Hypnagogic hallucinations and sleep paralysis are two associated features of narcolepsy that can also be found as isolated phenomena or within the context of other clinical conditions. Hypnagogic hallucinations are abnormal sensory perceptions experienced in the transition between wakefulness and sleep, whereas analogous hallucinations that occur upon awakening are called hypnopompic. Sleep paralysis is a transient paralysis of skeletal muscles associated with a clear waking mentation occurring in sleep–wake transitions. The two phenomena often occur together in narcoleptic subjects, provoking significant fear responses, especially when first experienced, because of the threatening and often terrifying nature of the hallucinations and the associated inability to move. Though underlying neurobiological mechanisms are still partly unknown, hypnagogic hallucinations and sleep paralysis are usually considered dissociated manifestations of REM sleep, with the former described as dreamlike intrusions into waking cognition and the latter considered to be the persistence of typical REM muscle atonia into wakefulness. Experimental evidence seems to point to the sleep-onset REM period typically found in narcoleptic subjects as a neurophysiological substrate for these phenomena; sleep paralysis has also been found to occur upon awakening during offset REM, confirming the hypothesis of an underlying dissociation of the REM stage in the transition between wakefulness and sleep. From a neurochemical point of view, an imbalance in the monoaminergic -cholinergic modulation of transitions among states of consciousness seems to underpin hypnagogic hallucinations and sleep paralysis by shifting the brain towards cholinergically driven hallucinatory cognition and inhibition of motility. The AIM state space model appears to further explain these REM-related phenomena by interpreting them in terms of varying levels of brain activation (A) and processing of internal–external inputs (I) in addition to neurochemical modulation (M). Though adequately structured clinical trials for evaluating the efficacy of medications for hypnagogic hallucinations and sleep paralysis are lacking, sodium oxybate and antidepressants such as clomipramine, venlafaxine and SSRIs are commonly used to alleviate the significant distress caused by these symptoms in narcoleptic subjects.

Hypnagogic hallucinations and sleep paralysis / A. D'Agostino, I. Limosani - In: Narcolepsy : a clinical guide / [a cura di] M. Goswami, S.R. Pandi-Perumal, M.J. Thorpy. - New York : Springer, 2010. - ISBN 978-1-4419-0853-7. - pp. 87-98 [10.1007/978-1-4419-0854-4_8]

Hypnagogic hallucinations and sleep paralysis

A. D'Agostino;I. Limosani
2010

Abstract

Hypnagogic hallucinations and sleep paralysis are two associated features of narcolepsy that can also be found as isolated phenomena or within the context of other clinical conditions. Hypnagogic hallucinations are abnormal sensory perceptions experienced in the transition between wakefulness and sleep, whereas analogous hallucinations that occur upon awakening are called hypnopompic. Sleep paralysis is a transient paralysis of skeletal muscles associated with a clear waking mentation occurring in sleep–wake transitions. The two phenomena often occur together in narcoleptic subjects, provoking significant fear responses, especially when first experienced, because of the threatening and often terrifying nature of the hallucinations and the associated inability to move. Though underlying neurobiological mechanisms are still partly unknown, hypnagogic hallucinations and sleep paralysis are usually considered dissociated manifestations of REM sleep, with the former described as dreamlike intrusions into waking cognition and the latter considered to be the persistence of typical REM muscle atonia into wakefulness. Experimental evidence seems to point to the sleep-onset REM period typically found in narcoleptic subjects as a neurophysiological substrate for these phenomena; sleep paralysis has also been found to occur upon awakening during offset REM, confirming the hypothesis of an underlying dissociation of the REM stage in the transition between wakefulness and sleep. From a neurochemical point of view, an imbalance in the monoaminergic -cholinergic modulation of transitions among states of consciousness seems to underpin hypnagogic hallucinations and sleep paralysis by shifting the brain towards cholinergically driven hallucinatory cognition and inhibition of motility. The AIM state space model appears to further explain these REM-related phenomena by interpreting them in terms of varying levels of brain activation (A) and processing of internal–external inputs (I) in addition to neurochemical modulation (M). Though adequately structured clinical trials for evaluating the efficacy of medications for hypnagogic hallucinations and sleep paralysis are lacking, sodium oxybate and antidepressants such as clomipramine, venlafaxine and SSRIs are commonly used to alleviate the significant distress caused by these symptoms in narcoleptic subjects.
AIM state space model; Consciousness; Dreaming; Hypnagogic-hypnopompic hallucinations; Sleep paralysis; SOREMP; Subjectivity
2010
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/69499
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