Pathophysiology of parasomnias

Abstract

Parasomnias are undesirable physical phenomena that intrude onto sleep. The pathophysiology of parasomnias has not been definitively established. They are hypothesized to result from sleep state dissociation, which is defined as the superimposition of elements of one state (non-rapid eye movement sleep, rapid eye movement sleep, or wakefulness) on to another. The basis for arousal parasomnias such as sleep walking, rhythmic movement disorder, and bruxism seems to be activation central pattern generators (CPGs). These are pacemaker-like networks of neurons and interneurons that are localized to the brainstem and spinal cord. They possess the ability to generate stereotyped movements. The clinical manifestations will depend upon the location of CPGs that have been activated. Sleep related breathing disorders and periodic limb movements in sleep can predispose to arousal parasomnias, probably via activation of CPGs. The expression of CPGs is controlled by genes that have been conserved during evolution. The present clinical classification of rhythmic parasomnias remains phenomenologically based. The application of whole genome analyses may advance the understanding of rhythmic motor phenomena of sleep. For example, the BTBD9 complex is associated with periodic limb movements in sleep. Increased activation of glutaminergic relative to GABAergic pathways may explain the appearance of NREM parasomnias in early childhood. Their gradual resolution over time may coincide with brain maturation. The pathophysiology of parasomnias of rapid eye movement sleep is less well understood.