Delay in the Execution of Voluntary Movement by Electrical or Magnetic Brain Stimulation in Intact Man

Experiments were undertaken to study the effect on voluntary movement of an electrical or magnetic stimulus delivered to the brain through the scalp. Subjects were trained to flex or extend their wrist rapidly in response to an auditory tone. A single brain stimulus (electrical or magnetic) delivered after the tone and before the usual time of onset of the voluntary reaction could delay the execution of the movement for up to 150 ms, without affecting the pattern of the agonist and antagonist EMG bursts. The delay increased with increasing stimulus intensity and with stimuli which were applied nearer to the usual time of onset of the voluntary reaction. A stimulus given after the onset of the first voluntary agonist EMG burst only delayed the onset of the first antagonist and later EMG bursts. Movement was not delayed when similar experiments were performed with supramaximal stimulation of the median nerve instead of the brain stimulus. The delay following a cortical shock was not due to spinal motoneurons being inaccessible to descending input during the delay period since a second brain stimulus, given in the middle of the delay period, was capable of producing a direct muscle response. Neither could the delay be explained by the brain stimulus altering the time of the subject's intention to respond since a stimulus delivered to one hemisphere before an attempted simultaneous bilateral wrist movement produced a far greater delay of the contralateral than the ipsilateral movement. We suggest that the brain stimulus delayed movement by inhibiting a group of strategically placed neurons in the brain (probably in the motor cortex) which made them unresponsive for a brief period to the command signals they receive which initiate the motor program of agonist and antagonist muscle activity. The results have implications for the issues of the storage of motor programs, internal monitoring of central movement commands and the site of organization of the antagonist EMG burst.