1349 REM Predominance on Polysomnography (58.7%)

Abstract Introduction Rapid eye movement (REM) sleep constitutes 20 to 25 percent of total sleep time (TST) in healthy adults. An increase in REM sleep, termed REM rebound or predominance, is typically observed after sleep deprivation, withdrawal of REM-suppressing agents, initiation of positive airway pressure therapy, or in major depressive disorder (MDD). We present a case with a striking REM-predominant hypnogram on overnight polysomnography, wherein multiple physiologic and behavioral contributors highlight the importance of detailed history taking. Report of case(s) A 57-year-old woman with a past medical history of MDD on desvenlafaxine, untreated moderate obstructive sleep apnea due to CPAP intolerance, and fibromyalgia was referred for nonrestorative sleep. Medications included as-needed lorazepam 1 mg for sleep onset insomnia and amphetamine-dextroamphetamine 20 mg twice a day for persistent daytime somnolence. Diagnostic polysomnography demonstrated a significantly elevated proportion of REM sleep (58.7%) with 224.5 minutes of REM sleep within 382.5 minutes of TST. REM latency was 53.5 minutes with multiple REM periods noted. Sleep latency was 6.5 minutes. Apnea-Hypopnea Index (AHI) was 27.6 events per hour. Retrospectively, the patient reported that she did not take lorazepam or her afternoon dose of amphetamine-dextroamphetamine on the night of the study. She endorsed stable MDD but substantial psychological stress in the weeks leading up to polysomnography and the demise of her significant other shortly after the study. No acute sleep deprivation was reported. Conclusion We postulate that intermittent stimulant use, significant psychological stress, and underlying MDD likely interacted to increase REM pressure in our patient. Stress physiology is an important yet under-recognized modulator of REM sleep. Mellman et al. reported that individuals who exhibited a robust REM rebound after traumatic events were less likely to develop PTSD than subjects with fragmented, short REM episodes. Suchecki et al. hypothesized that acute stress-induced serotonin release increases adrenocorticotropic hormone (ACTH) levels in the arcuate nucleus, with downstream metabolism into corticotropin-like intermediate lobe peptide, a significant inducer of REM sleep. These mechanisms indicate that stress-related pathways may augment classical causes of REM rebound, highlighting, as illustrated in our case, the need for careful history taking to identify multifactorial influences when interpreting REM rebound on polysomnography. Support (if any)