1356 Hypersomnia of Central Origin: Sequelae of Aneurysmal Rupture

Abstract Introduction Excessive daytime sleepiness (EDS) may occur due to insufficient sleep, sleep apnea, or primary central disorders of hypersomnolence. However, EDS may also occur following neurologic injury. Sleep–wake disturbances following subarachnoid hemorrhage (SAH) have been reported, yet missed in clinical practice. We present a case of severe hypersomnia following aneurysmal SAH complicated by persistent hydrocephalus with well-controlled obstructive sleep apnea (OSA). Report of case(s) 40-y/o male with hypertension, hyperlipidemia, and OSA on CPAP was referred for evaluation of profound hypersomnia following aneurysmal SAH one year prior, complicated by hydrocephalus. Neurosurgery recommended shunt placement, but the patient declined. After the SAH he had unrefreshing sleep, difficulty sustaining wakefulness, and unintentional dozing with functional impairment. Epworth Sleepiness Scale score was 15. OSA was effectively treated at 10 cm of water with PAP-generated AHI of 1.4. He denied using sedating prescription or over-the-counter medications. He underwent Multiple Sleep Latency Test (MSLT) preceded with PSG on CPAP at home setting. PSG documented a total sleep time of 466 minutes, with sleep architecture including N1 2.9%, N2 65.9%, N3 19.0%, and REM 12.2% (REM latency 125 minutes). MSLT demonstrated severe hypersomnia with sleep occurring in all five nap opportunities with a mean sleep latency of 2.5 minutes. One sleep-onset REM period (SOREMP) occurred (REM latency 12.5 minutes) in nap 1. In the context of SAH with persistent hydrocephalus and adequately treated OSA, findings supported a diagnosis of secondary hypersomnia likely related to post-hemorrhagic disruption of hypothalamic/brainstem arousal networks and associated neurophysiologic dysregulation. Conclusion This case underscores the importance of considering secondary neurologic causes of hypersomnolence. SAH, particularly when complicated by hydrocephalus, may disrupt central arousal systems and produce clinically significant hypersomnolence with severity similar to narcolepsy. Mechanistic support has been described in SAH cohorts reporting orexin/hypocretin abnormalities, including reported lower hypocretin-1/orexin-A levels following the SAH event, which may persist in some cases. Objective evaluation with PSG/MSLT may confirm pathological sleepiness, avoids diagnostic anchoring on treated OSA, and supports collaborative management and counseling regarding potentially modifiable contributors, including hydrocephalus. Support (if any)