Influence of asphyxia upon the responses of spinal motoneurons.

Observations have been made upon asphyxial and postasphyxial changes in the electrical responses of motoneurons to antidromic stimulation. Analysis has been aided by the use of a simple method for locating conduction blocks in the circumstances of volume conduction. Asphyxiation has been produced by suspending artificial ventilation. Regular practice has been to restore ventilation immediately after complete conduction block is established. This has permitted study of the postasphyxial state, but not of the effects of prolonged asphyxiation with the latter of which this paper is not concerned. With asphyxiation produced in the manner outlined a latent period of approximately 1 minute precedes the onset of asphyxial change. The initial change, to judge by the work of others (6, 7), is beginning central depolarization. At the same time there is a severe loss of somatic after-potential (Fig. 1). Through this loss the dendrites acquire the ability to carry two volleys in rapid succession (Fig. 13). These changes appear to reach completion within approximately 30 seconds. There follows a period of convulsive activity during which reciprocal amplitude changes in the response of axons and dendrites prove that a fluctuation in somatic responsivity is taking place (Fig. 11). Intermittent impulse discharge in ventral roots is seen (Fig. 1). Conduction block may be developing slowly throughout the period of convulsive activity (Fig. 11). Frequently there is a rather definite instant at which convulsive activity ceases and a rapid development of block begins. Usually the recorded amplitude of the dendritic response then increases to a peak (the preterminal increment) before final disappearance (Figs. 9 to 11, 13 to 15). A variety of reasons has been advanced to show that this preterminal increment represents not increased response, but rather a developing block (Figs. 11 to 13). When fully established, asphyxial block is located at the junction of the initial and myelinated axon segments (Figs. 5 to 7). It is a depolarization or cathodal block. On restoring ventilation a latency of less than 20 seconds antecedes the onset of postasphyxial change. Within the span of a few seconds membrane potential recovers and overshoots the normal level. At a critical stage of repolarization motoneurons are capable of conducting impulses, but again lapse into block (Figs. 9, 10, 14, and 15). The newly established block is due to hyperpolarization and is anodal in type. It is a somatic rather than an axonal block. Final recovery from the postasphyxial block requires some 20 minutes. As soon as motoneurons perform the rapid transition from asphyxial block through normal to postasphyxial block they will, upon reasphyxiation, pass through a new and complete asphyxial cycle with the one difference that a marked phase of incrementing response is experienced due to asphyxial mitigation of the postasphyxial block (Fig. 14). Barbiturate narcosis depresses the response of dendrites in a manner that resembles anodal depression for it is relieved rather than reinforced by asphyxial depolarization (Fig. 15). Asphyxial augmentation of response may acquire spectacular dimensions when written upon a state of barbiturate depression. Blocking time of the spinal motoneurons is on the average about 3.5 minutes. It may be shortened by prior asphyxiation (Fig. 14) and is lengthened by cooling of the preparation. Narcotization has not been observed to alter survival time significantly (Fig. 15).