Exploding Head Syndrome (EHS) is characterized by perception of sudden, loud noises or explosion-like sounds originating within the head, typically occurring as one falls asleep or wakes up [1,2]. While these experiences are not physically painful [1], they can cause significant psychological distress, leading to sudden awakenings and, when frequent, insomnia [3]. Although EHS is generally considered benign with a favorable prognosis [1,4], its rarity has limited comprehensive research. Furthermore, there are limited reports suggesting a potential link between EHS and obstructive sleep apnea (OSA) [4-6]. Here we present a middle-aged man with mild OSA. He frequently experienced EHS episodes, describing sensations of lightning accompanied by loud exploding sounds during sleep.

A 48-year-old man presented with a six-month history of perceptual symptoms during sleep, including vivid lightening-like sensations and perception of explosions in his head. These symptoms typically occurred when he was falling asleep, during sleep, or when napping. Although episodes were brief, they caused substantial anxiety and distress, often leaving him unable to resume sleep, further aggravating his sleep disruption. He denied headaches, nausea, and vomiting. He had no history of migraine. His medical history included hypertension, which was managed with medication. Neurological examination, laboratory tests, brain images, and electroencephalography were unremarkable. The patient was overweight (170 cm and 78 kg, body mass index 27.1 kg/m²). He snored gently and denied any witnessed apnea events. His Insomnia Severity Index score was 16 (range, 15–21, indicating moderate insomnia). His Epworth Sleepiness Scale score was 8 (range, 0–10, within normal range for sleepiness). His Beck depression inventory II score was 15 (range, 14–19, indicating a mild depressive mood). Polysomnography (PSG) revealed a total sleep time of 286.5 minutes, with a sleep latency of 16 minutes and a rapid eye movement (REM) sleep latency of 201 minutes. Sleep efficiency was 60.7%, with 169.5 minutes of waking after sleep onset. The PSG showed an apnea-hypopnea index (AHI) of 7.5/hour, indicating mild OSA (supine AHI: 13.7/hour, REM AHI: 14.3/hour, and supine REM AHI: 68.6/hour). The spontaneous arousal index was 20.3/hour and the total arousal index was 24.5/hour, showing no evidence of periodic limb movements. Notably, one episode of EHS occurred, coinciding with the end of a hypopnea event during N2 sleep (Fig. 1). These findings suggested that mild OSA could be a potential trigger for his EHS episodes. Initial treatment with continuous positive airway pressure (CPAP) at 6 cmH2O reduced, but did not entirely resolve, his difficulties with sleep maintenance. Adding clonazepam (1 mg) completely alleviated his nighttime EHS episodes, although his symptoms persisted during naps.

Due to its rarity and often benign nature, EHS is often underreported, contributing to the limited literature on this subject. This case provides insight into a possible relationship between EHS and OSA, specifically an episode of EHS associated with a hypopnea event during N2 sleep on PSG. Findings of this study suggest that even mild OSA may trigger or exacerbate EHS symptoms, such as auditory and visual sensations. Intermittent hypoxia and sleep fragmentation caused by OSA can disrupt sleep stage transitions [7], potentially triggering abnormal sensory experiences observed in EHS. In this case, the presence of mild OSA strengthened the potential link between sleep-disordered breathing and EHS, suggesting that OSA might play a role in the pathophysiology of EHS. However, it remains unclear how disrupted sleep stages might affect sensory perceptions characteristic of EHS.

The absence of symptoms indicative of OSA, other than mild snoring in the case, poses a significant challenge in establishing a definitive temporal relationship between EHS and OSA. However, the significant reduction in nighttime EHS symptoms following CPAP and clonazepam treatment might have addressed the underlying sleep-disordered breathing and helped manage EHS. CPAP can reduce the frequency of apneas and hypopneas, potentially reducing arousals and sensory disturbances that may trigger EHS episodes [8]. Additionally, anxiolytic and muscle relaxant effects of clonazepam might alleviate psychological impact of EHS and improve overall sleep quality [3,9]. However, the persistence of EHS during naps highlights a limitation of current treatments. CPAP is often impractical for short naps and daytime use of clonazepam is limited due to its sedative effects, which can impair daytime functioning. Although clonazepam was effective in this case, its long-term use carries risks of dependency and adverse effects. In addition, alternative or adjunctive therapies specifically targeting daytime episodes of EHS, which may involve less sedating interventions that would not interfere with daily activities, were not explored in this case. Moreover, studies have reported varying effectiveness of CPAP in treating EHS across different populations [4,8,10]. This variability highlights the need for more flexible treatment options that can address both nighttime and daytime EHS episodes without impairing daytime performance.

The chronic nature of the patient’s EHS over six months emphasizes the importance of early diagnosis and treatment in some cases. While many cases of EHS are self-limiting, a prolonged course in this patient suggests that EHS can become a long-term, distressing condition, especially when it is associated with underlying conditions such as OSA. Early identification and management of comorbidities, such as OSA, in early stages of EHS may reduce the risk of the condition becoming chronic, although the outcome may vary as suggested in previous literature. The persistence of symptoms during naps also highlights the complexity of EHS and the variability in response to treatment, suggesting that factors beyond OSA might contribute to EHS. Although EHS is known to be associated with psychological factors, a comprehensive assessment for coexisting psychological conditions such as life stress, anxiety disorders or depression was not studied in this case.

This case provides valuable preliminary insights supporting the link between OSA and EHS, with PSG revealing a direct association between a hypopnea event and an EHS episode. While this case suggests a possible link between EHS and hypopnea, multiple factors might have contributed to or been associated with EHS, including neurological, medication-related, and psychological factors such as stress or anxiety [1,4,10]. Brainstem or thalamocortical dysregulation may disrupt sensory processing. GABAergic or serotonergic medications could influence sleep-related hallucinations. Emotional stress, anxiety, and hyperarousal might exacerbate sensory disturbances [1,4,10]. The relative contribution of these factors is likely to vary among individuals, reflecting the complexity of EHS pathophysiology. Therefore, larger studies or case series are needed to confirm a consistent link between OSA and EHS. The resolution of symptoms with CPAP and clonazepam shows their efficacy of managing sleep-disordered breathing and improving sleep quality in reducing EHS episodes, particularly during nighttime sleep. Nonetheless, the persistence of EHS during naps suggests that further research is needed to better understand mechanisms of EHS in different sleep states.