The effect of closely spaced percutaneous stimuli (S1 and S2) on the early (R1) component of the human blink reflex was studied in three experiments. In all experiments, successive R1 components (called R1(1) and R1(2) here) were frequently elicited by S1-S2 pairs with stimulus onset asynchronies (SOAs) as brief as 4 msec. The successive R1s appeared to be under the separate control of S1 and S2, respectively. Experiment 1 (in which S1 was set at each subject's threshold for R1 elicitation and S2 was set at 80% of that threshold) and Experiment 2 (in which Sl was set at 80% of each subject's threshold for R1 elicitation and S2 was set at the threshold level) showed that S2 had no effect on either the probability or the amplitude of R1(1) but that S1 increased both the probability and the amplitude of R1(2) above control levels established by presentation of S2 alone. Augmentation of R1(2) was greatest at the shortest SOA tested (4 msec) and decayed to zero at an SOA of about 11-12 msec. Paired stimuli produced no systematic effect on the latency of either R1(1) or R1(2). Experiment 3 showed that the probability and amplitude of R1(1) increased with Sl intensity but were unaffected by S2 intensity over the range tested. The probability and amplitude of R1(2) increased with S2 intensity and were increased by the presence of S1; the augmentation produced by S1 was greater at the 4- than at the 8-msec SOA, and increased with S2 intensity. There were no systematic effects on the latency of either R1. Reflex augmentation in these experiments is not consistent with the model of temporal integration of stimulus energy. Instead, a percutaneous stimulus appears to evoke a transient excitation of the R1 pathway; a second percutaneous stimulus presented before the excitation decays is more likely to elicit an R1 than otherwise, and the R1 elicited will on the average be larger.
|Publication status||Published - 1993|