Presence and Absence of Muscle Contraction Elicited by Peripheral Nerve Electrical Stimulation Differentially Modulate Primary Motor Cortex Excitability

We have studied manual motor function in a man deafferented by a severe peripheral sensory neuropathy. Motor power was almost unaffected. Our patients could produce a very wide range of preprogrammed finger movements with remarkable accuracy, involving complex muscle synergies of the hand and forearm muscles. He could perform individual finger movements and outline figures in the air with high eyes closed. He had normal pre- and postmovement EEG potentials, and showed the normal bi/triphasic pattern of muscle activation in agonist and antagonist muscles during fast limb movements. He could also move his thumb accurately through three different distances at three different speeds, and could produce three different levels of force at his thumb pad when required. Although he could not judge the weights of objects placed in his hands without vision, he was able to match forces applied by the experimenter to the pad of each thumb if he was given a minimal indication of thumb movement. Despite his success with these laboratory tasks, his hands were relatively useless to him in daily life. He was unable to grasp a pen and write, to fasten his shirt buttons or to hold a cup in one hand. Part of hist difficulty lay in the absence of any automatic reflex correction in his voluntary movements, and also to an inability to sustain constant levels of muscle contraction without visual feedback over periods of more than one or two seconds. He was also unable to maintain long sequences of simple motor programmes without vision.

In humans, somatosensory stimulation results in increased corticomotoneuronal excitability to the stimulated body parts. The purpose of this study was to investigate the underlying mechanisms. We recorded motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) from abductor pollicis brevis (APB), first dorsal interosseous (FDI), and abductor digiti minimi (ADM) muscles. MEP amplitudes, recruitment curves (RC), intracortical inhibition (ICI), intracortical facilitation (ICF), resting (rMT) and active motor thresholds (aMT) were recorded before and after a 2-h period of ulnar nerve electrical stimulation at the wrist. Somatosensory input was monitored by recording somatosensory evoked potentials. To differentiate excitability changes at cortical vs. subcortical sites, we recorded supramaximal peripheral M-responses and MEPs to brainstem electrical stimulation (BES). In order to investigate the involvement of GABAergic mechanisms, we studied the influence of lorazepam (LZ) (a GABA(A) receptor agonist) relative to that of dextromethorphan (DM) (an NMDA receptor antagonist) and placebo in a double-blind design. We found that somatosensory stimulation increased MEP amplitudes to TMS only in the ADM, confirming a previous report. This effect was blocked by LZ but not by either DM or placebo and lasted between 8 and 20 min in the absence of (i) changes in MEPs elicited by BES, (ii) amplitudes of early somatosensory-evoked potentials or (iii) M-responses. We conclude that somatosensory stimulation elicited a focal increase in corticomotoneuronal excitability that outlasts the stimulation period and probably occurs at cortical sites. The antagonistic effect of LZ supports the hypothesis of GABAergic involvement as an operating mechanism.

Peripheral electrical stimulation (ES) is commonly used as an intervention to facilitate movement and relieve pain in a variety of conditions. It is widely accepted that ES induces rapid plastic change in the motor cortex. This leads to the exciting possibility that ES could be used to drive cortical plasticity in movement disorders, such as stroke, and conditions where pain affects motor control. This paper aimed to critically review the literature to determine which parameters induced cortical plasticity in healthy individuals using ES. A literature search located papers that assessed plasticity in the primary motor cortex of adult humans. Studies that evaluated plasticity using change in the amplitude of potentials evoked by transcranial magnetic stimulation of the motor cortex were included. Details from each study including sample size, ES parameters and reported findings were extracted and compared. Where data were available, Cohen's standardised mean differences (SMD) were calculated. Nineteen studies were located. Of the parameters evaluated, variation of the intensity of peripheral ES appeared to have the most consistent effect on modulation of excitability of corticomotor pathway to stimulated muscles. There was a trend for stimulation above motor threshold to increase excitability (SMD 0.79 mV, CI -0.10 to 1.64). Stimulation below motor threshold, but sufficient to induce sensory perception, produced conflicting results. Further studies with consistent methodology and larger subject numbers are needed before definitive conclusions can be drawn. There also appeared to be a time effect. That is, longer periods of ES induced more sustained changes in cortical excitability. There is insufficient evidence to determine the effect of other stimulation parameters such as frequency and waveform. Further research is needed to confirm whether modulation of these parameters affects plastic change. Copyright © 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.