Excitability of the pathways mediating the startle reaction before execution of a voluntary movement.

Studies with transcranial electrical or magnetic stimulation have shown a progressive increase of motor cortex excitability beginning at about 80 ms before the onset of electromyographic (EMG) activity in a voluntary movement. We studied whether a similar increase in excitability occurs in subcortical motor tracts before execution of a ballistic movement. In ten healthy volunteers, we examined the effects of a startling auditory stimulus (SAS) applied at various intervals following the imperative signal (IS) in a reaction time task experiment. We hypothesized that, if the excitability of the reticulospinal tract increases before onset of muscle activity, there would be a corresponding change in the size of the startle response elicited either in muscles responding to the SAS, the orbicularis oculi (OOc) and sternocleidomastoid (SCM), or in the agonist muscle for the reaction. A SAS was applied at intervals of 0, 20, 40, 60, 80, and 100 ms after IS in a reaction time task paradigm in which subjects had to perform a ballistic movement of wrist flexion. We measured the size of the EMG bursts recorded in the OOc and the SCM, as well as the size of the first EMG burst in the wrist flexors (WF). Comparisons were done with data obtained in baseline trials, in which unexpected SAS of the same intensity were delivered without preparation, and control trials, in which subjects performed the same motor task with no SAS. The size of the averaged OOc, SCM, and WF were larger in trials with SAS than in baseline or control trials, with significant differences in the SCM and in the WF (p<0.05). However, there were no effects of time interval on the size of OOc, SCM, or WF (p>0.05). These results indicate that, in the execution of a ballistic movement, the excitability of the subcortical motor tracts activated by a SAS is similarly enhanced at the time of the IS and 100 ms afterwards, just before the onset of EMG activity. We conclude that, in contrast with the reported progressive increase of excitability in the corticospinal tract, the excitability of the tracts activated by a SAS do not change between the IS and the onset of EMG activity.