Stimulation‐induced changes in lower limb corticomotor excitability during treadmill walking in humans

Abstract

Magnetic stimulation of human primary motor cortex (M1) paired with electrical stimulation of a peripheral motor nerve has been used to produce a lasting modulation of corticomotor (CM) excitability. This 'paired associative stimulation' (PAS) protocol has been used to induce bidirectional changes in excitability in upper limb CM pathways. The present study tested the hypothesis that temporally dependent PAS applied to the common peroneal nerve during the swing phase of walking would induce bidirectional changes in CM excitability consistent with the Hebbian principle of activity-dependent plasticity. Fourteen subjects with no known neurological disorder participated in two data collection sessions each. PAS was delivered as a single block of 120 pairs of stimuli delivered in a 10 min period during treadmill walking at 4.0 km h −1 . Changes in CM excitability were assessed by examining the size of motor potentials evoked by transcranial magnetic stimulation prior to and following PAS. Tibialis anterior motor-evoked potentials amplitude increased to 121% over baseline when the magnetic stimulus was delivered over M1 after the estimated arrival time of the afferent volley in sensorimotor cortex and decreased to 83% of baseline when the magnetic stimulus was delivered prior to the estimated afferent volley arrival. This extent of modulation was undiminished following a further 10 min period of walking without stimulation. The temporal nature of the bidirectional effects following PAS, their rapid evolution and subsequent persistence supported the study's hypothesis and were similar to the effects described by others in quiescent muscles of the upper limb.

Changes in Excitability of the Cortical Projections to the Human Tibialis Anterior After Paired Associative Stimulation

“…If this is the case, it is possible that an ISI of 34 ms would suffice to alter the excitability of the cortical projections to the TA because the coincident summation of the peripheral input with the generated MEP does not have to occur at the onset of the MEP. A second explanation of why Stinear and Hornby (2005) observed such low increases in the TA MEP amplitude after PAS may be that the task itself may have interfered with the induction of plastic changes after PAS. Stefan et al (2006) reported that dynamic motor training before PAS reduces the efficacy of PAS.…”

“…A number of these studies have reported that it was not possible to induce significant changes in all of the subjects tested , whereas in some studies, the increases in the peak-to-peak size of the motor-evoked potential (MEP) amplitude after PAS were comparatively small (Stinear and Hornby 2005). A possible explanation is that the interstimulus interval (ISI) used was not optimal for all subjects, because most studies have implemented a standard ISI (ϳ25 ms for the muscles of the hand).…”

“…The PAS protocol has been implemented to alter the excitability of the cortical projections to various hand muscles (Kujirai et al 2006;Ridding and Flavel 2006;Stefan et al 2000Stefan et al , 2002Stefan et al , 2006Weise et al 2006;Wolters et al 2003) and more recently to the lower limb muscle tibialis anterior (TA) (Prior and Stinear 2006;Stinear and Hornby 2005). A number of these studies have reported that it was not possible to induce significant changes in all of the subjects tested , whereas in some studies, the increases in the peak-to-peak size of the motor-evoked potential (MEP) amplitude after PAS were comparatively small (Stinear and Hornby 2005).…”

Noninvasive Neuromodulation in Poststroke Gait Disorders

“…These areas are less easily approached with NIBS techniques, especially when dealing with distal muscles. However, studies on healthy individuals have demonstrated that rTMS, tDCS, and PAS protocols are able to modulate the excitability of the leg motor cortex, 82,99,117 and a behavioral effect of anodal tDCS on lower-limb motor performance, as transient enhancement of maximal leg force, has been observed. 118 Because the pathophysiological reorganization of leg motor areas after stroke is still unclear, based on the model of interhemispheric competition after stroke established for the upper extremity, NIBS techniques have been mainly applied for inhibiting the unlesioned hemisphere or facilitating the lesioned hemisphere.…”

“…To achieve PAS-induced facilitation of corticospinal pathways, the TMS must be delivered at an ISI equivalent to the estimated MEP latency plus 5 ms. To achieve PAS-induced inhibition, the TMS must be delivered with an ISI 10 ms shorter than the estimated MEP latency. 82 …”