Disinhibition in the human motor cortex is enhanced by synchronous upper limb movements

Abstract

The phasic modulation of wrist flexor corticomotor disinhibition has previously been demonstrated during the flexion phase of rhythmical passive flexion-extension of the human wrist. Here we ask if rhythmical bimanual flexion-extension movements of the wrists of neurologically intact subjects, modulate inhibitory activity in the motor cortex. In the first experiment intracortical inhibition was assessed when one wrist was passively flexed and extended on its own, with the addition of the opposite limb voluntarily moving synchronously in a mirror symmetric pattern, and also in a near-symmetric asynchronous pattern. Two subsequent experiments investigated firstly the modulation of spinal reflex pathway activity during the same three movement conditions, and secondly the effect of contralateral wrist movement alone on the excitability of corticomotoneuronal pathways to a static test limb. When the wrist flexors of both upper limbs were shortening simultaneously (i.e. synchronously), intracortical inhibition associated with flexor representations was suppressed to a greater extent than when the two muscles were shortening asynchronously. The results of the three experiments indicate that modulation of inhibitory activity was taking place at the cortical level. These findings may have further application in the study of rehabilitation procedures where the effects of simultaneous activation of affected and unaffected upper limbs in hemiparetic patients are to be investigated.

Figure 1. EMG traces from FCR of one representative subject illustrating modulation of MEP amplitude

Top row, non-conditioned responses; bottom row, conditioned responses. Each panel contains an overlay of two responses.

Figure 2. Modulation of MEP amplitude by cycle phase from Experiment 1

Means of MEP amplitudes normalized to the maximum MEP amplitude for each subject. Black columns represent mid-flexion responses; open columns represent mid-extension responses. A and B, FCR non-conditioned and conditioned responses respectively; C and D, ECR non-conditioned and conditioned responses respectively. Error bars represent +1 s.e.m. *P = <0.05; **P = <0.01; ***P = <0.001. Levels of significance are from Student's one-tailed t tests, d.f. 1, 7.

Figure 3. Cortical disinhibition in the representation of FCR (A) and ECR (B) from Experiment 1

Mean MEP amplitudes of conditioned responses expressed as a percentage of non-conditioned responses. Black columns represent mid-flexion responses; open columns represent mid-extension responses; the hatched column represents static responses. Error bars represent +1 s.e.m. *P = <0.05; **P = <0.01, from Student's one-tailed t tests, d.f. 1, 7. The bracketed asterisk indicates there is a difference between inphase and novel means during flexion. The remaining levels of significance are from movement condition means compared with static means.

Figure 4. Modulation of H-reflexes from Experiment 2

Mean amplitude of H-reflex responses normalized to static values during mid-flexion responses (black columns) and mid-extension responses (open columns) for the three movement conditions. Error bars represent +1 s.e.m. *P = <0.05, indicating significance between flexion and extension responses. Levels of significance are from Student's one-tailed t tests, d.f. 1, 4.

Figure 5. Phasic modulation of MEP amplitudes from Experiment 3

A, from FCR. B, from ECR. Cycle phases 1–6 relate to contralateral hand movement. ○, conditioned responses; ♦, non-conditioned responses. Error bars represent 1 s.e.m. Brackets and asterisks above conditioned data points and below non-conditioned data points indicate significance between most potentiated and most inhibited cycle phases using Student's one-tailed t tests; d.f. 1, 6; *P < 0.05; **P < 0.01.