REM latency, suppress REM sleep, and may impair sleep continuity.
“While SSRI, SNRI, and activating TCA increase REM latency, suppress REM sleep, and may impair sleep continuity”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [3, 6, 7, 17 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
It may state two separate claims as one.
PremisecitationSedating antidepressants decrease sleep latency, improve sleep efficiency, increase SWS, and usually have little or no effect on REM sleep.
“sedating antidepressants decrease sleep latency, improve sleep efficiency, increase SWS, and usually have little or no effect on REM sleep [3, 6, 7, 17 ·· ].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [3, 6, 7, 17 ·· ]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
It may state two separate claims as one.
PremisecitationIn some patients, sleep-disrupting or sleep-promoting effects may persist, aggravating insomnia complaints or causing daytime somnolence.
“in some patients they may persist, aggravating insomnia complaints or causing daytime somnolence [18].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [18] Fava M. Daytime sleepiness and insomnia as correlates of depression. J Clin Psychiatry. 2004;65(Suppl 16):27–32.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
It may state two separate claims as one.
Premiseown dataSNRI and NRI may decrease sleep continuity, have no effect or increase SWS, increase REM latency, and decrease REM sleep.
“SNRI and NRI (e.g., venlafaxine, duloxetine, reboxetine) | ↓ | 0// ↑ | ↑ | ↓ | inhibition of serotonin and norepinephrine reuptake”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Table 2
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
It may state two separate claims as one.
InterpretationreasoningIn the short term, some antidepressants may impair sleep due to activating effects, while others may improve sleep due to sedative properties.
“However, in the short term, while some of them may impair sleep due to the activating effects, other may improve sleep due to the sedative properties.”
Quote in the paperSubstantial claimProbably not a substantial claim. The paper may give no reason why it holds.
Interpretationnone givenFor a sleep-promoting effect, it is sufficient to use a sedative antidepressant in a low dose.
“It is particularly noteworthy that for sleep-promoting effect, it is sufficient to use a sedative antidepressant in a low dose.”
Quote in the paperNot a substantial claimProbably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
Interpretationnone givenDisturbed sleep is a core symptom of depression and its normalization is necessary to achieve remission from the illness.
“Disturbed sleep is a core symptom of depression and its normalization is necessary to achieve remission from the illness.”
Quote in the paperNot a substantial claimProbably not a substantial claim.
InterpretationreasoningIn low dose, sedative antidepressants can be combined with other antidepressants as an alternative to hypnotic drugs, especially if there is a clinical necessity to promote sleep for longer than 2-4 weeks with a frequency higher than 3-4 times per week.
“In such dose, these drugs can be also combined with other antidepressants as an alternative to hypnotic drugs, especially if there is a clinical necessity to promote sleep for longer than 2 -4 weeks with a frequency higher than 3 -4 times per week.”
Quote in the paperSubstantial claim
The paper relies on this without support.
The sedating effect of sedative antidepressants becomes an increasing problem in long-term maintenance treatment, frequently requiring dose reduction.
“The sedating effect of those antidepressants is usually an increasing problem in long-term maintenance treatment, frequently resulting in a need to reduce the drug dose.”
The paper relies on this without support.
Combination treatment with benzodiazepines and SSRI/SNRI is often necessary to reduce anxiety and insomnia as early as the first week of treatment.
“Such an approach, combination treatment with benzodiazepines and SSRI/SNRI is often necessary to reduce anxiety and insomnia as early as in the first week of treatment.”
The paper relies on this without support.
Some antidepressants may worsen or induce primary sleep disorders like restless legs syndrome, sleep bruxism, REM sleep behavior disorder, nightmares, and sleep apnea.
“some antidepressants may worsen or induce primary sleep disorders like restless legs syndrome, sleep bruxism, REM sleep behavior disorder, nightmares, and sleep apnea”
The paper relies on this without support.
Antidepressant-induced weight gain may cause sleep apnea.
“which may result from an antidepressant-induced weight gain.”
The paper relies on this without support.
In daily clinical practice, the use of pharmacotherapy for insomnia is very common.
“However, in daily clinical practice, the use of pharmacotherapy for insomnia is very common.”
The paper relies on this without support.
The most frequently used drugs to treat insomnia aside from benzodiazepines and non-benzodiazepine hypnotics are sedative antidepressants.
“The most frequently used drugs to treat insomnia aside from benzodiazepines and non-benzodiazepine (eszopiclone/ zopiclone, zaleplon, zolpidem) hypnotics are sedative antidepressants.”
The paper relies on this without support.
Patients with comorbid mood or anxiety disorder are at increased risk of developing hypnotic dependency.
“The use of sedative antidepressants should be also considered when there is a comorbid mood or anxiety disorder because such patients are at increased risk of developing hypnotic dependency.”
The paper relies on this without support.
When a patient restricts time in bed and uses stimulus control technique, even low-dosage pharmacological treatment starts to work.
“When a patient restricts time in bed and uses stimulus control technique, even lowdosage pharmacological treatment starts to work.”
The paper relies on this without support.
Insomnia shares many features with depression.
“Although insomnia is not regarded as a severe mental disorder, it shares many features with depression.”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
FDA sleep-adverse-effect data attributed to the wrong reference
MinorThe text attributes FDA-register data on treatment-emergent insomnia to reference [16], but its own reference list identifies [16] as a paper on antidepressant onset of action. Reference [17] is the one described in the list as analyzing FDA-register data on sleep effects.
“Based on data from the US Food and Drug Administration (FDA) study register [16], the average prevalence of treatment-emergent insomnia in clinical trials with SSRI was 17% as compared to 9% out of patients randomized to the placebo arm.”
“16. Thompson C. Onset of action of antidepressants: results of different analyses. Hum Psychopharmacol. 2002;17(Suppl 1):S27 -32.”
Citations
Cites
Depression, chronic diseases, and decrements in health: results from the World Health Surveys
Moussavi, S., Chatterji, S., Verdes, E., Tandon, A., Patel, V., & Ustun, B. (2007) · The Lancet · doi:10.1016/s0140-6736(07)61415-9 · Cited by 4,070
The size and burden of mental disorders and other disorders of the brain in Europe 2010
Wittchen, H. U., Jacobi, F., Rehm, J., Gustavsson, A., Svensson, M., Jönsson, B., Olesen, J., Allgulander, C., Alonso, J., Faravelli, C., et al. (2011) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2011.07.018 · Cited by 3,754
Epidemiology of insomnia: what we know and what we still need to learn
Ohayon, M. M. (2002) · Sleep Medicine Reviews · doi:10.1053/smrv.2002.0186 · Cited by 3,743
Qaseem, A., Kansagara, D., Forciea, M. A., Cooke, M., Denberg, T. D., & for the Clinical Guidelines Committee of the American College of Physicians* (2016) · Annals of Internal Medicine · doi:10.7326/m15-2175 · Cited by 1,965
The hyperarousal model of insomnia: A review of the concept and its evidence
Riemann, D., Spiegelhalder, K., Feige, B., Voderholzer, U., Berger, M., Perlis, M., & Nissen, C. (2010) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2009.04.002 · Cited by 1,789
Sateia, M. J., Buysse, D. J., Krystal, A. D., Neubauer, D. N., & Heald, J. L. (2017) · Journal of Clinical Sleep Medicine · doi:10.5664/jcsm.6470 · Cited by 1,519
Sleep and mental disorders: a meta-analysis of polysomnographic research
Baglioni, C., Nanovska, S., Regen, W., Spiegelhalder, K., Feige, B., Nissen, C., Reynolds, C. F., & Riemann, D. (2016) · Psychological Bulletin · doi:10.1037/bul0000053 · Cited by 1,074
Hyperarousal and insomnia: state of the science
Bonnet, M. H., & Arand, D. L. (2010) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2009.05.002 · Cited by 914
Wilson, S., Nutt, D., Alford, C., Argyropoulos, S., Baldwin, D., Bateson, A., Britton, T., Crowe, C., Dijk, D.-J., Espie, C., et al. (2010) · Journal of Psychopharmacology · doi:10.1177/0269881110379307 · Cited by 634
Antidepressants and Body Weight: A Comprehensive Review and Meta-Analysis
Serretti, A., & Mandelli, L. (2010) · The Journal of Clinical Psychiatry · doi:10.4088/jcp.09r05346blu · Cited by 621
Antidepressants and Sleep: A Qualitative Review of the Literature
Wilson, S., & Argyropoulos, S. (2005) · Drugs · doi:10.2165/00003495-200565070-00003 · Cited by 392
Novel melatonin-based therapies: potential advances in the treatment of major depression
Hickie, I. B., & Rogers, N. L. (2011) · The Lancet · doi:10.1016/s0140-6736(11)60095-0 · Cited by 334
Restless legs syndrome as side effect of second generation antidepressants
Rottach, K. G., Schaner, B. M., Kirch, M. H., Zivotofsky, A. Z., Teufel, L. M., Gallwitz, T., & Messer, T. (2008) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2008.02.006 · Cited by 249
Hypersomnia across mood disorders: A review and synthesis
Kaplan, K. A., & Harvey, A. G. (2009) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2008.09.001 · Cited by 249
Daytime sleepiness and insomnia as correlates of depression.
Fava, M. (2004) · PubMed · Cited by 243
McClintock, S. M., Husain, M. M., Wisniewski, S. R., Nierenberg, A. A., Stewart, J. W., Trivedi, M. H., Cook, I., Morris, D., Warden, D., & Rush, A. J. (2011) · Journal of Clinical Psychopharmacology · doi:10.1097/jcp.0b013e31820ebd2c · Cited by 234
Schmid, D. A., Wichniak, A., Uhr, M., Ising, M., Brunner, H., Held, K., Weikel, J. C., Sonntag, A., & Steiger, A. (2006) · Neuropsychopharmacology · doi:10.1038/sj.npp.1300923 · Cited by 165
Self-citationTV exposure associated with sleep disturbances in 5‐ to 6‐year‐old children
Paavonen, E. J., Pennonen, M., Roine, M., Valkonen, S., & Lahikainen, A. R. (2006) · Journal of Sleep Research · doi:10.1111/j.1365-2869.2006.00525.x · Cited by 162
Antidepressants plus benzodiazepines for major depression
Furukawa, T. A., Streiner, D., Young, L. T., & Kinoshita, Y. (2001) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd001026 · Cited by 161
Treatment of insomnia associated with clinical depression
Jindal, R. D. (2003) · Sleep Medicine Reviews · doi:10.1016/s1087-0792(03)00025-x · Cited by 155
Mendlewicz, J. (2009) · The World Journal of Biological Psychiatry · doi:10.3109/15622970802503086 · Cited by 143
Mendelson, W. (2004) · Sleep Medicine Reviews · doi:10.1016/s1087-0792(03)00042-x · Cited by 142
Sleep and Antidepressant Treatment
Wichniak, A., Wierzbicka, A., & Jernajczyk, W. (2012) · Current Pharmaceutical Design · doi:10.2174/138161212803523608 · Cited by 142
Self-citationDepression, sleep, and antidepressants.
Thase, M. E. (1998) · PubMed · Cited by 134
Sleep as a biomarker for depression
Wichniak, A., Wierzbicka, A., & Jernajczyk, W. (2013) · International Review of Psychiatry · doi:10.3109/09540261.2013.812067 · Cited by 123
Self-citationAntidepressants for the Treatment of Insomnia: A Suitable Approach?
Wiegand, M. H. (2008) · Drugs · doi:10.2165/0003495-200868170-00001 · Cited by 108
Abad, V. C., & Guilleminault, C. (2005) · Dialogues in Clinical Neuroscience · doi:10.31887/dcns.2005.7.4/vabad · Cited by 102
Atypical antipsychotics for insomnia: a systematic review
Thompson, W., Quay, T. A. W., Rojas‐Fernandez, C. H., Farrell, B. J., & Bjerre, L. M. (2016) · Sleep Medicine · doi:10.1016/j.sleep.2016.04.003 · Cited by 97
Impact of the novel antidepressant agomelatine on disturbed sleep–wake cycles in depressed patients
Quera‐Salva, M., Lemoine, P., & Guilleminault, C. (2010) · Human Psychopharmacology: Clinical and Experimental · doi:10.1002/hup.1112 · Cited by 92
Onset of action of antidepressants: results of different analyses
Thompson, C. (2002) · Human Psychopharmacology: Clinical and Experimental · doi:10.1002/hup.386 · Cited by 92
Quera-Salva, M.-A., Hajak, G., Philip, P., Montplaisir, J., Keufer-Le Gall, S., Laredo, J., & Guilleminault, C. (2011) · International Clinical Psychopharmacology · doi:10.1097/yic.0b013e328349b117 · Cited by 91
Effects of Sertraline on Sleep Architecture in Patients With Depression
Jindal, R. D., Friedman, E. S., Berman, S. R., Fasiczka, A. L., Howland, R. H., & Thase, M. E. (2003) · Journal of Clinical Psychopharmacology · doi:10.1097/01.jcp.0000095345.32154.9a · Cited by 86
Vortioxetine: A review of the pharmacology and clinical profile of the novel antidepressant
Sowa-Kućma, M., Pańczyszyn-Trzewik, P., Misztak, P., Jaeschke, R. R., Sendek, K., Styczeń, K., Datka, W., & Koperny, M. (2017) · Pharmacological Reports · doi:10.1016/j.pharep.2017.01.030 · Cited by 86
The Effects of Antidepressants on Sleep: A Review
Gursky, J. T., & Krahn, L. E. (2000) · Harvard Review of Psychiatry · doi:10.1080/hrp.8.6.298 · Cited by 77
Insomnia is associated with suicide attempt in middle-aged and older adults with depression
Kay, D. B., Dombrovski, A. Y., Buysse, D. J., Reynolds, C. F., Begley, A., & Szanto, K. (2016) · International Psychogeriatrics · doi:10.1017/s104161021500174x · Cited by 76
Prevalence of self-reported insomnia in general population of Poland.
Nowicki, Z., Grabowski, K., Cubała, W., Nowicka-Sauer, K., Zdrojewski, T., Rutkowski, M., & Bandosz, P. (2016) · Psychiatria Polska · doi:10.12740/pp/58771 · Cited by 72
Adverse Effects of Psychotropic Medications on Sleep
Doghramji, K., & Jangro, W. C. (2016) · Psychiatric Clinics of North America · doi:10.1016/j.psc.2016.04.009 · Cited by 69
The Effects of Antidepressants on Sleep: A Review
Gursky, J. T. (2000) · Harvard Review of Psychiatry · doi:10.1093/hrp/8.6.298 · Cited by 55
Liu, Y., Xu, X., Dong, M., Jia, S., & Wei, Y. (2017) · Sleep Medicine · doi:10.1016/j.sleep.2017.03.007 · Cited by 44
Obstructive sleep apnea in severe mental disorders.
Szaulińska, K., Pływaczewski, R., Sikorska, O., Holka-Pokorska, J., Wierzbicka, A., Wichniak, A., & Śliwiński, P. (2015) · Psychiatria Polska · doi:10.12740/pp/32566 · Cited by 42
Self-citationUnmet need: what justifies the search for a new antidepressant?
Greden, J. F. (2002) · PubMed · Cited by 41
Wilson, S., Højer, A.-M., Buchberg, J., Areberg, J., & Nutt, D. J. (2015) · Journal of Psychopharmacology · doi:10.1177/0269881115599387 · Cited by 32
Low Risk for Switch to Mania during Treatment with Sleep Promoting Antidepressants
Wichniak, A., Jarkiewicz, M., Okruszek, Ł., Wierzbicka, A., Holka-Pokorska, J., & Rybakowski, J. (2015) · Pharmacopsychiatry · doi:10.1055/s-0034-1396802 · Cited by 28
Self-citationBonnet, M. H. (2009) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2009.07.003 · Cited by 23
Abad, V. C., & Guilleminault, C. (2009) · PubMed · Cited by 16
Contribution of sleep research to the development of new antidepressants
Bon, O. L. (2005) · Dialogues in Clinical Neuroscience · doi:10.31887/dcns.2005.7.4/olebon · Cited by 15
Frequent difficulties in the treatment of restless legs syndrome – case report and literature review
Narowska, D., Bożek, M., Krysiak, K., Antczak, J., Holka-Pokorska, J., Jernajczyk, W., & Wichniak, A. (2015) · Psychiatria Polska · doi:10.12740/pp/35395 · Cited by 13
Self-citationHashimoto, T., Shiina, A., Hasegawa, T., Kimura, H., Oda, Y., Niitsu, T., Ishikawa, M., Tachibana, M., Muneoka, K. T., Matsuki, S., et al. (2016) · Annals of General Psychiatry · doi:10.1186/s12991-016-0115-1 · Cited by 13
Mirtazapine Induces Nightmares in Depressed Patients
Buschkamp, J.-A., Frohn, C., & Juckel, G. (2017) · Pharmacopsychiatry · doi:10.1055/s-0043-105076 · Cited by 6
Sateia, M., Buysse, D., Krystal, A., Neubauer, D., & Heald, J. (2017) · Sleep · doi:10.1093/sleepj/zsx050.394
Flagged first, then by citations
Research works printed but not linked: 1
- Jernajczyk W, Sobańska A, Wierzbicka A, Wichniak A, Szatkowska E. The therapy of primary insomnia with citalopram. J Sleep Res. 2006;15(Suppl. 1):154.
Cited by
Sorted by citations
Sleep disturbance and psychiatric disorders
Freeman, D., Sheaves, B., Waite, F., Harvey, A. G., & Harrison, P. J. (2020) · The Lancet Psychiatry · doi:10.1016/s2215-0366(20)30136-x · Cited by 843
Sleep deficiency and chronic pain: potential underlying mechanisms and clinical implications
Haack, M., Simpson, N. S., Sethna, N. F., Kaur, S., & Mullington, J. M. (2019) · Neuropsychopharmacology · doi:10.1038/s41386-019-0439-z · Cited by 693
Sleep and anxiety: From mechanisms to interventions
Chellappa, S. L., & Aeschbach, D. (2022) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2021.101583 · Cited by 509
Selective Serotonin Reuptake Inhibitors and Adverse Effects: A Narrative Review
Edinoff, A. N., Akuly, H. A., Hanna, T. A., Ochoa, C. O., Patti, S. J., Ghaffar, Y. T., Kaye, A. D., Viswanath, O., Urits, I., Boyer, A. G., et al. (2021) · Neurology International · doi:10.3390/neurolint13030038 · Cited by 506
Clarifying the role of sleep in depression: A narrative review
Pandi-Perumal, S. R., Monti, J. M., Burman, D., Ramanujam, K., BaHammam, A. S., Spence, D. W., Brown, G. M., & Narashimhan, M. (2020) · Psychiatry Research · doi:10.1016/j.psychres.2020.113239 · Cited by 351
Difrancesco, S., Lamers, F., Riese, H., Merikangas, K. R., Beekman, A. T. F., van Hemert, A. M., Schoevers, R. A., & Penninx, B. W. J. H. (2019) · Depression and Anxiety · doi:10.1002/da.22949 · Cited by 226
The 5-HT1A receptor in Major Depressive Disorder
Kaufman, J., DeLorenzo, C., Choudhury, S., & Parsey, R. V. (2016) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2015.12.039 · Cited by 225
Ge, L., Liu, S., Li, S., Yang, J., Hu, G., Xu, C., & Song, W. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.1016578 · Cited by 187
SEP-363856, a Novel Psychotropic Agent with a Unique, Non-D2 Receptor Mechanism of Action
Dedic, N., JONES, P. G., Hopkins, S. C., Lew, R., Shao, L., Campbell, J. E., Spear, K. L., Large, T. H., Campbell, U. C., Hanania, T., et al. (2019) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.119.260281 · Cited by 179
Krahn, L. E., Arand, D. L., Avidan, A. Y., Davila, D., DeBassio, W. A., Ruoff, C. M., & Harrod, C. G. (2021) · Journal of Clinical Sleep Medicine · doi:10.5664/jcsm.9620 · Cited by 175
Effect of Electroacupuncture on Insomnia in Patients With Depression
Yin, X., Li, W., Liang, T., Lu, B., Yue, H., Li, S., Zhong, V. W., Zhang, W., Li, X., Zhou, S. Y., et al. (2022) · JAMA Network Open · doi:10.1001/jamanetworkopen.2022.20563 · Cited by 172
Lu, Y., Ho, C. S., Liu, X., Chua, A. N., Wang, W., McIntyre, R. S., & Ho, R. C. (2017) · PLOS ONE · doi:10.1371/journal.pone.0186700 · Cited by 164
Association Between Depressive Symptoms and Sleep Disturbances in Community‐Dwelling Older Men
Paudel, M. L., Taylor, B. C., Diem, S. J., Stone, K. L., Ancoli‐Israel, S., Redline, S. S., Ensrud, K. E., & for the Osteoporotic Fractures in Men Study Group (2008) · Journal of the American Geriatrics Society · doi:10.1111/j.1532-5415.2008.01753.x · Cited by 151
Babiloni, A. H., Bellemare, A., Beetz, G., Vinet, S.-A., Martel, M. O., Lavigne, G. J., & Beaumont, L. D. (2020) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2020.101381 · Cited by 129
Hutka, P., Krivosova, M., Muchova, Z., Tonhajzerová, I., Hamrakova, A., Mlyncekova, Z., Mokrý, J., & Ondrejka, I. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22031333 · Cited by 129
Sleep disturbance associated with the menopause
Maki, P. M., Panay, N., & Simon, J. A. (2024) · Menopause The Journal of The North American Menopause Society · doi:10.1097/gme.0000000000002386 · Cited by 116
A literature review of heart rate variability in depressive and bipolar disorders
Bassett, D. L. (2015) · Australian & New Zealand Journal of Psychiatry · doi:10.1177/0004867415622689 · Cited by 113
A critical review on recent trends on pharmacological applications of pyrazolone endowed derivatives
Mustafa, G., Zia‐ur‐Rehman, M., Sumrra, S. H., Ashfaq, M. A., Zafar, W., & Ashfaq, M. (2022) · Journal of Molecular Structure · doi:10.1016/j.molstruc.2022.133044 · Cited by 104
Trazodone for the treatment of insomnia: a meta-analysis of randomized placebo-controlled trials
Yi, X.-Y., Ni, S., Ghadami, M. R., Meng, H., Chen, M., Kuang, L., Zhang, Y., Zhang, L., & Zhou, X. (2018) · Sleep Medicine · doi:10.1016/j.sleep.2018.01.010 · Cited by 100
Antidepressants in inflammatory bowel disease
Mikocka-Walus, A., Ford, A. C., & Drossman, D. A. (2020) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-019-0259-y · Cited by 93
Neurodevelopmental Disorders Commonly Presenting with Sleep Disturbances
Shelton, A. R., & Malow, B. A. (2021) · Neurotherapeutics · doi:10.1007/s13311-020-00982-8 · Cited by 83
The Spectrum of Sleep Disorders in Parkinson Disease
Lajoie, A. C., Lafontaine, A., & Kamińska, M. (2020) · CHEST Journal · doi:10.1016/j.chest.2020.09.099 · Cited by 81
Novel Pharmacological Approaches to the Treatment of Depression
Elias, E., Zhang, A. Y., & Manners, M. T. (2022) · Life · doi:10.3390/life12020196 · Cited by 77
Weber, F. C., & Wetter, T. C. (2021) · Neuropsychobiology · doi:10.1159/000517329 · Cited by 74
Lim, R., Messineo, L., Grunstein, R. R., Carberry, J. C., & Eckert, D. J. (2021) · The Journal of Physiology · doi:10.1113/jp281912 · Cited by 71
Recent advances in sleep and depression
Mirchandaney, R., Asarnow, L. D., & Kaplan, K. A. (2022) · Current Opinion in Psychiatry · doi:10.1097/yco.0000000000000837 · Cited by 71
Role of trazodone in treatment of major depressive disorder: an update
Fagiolini, A. M., González-Pinto, A. M., Miskowiak, K. W., Morgado, P. F., Young, A. H., & Vieta, E. (2023) · Annals of General Psychiatry · doi:10.1186/s12991-023-00465-y · Cited by 68
De Diego-Adeliño, J., Crespo, J. M., Mora, F., Neyra, A., Iborra, P., Gutiérrez-Rojas, L., & Salonia, S. F. (2022) · Expert Opinion on Drug Safety · doi:10.1080/14740338.2022.2019705 · Cited by 67
Moon, E., Kim, K., Partonen, T., & Mantere, O. (2022) · Current Psychiatry Reports · doi:10.1007/s11920-022-01369-6 · Cited by 67
Akkaoui, M. A., Lejoyeux, M., d’Ortho, M., & Geoffroy, P. A. (2020) · Journal of Clinical Medicine · doi:10.3390/jcm9123990 · Cited by 67
Understanding genetic risk factors for common side effects of antidepressant medications
Campos, A. I., Mulcahy, A., Thorp, J. G., Wray, N. R., Byrne, E. M., Lind, P. A., Medland, S. E., Martin, N. G., Hickie, I. B., & Rentería, M. E. (2021) · Communications Medicine · doi:10.1038/s43856-021-00046-8 · Cited by 63
Identifying and integrating active ingredients for mental health
Wolpert, M., Pote, I., & Sebastian, C. L. (2021) · The Lancet Psychiatry · doi:10.1016/s2215-0366(21)00283-2 · Cited by 61
Insomnia disorder and its reciprocal relation with psychopathology
Lancel, M., Boersma, G. J., & Kamphuis, J. (2021) · Current Opinion in Psychology · doi:10.1016/j.copsyc.2021.02.001 · Cited by 61
The Neurobiological Basis of Sleep and Sleep Disorders
Joiner, W. J. (2018) · Physiology · doi:10.1152/physiol.00013.2018 · Cited by 59
Targeting Sleep Physiology to Modulate Glymphatic Brain Clearance
van Hattem, T., Verkaar, L., Krugliakova, E., Adelhöfer, N., Zeising, M., Drinkenburg, W. H. I. M., Claassen, J. A. H. R., Bódizs, R., Dresler, M., & Rosenblum, Y. (2024) · Physiology · doi:10.1152/physiol.00019.2024 · Cited by 57
Zheng, Y., Lv, T., Wu, J., & Lyu, Y. (2022) · Scientific Reports · doi:10.1038/s41598-022-18776-7 · Cited by 56
Endomba, F. T., Tchebegna, P. Y., Chiabi, E. N., Wouna, D. L. A., Guillet, C., & Chauvet-Gélinier, J. C. (2023) · European Geriatric Medicine · doi:10.1007/s41999-023-00862-2 · Cited by 55
Drug-Induced Insomnia and Excessive Sleepiness
Gastel, A. V. (2018) · Sleep Medicine Clinics · doi:10.1016/j.jsmc.2018.02.001 · Cited by 55
Hoyos, C. M., Gordon, C. J., Terpening, Z., Norrie, L. M., Lewis, S. J. G., Hickie, I. B., & Naismith, S. L. (2020) · BMC Psychiatry · doi:10.1186/s12888-020-02606-z · Cited by 53
Sun, A., & Wu, X. (2023) · Journal of Psychosomatic Research · doi:10.1016/j.jpsychores.2023.111435 · Cited by 52
Stress in obstructive sleep apnea
Wong, J. L., Martínez, F., Aguila, A. P., Pal, A., Aysola, R., Henderson, L. A., & Macey, P. M. (2021) · Scientific Reports · doi:10.1038/s41598-021-91996-5 · Cited by 51
Psilocin acutely alters sleep-wake architecture and cortical brain activity in laboratory mice
Thomas, C. W., Blanco‐Duque, C., Bréant, B. J. B., Goodwin, G. M., Sharp, T., Bannerman, D. M., & Vyazovskiy, V. V. (2022) · Translational Psychiatry · doi:10.1038/s41398-022-01846-9 · Cited by 49
Using genetic drug-target networks to develop new drug hypotheses for major depressive disorder
Gaspar, H. A., Gerring, Z. F., Hübel, C., Middeldorp, C. M., Derks, E. M., & Breen, G. D. (2019) · Translational Psychiatry · doi:10.1038/s41398-019-0451-4 · Cited by 50
Updates in insomnia diagnosis and treatment
Bragg, S. W., Benich, J. J., Christian, N., Visserman, J., & Freedy, J. R. (2019) · The International Journal of Psychiatry in Medicine · doi:10.1177/0091217419860716 · Cited by 50
Pharmacotherapy and the Role of Pharmacists in Rehabilitation Medicine
Yoshimura, Y., Matsumoto, A., & Momosaki, R. (2022) · Progress in Rehabilitation Medicine · doi:10.2490/prm.20220025 · Cited by 49
Rapid eye movements sleep as a predictor of functional outcome after stroke: a translational study
Pace, M., Camilo, M. R., Seiler, A., Duss, S. B., Mathis, J., Manconi, M., & Bassetti, C. L. (2018) · SLEEP · doi:10.1093/sleep/zsy138 · Cited by 49
Millan, M. J. (2022) · Therapeutic Advances in Psychopharmacology · doi:10.1177/20451253221105128 · Cited by 48
Zhou, S., Li, P., Lv, X., Lai, X., Liu, Z., Zhou, J., Liu, F., Tao, Y., Zhang, M., Yu, X., et al. (2023) · SLEEP · doi:10.1093/sleep/zsad177 · Cited by 48
Pruritus and sleep disturbances in patients with psoriasis
Hawro, T., Hawro, M., Zalewska-Janowska, A. M., Weller, K., Metz, M., & Maurer, M. (2019) · Archives of Dermatological Research · doi:10.1007/s00403-019-01998-7 · Cited by 48
Psychopharmacological properties and therapeutic profile of the antidepressant venlafaxine
Coutens, B., Yrondi, A., Rampon, C., & Guiard, B. P. (2022) · Psychopharmacology · doi:10.1007/s00213-022-06203-8 · Cited by 47
Mörkl, S., Narrath, M., Schlotmann, D., Sallmutter, M.-T., Putz, J., Lang, J., Brandstätter, A., Pilz, R., Lackner, H. K., Goswami, N., et al. (2025) · Gut Microbes · doi:10.1080/19490976.2025.2492377 · Cited by 47
Mundo-López, A., Hernández, O. O., San-Sebastián, A. P., Galiano‐Castillo, N., Rodríguez-Pérez, O., Arroyo-Luque, M. S., Arroyo‐Morales, M., Cantarero‐Villanueva, I., Fernández‐Lao, C., & Artacho‐Cordón, F. (2020) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph17113831 · Cited by 47
Automatic analysis of single-channel sleep EEG in a large spectrum of sleep disorders
Peter‐Derex, L., Berthomier, C., Taillard, J., Berthomier, P., Bouet, R., Mattout, J., Brandewinder, M., & Bastuji, H. (2020) · Journal of Clinical Sleep Medicine · doi:10.5664/jcsm.8864 · Cited by 46
Zambelli, Z., Halstead, E. J., Fidalgo, A. R., & Dimitriou, D. (2021) · Frontiers in Psychology · doi:10.3389/fpsyg.2021.668930 · Cited by 46
Inoue, T., Sasai, K., Kitagawa, T., Nishimura, A., & Inada, I. (2020) · Psychiatry and Clinical Neurosciences · doi:10.1111/pcn.12956 · Cited by 45
Adamo, D., Pecoraro, G., Coppola, N., Calabria, E., Aria, M., & Mignogna, M. D. (2020) · Oral Diseases · doi:10.1111/odi.13602 · Cited by 43
Yin, X., Li, W., Wu, H., Dong, B., Ma, J., Li, S., Lao, L., & Xu, S. (2020) · Nature and Science of Sleep · doi:10.2147/nss.s253320 · Cited by 43
Valomon, A., Riedner, B. A., Jones, S. G., Nakamura, K., Tononi, G., Plante, D. T., Benca, R. M., & Boly, M. (2021) · Scientific Reports · doi:10.1038/s41598-021-83980-w · Cited by 43
Mattingly, G. W., Ren, H., Christensen, M. C., Katzman, M. A., Polosan, M., Simonsen, K., & Hammer-Helmich, L. (2022) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2022.824831 · Cited by 43
Mo, L., Mansfield, D. R., Joham, A., Cain, S. W., Bennett, C., Blumfield, M., Teede, H., & Moran, L. J. (2019) · Clinical Endocrinology · doi:10.1111/cen.13922 · Cited by 42
Increased Aperiodic Neural Activity During Sleep in Major Depressive Disorder
Rosenblum, Y., Bovy, L., Weber, F. D., Steiger, A., Zeising, M., & Dresler, M. (2022) · Biological Psychiatry Global Open Science · doi:10.1016/j.bpsgos.2022.10.001 · Cited by 42
The relationship between sleep and depression and bipolar disorder in children and young people
Comsa, M., Anderson, K. N., Sharma, A., Yadav, V. C., & Watson, S. (2022) · BJPsych Open · doi:10.1192/bjo.2021.1076 · Cited by 42
Lee, S.-H., Kim, H.-B., & Lee, K.-W. (2019) · Journal of Affective Disorders · doi:10.1016/j.jad.2019.05.071 · Cited by 41
Neuroinflammation and Natural Antidepressants: Balancing Fire with Flora
Godoy, A. C. F., Frota, F. F., Araújo, L. P., Valenti, V. E., Pereira, E. D. S. B. M., Detregiachi, C. R. P., Galhardi, C. M., Caracio, F. C. C., Haber, R. S. A., Laurindo, L. F., et al. (2025) · Biomedicines · doi:10.3390/biomedicines13051129 · Cited by 41
Menown, S. J., & Tello, J. A. (2021) · Advances in Therapy · doi:10.1007/s12325-021-01900-w · Cited by 41
The Effects of Daytime Psilocybin Administration on Sleep: Implications for Antidepressant Action
Dudysová, D., Janků, K., Šmotek, M., Saifutdinová, E., Kopřivová, J., Bušková, J., Mander, B. A., Brunovský, M., Zach, P., Korčák, J., et al. (2020) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.602590 · Cited by 39
Pu, Z., Hou, Q., Yan, H., Lin, Y., & Guo, Z. (2022) · Journal of Affective Disorders · doi:10.1016/j.jad.2022.11.062 · Cited by 40
Halstead, S., Yap, C. X., Warren, N., Agarwal, S. M., Brand, B. A., Chan, S. K. W., Cipriani, A., Correll, C. U., Crossley, N. A., D’Ambrosio, E., et al. (2025) · The Lancet Psychiatry · doi:10.1016/s2215-0366(25)00162-2 · Cited by 39
Prevalence and Impact of Neuropathic and Nonneuropathic Pain in Chronic Spinal Cord Injury
Felix, E. R., Cardenas, D. D., Bryce, T. N., Charlifue, S. W., Lee, T. K., MacIntyre, B., Mulroy, S. J., & Taylor, H. B. (2021) · Archives of Physical Medicine and Rehabilitation · doi:10.1016/j.apmr.2021.06.022 · Cited by 39
Sleep time and efficiency in patients undergoing laboratory-based polysomnography
Harrison, E. I., Roth, R. H., Lobo, J. M., Kang, H., Logan, J. G., Patel, S. R., Kapur, V. K., & Kwon, Y. (2021) · Journal of Clinical Sleep Medicine · doi:10.5664/jcsm.9252 · Cited by 38
Effect of TAAR1/5-HT1A agonist SEP-363856 on REM sleep in humans
Hopkins, S. C., Dedic, N., & Koblan, K. S. (2021) · Translational Psychiatry · doi:10.1038/s41398-021-01331-9 · Cited by 38
Pathophysiology and Treatment of Non-motor Dysfunction in Amyotrophic Lateral Sclerosis
Mahoney, C., Ahmed, R. M., Huynh, W., Tu, S., Rohrer, J. D., Bedlack, R., Hardiman, O. M., & Kiernan, M. C. (2021) · CNS Drugs · doi:10.1007/s40263-021-00820-1 · Cited by 38
Dobrek, Ł. (2021) · Pharmaceutics · doi:10.3390/pharmaceutics13111915 · Cited by 37
Hsu, C., Tseng, W., Wang, L., Yang, Y., Kao, H.-Y., & Lin, P. (2021) · Journal of Affective Disorders · doi:10.1016/j.jad.2021.10.009 · Cited by 37
Sleep and psychiatric disorders: Bidirectional interactions and shared neurobiological mechanisms
Hyndych, A., Koval, K., Dzeruzhynska, N., & Mader, E. C. (2025) · PLOS mental health. · doi:10.1371/journal.pmen.0000531 · Cited by 36
Focusing on insomnia symptoms to better understand depression: A STAR*D report
Mason, B. L., Davidov, A., Minhajuddin, A., & Trivedi, M. H. (2019) · Journal of Affective Disorders · doi:10.1016/j.jad.2019.08.094 · Cited by 36
Wang, M., Zhang, B., Zhou, Y., Wang, C., Zheng, W., Liu, W., Zhan, Y., Lan, X., & Ning, Y. (2021) · Pharmacological Reports · doi:10.1007/s43440-020-00203-1 · Cited by 35
Cheng, Y., Tseng, P., Wu, M., Tu, Y., Wu, Y., Li, D., Chen, T., Su, K., Stubbs, B., Carvalho, A. F., et al. (2021) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2021.101469 · Cited by 35
Yin, J., Wang, H., Li, S., Zhao, L., You, Y., Yang, J., & Liu, Y. (2023) · BMC Psychiatry · doi:10.1186/s12888-023-05130-y · Cited by 35
Sleep disturbances and physical health problems in caregivers of children with ASD
Lovell, B., Elder, G. J., & Wetherell, M. A. (2021) · Research in Developmental Disabilities · doi:10.1016/j.ridd.2021.103932 · Cited by 34
Hein, M., Lanquart, J., Loas, G., Hubain, P., & Linkowski, P. (2017) · Journal of Psychosomatic Research · doi:10.1016/j.jpsychores.2017.10.004 · Cited by 34
Akers, K. G., Chérasse, Y., Fujita, Y., Srinivasan, S., Sakurai, T., & Sakaguchi, M. (2018) · Stem Cells · doi:10.1002/stem.2815 · Cited by 34
Psychotropic Drug-Associated Pneumonia in Older Adults
Rajamaki, B., Hartikainen, S. A., & Tolppanen, A. (2020) · Drugs & Aging · doi:10.1007/s40266-020-00754-1 · Cited by 34
Residual insomnia in major depressive disorder: a systematic review
Kwaśny, A., Włodarczyk, A., Dywel, A., Szarmach, J., Strandberg, O., & Cubała, W. J. (2023) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2023.1190415 · Cited by 33
Yoon, E. J., & Monchi, O. (2021) · npj Parkinson s Disease · doi:10.1038/s41531-021-00164-z · Cited by 33
Christensen, M. C., McIntyre, R. S., Florea, I., Loft, H., & Fagiolini, A. M. (2021) · CNS Spectrums · doi:10.1017/s1092852921000936 · Cited by 33
Non-REM sleep in major depressive disorder
Bovy, L., Weber, F. D., Tendolkar, I., Fernández, G., Czisch, M., Steiger, A., Zeising, M., & Dresler, M. (2022) · NeuroImage Clinical · doi:10.1016/j.nicl.2022.103275 · Cited by 33
Aishah, A., Loffler, K. A., Toson, B., Mukherjee, S., Adams, R., Altree, T. J., Ainge‐Allen, H. W., Yee, B. J., Grunstein, R. R., Carberry, J. C., et al. (2022) · Annals of the American Thoracic Society · doi:10.1513/annalsats.202206-492oc · Cited by 33
Effect of Ketamine on Sleep in Treatment-Resistant Depression: A Systematic Review
Kwaśny, A., Włodarczyk, A., Ogonowski, D., & Cubała, W. J. (2023) · Pharmaceuticals · doi:10.3390/ph16040568 · Cited by 32
Objective Sleep Duration in Older Adults: Results From The Irish Longitudinal Study on Ageing
Scarlett, S., Nolan, H., Kenny, R. A., & O’Connell, M. D. L. (2019) · Journal of the American Geriatrics Society · doi:10.1111/jgs.16177 · Cited by 32
Treatment of insomnia – effect of trazodone and hypnotics on sleep
Wichniak, A., Wierzbicka, A. E., & Jarema, M. (2021) · Psychiatria Polska · doi:10.12740/pp/125650 · Cited by 32
Self-citationMoon, E., Partonen, T., Beaulieu, S., & Mantere, O. (2022) · Neuropsychopharmacology · doi:10.1038/s41386-022-01278-5 · Cited by 32
Du, C., Hsiao, P. Y., Ludy, M., & Tucker, R. M. (2022) · Nutrients · doi:10.3390/nu14040775 · Cited by 32
Restraint stress induced anxiety and sleep in mice
Xu, Y., Liu, G., Ji, Z.-Z., Li, Y.-Y., Wang, Y., Wu, X., Liu, J.-L., Ma, D.-X., Zhong, M., Gao, C., et al. (2023) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2023.1090420 · Cited by 31
The Interaction between Stress and Inflammatory Bowel Disease in Pediatric and Adult Patients
Belei, O., Basaca, D.-G., Olariu, L., Pantea, M., Bozgan, D., Nanu, A.-M., Sîrbu, I., Mărginean, O., & Enătescu, I. (2024) · Journal of Clinical Medicine · doi:10.3390/jcm13051361 · Cited by 30
Ong, W. J., Tan, X. W., Shahwan, S., Satghare, P., Cetty, L., Ng, B. T., Tang, C. Y. Z., Verma, S. K., Chong, S. A., & Subramaniam, M. (2020) · Health and Quality of Life Outcomes · doi:10.1186/s12955-020-01367-3 · Cited by 30
The relationship between nightmares, depression and suicide
Hedström, A. K., Bellocco, R., Hössjer, O., Ye, W., Lagerros, Y. T., & Åkerstedt, T. (2020) · Sleep Medicine · doi:10.1016/j.sleep.2020.11.018 · Cited by 30
El-Solh, A., Lawson, Y., & Wilding, G. E. (2020) · Sleep And Breathing · doi:10.1007/s11325-020-02106-0 · Cited by 30
Brief psychotic disorder associated with quarantine and mild COVID-19
Haddad, P. M., Alabdulla, M., Latoo, J., & Iqbal, Y. (2020) · BMJ Case Reports · doi:10.1136/bcr-2020-240088 · Cited by 30
Price, G. D., Heinz, M. V., Zhao, D. Y., Nemesure, M. D., Ruan, F., & Jacobson, N. C. (2022) · Journal of Affective Disorders · doi:10.1016/j.jad.2022.08.013 · Cited by 30
Metadata
- Authors
- Wichniak, A., Wierzbicka, A., Walęcka, M., & Jernajczyk, W.
- Affiliations
- Institute of Psychiatry and Neurology (PL)
- Corresponding author
- Wichniak, Adam
- Venue
- Current Psychiatry Reports
- Published
- 2017-08-09
- Volume
- 19
- Issue
- 9
- Pages
- 63-63
- ISSN
- 1523-3812 (ISSN-L)
- 1535-1645
- PMC
- PMC5548844
- OpenAlex
- W2742814779
- Semantic Scholar
- 96a615c9109d6c7d744cd7ceebfb776593cdf0f4
- Cited by
- 557
- References
- 47
- Citations by year
- 2026: 71 · 2025: 87 · 2024: 62 · 2023: 66 · 2022: 72 · 2021: 74 · 2020: 47 · 2019: 50 · 2018: 20 · 2017: 4
- FWCI
- 4.24
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Current Psychiatry Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Keywords
- antidepressants, sleep, insomnia, depression, fluoxetine, venlafaxine, doxepin, mirtazapine, trazodone, cognitive behavioral therapy for insomnia, oversedation, restless legs syndrome, sleep bruxism, REM sleep behavior disorder, nightmares, sleep apnea, antidepressant-induced weight gain
- MeSH terms
- Antidepressive Agents, Depressive Disorder, Dose-Response Relationship, Drug, Drug Administration Schedule, Humans, Sleep, Sleep Wake Disorders, Time Factors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-11-07, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-11-07 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
