Hishikawa Y, Shimizu T
Department of Neuropsychiatry, Akita University School of Medicine, Japan.
Adv Neurol. 1995;67:245-71.
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.
产生肌肉张力缺失及快速眼动睡眠其他特征性现象的主要神经结构位于脑干中脑桥的背外侧部分。快速眼动睡眠的出现以及非快速眼动 - 快速眼动睡眠周期可能由胆碱能和胆碱感受性快速眼动睡眠开启神经元群体与单胺能快速眼动睡眠关闭神经元群体之间的平衡或相互作用所决定。在快速眼动睡眠中产生全身性肌肉张力缺失的神经活动主要起源于脑桥网状结构的背外侧部分，向下经过延髓和脊髓，并抑制脑干和脊髓中的运动神经元，从而导致姿势性肌张力缺失。猝倒症和睡眠瘫痪是快速眼动睡眠特征性全身性肌肉张力缺失的病理性、分离性表现。猝倒症由情绪刺激引发，可能是通过激活产生快速眼动睡眠肌肉张力缺失的神经结构。在持续性猝倒发作期间，发作性睡病患者在后一种睡眠状态中常经历睡眠瘫痪和生动的入睡幻觉。睡眠瘫痪是由在快速眼动睡眠期常出现的警觉水平与肌肉张力缺失之间的明显分离所引起的。发作性睡病患者和犬类频繁出现快速眼动睡眠期，可能是因为一些通常抑制快速眼动睡眠发生的产生觉醒和/或非快速眼动睡眠的神经机制异常薄弱，或者是促进快速眼动睡眠发生的神经机制过于敏感或活跃，或两者皆有。这两种异常情况都可能导致快速眼动睡眠期和睡眠瘫痪的发生，也会导致情绪引发猝倒症。快速眼动睡眠期的频繁出现似乎是猝倒症发生的前提条件，但并不充分。由情绪诱导的一些额外神经活动也通过抑制和/或激活与快速眼动睡眠期相关的紊乱神经机制而发挥作用。这些神经机制的异常可能涉及脑桥和脑桥以上结构中毒蕈碱胆碱能和/或胆碱感受性神经元群体的过度敏感或活跃，和/或脑桥和/或其他脑干结构中去甲肾上腺素能或5 - 羟色胺能神经元群体的活动异常减少。最后这个单胺能神经元群体可能对与全身性肌肉张力缺失和快速眼动睡眠产生相关的胆碱能和胆碱感受性神经元群体具有门控或抑制作用。尽管对快速眼动睡眠以及猝倒症和睡眠瘫痪有许多研究和已发表的报告，但我们仍远未完全理解在快速眼动睡眠中产生肌肉张力缺失的生理机制以及猝倒症和睡眠瘫痪的病理生理机制——尽管很明显这些机制密切相关。
