Abstract Introduction NREM parasomnias such as night terrors typically present in childhood and rarely recur in adulthood without identifiable triggers. Contributing factors include sleep deprivation, psychiatric stress, medications, or underlying sleep disorders. Glucagon-like peptide-1 (GLP-1) receptor agonists, including semaglutide, are increasingly used for metabolic disease and have recognized central nervous system effects with emerging reports of vivid dreaming and sleep disruption. However, their association with NREM parasomnias has not been described. We report a case of dose-dependent recurrence of night terrors following semaglutide initiation in an adult with remote childhood parasomnia. Report of case(s) A 42-year-old woman with class 2 obesity (BMI 36.8 kg/m²), migraine without aura, and mild generalized anxiety disorder presented with new nocturnal episodes occurring 60–90 minutes after sleep onset. Events involved sudden screaming, thrashing movements, marked confusion, and autonomic activation lasting several minutes followed by complete amnesia—consistent with night terrors. No dream enactment behaviors/ features of REM sleep behavior disorder were present. Her sleep schedule was stable (10 PM–6 AM) without shift work, substance use, or recent stressors. Two weeks before symptom onset, she began semaglutide 0.25 mg weekly, later titrated to 0.5 mg. Parasomnia frequency increased in parallel with dose escalation. Neurologic examination was normal. Laboratory evaluation (CBC, CMP, TSH, ferritin, vitamin B12, hemoglobin A1c) was unremarkable. Prior home sleep apnea testing showed no sleep-disordered breathing and she was not using SSRIs, TCAs, benzodiazepines, or hypnotics. Because of the temporal association, semaglutide was reduced to 0.25 mg weekly. Night terrors decreased immediately and resolved within 10 days. At three-month follow-up she remained asymptomatic at the lower dose. When she inadvertently resumed 0.5 mg weekly, symptoms recurred within 48 hours and again resolved after dose reduction, demonstrating a dose-dependent effect. Conclusion This case demonstrates a likely association between semaglutide and recurrence of NREM parasomnias in an adult supported by clear temporal and dose-dependent patterns. GLP-1–related effects on arousal regulation or N3 sleep stability may lower the threshold for parasomnia expression in predisposed individuals. As use of GLP-1 agonists expands, clinicians should monitor for new sleep-related behaviors and consider dose reduction when parasomnias occur as symptoms may resolve without discontinuing therapy. Support (if any)
Maithili Udupa (Fri,) studied this question.
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