Lingrui Meng1, Andrea Benedetti2, Anne-Louise Lafontaine3, Victoria Mery4, Ann Ross Robinson5, John Kimoff6, Priti Gros7, Marta Kaminska6. 1. Department of Epidemiology, Biostatistics & Occupational Health, McGill University, 942 Pine Ave W, Montreal, Quebec, H3A 1A2, Canada. Electronic address: Lingrui.Meng@mail.mcgill.ca. 2. Department of Epidemiology, Biostatistics & Occupational Health, McGill University, 942 Pine Ave W, Montreal, Quebec, H3A 1A2, Canada; Respiratory Epidemiology and Clinical Research Unit, Research Institute of the McGill University Health Centre, 5252 de Maisonneuve W, Montreal, Quebec, H4A 3S5, Canada. 3. Montreal Neurological Hospital, 3801 Rue Université, Montréal, Quebec, H3A 2B4, Canada. 4. Clinica Alemana de Santiago, Facultad de Medicina, Universidad Del Desarrollo, Región del Bío, Chile. 5. Respiratory Division & Sleep Laboratory, McGill University Health Centre, 1001 Decarie Blvd, Montreal, Quebec, H4A 3J1, Canada. 6. Respiratory Epidemiology and Clinical Research Unit, Research Institute of the McGill University Health Centre, 5252 de Maisonneuve W, Montreal, Quebec, H4A 3S5, Canada; Respiratory Division & Sleep Laboratory, McGill University Health Centre, 1001 Decarie Blvd, Montreal, Quebec, H4A 3J1, Canada. 7. Division of Neurology, University of Toronto, 6 Queen's Park Crescent West, Toronto, Ontario, M5S 3H2, Canada.
Abstract
INTRODUCTION: We aimed to assess, in patients with Parkinson's disease (PD), the association between obstructive sleep apnea (OSA), progression of motor dysfunction and the effect of OSA treatment. METHODS: Data were analysed from a prospective cohort study of idiopathic PD patients from a movement disorders clinic. Patients found to have OSA on polysomnography (apnea-hypopnea index [AHI] ≥15 events/h, OSA+) were offered treatment using continuous positive airway pressure (CPAP). CPAP+ was defined as an average ≥ 2 h/night use at each follow-up. Motor symptoms were assessed using the motor section of the Movement Disorder Society Unified Parkinson's Disease Rating Scale (mUPDRS) and the Timed-Up-And-Go (TUG). Follow-up times were 3, 6 and 12 months. Mixed models were constructed, adjusting for age, sex, body mass index, levodopa equivalent dose and comorbidities. RESULTS: We studied 67 individuals (61.2% male) of mean age 64.7 years (SD = 10.1). Baseline mUPDRS was higher in OSA+ compared to OSA- (24.5 [13.6] vs. 16.2 [7.2], p < 0.001). Motor dysfunction increased at comparable rates in OSA- and OSA+CPAP-. However, in OSA+CPAP+, mUPDRS change was significantly lower compared to OSA- (β = -0.01 vs. 0.61, p = 0.03; p = 0.12 vs. OSA+CPAP- [β = 0.39]) and TUG change was lower compared to OSA+CPAP- (β = -0.01 vs. 0.13, p = 0.002; p = 0.05 vs. OSA- [β = 0.02]). CONCLUSIONS: In this PD cohort, OSA was associated with higher baseline mUPDRS. In those with OSA, CPAP use was associated with stabilization of motor function (mUPDRS and TUG) over 12 months. These observations support further research to clarify the role of OSA in PD pathophysiology and motor dysfunction.
INTRODUCTION: We aimed to assess, in patients with Parkinson's disease (PD), the association between obstructive sleep apnea (OSA), progression of motor dysfunction and the effect of OSA treatment. METHODS: Data were analysed from a prospective cohort study of idiopathic PDpatients from a movement disorders clinic. Patients found to have OSA on polysomnography (apnea-hypopnea index [AHI] ≥15 events/h, OSA+) were offered treatment using continuous positive airway pressure (CPAP). CPAP+ was defined as an average ≥ 2 h/night use at each follow-up. Motor symptoms were assessed using the motor section of the Movement Disorder Society Unified Parkinson's Disease Rating Scale (mUPDRS) and the Timed-Up-And-Go (TUG). Follow-up times were 3, 6 and 12 months. Mixed models were constructed, adjusting for age, sex, body mass index, levodopa equivalent dose and comorbidities. RESULTS: We studied 67 individuals (61.2% male) of mean age 64.7 years (SD = 10.1). Baseline mUPDRS was higher in OSA+ compared to OSA- (24.5 [13.6] vs. 16.2 [7.2], p < 0.001). Motor dysfunction increased at comparable rates in OSA- and OSA+CPAP-. However, in OSA+CPAP+, mUPDRS change was significantly lower compared to OSA- (β = -0.01 vs. 0.61, p = 0.03; p = 0.12 vs. OSA+CPAP- [β = 0.39]) and TUG change was lower compared to OSA+CPAP- (β = -0.01 vs. 0.13, p = 0.002; p = 0.05 vs. OSA- [β = 0.02]). CONCLUSIONS: In this PD cohort, OSA was associated with higher baseline mUPDRS. In those with OSA, CPAP use was associated with stabilization of motor function (mUPDRS and TUG) over 12 months. These observations support further research to clarify the role of OSA in PD pathophysiology and motor dysfunction.