Abstract
In cats whose spinal cords had been asphyxiated for various periods of time, van Harreveld and Marmont 1 found that after recovery the hind legs could show an exaggerated extensor tone which usually stayed until death (in some experiments 3 weeks in total). Considering that after this time the acute effect of asphyxia will have disappeared, it was concluded that the high extensor tone is caused by a more or less selective damage of an inhibiting system present in the cord which normally keeps the tone in check.
A further study of these phenomena was made. A period of asphyxia for 30 minutes was usually followed within a few hours by the development of high extensor tone without abolishment of the flexor reflex. However, the effect of pinching the foot was not the same in all animals; sometimes it caused a regular flexor reflex with flexion in ankle and knee; in other experiments it caused, after the flexion, an extension of the leg, and in a few cases this stimulus caused instead of flexion an increase of the extensor tone.
When the contractions of the M. tibialis anterior and the triceps group were recorded simultaneously, it was often seen that stimulation of the N. peroneus superficialis caused a contraction in both of these antagonists. In other animals it was observed that the stimulation of the sciatic nerve caused a contraction in the quadriceps muscle of a Sherrington preparation instead of inhibiting the tone in this muscle.
By Sherrington's scheme for reciprocal innervation these observations can be best explained. Since, according to this scheme, the extensor motor neurones are inhibited during the flexor reflex, the simultaneous stimulation of afferent nerve fibers for extensor reflexes (e.g., for the extensor thrust) running in the stimulated branch of the sciatic nerve, normally remains without effect.
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