Physiology of REM sleep, cataplexy, and sleep paralysis.

The main neural structures generating muscle atonia and other phenomena characteristic of REM sleep are present in dorsolateral portions of the pons in the brainstem. Occurrence of REM sleep and the NREM-REM sleep cycle are probably determined by a balance or interaction between the cholinergic and cholinoceptive REM sleep-on neuronal populations and the monoaminergic REM sleep-off neuronal population. Neural activities producing generalized muscle atonia in REM sleep originate mainly in dorsolateral portions of the pontine reticular formation, descend through the medulla and spinal cord, and inhibit the motoneurons in the brainstem and spinal cord, bringing about postural atonia. Cataplexy and sleep paralysis are pathological, dissociated manifestations of the generalized muscle atonia characteristic REM sleep. Cataplexy is triggered by emotional stimuli, probably through activation of the neural structure generating the muscle atonia of REM sleep. During long-lasting cataplectic attacks, narcoleptic humans often experience sleep paralysis and vivid hypnagogic hallucinations in the latter sleep state. Sleep paralysis is caused by the marked dissociation between level of alertness and muscle atonia that often occurs in SOREM sleep episodes. Frequent SOREM sleep episodes in narcoleptic humans and dogs may occur when some of the neural mechanisms producing wakefulness and/or NREM sleep that normally inhibit the occurrence of REM sleep are abnormally weak, or when neural mechanisms facilitating the occurrence of REM sleep are hypersensitive or hyperactive, or both. Both abnormalities may contribute to the occurrence of SOREM sleep episodes and sleep paralysis, and also to the emotional triggering of cataplexy. Frequent occurrence of SOREM sleep episodes seems to be prerequisite but not sufficient for the occurrence of cataplexy. Some additional neural activities induced by emotion also contribute by inhibiting and/or activating the disturbed neural mechanisms related to SOREM sleep episodes. These abnormalities in neural mechanisms probably involve hypersensitivity or hyperactivity of muscarinic cholinergic and/or cholinoceptive neuronal populations in the pontine and suprapontine structures, and/or abnormally decreased activity of noradrenergic or serotonergic neuronal populations in the pons and/or other brainstem structures. This last monoaminergic neuronal population probably has a gating or inhibiting effect upon the cholinergic and cholinoceptive neuronal populations related to the generation of generalized muscle atonia and REM sleep. In spite of many studies and published reports on REM sleep, as well as on cataplexy and sleep paralysis, we are still far from a complete understanding of the physiological mechanisms producing muscle atonia in REM sleep and of the pathophysiological mechanisms of cataplexy and sleep paralysis--though it is apparent that these mechanisms are closely related.