Does the longer application of anodal-transcranial direct current stimulaton increase corticomotor excitability further? A pilot study

Introduction: Anodal transcranial direct current stimulation (a-tDCS) of the primary motor cortex (M1) has been shown to be effective in increasing corticomotor excitability.　Methods: We investigated whether longer applications of a-tDCS coincide with greater increases in corticomotor excitability compared to shorter application of a-tDCS. Ten right-handed healthy participants received one session of a-tDCS (1mA current) with shorter (10 min) and longer (10+10 min) stimulation durations applied to the left M1 of extensor carpi radialis muscle (ECR). Corticomotor excitability following application of a-tDCS was assessed at rest with transcranial magnetic stimulation (TMS) elicited motor evoked potentials (MEP) and compared with baseline data for each participant.　Results: MEP amplitudes were increased following 10 min of a-tDCS by 67% (p = 0.001) with a further increase (32%) after the second 10 min of a-tDCS (p = 0.005). MEP amplitudes remained elevated at 15 min post stimulation compared to baseline values by 65% (p = 0.02).　Discussion: The results demonstrate that longer application of a-tDCS within the recommended safety limits, increases corticomotor excitability with after effects of up to 15 minutes post stimulation.<br /

Primary sensory and motor cortex excitability are co-modulated in response to peripheral electrical nerve stimulation

Peripheral electrical stimulation (PES) is a common clinical technique known to induce changes in corticomotor excitability; PES applied to induce a tetanic motor contraction increases, and PES at sub-motor threshold (sensory) intensities decreases, corticomotor excitability. Understanding of the mechanisms underlying these opposite changes in corticomotor excitability remains elusive. Modulation of primary sensory cortex (S1) excitability could underlie altered corticomotor excitability with PES. Here we examined whether changes in primary sensory (S1) and motor (M1) cortex excitability follow the same timecourse when PES is applied using identical stimulus parameters. Corticomotor excitability was measured using transcranial magnetic stimulation (TMS) and sensory cortex excitability using somatosensory evoked potentials (SEPs) before and after 30 min of PES to right abductor pollicis brevis (APB). Two PES paradigms were tested in separate sessions; PES sufficient to induce a tetanic motor contraction (30–50 Hz; strong motor intensity) and PES at sub motor-threshold intensity (100 Hz). PES applied to induce strong activation of APB increased the size of the N20-P25 component, thought to reflect sensory processing at cortical level, and increased corticomotor excitability. PES at sensory intensity decreased the size of the P25-N33 component and reduced corticomotor excitability. A positive correlation was observed between the changes in amplitude of the cortical SEP components and corticomotor excitability following sensory and motor PES. Sensory PES also increased the sub-cortical P14-N20 SEP component. These findings provide evidence that PES results in co-modulation of S1 and M1 excitability, possibly due to cortico-cortical projections between S1 and M1. This mechanism may underpin changes in corticomotor excitability in response to afferent input generated by PES.Siobhan M. Schabrun, Michael C. Ridding, Mary P. Galea, Paul W. Hodges and Lucinda S. Chipchas

Corticomotor excitability during precision motor tasks

The aim of this preliminary study was to investigate motor cortex (cortical) excitability between a similar fine visuomotor task of varying difficulty. Ten healthy adults (three female, seven male; 20—45 years of age) participated in the study. Participants were instructed to perform a fine visuomotor task by statically abducting their first index finger against a force transducer which displayed the level of force (represented as a marker) on a computer monitor. This marker was to be maintained between two stationary bars, also displayed on the computer monitor. The level of difficulty was increased by amplifying the position of the marker, making the task more difficult to control. Cortical measures of motor evoked potential (MEP) and silent period (SP) duration in first dorsal interosseous (FDI) muscle were obtained using transcranial magnetic stimulation (TMS) while the participant maintained the ‘‘easy’’ or ‘‘difficult’’ static task. An 11.8% increase in MEP amplitude was observed when subjects undertook the ‘‘difficult’’ task, but no differences in MEP latency or SP duration. The results from this preliminary study suggest that cortical excitability increases reflect the demand required to perform tasks requiring greater precision with suggestions for further research discussed

Experimental muscle hyperalgesia modulates sensorimotor cortical excitability, which is partially altered by unaccustomed exercise

Impaired corticomotor function is reported in patients with lateral epicondylalgia, but the causal link to pain or musculotendinous overloading is unclear. In this study, sensorimotor cortical changes were investigated using a model of persistent pain combined with an overloading condition. In 24 healthy subjects, the effect of nerve growth factor (NGF)-induced pain, combined with delayed-onset muscle soreness (DOMS), was examined on pain perception, pressure pain sensitivity, maximal force, and sensorimotor cortical excitability. Two groups (NGF alone and NGF + DOMS) received injections of NGF into the extensor carpi radialis brevis (ECRB) muscle at day 0, day 2, and day 4. At day 4, the NGF + DOMS group undertook wrist eccentric exercise to induce DOMS in the ECRB muscle. Muscle soreness scores, pressure pain thresholds over the ECRB muscle, maximal grip force, transcranial magnetic stimulation mapping of the cortical ECRB muscle representation, and somatosensory-evoked potentials from radial nerve stimulation were recorded at day 0, day 4, and day 6. Compared with day 0, day 4 showed in both groups: (1) increased muscle soreness (P < 0.01); (2) reduced pressure pain thresholds (P < 0.01); (3) increased motor map volume (P < 0.01); and (4) decreased frontal N30 somatosensory-evoked potential. At day 6, compared with day 4, only the DOMS + NGF group showed: (1) increased muscle soreness score (P < 0.01); (2) decreased grip force (P < 0.01); and (3) decreased motor map volume (P < 0.05). The NGF group did not show any difference on the remaining outcomes from day 4 to day 6. These data suggest that sustained muscle pain modulates sensorimotor cortical excitability and that exercise-induced DOMS alters pain-related corticomotor adaptation

Differential corticomotor excitability responses to hypertonic saline-induced muscle pain in forearm and hand muscles

Experimental muscle pain inhibits corticomotor excitability (CE) of upper limb muscles. It is unknown if this inhibition affects overlapping muscle representations within the primary motor cortex to the same degree. This study explored CE changes of the first dorsal interosseus (FDI) and extensor carpi radialis (ECR) muscles in response to muscle pain. Participants (n=13) attended two sessions (≥48 hours in-between). Hypertonic saline was injected in the ECR (session one) or the FDI (session two) muscle. CE, assessed by transcranial magnetic stimulation (TMS) motor-evoked potentials (MEPs), was recorded at baseline, during pain, and twenty minutes postinjection together with pain intensity ratings. Pain intensity ratings did not differ between the two pain sites (p=0.19). In response to FDI muscle pain, the MEPs of the FDI muscle were reduced at 2 and 4 min postinjection (p≤0.03), but not after ECR muscle pain. No significant MEP change was detected for the ECR muscle (p=0.62). No associations between MEPs and pain intensity were found (p>0.2). The present results indicate that the output from overlapping cortical representations of two muscles differentially adapts to acute muscle pain