SINGLE-JOINT RAPID ARM MOVEMENTS IN NORMAL SUBJECTS AND IN PATIENTS WITH MOTOR DISORDERS

In normal subjects the execution of single rapid one-joint movements i s characterized by an electromyographic (EMG) pattern composed of thre e discrete bursts of activity: two bursts (first and second agonist bu rsts, or AG1 and AG2) are present in the agonist muscle separated by a n almost complete period of electrical silence. During this pause, ano ther burst (antagonist burst or ANT) occurs in the antagonist muscle. If a rapid movement is executed during tonic activation of the agonist muscle, tonic activity is inhibited just prior to AG1 onset (agonist inhibition). Similarly, if the movement is performed during tonic acti vation of the antagonist muscle, such activity is also inhibited prior to AG1 onset (antagonist inhibition). Antagonist inhibition also star ts prior to AG1 onset and lasts until ANT onset. A general descriptor of the kinematic features related to the EMG pattern described above i s a symmetrical and unimodal velocity profile that is bell-shaped and shows an acceleration time roughly equal to the deceleration time. Thi s holds true for movements performed under low accuracy constraints; a s accuracy demands become stricter and stricter the peak velocity decr eases but as long as the movement is made with one continuous trajecto ry the velocity profile remains roughly symmetrical. In general terms, the function of AG1 is to provide the impulsive force to start the mo vement; the function of ANT is to halt the movement at the desired end -point; and the function of AG2 is to dampen out the oscillations whic h might occur at the end of the movement. The timing and size of the b ursts vary according to the speed and amplitude of the movement. The o rigin of the EMG pattern is a central programme, but afferent inputs c an modulate the voluntary activity. In this paper we also review the E MG and kinematic abnormalities that are present during the execution o f single-joint, rapid arm movements in patients with Parkinson's disea se, Huntington's disease, Sydenham's chorea, dystonia, athetosis, cere bellar deficits, upper motor neuron syndrome, essential tremor and lar ge-fibre sensory neuropathy. The data from these studies lead us to th e following conclusions: (i) the basal ganglia have a role in scaling the size of AG1, reinforcing the voluntary command and inhibiting inap propriate EMG activity; (ii) the cerebellum has a role in timing the v oluntary bursts and probably in implementing muscle force phasically; (iii) the corticospinal tract has a role in determining spatial and te mporal recruitment of motor units; (iv) proprioceptive feedback is not necessary reproduce the triphasic pattern but it contributes to the a ccuracy of both the trajectory and the end-point of rapid movements.