Abstract Background Non-invasive ventilation (NIV) is a cornerstone of respiratory care in motor neurone disease (MND). The location in which ventilator settings are adjusted is a topic of debate. It is the current practice at our multidisciplinary MND clinic to facilitate an in-laboratory polysomnogram (PSG)-guided titration with close outpatient monitoring. Anecdotal experience suggests that NIV settings are frequently adjusted during follow-up. This raises important questions regarding the long-term utility of PSG-based titration as the initial setup method. The aim of this study is to describe current NIV titration practices and patient outcomes in individuals with MND attending a multidisciplinary MND clinic over a 12-month period. Methods Retrospective cohort study. It will include all adult patients (≥18 years old) diagnosed with MND who attended the multidisciplinary MND clinic between 1 May 2024 and 30 April 2025 and underwent in-laboratory NIV titration during the study period or were previously established on NIV. Progress to Date A research protocol has been submitted for an exemption from ethical review. Project timeline Intended outcome and impact Within Queensland, domiciliary NIV is provided by the Queensland Health Sleep Disorders Program (QHSDP). There remains a requirement for patients to undergo a PSG-guided titration in order to access a domiciliary device. The program requirements are currently under review, and it is intended that this project will provide insight into current NIV titration practices.

Abstract Introduction Studies have consistently demonstrated that hospitalised children sleep poorly, and that ward environments are disruptive, leading to poor quality sleep. To date, literature around potential interventions to improve sleep in hospitalised children has not been synthesised. This study aims to address this gap and provide guidance for future research. Methods A systematic review of the current literature pertaining to the interventions that have been evaluated to improve quality and duration of sleep for hospitalised children (age 0-18yrs) was undertaken, following PRIMSA guidelines. A detailed individual search strategy was developed and performed within PubMed, Embase, CINAHL, Web of Science and Cochrane Library databases. Title and abstract screening of identified articles was undertaken by one investigator, with a second investigator screening 50% (93% concordance between investigators). Results The initial search yielded 2474 studies regarding interventions to improve sleep in hospitalised children. 58 of these were deemed eligible for inclusion. Interventions studied included (i) Child focused interventions- use of music, mother’s voice, white noise, storybook reading, massage and acupressure (ii) Nursing focus interventions- decreasing overnight vital sign monitoring and clustering cares and (iii) Development of educational material to promote optimal sleep environments through reducing noise, light and screen time for patients. Full text screening of the included studies is now underway. Conclusion By providing a comprehensive review of the efficacy of existing interventions employed to improve sleep in hospitalised children, we hope to identify current gaps in knowledge and provide guidance around the optimal approach to reduce sleep disruption in hospitalised children.

Abstract Background Sedation and sleep have distinct electroencephalogram (EEG) properties. The presence of EEG patterns suggestive of sedation during sleep may have negative health effects. It has been shown that sedated intensive care unit (ICU) patients can be differentiated from matched sleep study patients not on Central Nervous System (CNS)-active medications using the amplitude criteria derived from cumulative frequency curves (CFCs). Aim To determine whether CFCs can be used to distinguish EEG patterns resembling sedation in patients with and without CNS-active medications. Methods Sleep study EEG data was analysed from 163 adult patients. Patients were categorised based on CNS medication status. 92 patients had no CNS medications, while 71 had CNS medications. Medications were sorted into the 7 CNS drug classes. Studies with poor signal quality, AHI > 5, were excluded. An automated analysis was applied to the left frontal lobe EEG trace and patients were compared on peak amplitude. Results Females and patients (<30yrs) spent more time at higher amplitudes. Patients with one or more CNS medications spent slightly more time (mean 7.46; SD 0.93 hours) asleep, vs unmedicated patients (mean 7.36; SD 1.01 hours; not statistically significant). Discussion Contrary to our original hypothesis, there was no significant difference in time at higher EEG amplitudes between CNS-medicated and non-medicated patients. It appears that in this population sample, CNS medications do not significantly affect sleep architecture but do slightly (not significantly) increase sleep duration. This study had limitations – we aim to use adequate sample sizes for each class of drug in future.

Abstract Introduction Charcot–Marie Tooth disease (CMT) describes a group of heterogeneous inherited peripheral neuropathies, affecting approximately 1 in 2500 children. While its primary motor and sensory symptoms are well understood, secondary symptoms including fatigue and sleep disorders are only beginning to emerge as significant comorbidities in the adult literature and remain under-investigated in children. This study aims to bridge that gap by investigating sleep quality and fatigue in Australian children with CMT. Methods We aim to recruit 30 children (= < 18 years) with CMT attending the neuromuscular clinic at the Royal Children’s Hospital, Melbourne. Depending on age, participants and their parent/guardian will complete up to 8 validated questionnaires assessing sleep, fatigue, physical activity, mood, pain and quality of life. Each child will also undergo an at-home overnight polysomnography (PSG) to assess for sleep disorders. Data will be analysed to examine the relationship between sleep, fatigue and other relevant factors. Results Recruitment commenced in April 2025 (currently n = 6; mean age 15.5 years). Preliminary data show 100% of participants reported elevated levels of fatigue (mean PedsQL-MFS total score of 33.78/100). The mean score on the SDSC was 59.7 consistent with significant sleep disturbance. Three PSG’s have been completed. Discussion Although recruitment ongoing, we anticipate that fatigue and sleep disorders will be prevalent and multifactorial, as seen in adult cohorts. In the absence of curative treatments for CMT, early identification and management of modifiable factors such as sleep may offer an opportunity to improve quality of life in affected children.

Abstract Introduction Obstructive sleep apnoea (OSA) frequently causes excessive daytime sleepiness (EDS). EDS impairs quality-of-life and can induce motor vehicle accidents or workplace injuries. Treatment dogma would suggest that CPAP (continuous positive airway pressure), the gold standard treatment, should abolish EDS, but up to 22% of CPAP-treated OSA patients can have residual EDS. Our tertiary health service serves a large catchment within the eastern coast of Australia. We aimed to examine the prevalence and precipitating causes of post-CPAP residual EDS in our local OSA population. Methods This was a single-centre retrospective study. Data set was compiled from the medical records of patients aged ≥18 years presenting to outpatients with OSA diagnosis in 2019-2024. Results Out of 354 patients, 35 (10%) had residual EDS on post-CPAP commencement follow-up. Median age was 58 years (IQR 54-75); 60% (n = 21) were males. Chronic pain and mental health co-morbidities were prevalent in 46%. Median Epworth Sleepiness Scale and Apnoea-Hypopnoea Index at diagnosis were 14 and 31.7, respectively. Most had home-based diagnostic study (n = 20) and lab-based CPAP titration (n = 24). 6 repeat in-lab titration studies and 3 vigilance tests were performed to evaluate residual EDS. Co-existing insomnia and CPAP-related issues were commonly identified as causing residual EDS. Conclusion OSA treatment is often undertaken to improve patients’ daytime somnolence and quality-of-life. Therefore, from the outset, patients should be informed about the CPAP acclimatisation process and of co-existing non-OSA conditions that may be perpetuating their EDS. Insomnia is not uncommon in modern society and should be screened for at index clinic reviews for OSA.

Abstract Background Long-term mechanical ventilation is often required following high spinal cord injury. Direct diaphragm pacing offers potential alternative ventilatory support in selected cases involving laparoscopic electrode implantation into the diaphragm’s abdominal surface. Reported benefits include improved quality of life and reduced healthcare utilisation with low rates of serious complications. This project aims to describe outcomes of patients assessed by our direct diaphragm pacing program and ability of pre-operative tests to predict successful diaphragm pacing. Methods Retrospective review of cases assessed between 2009-2024 will describe demographics, comorbidities, clinical outcomes (including dyspnoea scores, pacing utilisation, speech facilitation and achieved tidal volumes) and complications using non-parametric methods. Pre-operative tests include MRI spine and combined diaphragm assessment: phrenic nerve conduction studies with simultaneous measurement of diaphragm EMG and fluoroscopic response. Their relation to successful intraoperative stimulation of each hemidiaphragm and clinical outcomes will be assessed via Chi-squared testing, describing proportions for each category. Progress to date Literature review, protocol, power calculations and ethics application are complete. Preliminary data indicates nerve conduction studies and diaphragm screening closely relate to successful intraoperative pacing. Fluoroscopy could identify successful cases where nerve conduction indicated impairment. Intended outcome and impact With worldwide variation in approach, our study will describe the utility of protocol screening elements in relation to technical and clinical outcomes. Findings may be hypothesis-generating, informing future research towards improving ability to identify those who may benefit from direct diaphragm pacing and reduce unnecessary procedures in a vulnerable patient group with high healthcare utilisation risk.

Abstract Introduction Transcutaneous CO₂ (TcCO₂) monitoring helps detect hypoventilation during polysomnography, but sensor performance may deteriorate over time. We assessed whether a TcCO₂ sensor operating beyond the manufacturer’s stated useful life (old: >36 months) negatively impacts performance compared to a newer sensor (new: <12 months). Methods In this prospective, observational study, 19 patients undergoing polysomnography were monitored concurrently with both the same new and old TcCO₂ sensors. We measured mean TcCO₂ values, T90 response times, and subjective signal quality. Data analysis included paired t-tests, F-tests, Bland–Altman analyses, and Chi-Square tests. p<.05 was significant. Results Mean TcCO₂ values (n = 19) did not differ significantly between the new and the old sensors (40.6 ± 4.8 vs. 39.2 ± 4.9 mmHg, p=.17). The variance of the two sensors was also not significantly different (F-test ratio of 0.60; Levene’s test p=.975). Bland–Altman of TcCO₂ values (n = 19) showed only a small bias with a mean difference of +1.25 mmHg, but with wide limits of agreement (-6.31 to +8.92 mmHg), indicating substantial variability between the two sensors. The new sensor demonstrated a faster T90 response time (45.0 ± 4.9 vs. 95.9 ± 14.4 s, p<.0001) and better subjective signal quality (84.2% vs. 47.4% good quality, X2 = 5.73, p=.017) compared to the old sensor. Conclusion TcCO₂ values showed no significant difference between a new and old sensor, despite relatively large variability in agreement. However, deterioration in response time and subjective signal quality demonstrate a worse performance of the old sensor. Further research using multiple TcCO₂ sensor pairs is needed to determine if findings are consistent and broadly applicable.

Abstract STUDY OBJECTIVES The microbiome is proposed as a contributor to the adverse health impacts from altered sleep. The oral microbiome is a multifaceted microbial community that influences many health functions. However, data on the relationship between sleep and the oral microbiome are limited, and no studies have incorporated lifestyle and environmental exposures. METHODS Within a subset (N=1,139) of the NIH-AARP cohort, we examined the association between self-reported sleep duration and the oral microbiome via 16S rRNA gene amplicon sequencing. Statistical models were adjusted for demographic characteristics. Additional models examined the role of various lifestyle and neighborhood exposures on the sleep-oral microbiome association. RESULTS Compared to participants reporting the recommended 7-8 hours average sleep duration (n=702), those reporting short sleep (6 or fewer hours, n=284) had consistently decreased within-sample oral microbial diversity [e.g. number of observed amplicon sequence variants difference -8.681, p-value=0.009]. Several bacterial genera were more likely to be absent in the short sleep group. We found a higher relative abundance of Streptococcus and Rothia, and lower abundance of Fusobacterium, Atopobium, and Campylobacter in the short compared to the recommended sleep duration group. Results were consistent when controlling for lifestyle and neighborhood factors. CONCLUSIONS Our findings provide evidence for an association of short sleep duration with oral microbial diversity and composition. This suggests that oral bacteria may play a possible mechanistic role related to sleep health. Improved understanding of physiological pathways can aid in the design of interventions that may beneficially improve overall sleep health.

Abstract Aims Laboratory studies suggest that caffeine consumption has clear and consistent adverse effects on sleep, but epidemiological studies have yielded mixed findings. This study aimed to examine temporal associations between sleep and caffeine consumption in young adults. Methods Fifty-one New Zealand young adults (aged 18-25 years) wore an actigraph and completed a sleep diary for 7 days to capture objective and self-reported measures of sleep and self-reported caffeine intake, providing 355 observations. Mixed linear models were conducted to assess temporal associations between caffeine intake (dose and timing) and the subsequent night’s sleep. Lagged models were conducted to assess temporal associations between sleep characteristics and next-day caffeine dose. Independent variables for caffeine and sleep were included in models as within-person and between-person variances from the mean. Results Between participants, those who consumed more caffeine per day than the group average had shorter total night time (β=-0.12; p=0.02) and daily (β=-0.12; p=0.02) sleep durations in the subsequent sleep period(s). Conversely, between participants, those with shorter night time (β=-0.06; p=0.004) and daily (β=-0.06; p=0.01) sleep durations consumed more caffeine in total the following day. Within participants, on days with longer night time (β=0.07; p=0. 001)and daily (β=0.05; p=0.02) sleep durations than their personal average, they consumed more caffeine the next day. Conclusion There may be a cycle of activity in young adults whereby higher caffeine consumption leads to shorter sleep, which leads to higher caffeine consumption. Further research that accounts for prior sleep history is needed to elucidate associations with sleep characteristics.

Abstract Evening light exposure is disruptive to sleep and circadian rhythms. This disruption may be amplified for people taking Selective-Serotonin Reuptake Inhibitors (SSRIs), as SSRIs increase sensitivity to the non-visual effects of light. Minimising the amount of evening light exposure may therefore improve antidepressant treatment responses by minimising disruption and improving sleep and mood. We investigated the potential of a home-lighting intervention focused on minimising evening light to reduce depressive symptoms in individuals taking an SSRI. Individuals taking an SSRI who reported moderate or high levels of depressive symptoms, assessed via the Beck Depression Inventory, were recruited (N=24). After completing a baseline week of at-home monitoring of sleep, light, and mood, participants were randomly allocated to four weeks of a smart light intervention (n=12) or a control condition (n=11). Participants in the light intervention group were asked to replace their existing evening lighting with dimmed/warm smart lights. There was no difference in depressive symptoms between groups during the baseline week. Following the intervention period, participants in the intervention group reported significantly reduced depressive symptoms compared to those in the control group, with a large effect (d=2.11) and an average shift from severe to mild depressive symptoms. The intervention group showed a significant reduction in evening light following the intervention, averaging a 21 lux difference in change scores compared to the control group (d=1.11). We conclude that at-home light interventions that reduce evening light exposure hold promise as an adjunctive treatment for individuals experiencing depression while taking SSRIs.