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.