Introduction Atonia of Skeletal Muscles Is One of the Cardinal Features of Rapid Eye Movement

ATONIA OF SKELETAL MUSCLES IS ONE OF THE CARDINAL FEATURES OF RAPID EYE MOVEMENT (REM) SLEEP. Superimposed on this atonia is intermittent activity in both axial and limb muscles. REM sleep behavior disorder (RBD) is characterized by excessive motor activity during REM sleep with acting out of dreams.1 The diagnosis of RBD is made by the appearance of elevated submental electromyogram (EMG) tone during REM and/or excessive phasic submental or anterior tibialis EMG activity, combined with polysomnographic documentation or a history of frank movements during REM sleep.2 RBD is more common in elderly men, and at least half of those followed for 10 years develop Parkinson disease.3 Muscle-tone abnormalities in REM sleep may consist along a spectrum, with maintenance of full atonia at one end and full RBD at the other end. REM sleep without atonia has been described as an intermediate condition, in which REM sleep atonia is reduced on polysomnography, in the absence of reports of abnormal behaviors by the patient or bed partner. This polysomnographic finding has also been called “subclinical” RBD. Eisensehr’s recent report4 demonstrating that those patients with subclinical RBD have an intermediate reduction of striatal dopamine transporters, roughly halfway between normal individuals and those with RBD, establishes the potential importance of this disorder. Antidepressants have substantial effects on REM sleep. Many studies show that they prolong REM sleep latency and suppress REM sleep time.5 They are also associated with reports of “vivid” dreams.6 In addition, case reports dating back 30 years show that antidepressants can induce RBD7 or reduce REM sleep atonia.8 In fact, medications with a wide variety of mechanisms of action have been implicated in producing loss of REM sleep atonia, including serotonergic reuptake blockers such as fluoxetine,9 monoamine oxidase inhibitors,10 β-adrenergic receptor blockers,11 the noradrenergic and 5-HT1A-mediated serotonergic enhancer mirtazapine,12 and the tricyclic antidepressants.13 However, no study has systematically assessed EMG tone during REM sleep in individuals chronically taking antidepressants. Given the number of individuals taking these medications, this issue is potentially of substantial public health importance. The objective of this study was to compare tonic and phasic EMG during REM sleep in individuals without a complaint of abnormal behavior during sleep who were taking serotonergic antidepressants with the REM characteristics of matched controls not taking such medications. We hypothesize that serotonergic antidepressants will increase tonic and phasic submentalis and anterior tibialis EMG activity during REM sleep compared to the control population not taking such medications.