1390 Comorbid Insomnia and Obstructive Sleep Apnea in Huntington’s Disease: A Case Report

Abstract Introduction Sleep disturbances are common in Huntington’s disease (HD), including insomnia, circadian delay, and obstructive sleep apnea (OSA). Comorbid insomnia and sleep apnea (COMISA) is associated with greater symptom burden, reduced positive airway pressure (PAP) adherence, and impaired daytime function. Treatment is particularly challenging in neurodegenerative diseases, where fatigue, chorea and cognitive hyperarousal may hinder behavioral interventions. We describe a patient with HD and moderate OSA who achieved rapid insomnia remission using measurement-guided cognitive behavioral therapy for insomnia (CBT-I) with adaptations for fatigue. Report of case(s) A 37-year-old woman with genetically confirmed HD presented with long-standing insomnia, excessive daytime sleepiness, and loud snoring. Baseline assessments included ISI 23, ESS 11, evening chronotype, pronounced sleep inertia, cognitive hyperarousal, and sleep extension (time-in-bed 11.5 h). Home sleep testing showed moderate–severe OSA (AHI 36.2). PAP had been initiated previously but was poorly tolerated. Measurement-based CBT-I was started with an initial 8.5-hour sleep window (01:00–09:30), weekly titration contingent on sleep efficiency ≥85%, stimulus control, constructive worry, and relaxation training. Because of HD-related excessive sleepiness and fatigue, we incorporated scheduled daytime power naps (≤30 min, ending by 16:00) while enforcing strict behavioral contingencies to maintain sleep drive. Rapid improvement was noted. Within four weeks, ISI decreased from 23 to 12; by week seven, ISI reached 4. Sleep-diary metrics normalized (SOL 60→10 min; WASO 60→5 min; awakenings 3→1; SE 69.6%→93%). ESS improved from 11 to 4, and functional outcomes improved (FOSQ 16→22). Sleep quality rose from 1 (poor) to 3.5 (good). Short, planned naps prevented fatigue without disrupting nocturnal sleep. No adverse effects occurred, and mood screens remained negative. Conclusion In a patient with HD and COMISA, tailored CBT-I produced rapid and durable insomnia remission despite ongoing OSA and neurologic comorbidity. Strict titration of sleep opportunity, structured daytime napping, and targeted reduction of cognitive hyperarousal were central to treatment success. Behavioral therapy should be considered early in COMISA involving neurodegenerative disease, with pragmatic adaptations to support adherence and functional stability. Support (if any) None