Sleep paralysis is classified as a parasomnia associated with rapid-eye-movement periods (REMPs). The paralysis is consistent with atonia observed during normal REMPs produced by hyperpolarization of the spinal motoneurons originating in cholinoceptive neurons in dorsolateral regions of the pontine reticular formation. Estimates of RISP prevalence vary dramatically, yielding estimates between 6% and 40%. Sleep paralysis is often considered as a sleep-onset problem under the assumption that episodes occur at the beginning of the sleep period during Sleep Onset REM Period (SOREMP). Multiphase sleep-wake schedule (MPS) regimes likely produce high level of cognitive arousal precipitating episodes by increasing potential for waking during immediate post-interruption REMPs. Vestibular-motor (V-M) hallucinations likely arise via interactions between subcortical and cortical vestibular centers. RISP associated with a variety of affective disorders including depression, panic disorder, PTSD, and social anxiety. RISP has typically been thought to reflect anomalies of the functioning of monoaminergic and/or cholinergic neural systems.

Arousal parasomnias occur mainly during non-rapid eye movement (NREM) sleep. This group consists of confusional arousals, sleepwalking and sleep terrors. Sleepwalking and sleep terrors can be triggered by stress, sleep deprivation, alcohol ingestion, and almost all sedative medications. This group of parasomnias is composed of three disorders occurring essentially during rapid eye movement (REM) sleep. Sleep paralysis is one of the main symptoms associated with narcolepsy, but it can also occur individually. REM sleep behavior disorder is characterized by a loss of generalized skeletal muscle REM-related atonia and the presence of physical dreamenactment. Polysomnographic recordings of individuals with RBD showed a reduction of the tonic phenomena of REM sleep and the activation of the phasic phenomena. Parasomnias are frequent in the general population; more than 30% of individuals experiences at least one type of parasomnia. At the genetic level, there is growing evidence that many parasomnias have a genetic component.