Using a startling acoustic stimulus to investigate underlying mechanisms of bradykinesia in Parkinson's disease.

Delays in the initiation of a movement response and slowness during movement are among the hallmark motor symptoms in patients with Parkinson's disease (PD). These impairments may result from deficits in neural structures related to perception, response programming, response initiation, or a combination of all three. However, the relative impact of each process on movement control in PD is still unclear. The present study investigated which processes might be responsible for the observed slowness. Patients performed a simple reaction time (RT) task involving arm extension where the normal 82 dB acoustic "go" signal was unexpectedly replaced with a 124 dB startling acoustic stimulus (SAS) on selected trials. The SAS was used as a probe of motor preparatory state since it has been shown to act as a subcortically-mediated involuntarily trigger for actions that are sufficiently prepared and waiting to be initiated by normal cortical processes. It was expected that release of the voluntary response by startle would not occur in PD patients if bradykinetic symptoms were attributable primarily to motor programming deficits. In contrast, results clearly showed that when a SAS was presented, the prepared response was elicited at a significantly shorter latency. In addition, the amplitude and timing pattern of EMG output appeared to be improved compared to control, resulting in a faster, more normalized movement. These results suggest that in PD patients motor programming processes are relatively intact, while the dysfunctional basal ganglia likely assert an inhibitory effect on the thalamo-cortical connections responsible for the initiation of motor acts.