The sense of movement elicited by transcranial magnetic stimulation in humans is due to sensory feedback.

It has been claimed that transcranial magnetic stimulation (TMS) of the human motor cortex can produce a sense of movement of the contralateral hand, even when the hand is paralysed. The sense of movement was equated with a 'corollary discharge', a nulling mechanism originally posited for maintaining constancy of the visual field during eye movements. Our experiments were designed to test whether the sensation that accompanies TMS-evoked finger movements is generated centrally or whether it arises as a result of sensory feedback. Matched twitches of the left and right fingers were elicited either by bilateral electrical stimulation of forearm extensor muscles, or by a combination of TMS of left motor cortex (eliciting twitches of the right forefinger), and electrical stimulation of the left forearm muscles (eliciting twitches of the left forefinger). The time interval between stimuli activating left and right twitches was varied randomly (range +/- 90 ms) from trial to trial. Subjects reported whether they sensed that the left or the right movement occurred first, or if they could detect no difference. The left and right movements evoked by bilateral electrical stimulation of muscles were sensed as near simultaneous when there was zero delay between them. When TMS was applied in conjunction with unilateral muscle stimulation, the TMS-evoked movement was felt, on average, 20 ms after the movement evoked by muscle stimulation. Similar results were obtained when the skin under the cathodal electrodes was anaesthetized. Since the TMS-evoked movements were felt later rather than earlier than the electrically evoked movements, the results do not support the idea that the sensation of movement was elicited centrally by TMS. Rather, they favour sensory feedback as the source of the sense of movement. The earlier perception of electrically evoked versus TMS-evoked movements was probably due to earlier sensory responses in the periphery rather than a suppression of the excitability of somatosensory cortex.