Common Antidepressants Disrupt the Sleep Paralysis That Keeps Dreamers Still

Every night, as healthy sleepers slip into rapid eye movement (REM) sleep, the brain performs a remarkable trick: it paralyzes nearly every muscle in the body. This state of atonia prevents us from physically acting out our dreams. But in some people, that paralysis fails, and the electromyographic signature of that failure—known as REM sleep without atonia, or RSWA—can be measured on a sleep study. Now, one of the largest investigations ever conducted has found that not all antidepressants interfere with this protective paralysis equally. The findings, published in the Journal of Clinical Sleep Medicine, carry important implications for how sleep physicians interpret polysomnograms in the millions of patients taking these medications.

A team of sleep neurologists at the Cleveland Clinic Sleep Disorders Center analyzed 1,474 video polysomnograms performed between September 2018 and October 2023, drawing on the center’s STARLIT registry. Of these patients, 624—about 42 percent—were taking antidepressants, while 850 were not. The researchers manually scored RSWA using chin (submentalis) and bilateral flexor digitorum superficialis (FDS) electromyography, following the American Academy of Sleep Medicine’s current scoring criteria. Unlike many earlier studies that relied on leg muscles prone to artifact, this approach captured the upper limb signals now considered the most accurate diagnostic markers for REM sleep behavior disorder.

The technical rigor of the scoring matters. RSWA was flagged when any of three criteria were met: tonic activity, in which chin EMG amplitude runs at least twice the atonia level for at least half of a 30-second epoch; phasic activity, in which at least five of ten consecutive three-second mini-epochs contain brief bursts of doubled-amplitude muscle activity in the chin or forearm muscles; or any sustained EMG activity meeting amplitude thresholds regardless of duration. To avoid confounding by sleep apnea, REM epochs during or within 30 seconds of a respiratory event were excluded from analysis.

The headline result is a clear class effect. After adjusting for age, body mass index, gender, and race, patients on selective serotonin reuptake inhibitor (SSRI) monotherapy showed a 3.39 percent increase in the proportion of REM epochs containing RSWA compared with medication-free patients, while those on serotonin norepinephrine reuptake inhibitors (SNRIs) showed a substantially larger 6.66 percent increase. Both findings were statistically significant. In striking contrast, tricyclic antidepressant (TCA) monotherapy was not associated with any increase in RSWA—in fact, the point estimate trended downward, though it did not reach significance.

Combination therapies produced the highest estimates of all. Patients taking both an SSRI and an SNRI showed a 10.44 percent increase in RSWA, and those combining an SNRI with a TCA showed a 12.81 percent increase, although the authors caution that these combination subgroups were small—14 and 9 patients respectively—and the results did not reach conventional statistical significance. Overall, mean RSWA was significantly higher among antidepressant users than non-users, at 15.0 percent versus 9.7 percent of REM epochs, and 18.9 percent of medicated patients crossed the 27 percent RSWA threshold used to diagnose REM sleep behavior disorder on polysomnography, compared with 11.4 percent of non-users.

Why would serotonergic and noradrenergic drugs loosen the grip of sleep paralysis? The answer lies in the brainstem circuitry that governs REM atonia. Glutamate-releasing neurons in the pontine sublaterodorsal nucleus activate inhibitory premotor neurons in the ventral medulla, which in turn silence spinal motor neurons during REM sleep. SSRIs and SNRIs boost serotonin and norepinephrine signaling, and the study’s authors suggest that activation of the dorsal raphe serotonergic and locus coeruleus noradrenergic nuclei during REM may interfere with this normal inhibitory cascade, allowing muscle tone to leak back into dreaming sleep.

The clinical stakes are high because RSWA is the polysomnographic biomarker of REM sleep behavior disorder (RBD), a parasomnia in which patients physically enact their dreams—punching, kicking, and shouting—sometimes injuring themselves or their bed partners. Isolated RBD in older adults is one of the strongest known harbingers of neurodegenerative disease, frequently preceding Parkinson’s disease, dementia with Lewy bodies, or multiple system atrophy by years or even decades. Yet increased REM muscle tone is not specific to neurodegeneration. It also appears with antidepressant exposure, psychiatric illness, and narcolepsy, which creates a genuine diagnostic dilemma for sleep physicians evaluating a depressed patient on an SSRI who also shows excessive REM EMG activity.

One emerging hypothesis, supported by the new data, is that antidepressants do not create RBD from scratch but rather unmask a pre-existing, subclinical neurodegenerative process. Patients with antidepressant-associated RBD have been found to harbor markers of neurodegeneration—olfactory impairment, color vision deficits, and autonomic dysfunction—that cannot be explained by the medications alone. If serotonergic drugs simply reveal an underlying tendency toward RSWA, then a patient whose sleep study shows drug-associated muscle activity may still warrant closer neurological follow-up rather than reassurance that the finding is merely a side effect.

The Cleveland Clinic study is not without caveats, and the authors are candid about them. The cohort was clinically selected: RSWA scoring was performed only for studies with suspected parasomnia or observed dream enactment, enriching the sample for muscle activity and inflating absolute percentages relative to an unselected sleep laboratory population. The cross-sectional design precludes causal inference, potential confounders such as melatonin use could not be assessed, and the software could not distinguish tonic from phasic RSWA. The cohort was also predominantly White, and the medicated group skewed female and slightly younger, limiting generalizability. Formal inter-reader reliability testing was not performed, though average RSWA percentages did not differ significantly across the four scorers.

Even with those limitations, the study stands as the largest to date to quantify RSWA with modern AASM criteria and the SINBAR-style montage incorporating upper extremity EMG, and its message is unambiguous: SSRIs and SNRIs, but not TCAs, are associated with measurably more REM sleep without atonia in patients evaluated for parasomnia. For clinicians, the practical takeaway is that medication history must be weighed carefully when interpreting a sleep study suggestive of RBD, particularly since the proportion of patients meeting electrodiagnostic criteria for RBD was higher among antidepressant users in this cohort. For the millions of people taking these widely prescribed drugs, the findings are not a reason to stop treatment—but they are a reason for sleep medicine to look more closely at what antidepressants do to the sleeping brain, and at what those changes might reveal about the decades to come.

Subject of Research: Differential effects of antidepressant classes on REM sleep without atonia measured by chin and upper extremity EMG

Article Title: Antidepressant medications have differential effects on REM sleep without atonia quantified by chin and upper extremity EMG

Article References: Ahdab, J. E., Rodriguez, C. L., Grigg-Damberger, M., Araujo, M. L. D., Andrews, N. D., Thanaviratananich, S., & Foldvary-Schaefer, N. (2026). Antidepressant medications have differential effects on REM sleep without atonia quantified by chin and upper extremity EMG. Journal of Clinical Sleep Medicine, 22(1), Article 109. https://doi.org/10.1007/s44470-026-00127-2

Image Credits: AI Generated

DOI: 10.1007/s44470-026-00127-2

Keywords: REM sleep without atonia, REM sleep behavior disorder, antidepressants, SSRIs, SNRIs, tricyclic antidepressants, polysomnography, electromyography, sleep medicine, neurodegeneration, Parkinson's disease, parasomnia