• David P Breen, Romina Vuono, Upekshani Nawarathna, Kate Fisher, John M Shneerson, Akhilesh B Reddy, and Roger A Barker.
• John van Geest Centre for Brain Repair, University of Cambridge, Cambridge, England (Breen, Vuono, Fisher, Barker); Respiratory and Sleep Support Centre, Papworth Hospital, Cambridge, England (Nawarathna, Shneerson); Institute of Metabolic Science, University of Cambridge, Cambridge, England (Reddy).
• JAMA Neurol. 2014 May 1; 71 (5): 589-595.

ImportanceSleep disturbances are recognized as a common nonmotor complaint in Parkinson disease but their etiology is poorly understood.ObjectiveTo define the sleep and circadian phenotype of patients with early-stage Parkinson disease.Design, Setting, And ParticipantsInitial 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 MeasuresSleep 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. 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 RelevanceSleep dysfunction seen in early Parkinson disease may reflect a more fundamental pathology in the molecular clock underlying circadian rhythms.

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