Abstract Study Objectives The purpose of this cross-sectional study was to survey awareness, attitudes, and clinical practices regarding the screening of sleep-disordered breathing (SDB) among orthodontists in Australia. Methods A pilot-tested electronic survey was distributed to 485 full members of the Australian Society of Orthodontists. Questions were related to demographics, screening methods, perceived barriers, and attitudes toward education and interdisciplinary collaboration. Results were summarised using item-specific denominators, with multiple-response percentages based on the number of respondents answering each item. Results The analysable response rate was 31.8% (154/485). Most participants (139/154, 90.3%) practiced primarily in private settings and in urban or suburban areas (138/154, 89.6%). Only a small proportion (25.2%) reported routine SDB screening, while 45.0% screened only in selected cases. Among respondents answering the screening-method questions, informal questions (83/104, 79.8%) and clinical examination (64/104, 61.5%) were most common. The Pediatric Sleep Questionnaire and STOP-Bang Questionnaire were used by 25/104 (24.0%) and 22/104 (21.2%), respectively. The main barriers to routine screening were insufficient training, lack of standardized screening protocols, and limited collaboration with medical professionals. Most respondents supported continuing professional development training (102/146, 69.9%) and inclusion of SDB teaching in the Doctor of Clinical Dentistry curriculum (127/146, 87.0%). Conclusions Among Australian orthodontists, routine SDB screening was limited and predominantly informal. In the Australian setting, professional bodies and orthodontic training programs should prioritise validated screening protocols, education, and clear interdisciplinary referral pathways.
Abstract Study Objectives Sleep slow-wave activity (SWA) shows regional and hemispheric variation reflecting local cortical regulation. Obstructive sleep apnea (OSA) introduces recurrent respiratory instability and arousals that may alter cortical dynamics during sleep. It remains unclear whether continuous positive airway pressure (CPAP) affects hemispheric SWA balance. Methods In this retrospective observational study, we included adult patients who underwent diagnostic polysomnography followed by a CPAP titration study on a separate night. Frontal delta power during N3 sleep was calculated from F3-A2 and F4-A1 using spectral analysis. Hemispheric asymmetry was quantified using a normalized asymmetry index (F4 − F3) / (F4 + F3). Sleep, respiratory, and EEG parameters were compared using paired nonparametric tests. Results A total of 143 patients were included (median age 47 years, 76% male). CPAP improved respiratory parameters, with median apnea-hypopnea index decreasing from 27.4 to 3.2 events/h (P < .001). Frontal delta power decreased at both F3 and F4 during CPAP (P < .001). Absolute asymmetry index decreased from 9.35% to 7.55% (P = .008). Signed asymmetry shifted toward left hemispheric dominance (P < .001). Right-dominant patterns were more frequent during the diagnostic night, whereas left-dominant patterns predominated during CPAP. Among patients with non-neutral asymmetry on both nights, dominance direction changed significantly (McNemar P = .008), mainly from right to left. Conclusion CPAP is associated with reduced frontal delta power and attenuation of hemispheric SWA asymmetry during deep sleep, suggesting that respiratory stabilization may influence cortical organization. These findings should be interpreted considering potential night-to-night effects.
Abstract Adolescent sleep insufficiency is increasingly prevalent, but whether repeated insufficient sleep during this developmental period promotes addiction vulnerability remains unclear. Here, we investigated the effects of chronic sleep restriction (CSR) imposed during adolescence, from 4 to 7 weeks of age, on the mesocorticolimbic dopamine (DA) system and addiction-related behaviors in mice. Behavioral and neuronal responses in the mesolimbic pathway to the psychostimulant Amphetamine (Amph) were examined. Also, DA-related molecular and structural components, including DA receptors, DA turnover, and developmental regulators such as Netrin-1/deleted in colorectal cancer (DCC), were assessed. Our results identified that adolescent CSR induces a hypodopaminergic profile characterized by reduced neuronal activity in the core regions of the mesolimbic DA circuit at baseline and upon acute Amph stimulation, downregulated striatal DA receptors, and reduced DA axon innervation in the ventral striatum. Altered Netrin-1/DCC signaling and mesocortical DA synthesis further suggest that sleep loss during adolescence disrupts ongoing maturation of DA circuitry. Furthermore, these neurobiological profiles were accompanied by enhanced Amph-induced conditioned place preference (CPP). Together, these findings indicate that chronic adolescent sleep insufficiency induces a constellation of behavioral and neurobiological adaptations relevant to addiction susceptibility. In contrast to prior acute sleep-loss paradigms that mainly capture transient DA activation, our data support a model in which repeated sleep restriction imposes cumulative allostatic load and promotes longer-term maladaptive remodeling of reward circuitry. These results identify insufficient sleep during adolescence as a potential risk factor for addiction vulnerability.
Abstract Insomnia disorder (ID) has become a prevalent sleep disorder worldwide, yet its underlying neural mechanisms remain unclear due to heterogeneous neuroimaging findings and uncertain network localization. We identified brain structural and functional abnormality locations associated with ID from 63 published neuroimaging studies, including 3391 patients and 3433 healthy controls. Using coordinate network mapping combined with a normative connectome database, we mapped these abnormalities to large-scale brain networks of ID across imaging modalities and further decoded them by integrating microscale chemo-architectural, cellular, and cognitive maps. The structural network widely involved the ventral attention (VAN), sensorimotor (SMN), dorsal attention (DAN) and default mode network (DMN); the task-induced network showed a similar but less extensive pattern, predominantly implicating the VAN, DMN, SMN and subcortical network (SCN); in contrast, the resting-state network was largely confined to the left middle frontal gyrus and the bilateral mid-cingulate cortex. Molecular mapping revealed both shared and distinct neurotransmitter signatures across the three networks, involving cholinergic, histaminergic, glutamatergic, noradrenergic, and opioid systems. Cellular decoding showed relatively selective associations of the structural and task-based networks with glial cells and excitatory neurons, whereas the resting-state network exhibited broader associations with glial cells and multiple excitatory and inhibitory neuronal subtypes. Cognitive decoding linked structural and task-based networks to sensorimotor processing and the resting-state network to memory-related functions. Our findings reconcile heterogeneous neuroimaging results and reveal neurobiological substrates of ID from a network perspective, providing a promising biomarker and paving the way for circuit-based precision therapies of ID.
