1342 A Multidisciplinary Sleep–Psychiatry Approach to Exploding Head Syndrome in a Veteran with PTSD

Abstract Introduction Exploding Head Syndrome (EHS) is a benign parasomnia characterized by sudden sensory “explosions” at sleep–wake transitions, which can aggravate insomnia and PAP intolerance in PTSD. Report of case(s) We report a 79-year-old veteran with chronic obstructive and central sleep apnea, long-standing PTSD, and depression, who experienced nightly episodes of explosive sounds accompanied by flashes of light, myoclonic jerks, tachycardia, and panic, leading to removal of positive airway pressure (PAP) equipment. Earlier records (2007–2008) described poor sleep hygiene, insomnia linked to PTSD/depression, parasomnia-like symptoms, and evolving PAP intolerance. After being lost to follow-up, he re-presented in 2023 with severe sleep fragmentation and recurrent “gunshot-like” awakenings consistent with EHS. Polysomnography (1/12/2024) captured an event at the transition from wakefulness to N2 sleep and revealed an AHI of 66.2/hour (central 45.4/hour; SpO₂ nadir 85%). PAP titration to 13 cm H₂O normalized breathing (residual AHI 0/hour). Two-week actigraphy (10/21–11/03/2024) showed ~5 hours of sleep, 74% efficiency, ~20 awakenings/night, and an irregular sleep schedule. A multidisciplinary plan included structured psychiatric interviews, sleep diaries, and measurement-based care. Sleep psychiatry optimized sertraline (200 mg/day) and added buspirone (7.5 mg TID) and gabapentin (900 mg BID) to reduce anxiety and hyperarousal. Behavioral sleep medicine delivered CBT-I tailored to PTSD triggers with PAP desensitization, emphasizing stimulus control, relaxation, and gradual sleep-window extension. Mindfulness and alpha-frequency cranial stimulation were adjuncts. Over eight months, EHS frequency decreased from nightly (~7/week) to 1–2/week with reduced intensity. Sleep efficiency improved to ~94% with 2–3 awakenings/night, and Insomnia Severity Index dropped from 26 to 7. Nightmares declined, and PAP adherence temporarily improved before later relapse due to PTSD-related distress, prompting hypoglossal nerve stimulation implant evaluation. At one-year follow-up, EHS symptoms remained improved without adverse effects. Conclusion In this veteran with PTSD and severe sleep-disordered breathing, EHS improved with integrated pharmacologic anxiety modulation and CBT-I with PAP desensitization. Collaborative sleep-psychiatric and behavioral care reduced arousal sensitivity and produced durable improvements in symptoms and sleep quality, even as alternative therapies were pursued for persistent sleep apnea. Support (if any)