2026-07-08 | Locked in Lucid Rhythms: A Case of Rhythmic Movement Disorder in Rapid Eye Movement (REM) Sleep.

Sleep-related rhythmic movement disorder (SRRMD) is uncommon in adults. It can closely mimic nocturnal epilepsy and rapid eye movement (REM) sleep behavior disorder (RBD), creating significant diagnostic challenges. We report the case of a man in his mid-20s presenting with chief complaints of nightly head movements during sleep occurring multiple times each night. He intentionally shook his head to terminate these episodes, a volitional strategy he had developed to escape lucid dreams. Video-electroencephalogram (EEG) monitoring over two nights excluded epilepsy. Polysomnography (PSG) confirmed stereotyped lateral head rolling exclusively during REM sleep at approximately 1 Hz, without any loss of REM sleep atonia, thereby excluding RBD. Comorbid mild obstructive sleep apnea (apnoea-hypopnoea index (AHI) 8.7 events/hour) was also identified. Nasal septoplasty partially improved symptoms. He reported excessive daytime sleepiness, with an initial Epworth Sleepiness Scale (ESS) score of 22. Due to the presence of excessive daytime sleepiness, two Multiple Sleep Latency Tests (MSLTs) were performed at different time points to evaluate for a primary hypersomnia disorder. However, both studies were conducted under suboptimal conditions. The first was performed in the presence of untreated mild sleep apnea, and the second while the patient was receiving medications known to suppress REM sleep. Neither study demonstrated sleep-onset REM periods, and mean sleep latencies of 7.2 and 12 minutes did not meet the diagnostic criteria for narcolepsy. Nevertheless, narcolepsy could not be definitively excluded because of the suboptimal testing conditions. The patient did not report symptoms suggestive of cataplexy. He experienced rare episodes of isolated sleep paralysis and a single episode of hypnopompic hallucination. The patient denied experiencing sleep attacks. He managed daytime sleepiness by scheduling daytime naps, which could last up to one to two hours. Sequential pharmacotherapy with amitriptyline, followed by nortriptyline, and subsequently the addition of venlafaxine and bupropion, achieved complete resolution of rhythmic movements and excessive daytime sleepiness. We identified no previous reports describing a patient with successful management of rhythmic head movements during REM sleep using sequential tricyclic antidepressant (TCA), selective serotonin reuptake inhibitor (SSRI), and serotonin-norepinephrine reuptake inhibitor (SNRI) therapy for this condition. At the six-month follow-up, the patient's ESS score improved from 22 to 3.

Open article ↗

2026-07-08 | GABA neurons in the sublaterodorsal tegmental nucleus suppress wakefulness in healthy and narcoleptic mice.

The sleep-wake cycle is generated by competing neural circuits that control the oscillation between wakefulness, rapid eye movement (REM) sleep, and non-REM (NREM) sleep. While the sublaterodorsal tegmental nucleus (SLD) is recognized for its role in REM sleep generation, the functional contribution of its GABAergic neurons (SLDGABA) to sleep-wake regulation remains poorly understood. Here, we found that SLDGABA neurons function as a suppressor of wakefulness in both healthy (i.e., orexin+/+) and narcoleptic (i.e., orexin-/-) mice. In healthy mice, optogenetic silencing of SLDGABA neurons rapidly induced robust wakefulness, while enhancing cortical and motor activity. Conversely, optogenetic activation of these neurons suppressed wakefulness and promoted NREM sleep. We found traces of SLDGABA axonal projections to wake-promoting brain regions, providing an anatomical basis for their wake-suppressing effects. Importantly, we discovered that SLDGABA neurons play a pathological role in narcolepsy: their activation in orexin-deficient narcoleptic mice triggered characteristic sleep attacks-rapid intrusions of NREM sleep during active wakefulness-while silencing these neurons rescued animals from both sleep attacks and cataplexy. Collectively, these findings establish SLDGABA neurons as a key regulator of arousal state transitions and identify them as a novel therapeutic target for the treatment of narcolepsy.

Open article ↗

2026-07-03 | Adipsic hypernatremia associated with hypothalamic dysfunction and sleep disorders.

Adipsic hypernatremia is a rare hypothalamic disorder characterized by impaired thirst despite preserved renal concentrating ability and may coexist with multisystem neuroendocrine and sleep disturbances. We report a 20-year-old male with beta-thalassemia minor presenting with severe hypernatremia with serum sodium of 170 mEq/L (SI: 170 mmol/L) (reference range 133-146 mEq/L [SI: 133-146 mmol/L]), absent thirst, weight loss, fatigue, hypogonadotropic hypogonadism, and hyperprolactinemia, along with excessive daytime sleepiness, hypnagogic hallucinations, and emotion-triggered cataplexy. Laboratory evaluation confirmed preserved renal concentrating ability, and pituitary magnetic resonance imaging was normal. Findings were consistent with adipsic hypernatremia due to functional hypothalamic dysfunction, with coexisting severe obstructive sleep apnea confirmed on polysomnography (apnea-hypopnea index [AHI] 35.9 events/hour) and presumed narcolepsy with cataplexy. Management included structured fluid intake, testosterone replacement, cabergoline, wake-promoting agents (modafinil, methylphenidate), and continuous positive airway pressure therapy. This case underscores the complex interplay between hypothalamic dysfunction, endocrine abnormalities, and sleep disorders, highlighting the importance of early recognition and structured management to prevent recurrent hypernatremia and optimize clinical outcomes.

Open article ↗