Service de Physiologie - Explorations Fonctionnelles, Hôpital Henri-Mondor, AP-HP; EA 4391, Excitabilité Nerveuse Et Thérapeutique

Author Of 1 Presentation

Imaging Poster Presentation

P0576 - Exploring the Corticospinal Tract in Progressive Multiple Sclerosis: A Transcranial Magnetic Stimulation and Magnetic Resonance Imaging Study (ID 1446)

Speakers
Presentation Number
P0576
Presentation Topic
Imaging

Abstract

Background

Progressive multiple sclerosis (MS) phenotypes are associated with important clinical disability. Yet, moderate lesion burden is usually reported using conventional magnetic resonance imaging (MRI), suggesting other mechanisms at the basis of disability (e.g., motor cortical lesions, alteration of corticospinal tract (CST) function and integrity). Transcranial magnetic stimulation (TMS) permits a noninvasive exploration of corticospinal function. MRI allows a precise assessment of cortical (double inversion recovery (DIR) sequence) and CST structural integrity (diffusion tensor imaging (DTI)).

Objectives

This work aimed to assess the correlation between TMS and MRI-derived measures of CST and motor cortex. This might give complementary insight on neurophysiological and neuroanatomical characteristics of CST.

Methods

Adult patients with progressive MS were included. Patients were not included if they had a relapse in the last three months, change in MS treatments in the last two months, absence of motor evoked potentials, presence of contraindications for TMS/MRI performance, or presence of other neuropsychiatric diagnoses. TMS measures included short interval intracortical inhibition and facilitation. MRI protocol included DTI and DIR sequences to generate measures of CST integrity (volume, fractional anisotropy, apparent diffusion coefficient (ADC), axial diffusivity and radial diffusivity (RD)) and motor cortical lesions load. Correlation analysis was performed.

Results

Twenty-five patients completed the evaluations (13 females, mean age: 56 ± 11 years). Significant inverse correlations between percentages of intracortical facilitation and each of CST RD (p<0.01) and CST ADC (p<0.05) were observed.

Conclusions

High ADC and RD have been previously found among patients with MS and reflect high structural damage of the CST (demyelination as reflected by high RD, or both axon/myelin pathology as reflected by high ADC). In addition, low intracortical facilitation was previously suggested to reflect a deficient synaptic transmission and would hint towards an exhaustion of the compensatory mechanisms that are usually deployed to overcome the MS-related functional decline. The current findings would suggest a concomitant impairment of CST and intracortical facilitatory circuits that takes place at an advanced stage of MS. Intracortical facilitation and RD/ADC could constitute potential biomarkers to monitor disease evolution and response to interventions.

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