Evidence from the use of vibration that the human long-latency stretch reflex depends upon spindle secondary afferents.

Abstract

The electromyographic [EMG] activity of flexor pollicis longus was recorded in normal human subjects on moving the tip of the thumb with the proximal phalanx clamped. On stretching the muscle the usual combination of short-latency and long-latency components of response were observed. The short-latency response progressively predominated as the velocity was increased. One subject still showed only a long-latency response with the fastest stretch, arguing that it is a distinct reflex entity. During vibration a short-latency response was regularly obtained, but any long-latency response was always small in relation to that elicited by stretch. This was equally so when the short-latency responses to the 2 types of stimulation was matched by using appropriate parameters of stimulation. The time course of the vibration response did not change appreciably with change of amplitude of vibration, so that its temporal profile was always quite different from that of the stretch response. Apparently the spindle group II afferents produce the long-latency excitation, with the time lost peripherally in afferent conduction rather than centrally. In relation to the strength of their Ia excitatory actions, stretch is known to excite secondary afferents more powerfully than does vibration. Findings do not support the hypothesis that the long-latency response is a transcortical reflex elicited by the initial Ia input, since vibration should then also have had a powerful long-latency action. Similar responses to vibration were obtained when it was applied percutaneously to the tendon of flexor pollicis longus 6 cm above the wrist. Those elicited by thumb vibration persisted largely unchanged when the thumb was anesthetized. This confirms that they were dependent upon the excitation of receptors in flexor pollicis longus, presumably the Ia afferents, rather than upon cutaneous or joint receptors in the thumb. The stretch responses also depended upon muscle receptors, since they too survived anesthesia. Upon termination of a pre-existing stretch or vibration, differences similar to those seen at their onset were found. Cessation of vibration led to a moderate short-latency reduction of activity and no appreciable extra component of long-latency reduction. Terminal of stretch (let go) normally failed to produce a detectable short-latency effect above the noise, but it was regularly followed by a large long-latency reduction of EMG activity. This powerfully supports the group II hypothesis; these differences, unlike those at the onset of stimulation, cannot readily be explained by postulating appropriately different patterns of Ia firing for stretch and for vibration with corresponding differences in their short-latency reflex actions. The weakness of the short-latency Ia off effects is notable but not entirely surprising. The long-latency reduction of activity seen on releasing stretch was due to a withdrawal of excitation rather than to an inhibition, as might arise from the concomitant stretch of the antagonists. This was shown by comparing the response to ramp stretches lasting 15-30 ms with that to continued stretch. The reduction of activity again occurred with a long latency. But now there was increased activity above the base-line level in the period after the expected cessation of short-latency activity, which can only have been due to continuing long-latency excitation. The only available single unifying explanation for the various findings is that in addition to its short-latency actions stretch evokes a distinct reflex with a longer latency. This is evidently attributable to the spindle group II afferents exerting a powerful autogenetic excitatory action.