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. 2014 Aug 1;37(8):1393. doi: 10.5665/sleep.3938

Antidepressants Trigger an Early Clinical Presentation of REM Sleep Behavior Disorder: The Jury is Still Out

Bhanu Prakash Kolla 1,✉, Meghna Prabhdas Mansukhani 1
PMCID: PMC4096209  PMID: 25083020

In their interesting prospective cohort study addressing an important clinical issue, Postuma1 et al. evaluate the relationship between antidepressant use and idiopathic rapid eye movement sleep behavior disorder (iRBD). Their cohort comprises 100 patients who present to a sleep clinic and are found to have iRBD. After comparing patients with iRBD who are on antidepressants with healthy controls as well as other patients with iRBD who are not on antidepressants, the authors conclude that “antidepressants primarily trigger early clinical presentation of an RBD that is nonetheless still due to underlying neurodegeneration.”

The authors posit that because the patients in their cohort with antidepressant-associated RBD had markers for neurodegeneration and lower rates of developing neurodegenerative disorders, antidepressants primarily trigger an early clinical presentation caused by an underlying degenerative disorder. Based on the current data, we believe that this conclusion may be premature.

In the introduction, the authors acknowledge that antidepressant use could be a proxy marker for depression, a prodromal symptom for neurodegeneration. This possibility is discounted in the discussion because patients with antidepressant-associated iRBD had lower rates of developing neurodegeneration at the end of the study period. Depression can predate neurodegeneration by many years.2,3 The study population was followed for 8 y, and patients with a possible temporal relationship between antidepressant use and iRBD were significantly younger than the no-antidepressant group (62.0 ± 10.9 versus 67.8 ± 9.7; P = 0.03; Table S1); if the antidepressant group were followed for a longer duration, neurodegeneration could possibly develop at similar rates. Thus, the possibility that antidepressant use is a proxy measure of depression remains a viable explanation.

Additionally, this study relies on subject recall to determine the relationship between antidepressant use and the onset of iRBD. This is prone to recall bias and hence the temporal relationship between the onset of iRBD, and antidepressant use is not certain. Also, the authors state that iRBD was diagnosed based on either polysomnography (PSG) findings or clinical history, and it is not clear how many patients provided a history of dream enactment behavior versus the number of patients in whom the diagnosis was made based entirely on PSG findings.

Finally, another plausible explanation for the aforementioned results is that antidepressants are in fact neuroprotective. There is a body of research showing that antidepressants increase neuronal proliferation and inhibit neural cell destruction.4–6 Antidepressants, through their neuroprotective mechanisms, may therefore reduce the rates of developing a neurodegenerative disorder or delay the course of neurodegeneration in patients who are otherwise at risk.

CITATION

Kolla BP, Mansukhani MP. Antidepressants trigger an early clinical presentation of REM sleep behavior disorder: the jury is still out. SLEEP 2014;37(8):1393.

DISCLOSURE STATEMENT

The authors have indicated no financial conflicts of interest.

REFERENCES

  • 1.Postuma RB, Gagnon JF, Tuineaig M, et al. Antidepressants and REM sleep behavior disorder: isolated side effect or neurodegenerative signal? Sleep. 2013;36:1579–85. doi: 10.5665/sleep.3102. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2.Shiba M, Bower JH, Maraganore DM, et al. Anxiety disorders and depressive disorders preceding Parkinson's disease: a case-control study. Mov Disord. 2000;15:669–77. doi: 10.1002/1531-8257(200007)15:4<669::aid-mds1011>3.0.co;2-5. [DOI] [PubMed] [Google Scholar]
  • 3.Schuurman AG, van den Akker M, Ensinck KT, et al. Increased risk of Parkinson's disease after depression: a retrospective cohort study. Neurology. 2002;58:1501–4. doi: 10.1212/wnl.58.10.1501. [DOI] [PubMed] [Google Scholar]
  • 4.Czeh B, Muller-Keuker JI, Rygula R, et al. Chronic social stress inhibits cell proliferation in the adult medial prefrontal cortex: hemispheric asymmetry and reversal by fluoxetine treatment. Neuropsychopharmacology. 2007;32:1490–503. doi: 10.1038/sj.npp.1301275. [DOI] [PubMed] [Google Scholar]
  • 5.Kodama M, Fujioka T, Duman RS. Chronic olanzapine or fluoxetine administration increases cell proliferation in hippocampus and prefrontal cortex of adult rat. Biol Psychiatry. 2004;56:570–80. doi: 10.1016/j.biopsych.2004.07.008. [DOI] [PubMed] [Google Scholar]
  • 6.Lucassen PJ, Fuchs E, Czeh B. Antidepressant treatment with tianeptine reduces apoptosis in the hippocampal dentate gyrus and temporal cortex. Biol Psychiatry. 2004;55:789–96. doi: 10.1016/j.biopsych.2003.12.014. [DOI] [PubMed] [Google Scholar]

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