Timing-specific associative plasticity between supplementary motor area and primary motor cortex in humans

• Published in: Klinische Neurophysiologie
• Main Authors: Müller-Dahlhaus, F, Arai, N, Bliem, B, Lu, MK, Ziemann, U
• Format: Conference Proceeding
• Language: English; German
• Published: 02.03.2010
• ISSN: 1434-0275; 1439-4081
• DOI: 10.1055/s-0030-1250955

Introduction: The supplementary motor area (SMA) is essential for preparation and execution of voluntary movements. Anatomically, SMA shows dense reciprocal connections to primary motor cortex (M1), yet the functional connectivity within the SMA-M1 network is not well understood. Here we modulated the SMA-M1 network using multifocal transcranial magnetic stimulation (TMS) and detected changes in functional coupling by electroencephalography (EEG) as well as corticospinal output changes by motor evoked potentials (MEPs). Material and Methods: Twenty-four right-handed subjects aged 19–43 years participated in the study. MEPs were recorded from right and left first dorsal interosseous muscles. Left and right M1 were stimulated near-simultaneously (delta t: 0.8ms) in nine blocks of 50 trials each with an intertrial interval of five seconds (Pre1–3, Cond1–3, Post1–3). In blocks Cond1–3 an additional TMS pulse was applied over SMA at an ISI of -6ms (SMA stimulation prior to bilateral M1 stimulation) or +15ms (SMA stimulation following bilateral M1 stimulation). TMS intensity for SMA stimulation equaled 140% of the individual active motor threshold. M1 stimulation intensity was adjusted to produce an unconditioned MEP of 1–1.5mV. In a second set of experiments scalp-EEG was recorded during rest at baseline (B0), after near-synchronous bilateral M1 stimulation (B1), and after associative SMA and M1 stimulation (P1, P2). Results: Associative SMA and M1 stimulation at an ISI of -6ms long-lastingly increased MEP amplitudes in left (F(8,64)=3.04, p=0.006) and right M1 (F(8,64)=2.66, p=0.014), whereas at an ISI of +15ms MEP amplitudes were decreased in right M1 only (left M1: F(8,64)=1.07, p=0.40; right M1: F(8,64)=2.20, p=0.039). These effects were critically dependent on the ISI between SMA and M1 stimulation as well as SMA stimulation intensity and site. Importantly, MEP amplitude changes could not be induced by associative SMA and M1 stimulation without prior bilateral near-synchronous M1 stimulation during Pre1–3 trials. Partial coherence analysis of EEG data revealed significant coherence changes (B1 vs. B0) in the low and high alpha band in a distributed motor network including SMA and M1. These EEG coherence changes were predictive for MEP amplitude changes in dominant (left) M1 after associative SMA and M1 stimulation. Conclusion: Our findings demonstrate that priming of cortical motor networks may induce specific changes in coherent oscillatory activity in these networks which are both necessary and predictive for subsequent occurrence of stimulus-induced associative plasticity between SMA and M1. The present results suggest a role for functional coupling of cortical areas to promote associative plasticity, for instance in the context of learning.