Hanna is investigating sleep disorders and sleep disruption in people with Multiple Sclerosis (MS). MS is an auto-immune and neurodegenerative disease that is most commonly diagnosed in young adults between 20-40 years, in Australia over 23.000 people are affected and worldwide over 2 million people are diagnosed. It causes a broad scope of symptoms with increasing morbidity and disability. Fatigue is one of the most common and debilitating symptoms, affecting about 70% of the people with MS. Fatigue is very difficult to treat and all current therapies are either ineffective or only partially effective in relieving this debilitating symptom. Poor sleep and sleep disruption are also common in people with MS and can contribute to fatigue and impair cognitive function. The first aim of my PhD is to define the prevalence of sleep disorders and sleep disruption in people with MS and determine the relationship with fatigue and other symptoms of the disease. The second aim is to trial targeted therapies to determine if treating sleep problems can improve fatigue and cognitive function in people with MS. I hope that by carefully diagnosing and treating sleep problems this work will reduce fatigue and improve cognitive function to increase quality of life, productivity and wellbeing in people with MS.
This project focuses on sleep in people with multiple sclerosis (MS). It is a sub-study which is part of a larger clinical trial in people with MS to define is home based exercises can improve balance and reduce falls in people with MS. The sleep sub-study includes the performance of two home based sleep studies (before and after intervention) and several questionnaires. It will inform us how common sleep disorders and sleep disruptions are in people with MS and how sleep is associated with symptoms of the disease (e.g. fatigue and cognitive impairment).
DR PETER BURKE Postdoctoral fellow
RICHARD LIM Honours student
DR AHMAD BAMAGOOS PhD student
DR CHINH NGUYEN NeuroSleep NHMRC CRE Postdoctoral Fellow
AMAL OSMAN PhD student
Sleep Lab Manager
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DR NIRU WIJESURIYA Postdoctoral Fellow
DR JAYNE CARBERRY NeuroSleep NHMRC CRE Postdoctoral Fellow
This study assessed the effects of inhaled lignocaine to reduce upper airway surface mechanoreceptor activity on 1) basal genioglossus and tensor palatini EMG, 2) genioglossus reflex responses to large pulses (∼10 cmH2O) of negative airway pressure, and 3) upper airway collapsibility in 15 awake individuals. Genioglossus and tensor palatini muscle EMG and airway pressures were recorded during quiet nasal breathing and during brief pulses (250 ms) of negative upper-airway pressure. Lignocaine reduced peak inspiratory (5.6 ± 1.5 vs. 3.8 ± 1.1% maximum; mean ± SE, P < 0.01) and tonic (2.8 ± 0.8 vs. 2.1 ± 0.7% maximum; P < 0.05) genioglossus EMG during quiet breathing but had no effect on tensor palatini EMG (5.0 ± 0.8 vs. 5.0 ± 0.5% maximum; P = 0.97). Genioglossus reflex excitation to negative pressure pulses decreased after anesthesia (60.9 ± 20.7 vs. 23.6 ± 5.2 μV; P < 0.05), but not when expressed as a percentage of the immediate prestimulus baseline. Reflex excitation was closely related to the change in baseline EMG following lignocaine (r(2) = 0.98). A short-latency genioglossus reflex to rapid increases from negative to atmospheric pressure was also observed. The upper airway collapsibility index (%difference) between nadir choanal and epiglottic pressure increased after lignocaine (17.8 ± 3.7 vs. 28.8 ± 7.5%; P < 0.05). These findings indicate that surface receptors modulate genioglossus but not tensor palatini activity during quiet breathing. However, removal of input from surface mechanoreceptors has minimal effect on genioglossus reflex responses to large (∼10 cmH2O), sudden changes in airway pressure. Changes in pressure rather than negative pressure per se can elicit genioglossus reflex responses. These findings challenge previous views and have important implications for upper airway muscle control.