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The diagnosis of rapid eye movement (REM) sleep behavior disorder (SBD) requires videopolysomnography detection of excessive electromyographic activity during REM sleep, which is time consuming and difficult. An easier, faster, reliable, and reproducible methodology is needed for its diagnosis. The isolated form of RBD represents an early manifestation of the synucleinopathies Parkinson disease and dementia with Lewy bodies. There is a need to find neuroprotective drugs capable of preventing parkinsonism and dementia onset in isolated RBD. Clonazepam and melatonin ameliorate the RBD symptoms, but therapeutic alternatives are needed when these medications fail or show produce side effects.

The diagnosis of rapid eye movement (REM) sleep behavior disorder (SBD) requires videopolysomnography detection of excessive electromyographic activity during REM sleep, which is time consuming and difficult. An easier, faster, reliable, and reproducible methodology is needed for its diagnosis. The isolated form of RBD represents an early manifestation of the synucleinopathies Parkinson disease and dementia with Lewy bodies. There is a need to find neuroprotective drugs capable of preventing parkinsonism and dementia onset in isolated RBD. Clonazepam and melatonin ameliorate the RBD symptoms, but therapeutic alternatives are needed when these medications fail or show produce side effects.

Sleep paralysis is rare in the elderly but may occur particularly in families suffering from this phenomenon. In a minority of patients with disorders of arousal, the episodes persist until the age of 70. Zolpidem and other medications may induce sleepwalking and sleep eating-related syndrome. Most patients with idiopathic REM sleep behavior disorder (RBD) eventually develop Parkinson disease and dementia with Lewy bodies. Anti-IgLON5 disease includes abnormal behaviors in both nonrapid eye movement sleep and rapid eye movement sleep (REM) sleep. Restless legs syndrome prevalence increases with age until the sixth decade. A severe form of periodic limb movements in sleep may clinically mimic REM sleep behavior disorder (RBD).

In recent years, the diagnostic approach to rapid eye movement (REM) sleep behavior disorder (RBD) has become more objective and accurate. This was achieved mainly by introduction of methods to exactly quantify electromyographic (EMG) activity in various muscles during REM sleep. The most established muscle combination for RBD diagnosis is the mentalis and upper extremity EMG. Computer-assisted systems for this analysis have been described, and an increasing number of studies looked into analysis of video events. Recently, prodromal phases of isolated RBD have been recognized.

Disorders of sleep are an integral part of neurodegenerative diseases and include insomnia, sleep-wake cycle disruption, excessive daytime sleepiness that may be manifested as persistent somnolence or sudden onset of sleep episodes, obstructive and central sleep apnea, rapid eye movement sleep behavior disorder, and restless legs syndrome. The origin of these sleep disorders is multifactorial including degeneration of the brain areas that modulate sleep, the symptoms of the disease, and the effect of medications. Treatment of sleep disorders in patients with neurodegenerative diseases should be individualized and includes behavioral therapy, sleep hygiene, bright light therapy, melatonin, hypnotics, waking-promoting agents, and continuous positive airway pressure.

Sleep disorders are common in multiple system atrophy (MSA) and they should be recognized as an integral part of the disease. Problems with sleep vary in their frequency, severity, and characteristics and may be the first manifestation of the disease. Parasomnias, breathing dysfunction during sleep, sleep fragmentation, and hypersomnia have all been described in MSA. Although many questions remain to be answered, this article reviews what is known about the different sleep disorders occurring in MSA.

Parkinson’s disease (PD) is the most frequent progressive neurodegenerativemovement disorder with a prevalence of 1% to 2% in people over 55 years of age. The cause of PD is unknown, although damage to the dopaminergic central nervous system is implicated in its pathophysiology. The cardinal clinical signs of PD are tremor, rigidity, bradykinesia, and postural and gait abnormalities. In addition, PD patients frequently present with different nonmotor manifestations including mood disorders, anxiety, cognitive impairment, autonomic failure, and sleep disorders. Sleep complaints in PD are frequent and in some cases they are the initial manifestation of the disease [1]. As many as 60% of parkinsonian patients are affected by sleep disturbances that may have a negative impact on their quality of life. Complaints amongPDpatients include initial insomnia, frequent awakenings during the night, early awakening, nocturnal akathisia, nocturia, back pain, stiffness, difficulties in turning over in bed, painful cramps, leg jerks, nightmares, vigorous motor and vocal dreamenacting behaviors, visual hallucinations, confusional awakenings, restless legs interfering with sleep initiation andmaintenance, loud snoring, witnessed apnea by the bed partner, painful earlymorning dystonia, and daytime sleepiness. Nocturnal polysomnography (PSG) may detect poor and reduced sleep architecture; decreased amounts of slow wave sleep and rapid eye movement (REM) sleep stages; reduction or loss of spindles and K complexes; periodic leg movements during sleep (repetitive stereotyped jerks of the legs and feet that may disrupt sleep continuity); obstructive or central sleep apnea; and REM sleep behavior disorder (a parasomnia consisting of potentially harmful dreamenacting behaviors associated with nightmares, such as being attacked or chased by unknown people and lack of REM sleep muscle atonia). All these sleep complaints and PSG abnormalities have been related to several conditions, such as damage of the brain structures and mechanisms involved in sleep origin and maintenance; the effects of antiparkinsonian drugs; poor control of parkinsonism; comorbid conditions, such as anxiety, depression, and dementia; aging; and individual genetic susceptibility. In general, sleep disturbances gradually worsen with the invariable progression of the disease. This article briefly reviews the epidemiology, characteristics, etiology, and management of sleepiness in PD.