This chapter focuses on primary sleep disorders in Parkinson's disease (PD) and multiple system atrophy (MSA) and insights provided by functional neuroimaging research. Specific disorders to be considered include excessive daytime sleepiness (EDS), sleep disordered breathing, restless legs syndrome/periodic limb movements in sleep (RLS/PLMS), and rapid eye movement (REM) sleep behavior disorder (RBD). The chapter reviews the relevant neurochemical pathways in PD and MSA, and discusses specific sleep disorders. It explains the neurotransmitter in more detail, as it relates to PD, MSA, and sleep circuits. The neurotransmitter dopamine may play a role in REM sleep control, but there is limited direct evidence for this. Dopamine may also play a role in regulation of the sleep/wake cycle with a wakefulness promoting effect that is similar to histamine and hypocretin. In the future, a greater focus should be placed on non-dopaminergic pathways to evaluate sleep disorders in PD and MSA.

Transcranial B-mode sonography (TCS) is a widely available, non-invasive and cost-effective diagnostic instrument. By convention and due to the resolution of the ultrasound waves in proximity of the probe, structures that are close to the midline are assessed from the ipsilateral side whereas structures that are located distant to the midline are examined from the contralateral side. Most data on TCS in disorders associated with insomnia or parasomnias have been evaluated from the movement disorder perspective and did not address diagnosis or differential diagnosis of sleep disorders directly. Some interesting findings indicate that TCS is valuable for the evaluation of sleep disorder patients with suspected restless legs syndrome (RLS), depressive disorder, or rapid eye movement (REM) sleep behavior disorder (RBD). In a patient complaining about disturbed sleep a TCS demonstrating substantia nigra (SN) hypoechogenicity, raphe hypoechogenicity, and red nucleus (RN) hyperechogenicity may help to support a suspected diagnosis of RLS.

Rapid eye movement (REM) sleep behavior disorder (RBD) was first formally identified in 1986 by Schenck and Mahowald in five elderly subjects presenting similar motor behavioral patterns during REM sleep consisting of violent dream-enacting behaviors. The clinical manifestations of RBD are typically dream-related motor-behavioral manifestations that appear to be the enactment of a fight. Subclinical or preclinical RBD, status dissociatus and parasomnia overlap syndrome are the clinical-pathophysiological subtypes of RBD, according to ICSD-2. The literature contains anecdotal reports of co-existing RBD and narcolepsy in both adults and children, in some cases with the RBD episodes as the presenting symptoms. The parasomnia and non-parasomnia disorders are taken into account in the differential diagnosis of RBD. In humans, RBD has been associated with several etiologies and abnormalities. Anecdotal reports and uncontrolled, retrospective studies of small patient series suggest that levodopa and pramipexole (D3 agonist) reduce RBD manifestations.