Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder modulated by genetic and environmental factors. Approximately 20-55% of individuals with ADHD experience concurrent sleep disturbances, yet the dynamic relationship between the two and their shared genetic mechanisms remain unclear. This study analyzed 11,288 participants (52.1% male) from the Adolescent Brain Cognitive Development Study using the Sleep Disturbance Scale for Children. We found a robust positive correlation between ADHD and sleep traits, though ADHD medication weakened this relationship. Latent growth curve modeling revealed that ADHD symptoms significantly impacted sleep traits with a lag effect. Polygenic risk score analyses showed significant but very small associations (explained variance ~0.28-0.30%). Pleiotropic analyses identified two loci associated with ADHD and excessive somnolence (implicating 30 genes), and cross-cohort comparisons with UK Biobank insomnia data uncovered 12 additional pleiotropic loci (98 genes) enriched in brain tissue. Functional enrichment analysis highlighted excitatory and inhibitory neuronal subtypes in visual and frontal cortices, suggesting roles in synaptic transmission and neural circuit development. Protein-protein interaction network analysis identified 10 hub genes involved in cell growth regulation and neurodevelopmental processes. This study demonstrates robust ADHD-sleep associations, with medication moderating this link, and provides preliminary insights into their shared genetic architecture.

Daytime sleepiness and excessive sleep are frequent symptoms. When these symptoms are recognized, they are often attributed to comorbid depression or, following ambulatory screening, to obstructive sleep apnea (OSA). While OSA affects 20-50% of the population, more frequently in men, its contribution to sleepiness in the general population is modest, and subjective sleepiness shows stronger associations with depression, insufficient sleep, and shift work. As a result, mild OSA in the presence of sleepiness is often overtreated. Further, stimulants are used as adjunct therapy in depression despite limited evidence. When referred to sleep disorder specialists, after exclusion of OSA, these patients are typically evaluated using a daytime nap test, the Multiple Sleep Latency Test (MSLT). The MSLT is used to diagnose Narcolepsy or Idiopathic Hypersomnia. Problematically, the MSLT performs well only to confirm narcolepsy type 1, a disorder with cataplexy and caused by orexin deficiency. A high false positive rate occurs in the absence of cataplexy, leading to questionable diagnoses of narcolepsy type 2 and idiopathic hypersomnia. A return to four historical subtypes of central nervous system hypersomnolence independent of MSLT testing is proposed. Narcolepsy Type 1: cataplexy, refreshing naps, sleep-onset REM periods. It is caused by orexin deficiency, responds to oxybate, antidepressants, stimulants, and low dose orexin receptor 2 agonists (in development). Narcolepsy-like hypersomnolence: Irresistible sleep attacks with short, refreshing naps. Insufficient Sleep must be excluded. It is often responsive to modafinil. Idiopathic Hypersomnia with sleep inertia and unrefreshing sleep: Excessive sleep amounts, severe sleep inertia, and long, unrefreshing naps. Association with psychiatric comorbidities, notably resolved depression, is frequent. Sodium oxybate can be transformative. Kleine-Levin Syndrome: periodic extreme hypersomnia with apathy and derealization. Responds to lithium in ∼50% of cases. A pathophysiological overlap with bipolar disorder is likely. A greater collaboration between psychiatry and sleep medicine is needed considering the emergence of orexin receptor agonists as potential therapies for hypersomnia.

Obstructive sleep apnoea-hypopnea syndrome (OSAHS) is characterized by the recurrent occurrence of apnoea and hypopneas during sleep. OSAHS is an independent risk factor for cardiovascular diseases, including hypertension, coronary artery disease, arrhythmias, and stroke. The high prevalence of OSAHS among patients with psychiatric disorders, along with the reciprocal links between these two categories of conditions, deserve emphasis. This association indeed carries diagnostic, prognostic, and therapeutic implications. Diagnosis poses specific challenges, including difficulties to perform sleep recording, and intricated causes of excessive daytime sleepiness. Emphasis should be made on reducing daytime sleepiness, nocturnal symptoms, and psychiatric symptoms. Data exist on the efficacy of continuous positive airway pressure (CPAP) in reducing anxiety and depression.

This paper presents an overview of current pharmacological and non-pharmacological treatment options available for narcolepsy. Antidepressant medications, including selective serotonin reuptake inhibitors and selective serotonin and norepinephrine reuptake inhibitors, have demonstrated efficacy in mitigating cataplexy episodes. Additionally, various pharmaceutical agents, including psychostimulants and anesthetics, are effective in alleviating excessive daytime sleepiness. Among the behavioral interventions for narcolepsy, adherence to a consistent sleep schedule and the incorporation of scheduled naps throughout the day remain the most widely implemented strategies.

This review consolidates current findings concerning the epidemiology, pathophysiology, and clinical characteristics of sleep disorders in women. The discussion encompasses gender disparities in sleep architecture and circadian rhythms, as well as the influence of reproductive stages - including the menstrual cycle, pregnancy, and menopause - on the emergence and progression of disorders such as insomnia, restless legs syndrome, snoring, obstructive sleep apnea, hypersomnias, and parasomnias. Special emphasis is placed on diagnostic and therapeutic approaches that address physiological changes throughout various stages of a woman's life, particularly during pregnancy and lactation. The necessity for a personalized approach and interdisciplinary collaboration for the prompt diagnosis and effective treatment of these conditions is underscored.

Sleep inertia impairs performance upon awakening and may be assessed using the psychomotor vigilance task (PVT). This study aimed to determine optimal PVT lapse cut-offs at awakening to objectively measure sleep inertia by comparing patients with idiopathic hypersomnia (IH) and severe sleep inertia to patients with other sleep disorders (OSD) without sleep inertia, to assess the discriminative performance of these thresholds in OSD patients with sleep inertia; and to explore factors associated with PVT lapses. 350 drug-free consecutive patients (227 females, 30.7 ± 11.0 y.o.) were included: 131 IH and 219 OSD (75 non-specified hypersomnolence, 54 narcolepsy, 50 obstructive sleep apnea, 40 others). All patients performed two 5-min PVTs at 07:00 pm and 07:00 am upon awakening. Sleep inertia was self-reported with the Idiopathic Hypersomnia Severity Scale. Receiver operating characteristic analyses were used to determine optimal cut-offs for 7:00 am PVT lapses and the change between 07:00 am and 07:00 pm in IH patients with severe sleep inertia (n = 73) and OSD patients without sleep inertia (n = 84). Optimal PVT cut-offs were ≥ 4 for 7 am-Lapses (sensitivity 72.6%, specificity 69.1%) and ≥ 4 for Delta 7 am-7 pm-Lapses (sensitivity 50.9%, specificity 83.3%). Across all 350 participants, 56.9% exhibited 7 am-Lapses ≥ 4, while 39.7% had Delta 7 am-7 pm Lapses ≥ 4. In conclusion, a threshold of ≥ 4 PVT lapses at 07:00 am, along with an increase of ≥ 4 lapses from 07:00 pm to 07:00 am best capture sleep inertia-related performance impairment in IH, supporting their use as objective markers in clinical practice and research settings.