The patient’s mother reported that the child had experienced frequent episodes of confusional arousal characterized by abrupt partial awakenings from sleep accompanied by nocturnal screaming, disorientation, confused behavior, and inconsolable agitation. These episodes occurred three to four times per week for approximately 1 year and were accompanied by habitual snoring and mouth breathing during sleep. There were no prominent features of intense fear or marked autonomic activation, and the patient had complete amnesia for the events the following morning, findings that helped distinguish these episodes from night terrors. These clinical features were consistent with confusional arousal, a type of non-rapid eye movement (NREM) parasomnia. She subsequently presented to our clinic for evaluation of these sleep-related symptoms.

Approximately 3 months before this visit, the patient had been evaluated for a 3-day history of dull frontal headache accompanied by postnasal drip and nasal congestion. Her height, weight, and body mass index were 107 cm (25th percentile), 18.5 kg (25th percentile), and 16 kg/m², respectively. At that time, physical examination revealed bilateral grade 3 tonsillar hypertrophy, and adenoid hypertrophy was incidentally identified on lateral neck radiography (Fig. 1). She was diagnosed with headache attributed to acute rhinosinusitis (International Classification of Headache Disorders–3 code 11.5.1), which resolved with short-term medical treatment [4].

The patient had no history of epilepsy or other medical conditions. Because of the unusually frequent confusional arousals and the exclusion of other nocturnal paroxysmal events, polysomnography was performed. The total recording time was 391 minutes, and the total sleep time was 368 minutes, yielding a sleep efficiency of 94.2%. Sleep latency was 10 minutes, and rapid eye movement (REM) sleep latency was 135.5 minutes. During sleep, five apneic episodes and 24 hypopnea episodes were recorded. Respiratory effort–related arousals were not scored in this study. The apnea-hypopnea index (AHI) was 4.7 events/hr, with an AHI of 4.3 events/hr during NREM sleep and 6.8 events/hr during REM sleep. All apnea events were obstructive in nature, and no central apnea was observed. No electroencephalographic abnormalities or parasomnia episodes were recorded during polysomnography. However, the diagnosis of frequent confusional arousals was based on the characteristic clinical history, including recurrent abrupt awakenings with nocturnal screaming occurring several times per week for 1 year, because parasomnia episodes are not always captured during a single-night polysomnographic study. These findings were consistent with obstructive sleep apnea.

Based on the clinical history and polysomnographic findings, obstructive sleep apnea was considered a triggering and exacerbating factor for the patient’s frequent confusional arousals. In addition to bilateral grade 3 tonsillar hypertrophy identified on physical examination, adenoid hypertrophy had been identified on lateral neck radiography obtained during a headache evaluation two months prior to surgery (Fig. 1), demonstrating narrowing of the nasopharyngeal airway. The patient therefore underwent tonsillectomy and adenotonsillectomy. During 3 months of postoperative follow-up, the caregiver reported that the frequency of night awakenings associated with confusional arousal decreased by more than 80% compared with the preoperative period. The patient occasionally experienced more frequent episodes of confusional arousal accompanied by nasal congestion; however, these episodes were subtle and brief compared with the pre-adenotonsillectomy state.

Nocturnal paroxysmal events are common in children and usually resolve spontaneously with age [5]. Although the frequency of parasomnias varies considerably, they generally do not occur on a nightly basis [6]. Several studies have demonstrated that OSAS can trigger recurrent cortical arousals and sleep fragmentation, thereby exacerbating both NREM and REM parasomnias [7,8]. NREM parasomnias are more prevalent in childhood because immature sleep–wake regulatory mechanisms and a higher proportion of slow-wave sleep predispose children to incomplete arousals and sleep–wake state dissociation. In addition to OSAS, factors such as sleep deprivation, febrile illness, psychological stress, irregular sleep schedules, and other conditions that cause sleep fragmentation have been reported to worsen parasomnias in children [5,9]. In children, OSAS is defined as an AHI ≥1, and adenotonsillar hypertrophy is the most common underlying cause. Tonsillectomy and adenotonsillectomy are considered first-line treatments in such cases [10].

Nocturnal paroxysmal events are often difficult to diagnose based solely on a patient’s history. Although most parasomnias are benign and tend to resolve spontaneously with age, polysomnography is recommended when episodes occur with unusual frequency because it may help identify the underlying cause.

The requirement for informed consent for publication was waived by the Institutional Review Board (IRB) of Bundang Jesaeng Hospital. (IRB No. 2025-09-004). All patient information was anonymized, and no identifiable personal data are included in this article.