Cortical activation to voluntary movement in amyotrophic lateral sclerosis is related to corticospinal damage: Electrophysiological evidence

Riva, N.; Falini, A.; Inuggi, A.; Gonzalez-Rosa, J.J.; Amadio, S.; Cerri, F.; Fazio, R.; Del Carro, U.; Comola, M.; Comi, G.; Leocani, L.

doi:10.1016/j.clinph.2011.12.013

« BackClinical Neurophysiology

Article in Press

Cortical activation to voluntary movement in amyotrophic lateral sclerosis is related to corticospinal damage: Electrophysiological evidence

N. Riva
- Scientific Institute and Vita-Salute University San Raffaele, INSPE – Department of Neurology, Milan, Italy
A. Falini
- Scientific Institute and Vita-Salute University San Raffaele, CERMAC – Department of Neuroradiology, Milan, Italy
A. Inuggi
- Scientific Institute and Vita-Salute University San Raffaele, INSPE – Department of Neurology, Milan, Italy
J.J. Gonzalez-Rosa
- Scientific Institute and Vita-Salute University San Raffaele, INSPE – Department of Neurology, Milan, Italy
S. Amadio
- Scientific Institute and Vita-Salute University San Raffaele, INSPE – Department of Neurology, Milan, Italy
F. Cerri
- Scientific Institute and Vita-Salute University San Raffaele, INSPE – Department of Neurology, Milan, Italy
R. Fazio
- Scientific Institute and Vita-Salute University San Raffaele, INSPE – Department of Neurology, Milan, Italy
U. Del Carro
- Scientific Institute and Vita-Salute University San Raffaele, INSPE – Department of Neurology, Milan, Italy
M. Comola
- Scientific Institute and Vita-Salute University San Raffaele, INSPE – Department of Neurology, Milan, Italy
G. Comi
- Scientific Institute and Vita-Salute University San Raffaele, INSPE – Department of Neurology, Milan, Italy
L. Leocani
- Scientific Institute and Vita-Salute University San Raffaele, INSPE – Department of Neurology, Milan, Italy
- Corresponding author. Address: Department of Clinical Neurophysiology, Hospital San Raffaele, Via Olgettina 60, 20132 Milan, Italy. Tel.: +39 02 2643 3092; fax: +39 02 2643 3085.

Accepted 5 December 2011. published online 13 February 2012.
Corrected Proof

Highlights

► Movement-related cortical overactivation in ALS as revealed by analysis of sensorimotor EEG rhythms occurs in the post-movement phase and not in the pre-movement phase. ► The amount of movement-related cortical overactivation in ALS, measured with analysis of sensorimotor EEG rhythms, is proportional to the amount of corticospinal damage evident at MRI and TMS measures. ► Motor cortical overactivation in ALS patients may be related to reduced cortical inhibition or idling rather than to generalized hyperexcitability.

Abstract

Objectives

The time course of mu and beta sensorimotor rhythms, with event-related desynchronisation (ERD) to preparation and execution of voluntary movement followed by synchronisation (ERS) after movement, is considered to indicate cortical activation and idling, respectively. We investigated ERD and ERS in amyotrophic lateral sclerosis (ALS) patients and the relationship with anatomical and neurophysiological measures of corticospinal tract damage.

Methods

Pre-movement mu and beta ERD, and post-movement beta ERS were analysed in 16 ALS patients and 15 healthy controls performing self-paced brisk right thumb extensions. Apparent diffusion coefficient (ADC) of corticospinal tract was measured with magnetic resonance imaging (MRI). Motor-evoked potentials (MEPs) to the right abductor pollicis brevis were obtained using transcranial magnetic stimulation (TMS).

Results

Movement-related electromyographic activity was similar in the two groups. Post-movement ERS was significantly reduced in ALS group and negatively correlated with the amount of corticospinal damage as from MRI and TMS measures. ERD did not significantly differ between groups.

Conclusions

Alterations of cortical activity in ALS patients were limited to the post-movement phase, as indicated by reduced ERS, and could be linked to reduced cortical inhibition rather than to generalised hyperexcitability.

Significance

The correlation between ERS and corticospinal damage severity might be interpreted as a functional compensation or dysfunction of inhibitory systems paralleling corticospinal damage.

Keywords: Motor neuron disease, Amyotrophic lateral sclerosis, EEG, Neurophysiology, DWI, TMS, Cortico-spinal tract