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, sponsored by MS research Australia, focuses on sleep apnoea in people with multiple sclerosis (MS). Our recent study, amongst other studies, suggests that sleep apnoea rates are higher in people with MS. However little is known about the causes of sleep apnoea in people with MS and how they might be different from people without MS. This project involves a sleep study including physiological measurements to identify differences in the causes of sleep apnoea between people with and without MS.
Approximately 1/3 of all obstructive sleep apnoea (OSA) patients have poor upper airway muscle activity during sleep which contributes to the repetitive narrowing or closure of the airway during sleep. This leads to abrupt arousals and disruption of sleep throughout the night which can lead to various health problems including diabetes, cardiovascular diseases, obesity, high blood pressure, impaired cognitive function, decreased quality of life and patients are more likely to be involved in motor vehicular accidents.
Recent studies have found that combination of these noradrenergic and antimuscarinic agents help to improve upper airway muscle activity during sleep. Therefore, this clinical study will focus on determining the effects of these agents on the severity of sleep apnoea in OSA patients in hopes to improve treatment outcomes for OSA patients in the future. The study also aims to determine the effects of these combination of agents on cognitive alertness and other sleep parameters which are impaired in patients with OSA.
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
AMAL OSMAN PhD student
Sleep Lab Manager
: 9399 1886
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.