Research reportSelective modulation of left primary motor cortex excitability after continuous theta burst stimulation to right primary motor cortex and bimanual training

- Theta burst stimulation (TBS) to right primary motor cortex (rM1) and bimanual training (BMT).
- TBS to rM1 and BMT caused a greater shift in centre of gravity and prolonged increased spatial map.
- TBS to rM1 and BMT individually increased map volume and spatial map.
- Modulation of rM1 with rehabilitation may be useful in enhancing excitability in damaged cortex.

Bimanual movement training (BMT) enhances the excitability of human preparatory premotor and primary motor (M1) cortices. We have shown that activity in M1 is enhanced after BMT involving simultaneous activation of homologous muscles (in-phase). Potential neural mechanisms underlying this effect could be input from premotor areas (i.e. dorsal premotor cortex (PMd)) and/or the homologous M1 representation. Recently, we showed that increasing PMd activity using theta burst stimulation (TBS) followed by BMT enhanced the corticospinal excitability of M1 compared to BMT alone. The purpose of this study was to investigate the effects of continuous TBS (cTBS) to right hemisphere M1 (rM1) on the homologous wrist extensor representation in left M1 (lM1), and its potential combined effects when followed by BMT. We used transcranial magnetic stimulation (TMS) to measure cortical excitability of extensor carpi radialis (ECR) representation at multiple time points in three conditions: (1) BMT, (2) cTBS to rM1 or (3) cTBS to rM1 and BMT. The combination of cTBS to rM1 and BMT resulted in an increased shift in the centre of gravity (CoG) compared to either intervention alone, along with an increased muscle topographical representation up to 60 min when cTBS to rM1 was combined with BMT compared to cTBS to rM1 alone. These results suggest that modulation of M1 may reduce ongoing interhemispheric inhibition (or increase facilitation indirectly) to the opposite homologous M1 region in healthy individuals via transcallosal or subcortical connections. Critically, this work may guide rehabilitation training and stimulation techniques that modulate cortical plasticity after brain injury.