ArticleCureus2026
Rapid Eye Movement (REM)-Predominant Obstructive Sleep Apnea (OSA) Coexisting With and Initially Obscuring Narcolepsy Type 1: A Nine-Year Longitudinal Case Report.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Obstructive sleep apnea (OSA) is a common disorder whose clinical expression and daytime sleepiness may evolve over time, particularly in the presence of coexisting sleep disorders. We report a nine-year longitudinal case of a 29-year-old man presenting initially with severe excessive daytime sleepiness (EDS) (Epworth Sleepiness Scale (ESS) score: 19/24) and mild OSA (apnea-hypopnea index (AHI): 10 events/h), who represented nine years later with disabling sleepiness, weight gain (body mass index: 30.2 kg/m²), and typical cataplexy. No documented sleep medicine follow-up or OSA treatment was available during the intervening nine-year period. Repeat polysomnography demonstrated moderate, rapid eye movement (REM)-predominant OSA (AHI: 20.4 events/h; REM-AHI: 52.9 events/h; non-REM (NREM)-AHI: 9.4 events/h; REM-AHI/NREM-AHI ratio: 5.6), with increased sleep fragmentation. The Multiple Sleep Latency Test (MSLT), performed after diagnostic polysomnography and before continuous positive airway pressure (CPAP) optimization, showed severe objective sleepiness (mean sleep latency: 3.7 minutes) with sleep-onset REM periods in all five nap opportunities. In the setting of typical cataplexy, these findings strongly supported a diagnosis of narcolepsy type 1; however, untreated OSA and sleep fragmentation at the time of testing were acknowledged as potential confounders in the interpretation of the MSLT. Management included fixed-pressure CPAP at 8 cm H₂O, sertraline for cataplexy, and modafinil for EDS. At 30-day follow-up, CPAP downloads showed use on 60% of nights, with a residual AHI of 3.1 events/h and mean leak of 35 L/min, indicating effective control of respiratory events when therapy was used, but suboptimal adherence and mask leak likely limiting clinical benefit. This case highlights three key clinical messages: EDS disproportionate to OSA severity should prompt evaluation for a coexisting central disorder of hypersomnolence; REM-predominant OSA can coexist with narcolepsy type 1 without implying a causal relationship between the two disorders; and their relative contributions to sleepiness may change over time. When MSLT is required in a patient with OSA, effective treatment of OSA and adequate documentation of prior sleep are important for reliable interpretation. Management should address both OSA and narcolepsy and include periodic reassessment as the clinical phenotype evolves.
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