Modulation of corticospinal output in agonist and antagonist proximal arm muscles during motor preparation

Abstract

Previous studies have shown modulation of corticospinal output of the agonist muscle when a known-movement is prepared but withheld until a response signal appearance, reflecting motor preparation processes. However, modulation in the antagonist muscles has not been described, despite the fact that reaching movements require precise coordination between the activation of agonist and antagonist muscles. In this study, participants performed an instructed-delay reaction time (RT) task, with randomized elbow flexion and extension movements. The aim was to assess the time course modulation of corticospinal output in two antagonist muscles, by simultaneously quantified the amplitude of motor evoked potentials (MEPs) in biceps brachii and triceps brachii, and the amplitude and direction of elbow movements evoked by transcranial magnetic stimulation (TMS). Depending on the prepared movement direction, a specific modulation of corticospinal output was observed, MEPs and TMS-evoked movements amplitude being relatively greater for extension compared to flexion. At the end of motor preparation, a decrease in MEPs amplitude was observed for both biceps brachii and triceps brachii, regardless of the prepared movement direction. In contrast, the probability of evoking movement in the flexion direction and the amplitude of TMS-evoked movement decreased at the end of preparation for flexion, but not for extension. Together, these results confirm the existence of inhibitory processes at the end of the motor preparation, probably to avoid a premature motor response. Moreover, they provide evidence of differences in the corticospinal control of elbow flexor and extensor muscles with patterns of modulation that are not necessarily reciprocal during motor preparation.

Effect of movement‐related pain on behaviour and corticospinal excitability changes associated with arm movement preparation

“…Finally, as previously observed in a study using a similar motor preparation paradigm (without pain) (Neige et al . ), no difference in RT and peak velocity was observed between Flexion and Extension movements during the No‐Pain Testing phase (all P > 0.354).…”

“…EMG activity was recorded from the middle portion of the right BB for MEP and RT measures and lateral head of the right triceps brachii (TB) for RT only, MEPs being difficult to evoke in this muscle in this arm posture (Neige et al 2017). Pairs of surface Ag/AgCl electrodes (Kendall Medi-trace 200, Covidien, Dublin, Ireland) were placed in bipolar configuration over the muscle belly.…”

“…) and the modulation of corticospinal output (Neige et al . ), the second objective was to determine the effect of pain‐eliciting movement direction on the modulation of corticospinal excitability. Finally, the third objective was to confirm that movement‐related pain anticipation affects movement initiation (i.e.…”

“…Because previous studies provide evidence that pain or the expectation of pain modulates activity in the motor cortex, the main objective of the present study was to investigate the effect of movement-related pain anticipation on the modulation of corticospinal excitability during preparation of arm movements. Based on previous studies showing that during motor preparation the agonist/antagonist role of the muscle and the direction of movement both influence the effect of pain on muscle activity (Lund et al 1991;Graven-Nielsen et al 1997;Falla et al 2006) and the modulation of corticospinal output (Neige et al 2017), the second objective was to determine the effect of pain-eliciting movement direction on the modulation of corticospinal excitability. Finally, the third objective was to confirm that movement-related pain anticipation affects movement initiation (i.e.…”

Split elbow sign: more evidence for the importance of cortical dysfunction in ALS

“…Although the biceps brachii has been traditionally regarded as an antipyramidal muscle, transcranial magnetic stimulation (TMS) studies have established a greater density of corticomotoneuronal inputs to the biceps brachii muscle when compared with the triceps 10. Given that cortical hyperexcitability is an important pathophysiological mechanism in ALS,11 12 and that the bicep brachii receives a greater corticomotoneuronal input, it could be argued that the split elbow sign is mediated by corticomotoneuronal hyperexcitability.…”