Dopamine cell death attending Parkinson's disease (PD) profoundly alters the sleep-wake state which can be classified into disturbances of: nocturnal movement, and thalamocortical arousal state. Diurnal rhythms in the content, turnover, release and behavioral responsiveness of the brain's principal dopamine systems are well established. Clinicians have long relied upon the wake-promoting effects of dopaminomimetics inclusive of traditional psychostimulants. Apart from the neurobiological substrates governing PD, genetic and disease factors may also influence expression of sleepiness and sleep onset rapid-eye-movement sleep (SOREMs). The utility of the multiple sleep latency test (MSLT), and other objective and subjective measures of sleepiness in PD has been reviewed. The clinician treating sleepiness in the parkinsonian patient is in the unenviable position of weighing the potential positive impact of dopaminomimetics upon sleep as it relates to daytime motor function, against the real possibility of adverse effects upon daytime alertness.