Successful Treatment of Exploding Head Syndrome With Ketamine.
Luiza Haruyunyan, Mitchell Liester, Bertrand Liang
Cureus November 23, 2025 DOI: 10.7759/cureus.97558 via PubMed Central
Summary
AI-generated from the abstractA 75-year-old man with chronic exploding head syndrome—loud internal noises, lightning-like sensations, and sleep paralysis for over five years—failed multiple standard medications. Sublingual ketamine, starting at 25 mg every third night and increasing to nightly, reduced episodes from 3-4 times weekly to once every two weeks after one month, monthly by three months, and resolved completely by six months, with only occasional sleep paralysis remaining. The treatment improved quality of life. Ketamine may work through NMDA receptor modulation and neuroplasticity. This case suggests a potential new approach for this difficult-to-treat sleep disorder.
Study at a glance
| Characteristics | Case report Peer reviewed |
|---|---|
| Sample size | 1 |
| Population | A 75-year-old man with chronic exploding head syndrome |
| Intervention | sublingual ketamine |
| Dose | 25 mg every third night escalating to nightly dosing |
| Duration | 6-month follow-up |
| Key finding | Sublingual ketamine led to complete resolution of exploding head syndrome episodes within six months in a patient who had failed multiple prior treatments. |
Abstract
Exploding head syndrome (EHS) is a parasomnia characterized by the perception of loud noises originating from inside the head during sleep transitions, often accompanied by visual phenomena and fear. Treatment remains challenging due to unknown etiology and limited therapeutic options. We report a 75-year-old man with chronic exploding head syndrome experiencing lightning-like sensations, thunder-like sounds, sleep paralysis, and intense fear during sleep onset. Episodes occurred multiple times weekly for over five years. Initial treatments, including gabapentin, valproic acid, amitriptyline, and buspirone, proved ineffective. The patient was subsequently treated with sublingual ketamine, starting at 25 mg every third night and escalating to nightly dosing. After one month, episode frequency decreased from 3-4 times weekly to once every two weeks. By three months, episodes occurred monthly with reduced intensity. After six months, the patient experienced only occasional sleep paralysis with the complete resolution of exploding head syndrome and reported improved quality of life. Ketamine's mechanism likely involves N-methyl-D-aspartate (NMDA) receptor modulation, brain-derived neurotrophic factor release, and σ1 receptor agonism, promoting neuroplasticity and sleep regulation. This case represents a reported successful treatment of exploding head syndrome with ketamine, suggesting a potential therapeutic approach for this refractory parasomnia. Further studies are warranted to evaluate ketamine's efficacy in exploding head syndrome treatment.