The Effects of Bilateral Priming on Motor Cortex Function in Healthy Adults

Abstract

Bilateral priming is an adjuvant that has shown potential to assist upper limb motor recovery at both the subacute and chronic stage post-stroke. It involves the use of a table-top device to couple the upper limbs together such that active flexion and extension of one wrist leads to passive movement of the opposite wrist in a mirror symmetric pattern. Bilateral priming increases corticomotor excitability (CME) in the primary motor cortex (M1) controlling the passively driven limb, however the neurophysiological mechanisms underlying this CME increase remain unclear. The aim of this study was to explore these mechanisms using transcranial magnetic stimulation to investigate two forms of facilitation within the passively driven M1: intracortical facilitation (ICF) and short-interval intracortical facilitation (SICF). ICF was recorded using posterior-anterior (PA) current stimulation while CME and SICF were recorded using both PA and anterior-posterior (AP) current stimulation. Motor evoked potentials were recorded from the left extensor carpi radialis (ECR) and first dorsal interosseous (FDI) muscles of 23 healthy adults before priming (Baseline) and again five minutes and 35 minutes after a single 15-minute session of priming (Post5 and Post35, respectively). Participants completed two separate experimental sessions, a bilateral priming session and a unilateral priming session in which their left arm remained stationary while the right arm actively moved during priming. Priming increased PA CME at Post35 and this remained elevated until the end of the experiment, while AP SICF was facilitated at both Post5 and Post35. Priming had no effect on AP CME, ICF and PA SICF, and there were no differences between the bilateral and unilateral priming sessions for any measures. Despite increasing AP SICF, this is most likely not the mechanism underlying the increased PA CME due to the differing timelines of their effects and the separate interneuron circuits activated by the PA and AP stimulation. These results suggest priming does not increase CME through alterations of intracortical facilitatory circuits.