A 45-year-old woman presenting with five concurrent primary sleep disorders — mixed OSA/CSA, NREM parasomnia (night terrors), sleep-related eating disorder (SRED), nightmare disorder with REM behavior-like symptoms, central hypersomnolence, and delayed sleep-wake phase disorder — required individualized multimodal therapy over two decades. Among wake-promoting agents, pitolisant and solriamfetol produced the most durable improvement in excessive daytime sleepiness; melatonin plus clonazepam reduced parasomnia burden. Notably, GLP-1 receptor agonist therapy initiated for obesity preceded substantial weight loss and coincident SRED resolution, though causality remains confounded by simultaneous PAP optimization and behavioral changes.
The GLP-1 observation is the most scientifically provocative element here. Incretin-pathway signaling influences hypothalamic feeding circuits and reward-dopamine pathways — precisely the systems implicated in nocturnal bingeing behaviors. While this single case cannot establish mechanism, it aligns with emerging metabolic neuroscience suggesting GLP-1 agonists modulate compulsive feeding drives independent of caloric restriction alone. For clinicians managing SRED — a notoriously difficult-to-treat parasomnia associated with weight gain, injury, and medication side effects — this signal warrants prospective investigation.
As a case report, this carries the lowest evidential weight in the hierarchy of clinical research. Its value lies in hypothesis generation rather than practice change. Still, given the rapid expansion of GLP-1 agonist prescribing, systematic collection of sleep-behavior outcomes in these patients represents a low-cost, high-yield research opportunity. An incremental but genuinely interesting clinical observation.