1339 Recurrent Injurious Nocturnal Hypermotor Episodes: Diagnostic Assessment of Parasomnia Overlap Syndrome and Sleep-Related Hypermotor Epilepsy

Abstract Introduction Sleep-Related Hypermotor Epilepsy (SHE) and parasomnias often present with overlapping hypermotor behaviors, complicating diagnosis. We report a case of a stereotyped, injurious nocturnal motor disorder in which sequential polysomnography (PSG) and extended video-EEG monitoring ultimately supported a diagnosis of parasomnia overlap syndrome. Report of case(s) A 49-year-old male with well-controlled obstructive sleep apnea presented with recurrent injurious nocturnal hypermotor episodes, culminating in right tibia-fibula fracture requiring surgical fixation. He described several years of 5–7 nightly, 30-second episodes of abrupt arousal, leaving the bed, and uncontrolled limb movements, with partial awareness. History included childhood somnambulism which resolved at age twelve and remote dream enactment behavior. Neurologic exam, MRI, and baseline EEG were unremarkable. PAP-titration polysomnography captured eight stereotyped hypermotor episodes during N3 sleep, featuring dystonic posturing, hyperkinetic limb movements, and semi-purposeful CPAP manipulation, lasting 45–90 seconds. Some episodes were preceded by rhythmic theta activity; periodic limb movement index was 40/hr. Clonazepam (1 mg nightly) prevented further falls but did not significantly reduce event frequency. Epilepsy Monitoring Unit (EMU) admission (off clonazepam) recorded 3 push button events arising from N3 sleep with paroxysmal arousals, rapid autonomic activation, and limb shaking, but no ictal EEG activity. EMU assessment was low likelihood of SHE. Subsequent PSG with CPAP demonstrated REM sleep without atonia. A FLEP (frontal lobe epilepsy and parasomnia) score of +2 was suggestive of epileptic hypermotor events, possibly corroborated by rhythmic theta, though this can be a normal variant. Transition from desvenlafaxine to bupropion and resumption of clonazepam correlated with near resolution of events. Conclusion This case illustrates diagnostic complexity of nocturnal hypermotor events, where clinical features and nondiagnostic EEG blur distinctions among NREM parasomnia and SHE. Parasomnia overlap syndrome was favored given evidence of both REM and NREM parasomnias with negative seizure evaluation. Negative scalp EEG is supportive rather than diagnostic, since only 10-50% of awake and 50% of asleep patients with SHE show interictal abnormalities. The case underscores the limitations of scalp EEG and scoring tools, and highlights the importance of longitudinal assessment, PAP and medication optimization, and safety. Support (if any)