Clinical neurophysiology of REM parasomnias: Diagnostic aspects and insights into pathophysiology

Highlights

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  RBD presents REM sleep without atonia, EEG slowing, impaired functional connectivity, microstructural sleep EEG changes, among others.

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  During sleep paralysis there is a REM-wake dissociation - an intermediate state between REM and wakefulness, REM sleep or EEG alpha frequencies.

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  Nightmare disorder shows reduced sleep, increased awakenings, reduced SWS, increased respiratory and heart rate, and high alpha power in REM sleep.

Abstract

Parasomnias are due to a transient unstable state dissociation during entry into sleep, within sleep, or during arousal from sleep, and manifest with abnormal sleep related behaviors, perceptions, emotions, dreams, and autonomic nervous system activity.

Rapid eye movement (REM) parasomnias include REM sleep behavior disorder (RBD), isolated recurrent sleep paralysis and nightmare disorder. Neurophysiology is key for diagnosing these disorders and provides insights into their pathophysiology.

RBD is very well characterized from a neurophysiological point of view, also thank to the fact that polysomnography is needed for the diagnosis. Diagnostic criteria are provided by the American Academy of Sleep Medicine and video-polysomnography guidelines for the diagnosis by the International REM Sleep Behavior Disorder Study Group. Differences between the two sets of criteria are presented and discussed. Availability of polysomnography in RBD provides data on sleep electroencephalography (EEG), electrooculography (EOG) and electromyography (EMG). Sleep EEG in RBD shows e.g. changes in delta and theta power, in sleep spindles and K complexes. EMG during REM sleep is essential for RBD diagnosis and is an important neurodegeneration biomarker. RBD patients present alterations also in wake EEG, autonomic function, evoked potentials, and transcranial magnetic stimulation.

Clinical neurophysiological data on recurrent isolated sleep paralysis and nightmare disorder are scant. The few available data provide insights into the pathophysiology of these disorders, demonstrating a state dissociation in recurrent isolated sleep paralysis and suggesting alterations in sleep macro- and microstructure as well as autonomic changes in nightmare disorder.