INTRODUCTION
Disorders of arousal (DoA) are sleep disorders arising from incomplete awakening from slow-wave sleep during non-rapid eye movement (NREM) sleep, presenting with abnormal mental and motor behaviors such as confusional arousals, sleepwalking, and sleep terrors. These events are most common in childhood and typically decline with age through adolescence and adulthood [1]. Episodes generally occur during the first half of the night, when slow-wave sleep predominates, and are characterized by a confusional state and reduced responsiveness to external stimuli. Most patients do not recall these events the following day, and sleep deprivation and stress are recognized triggers [2].
DoA in older adults is rare, usually beginning in adolescence or early adulthood and often associated with a family history [3]. Herein, we report a patient who developed DoA in the mid-60s without any family history of parasomnia.
CASE REPORT
A 66-year-old male was referred because of nocturnal paroxysmal behaviors of 2 years’ duration. According to his spouse, he experienced nocturnal awakenings between midnight and 2 am, occurring two to three times per month. Episodes were characterized by inappropriate verbalizations and behaviors, such as wandering toward the boiler room while claiming it was operating or aimlessly searching his surroundings. During the episodes, he remained verbally interactive but demonstrated emotional responses to the spouse’s attempts at redirection. Post-episode recall was inconsistent: he occasionally remembered events the following morning if his spouse intervened but had no memory when left undisturbed. He denied dream recall during these episodes. He reported snoring, witnessed apneas, and excessive daytime sleepiness, but denied leg discomfort or periodic limb movements. There was no family history of parasomnia.
The patient had experienced gait disturbance with frequent falls for approximately one year and had been diagnosed with progressive supranuclear palsy. His medications included mirabegron, bethanechol, solifenacin, tamsulosin/dutasteride, losartan/ hydrochlorothiazide, and ezetimibe/rosuvastatin. Examination revealed slow vertical saccades and generalized bradykinesia. Laboratory tests were unremarkable, and brain magnetic resonance imaging (MRI) showed midbrain atrophy without other abnormalities. Body mass index was 26.7 kg/m2. Cognitive assessment using the Korean Mini-Mental State Examination and Clinical Dementia Rating yielded scores of 24 and 0.5, respectively.
Polysomnography was performed while the patient continued his usual medications. Sleep latency was 4 minutes, total sleep time was 309 minutes, and sleep efficiency was 67.1%. Sleep architecture showed increased NREM stage 1 sleep (25.3%) and reduced NREM stage 2 (41.0%) and rapid eye movement (REM) sleep (13.9%). The apnea-hypopnea index was 32.1/hour, with a nadir oxygen saturation of 87%. Two habitual nocturnal events were observed, one in each half of the night, resembling those described in the clinical history. In the first event, alpha rhythm emerged within ongoing slow waves in NREM stage 3 sleep. Six seconds later, the patient opened his eyes, raised his upper body, and vocalized incomprehensible speech (Fig. 1). He initially did not respond to the technologist but gradually recognized the setting and returned to sleep. The second event followed a similar pattern, with persistent disorientation despite repeated questioning. The patient had no recollection of either event the next morning.
Treatment targeted severe obstructive sleep apnea with continuous positive airway pressure therapy, which the patient discontinued after 3 weeks because of unintentional mask removal during sleep. Device-recorded data demonstrated normalization of the apnea-hypopnea index, although he remained uncertain whether the nocturnal events had improved. He was prescribed clonazepam 0.25 mg at bedtime and encouraged to retry PAP therapy, but adherence was limited, and further follow-up was scheduled on an as-needed basis.
This study was approved by the Institutional Review Board of Chungnam National University Hospital (IRB no. 2026-01-033) with a waiver of written informed consent.
DISCUSSION
The clinical presentation of recurrent nocturnal behaviors in a mid-60s patient without family history of parasomnia suggested DoA. Polysomnography did not capture the bed-leaving episode reported in the history; however, other events consistent with the clinical history were observed, and the patient had no recall of these events, findings compatible with DoA.
Loddo et al. [3] reported four older men with DoA, with onset in adolescence or early adulthood, and sometimes in the 60s with a family history. In all reported cases, habitual nocturnal events arose from NREM sleep stage 3, as in this patient, though the late onset and absence of family history distinguish this case from typical DoA patterns. Electroencephalographic (EEG) features of DoA often include hypersynchronous delta activity exceeding 150 μV with frontocentral predominance at or immediately before arousal from slow-wave sleep [4], with alpha and beta rhythms sometimes superimposed on high-amplitude slow waves during episodes [5]. In this patient, these EEG patterns were not clearly observed.
Differential diagnoses included transient confusion related to sleep inertia, which may be pronounced in cognitive impairment [6]. The late-onset symptoms and suspected mild cognitive impairment (MCI) support this, but the stereotyped nature, exclusive occurrence during NREM sleep stage 3, and lack of recall after polysomnography argue against a generalized sleep inertia explanation. Wandering in cognitively impaired patients usually involves purposeless ambulation and occurs in advanced cognitive decline [7]. Although the patient’s nocturnal behavior of going to the boiler room, as reported in the clinical history, could suggest this possibility, it is unlikely given his suspected MCI and lack of bed-leaving during polysomnography.
REM sleep behavior disorder was excluded, as events occurred in NREM stage 3 sleep without REM sleep without atonia. While obstructive sleep apnea was documented, respiratory events or hypoxemia did not coincide with the habitual nocturnal events. Ohayon et al. [8] reported that confusional arousals, a subtype of DoA, are more frequently observed in older adults with sleep-disordered breathing. No clinical history or polysomnographic findings suggested epileptic seizures [9]. Although a full international 10–20 EEG montage was not applied, no epileptiform activity was observed before, during, or after the habitual nocturnal events. Blood tests and brain MRI showed no abnormalities causing acute deconditioning, making delirium unlikely.
The patient’s presentation aligns most closely with DoA, although atypical features suggest an unusual case. This case illustrates that DoA may manifest de novo in older adults even without a family history and highlights the importance of thorough history-taking and detailed polysomnographic analysis.
PDF Links
PubReader
ePub Link
XML Download
Full text via DOI
Download Citation 
Print 
