Gen Shiraishi

Effect of stimulus intensity and voluntary contraction on corticospinal potentials following transcranial magnetic stimulation

Following magnetic transcranial stimulation, motor-evoked potentials (MEPs) from the abductor digiti minimi muscle, and evoked spinal cord potentials (ESCPs) from the cervical epidural space were recorded simultaneously in 9 subjects in the awake and anesthetized condition. In the awake condition, during voluntary contraction, one (n = 5) or two (n = 4) components of the ESCPs were elicited at the threshold stimulus intensity of the MEPs. As the stimulus intensity increased, an early response (n = 7) and multiple late components were recorded. The first component at high stimulus output (average 80%) preceded the small potentials elicited at threshold stimulus intensity. The latency of each component of the ESCPs during voluntary contraction was the same as that during the resting condition. In addition, the enhancement of amplitude of the ESCPs during voluntary contraction was not significant compared with that recorded at rest. During general anesthesia with volatile anesthetics, the first component of the ESCPs could be elicited at high stimulus intensity, but later components were markedly attenuated. In paired transcranial magnetic stimulation, the amplitude of this first potential following the test stimulus completely recovered within the 2 ms interstimulus interval. From these results, we hypothesized that the first component was generated non-synaptically (D-wave), but later components were generated transsynaptically (I-waves). Compound muscle action potentials (CMAPs) and F-waves also were recorded following supramaximal ulnar nerve stimulation at the wrist. Peripheral conduction time, which included synaptic delay in spinal motor neurons, was measured as follows (latency of CMAPs+ latency of F-wave + 1)/2 (ms). The central motor conduction time (CMCT) was measured by subtracting the peripheral conduction time from the onset latency of the MEP at high stimulus intensity in the awake state. During voluntary contraction, the calculated CMCT (4.9 +/- 1.0 ms) was the same as the onset latency of the second component of the ESCPs (I-wave, 4.3 +/- 0.2 ms) recorded from the C6-C6/7 epidural space. These results suggest that transcranial magnetic stimulation generates I-waves preferentially when the stimulus intensity was set at just the threshold level of the MEPs during voluntary contraction in the awake condition. At high stimulus intensity, transcranial magnetic stimulation can elicit both D- and I-waves, but most spinal cells require I-wave activation to fire. Facilitatory effects of voluntary contraction on the muscle response following transcranial magnetic stimulation mainly originates at a spinal level.

Topographic analyses of somatosensory evoked potentials following stimulation of tibial, sural and lateral femoral cutaneous nerves

Using topographic maps, we studied the scalp field distribution of somatosensory evoked potentials (SEPs) in response to the stimulation of the tibial (TN), sural (SN) and lateral femoral cutaneous (LFCN) nerves in 24 normal volunteers. Cortical peaks, i.e., N35, P40, N50 and P60 were generally dominant in the contralateral hemisphere for the LFCN-SEP, whereas all peaks except N35 had dominance in the ipsilateral hemisphere to TN- and SN-SEPs. The findings imply that ipsilateral or contralateral peak dominance for the lower extremity SEP is determined by where the cortical leg representation occurs. As a result, mesial hemisphere representation results in peak dominance projected to the hemisphere ipsilateral to stimulation. Representations at the superior lip of the interhemispheric fissure or lateral convexity lead to midline or contralateral peak dominance. These findings also suggest that the paradoxically lateralized P40 is not the result of a positive field dipole shadow generated by the primary negative wave in the mesial hemisphere, but is the primary positive wave, analogous to P26 of the median nerve SEP. Accordingly, contralaterally dominant N35 is likely equivalent to the first cortical potential of N20 in the median nerve SEP. The difference in vector directions of potential fields between N35 and P40 may account for the opposite hemispheric dominance for these peaks in TN- and SN-SEPs.