Abstract

The effect of a second stimulus presented after the reflex elicitor on the two successive EMG components of the cutaneous blink reflex in normal human subjects was examined. An acoustic stimulus presented up to 6 msec after the eliciting stimulus had no effect on size or latency of the first component recorded ipsilateral to the eliciting stimulus (R1), but the size of the second component recorded contralateral to the eliciting stimulus (CR2) was increased and its latency decreased. Enhancement of CR2 was independent ofthe stimulus onset asynchrony (SOA) of the two stimuli and was an increasing function of the intensity of the acoustic stimulus. CR2 enhancement was present when the second stimulus was by itself below threshold for reflex elicitation. A second percutaneous stimulus that appeared up to 8 msec after the eliciting stimulus increased the size of RI at all SOAs and increased its latency at the longest SOA tested. CR2 amplitude was unaffected and there was only a small effect on CR2 latency. The components of the blink reflex are not determined fully at the time ofreflex elicitation, but are sensitive to low-Ievelstimuli that occur in the reflex latency. This sensitivity was restricted to percutaneous stimuli for RI, indicating that acoustic stimuli do not have direct access to the R1 pathway. The results show an inverse relationship between the size of R1 and the size of CR2, which may be a compensatory reduction in CR2 following closure of the eyelid initiated by large R1 components.

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