Clinical Value of the Assessment of Changes in MEP Duration with Voluntary Contraction.

Marisa Brum,Christopher Cabib,Josep Valls-Solé

doi:10.3389/fnins.2015.00505

Abstract

Transcranial magnetic stimulation (TMS) gives rise to muscle responses, known as motor evoked potentials (MEP), through activation of the motor pathways. Voluntary contraction causes facilitation of MEPs, which consists of shortening MEP latency, increasing MEP amplitude and widening MEP duration. While an increase in excitability of alpha motorneurons and the corticospinal tract can easily explain latency shortening and amplitude increase, other mechanisms have to be accounted for to explain the increase in duration. We measured the increase in duration of the MEP during contraction with respect to rest in a group of healthy volunteers and retrospectively assessed this parameter in patients who were examined in a standardized fashion during the past 5 years. We included 25 healthy subjects, 21 patients with multiple sclerosis, 33 patients with acute stroke, 5 patients with hereditary spastic paraparesis, and 5 patients with signs suggesting psychogenic paresis. We found already significant differences among groups in the MEP duration at rest, patients with MS had a significantly longer duration, and patients with stroke had significantly shorter duration, than the other two groups. The increase in MEP duration during voluntary contraction was different in patients and in healthy subjects. It was significantly shorter in MS and significantly longer in stroke patients. It was absent in the five patients with suspected psychogenic weakness. In patients with HSP, an abnormally increase in duration occurred only in leg muscles. Our results suggest that the increase in duration of the MEP during contraction may reveal the contribution of propriospinal interneurons to the activation of alpha motorneurons. This mechanism may be altered in some diseases and, therefore, the assessment proposed in this work may have clinical applicability for the differential diagnosis of weakness.

Highlights

Transcranial magnetic stimulation (TMS) gives rise to muscle responses, known as motor evoked potentials (MEP), through activation of the motor pathways (Amassian et al, 1987; Day et al, 1987, 1989; Rothwell et al, 1987, 1991)
We reasoned that, when an MEP is elicited during voluntary contraction, inhibitory inputs generated at spinal level or by the descending volleys should counteract the excitatory commands to effectively end the ongoing EMG activity and give way to the silent period. This may take some time and, the EMG activity will not be suppressed. We considered that such “MEPtail,” i.e., the EMG activity that follows the MEP peak and ends at the beginning of the silent period, should indicate the relationship between the strength of the excitatory inputs reaching the alpha motorneurons during voluntary contraction and the inhibitory inputs derived from the synchronized activation of alpha motorneurons at the time of the MEP
We performed a retrospective study of the recordings obtained within the last 5 years in healthy subjects and patients in whom we examined facilitation of the MEP in the first dorsal interosseous muscle (FDI), using a standardized method

Summary

Introduction

Transcranial magnetic stimulation (TMS) gives rise to muscle responses, known as motor evoked potentials (MEP), through activation of the motor pathways (Amassian et al, 1987; Day et al, 1987, 1989; Rothwell et al, 1987, 1991). Clinical Value of MEP Duration Analysis shortening and amplitude increase can be well explained by assuming that voluntary contraction put more motorneurons near the firing threshold, the rationale behind the increase in MEP duration is less clear. Motorneurons should be firing earlier and more synchronously to give rise to the shortening of latency and increase in peak amplitude. Some motorneurons should receive excitatory inputs with latency longer than at rest. This could be due to activation of slow conducting corticospinal fibers or to the generation of excitatory inputs at spinal level (Brasil-Neto et al, 1992; Di Lazzaro et al, 1999, 2001), but it seems contradictory that slow conducting corticospinal fibers are recruited during voluntary contraction. Even if some inhibitory activity may be temporarily switched off during contraction, this does not justify the presence of EMG activity at a time when there are no identifiable excitatory inputs

Methods

Results

Conclusion