Narcolepsy is a neurological sleep disorder affecting occupational functioning; however, occupational therapy is rarely found in the interdisciplinary care of narcolepsy and occupation-based assessments specific to narcolepsy are limited. This study examined the preliminary performance of the Wilder-Addison Narcolepsy Function Scale (WANFS), a performance measure designed to detect functional disruption associated with narcolepsy symptoms. A cross-sectional survey design was employed. Participants with Narcolepsy Type 1 (n = 63), Narcolepsy Type 2 (n = 58), and control participants without narcolepsy (n = 51) completed the WANFS. Descriptive statistics, internal consistency reliability, and known-groups validity analyses were conducted. The WANFS demonstrated excellent internal consistency (Cronbach's α = .96). Participants with narcolepsy reported significantly higher functional disruption across domains compared with controls (p < .001). Findings provide preliminary evidence supporting the WANFS as an occupation-based assessment of narcolepsy-related functional disruption and highlight the relevance of occupational therapy perspectives in sleep disorder care.

Kleine–Levin syndrome (KLS), also known as "Sleeping beauty syndrome," is a rare yet devastating parasomnia that includes recurrent episodes of hypersomnia, along with behavioral or cognitive abnormalities, coupled with compulsive eating and hypersexuality.[1] In 1862, Brierre de Boismont reported the first apparent case of Kleine–Levin syndrome. The condition is named after Willi Kleine, who documented several cases of periodic hypersomnia in 1925, and Max Levin, who, in 1930, noted a case of periodic hypersomnia paired with hyperphagia.[2]  Critchley and Hoffman actually defined the syndrome in 1942 and gave it its name after the publication of the classic paper, “The Syndrome of Periodic Somnolence and Morbid Hunger (Kleine–Levin syndrome)."[3]  It predominantly affects adolescent males with episodes usually lasting up to a few weeks and result in complete recovery.[2] Those who are affected are asymptomatic between these episodes; however, multiple relapses may occur.[1] Each episode can last from a week to 1 to 2 months.[3] The duration of Kleine–Levin syndrome can vary based on the clinical manifestation of the syndrome.

In an extraordinary convergence, Emmanuel Mignot and Masashi Yanagisawa employed two entirely different approaches to establish the pathogenesis of narcolepsy, a devastating sleep disorder associated with overwhelming sleep attacks, cataplexy, episodes with sudden loss of muscle tone, and hallucinations resulting from dreaming while awake. Yanagisawa purified brain ligands for orphan G protein-coupled receptors identifying a peptide, orexin, and then used reverse genetics to show that a knockout of the neuropeptide caused narcolepsy in mice. Mignot used forward genetics to identify genetic defects in the orexin receptor 2 in a hereditable form of canine narcolepsy. Together, they showed that orexin signaling in the brain maintains wakefulness and that orexin deficiency causes narcolepsy. This has led to new, effective treatments to induce sleep or maintain wakefulness. Their discoveries have elucidated a novel neural and molecular mechanism that maintains arousal, suppresses sleep, and controls the onset of our dreams.

ObjectiveAs the first oral treatment FDA-approved for postpartum depression, the long-term adverse effects of zuranolone have not been fully investigated. This study aims to characterize the real-world safety profile of zuranolone.MethodsFAERS data from the third quarter of 2023 to the second quarter of 2025 were retrieved, covering adverse event (AEs) reports related to zuranolone. Signal detection was performed using ROR, PRR, BCPNN, and MGPS algorithms.FindingsOur study identified a total of 299 Preferred Terms with zuranolone as the primary suspect drug, involving 648 patients. Among the 24 identified System Organ Classes, nervous system disorders and psychiatric disorders were the most frequently reported AEs associated with zuranolone. Beyond the AEs already listed in the drug label, intrusive thoughts and feeling drunk exhibited strong signal intensity, though these findings require cautious interpretation. Our study identified unexpected safety concerns, including panic attack, tachyphrenia, suicidal ideation, dissociation, brain fog, and dysphemia, suggesting potential risks of depression switching to mania, suicide, addiction, and cognitive or speech-related impairments. The signal of exposure via breast milk highlights a unique population concern. Sleep-related AEs, such as somnolence, hypersomnia, and initial insomnia, highlight the central nervous system effects of zuranolone. Additionally, rare movement symptom-related AEs were observed, including tremor, muscle twitching, and motor dysfunction.ConclusionOur findings suggest that safety concerns associated with traditional GABAkines may persist in zuranolone. Given the specific patient population for zuranolone, clinicians should be particularly vigilant about its potential risks in certain clinical contexts, particularly breast milk exposure and the potential risk of sedation. Prospective clinical studies are warranted for continued monitoring of rare or long-term AEs. Further safety evaluations and clinical management strategies are essential.

Narcolepsy is a long-term brain disorder caused by disrupted orexin signaling. Orexin neurons sit in the hypothalamus and control the sleep-wake cycle; damage to these neurons leads to narcolepsy. Early evidence pointed to an autoimmune attack on orexin neurons as the main cause. Current treatments - stimulants, antidepressants, sodium oxybate, and scheduled naps - ease symptoms but do not stop the disease, and they often cause side effects such as anxiety, insomnia, and heart problems. Most of these drugs also cannot cross the blood-brain barrier (BBB) to act directly on the hypothalamus. This review examines the autoimmune basis of orexin neuron loss in narcolepsy and looks at how nanotechnology-based delivery systems could carry orexin peptides, genes, or antibodies across the BBB. We highlight priorities for future work: nano-enabled drug delivery, gene and peptide-based therapies, long-term safety data, and treatment approaches tailored to each patient. Progress in this area could shift narcolepsy care from symptom control toward real disease-modifying therapy.

Objective: Greater severity of posttraumatic stress disorder (PTSD) symptoms has been linked to elevated C-reactive protein (CRP), a marker of systemic inflammation. The association between PTSD symptoms and CRP levels has been difficult to interpret due to confounding associations between CRP levels and medical comorbidities associated with PTSD and heterogeneity of trauma exposures and PTSD symptoms. The objective of this study was to characterize the relation between clinician-rated PTSD symptom dimensions, medical conditions, and CRP levels among individuals exposed to the World Trade Center (WTC) attacks. WTC rescue, recovery, and clean-up workers were recruited from the WTC Health Program General Responder Cohort.

DA is an uncommon psychocutaneous disorder in which the patient intentionally induces lesions to satisfy a subconscious psychological need and, at the same time, denies self-harm. DA typically presents as bizarre, well-demarcated lesions in accessible areas. Diagnosis is based on the suspicion and exclusion of organic causes. A 27-year-old married woman presented with painful, slow-healing ulcers on the dorsum of both hands and forearms for 2 months, along with body pain and progressive hair loss. The patient had epilepsy, which was controlled with sodium valproate and carbamazepine, although she had occasional psychogenic non-epileptic seizures (PNES). She denied systemic symptoms, like fever or arthralgia. Examination revealed irregular punched-out ulcers with erythematous borders, crusting, and post-inflammatory hyperpigmentation and infection or signs of systemic illness. Investigations revealed leukocytosis (TLC 19.1 × 10[9]/L), while the brain CT was normal. Skin biopsy revealed epidermal ulceration, necrosis, and mixed inflammatory infiltrates without vasculitis or pathogenic organisms. The patient was admitted to the hospital to manage her lesions when experiencing anxiety attacks, thereby confirming DA. This case represents the typical features of DA: self-inflicted geometric lesions on accessible sites in a young woman with psychological stressors. The coexistence of epilepsy and pseudoseizures reflects a psychoneurological interaction whereby chronic illness and emotional instability may be the instigators of maladaptive behavior. Management requires a multidisciplinary approach involving dermatology, psychiatry, and neurology. Supportive topical therapy and cognitive-behavioral therapy resulted in better emotional regulation, adequate sleep, and ulcer healing. Empathetic, integrated management ensures recovery and prevents the recurrence of DA.

Several children living with Tourette syndrome (TS) also present with recurrent episodes of sudden and intense anger, which are known as explosive outbursts. Nevertheless, individual characteristics influencing the onset of such outbursts remain poorly understood. In adults, impulsivity has been found to be a risk factor for explosive outbursts, but there are no such data among children. Additionally, behavioral inflexibility, which is conceptualized as a pattern of rigid, inflexible behavior in situations where it would be beneficial to adapt one's behavior to external demands, constitutes a trigger for anger outbursts in other neurodevelopmental conditions. However, its role in TS has not been studied yet. Therefore, the aim of this study was to assess whether impulsivity and behavioral inflexibility were associated with explosive outbursts. Three hundred and seventeen (317) parents of children (aged 6-14, 74.8% male) living with TS completed a series of online questionnaires. Parents completed the Behavioral Inflexibility Scale (BIS), the short-version of the UPPS-P Impulsivity Inventory, and the Rage Attack Questionnaire-Revised (RAQ-R) to assess behavioral inflexibility, impulsivity, and explosive outbursts, respectively. Parents also reported on socio-demographic and clinical characteristics of their child. Parent-rated impulsivity and behavioral inflexibility were significantly associated with explosive outbursts, as assessed with the RAQ-R. However, their interaction was not a significant predictor of explosive outbursts. Exploratory analyses also identified that several clinical characteristics, including tic severity and specific co-occurring conditions such as internalizing disorders, learning disorders, and sleep problems, were associated with explosive outbursts. Our results revealed that behavioral inflexibility, impulsivity, as well as several clinical characteristics were risk factors for explosive outbursts. Explosive outbursts are highly detrimental to the individual and familial functioning. Therefore, identifying risk factors for such outbursts is important given that it may lead to new targets for interventions aiming to decrease the frequency and intensity of explosive outbursts.