Katayama Y, Young H F, Dunbar J G, Hayes R L
Department of Neurological Surgery, Nihon University, Tokyo, Japan.
Brain Inj. 1988 Jan-Mar;2(1):51-66. doi: 10.3109/02699058809150931.
In the preceding paper we reported that concussive levels of fluid-percussion head injury can produce transient flaccidity of postural muscles associated with other indices of coma. This reversible coma associated with flaccidity follows an initial period of generalized areflexia and occurs in the absence of EEG slow waves. The present study investigated the physiological mechanisms underlying the flaccidity following concussive head injury be recording dorsal and ventral root potentials of the spinal cord. Studies indicated that, during the initial period of generalized areflexia, afferent input transmission was depressed although the excitability of motoneuronal pools was increased. In contrast, during periods of flaccidity, spinal cord somatomotor functions were depressed while transmission of afferent inputs was recovering. Systematic transection of the brain stem showed that activity within structures lying between collicular and midpontine levels is necessary to produce this latter condition. Cholinergic activation of pontine inhibitory areas within this same region of the rostral pons can produce profound descending inhibitory influences on postural somatomotor function in conjunction with other features of coma including suppression of eye-opening responses. Such effects occur without EEG slow waves. Moreover, other data indicate that local rates of glucose utilization within this pontine inhibitory area increase following concussive head injury. Thus, it is possible that a predominance of activity within the pontine inhibitory area could provide at least one neural basis for the reversible comatose state following concussive head injury characterized by close association between flaccidity and other indices of coma. Possible relationships of these data to clinically observed features of concussion are discussed.
在前一篇论文中，我们报道了流体冲击性头部损伤的震荡水平可导致与其他昏迷指标相关的姿势肌肉短暂性松弛。这种与松弛相关的可逆性昏迷发生在最初的全身性无反射期之后，且在脑电图慢波缺失的情况下出现。本研究通过记录脊髓的背根和腹根电位，探讨了震荡性头部损伤后肌肉松弛的生理机制。研究表明，在全身性无反射的初始阶段，虽然运动神经元池的兴奋性增加，但传入输入的传递受到抑制。相反，在肌肉松弛期间，脊髓躯体运动功能受到抑制，而传入输入的传递正在恢复。对脑干进行系统性横切显示，在中脑丘系和脑桥中部水平之间的结构内的活动对于产生后一种情况是必要的。在脑桥前部的同一区域内，对脑桥抑制区进行胆碱能激活，可对姿势躯体运动功能产生深远的下行抑制影响，并伴有包括睁眼反应抑制在内的其他昏迷特征。这种效应在没有脑电图慢波的情况下发生。此外，其他数据表明，震荡性头部损伤后，该脑桥抑制区内的局部葡萄糖利用率会增加。因此，脑桥抑制区内的活动占优势可能至少为震荡性头部损伤后以肌肉松弛与其他昏迷指标密切相关为特征的可逆性昏迷状态提供了一种神经基础。本文还讨论了这些数据与临床上观察到的脑震荡特征的可能关系。
