Disturbances of sleep and wake are among the most common and disabling nonmotor manifestations of Parkinson disease (PD), affecting as many as 90% of patients.^1,2 Disrupted sleep-wake cycles contribute to poor quality of life and increased risk for accidents, leading to increased morbidity and mortality in the PD population.^3-5 Current treatment options for disturbed sleep and alertness in PD are very limited and are associated with undesirable adverse effects. Therefore, the need to understand the mechanisms leading to sleep-wake dysfunction in PD and to develop innovative treatment modalities is great. The exact pathophysiological features of sleep-wake disturbances in PD remain largely unknown, but the cause is likely to be multifactorial, including the effect of motor symptoms on sleep, primary sleep disorders (sleep apnea and Rapid Eye Movement Sleep Behavior Disorder), adverse effects of medications, and neurodegeneration of central sleep-wake regulatory systems.^6-9

ADVANCED SLEEP phase syndrome (ASPS) is characterized by persistent advanced sleep onsets and awakenings that are earlier than desired.^1-3 Individuals with ASPS typically experience sleepiness in the early evening, when other people are active, and early morning awakening, when most are still sleeping. Therefore, individuals with ASPS sometimes find it difficult to maintain a normal social and work life. It has been postulated that ASPS is a circadian rhythm disorder in which the phase of the circadian rhythm of sleep and wake is advanced in relation to the "normal timing," which is synchronized, to the external environment.^2,3

Circadian rhythm sleep disorders occur when individuals attempt to sleep at the wrong circadian time. The misalignment between the internal circadian timing system and the external environment is typically due to either an alteration in the functioning of the circadian timing system (e.g., delayed or advanced sleep phase disorder) or to changes in the external environment (e.g., jet lag). However, the clinical presentation of most of the circadian rhythm sleep disorders is influenced by a combination of physiologic, behavioral, and environmental factors. These disorders lead to complaints of insomnia and excessive daytime sleepiness, with impairment in important areas of functioning and quality of life. Current treatments, such as timed exposure to bright light and exogenous melatonin, primarily serve to align the timing of circadian rhythms or increase the strength of the circadian signal. Although these treatments are effective, their use in clinical practice has been limited by the availability of adequate diagnostic tools and large-scale randomized controlled clinical trials. The rapid advances in our understanding of the molecular, cellular, and physiologic basis of circadian regulation and the pathophysiology of these disorders will lead to more targeted and effective treatments.