IMPORTANCE Sleep disturbances are recognized as a common nonmotor complaint in Parkinson disease but their etiology is poorly understood. OBJECTIVE To define the sleep and circadian phenotype of patients with early-stage Parkinson disease. DESIGN, SETTING, AND PARTICIPANTS Initial assessment of sleep characteristics in a large population-representative incident Parkinson disease cohort (N=239) at the University of Cambridge, England, followed by further comprehensive case-control sleep assessments in a subgroup of these patients (n=30) and matched controls (n=15). MAIN OUTCOMES AND MEASURES Sleep diagnoses and sleep architecture based on polysomnography studies, actigraphy assessment, and 24-hour analyses of serum cortisol, melatonin, and peripheral clock gene expression (Bmal1, Per2, and Rev-Erbα). RESULTS Subjective sleep complaints were present in almost half of newly diagnosed patients and correlated significantly with poorer quality of life. Patients with Parkinson disease exhibited increased sleep latency (P = .04), reduced sleep efficiency (P = .008), and reduced rapid eye movement sleep (P = .02). In addition, there was a sustained elevation of serum cortisol levels, reduced circulating melatonin levels, and altered Bmal1 expression in patients with Parkinson disease compared with controls. CONCLUSIONS AND RELEVANCE Sleep dysfunction seen in early Parkinson disease may reflect a more fundamental pathology in the molecular clock underlying circadian rhythms.

AimSleep disturbances are recognised as a common non-motor complaint in Parkinson's disease but their aetiology is poorly understood. We set out to define the sleep and circadian phenotype of early-stage Parkinson's disease patients.MethodsWe began by assessing the sleep characteristics of a large population-representative incident Parkinson's disease cohort (n=239) at the University of Cambridge. We went on to carry out more comprehensive case-control sleep assessments in a subgroup of these patients (n=30) and matched controls (n=15). Outcome measures were sleep diagnoses and sleep architecture based on polysomnography studies; actigraphy assessment; and 24-hour analyses of serum cortisol, melatonin and peripheral clock gene expression (Bmal1, Per2, and Rev-Erbα).ResultsSubjective sleep complaints were present in almost half of newly-diagnosed patients and correlated significantly with poorer quality of life. Parkinson's disease patients exhibited increased sleep latency, reduced sleep efficiency and reduced REM sleep. In addition, there was a sustained elevation of serum cortisol levels, reduced circulating melatonin levels, and altered Bmal1 expression in Parkinson's disease patients compared to controls.ConclusionsThe sleep dysfunction seen in early Parkinson's disease may reflect a more fundamental pathology in the molecular clock underlying circadian rhythms.