MRI shows thickening and altered diffusion in the median and ulnar nerves in multifocal motor neuropathy

Wieke Haakma,Jeroen Hendrikse,Clemens Bos,H Stephan Goedee,Martijn Froeling,Alexander Leemans,Leonard H Van Den Berg,Bas A Jongbloed,W Ludo Van Der Pol

doi:10.1007/s00330-016-4575-0

Wieke Haakma, Jeroen Hendrikse + Show 7 more

Open Access

https://doi.org/10.1007/s00330-016-4575-0

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Abstract

ObjectivesTo study disease mechanisms in multifocal motor neuropathy (MMN) with magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI) of the median and ulnar nerves.MethodsWe enrolled ten MMN patients, ten patients with amyotrophic lateral sclerosis (ALS) and ten healthy controls (HCs). Patients underwent MRI (in a prone position) and nerve conduction studies. DTI and fat-suppressed T2-weighted scans of the forearms were performed on a 3.0T MRI scanner. Fibre tractography of the median and ulnar nerves was performed to extract diffusion parameters: fractional anisotropy (FA), mean (MD), axial (AD) and radial (RD) diffusivity. Cross-sectional areas (CSA) were measured on T2-weighted scans.ResultsForty-five out of 60 arms were included in the analysis. AD was significantly lower in MMN patients (2.20 ± 0.12 × 10-3 mm2/s) compared to ALS patients (2.31 ± 0.17 × 10-3 mm2/s; p < 0.05) and HCs (2.31± 0.17 × 10-3 mm2/s; p < 0.05). Segmental analysis showed significant restriction of AD, RD and MD (p < 0.005) in the proximal third of the nerves. CSA was significantly larger in MMN patients compared to ALS patients and HCs (p < 0.01).ConclusionsThickening of nerves is compatible with changes in the myelin sheath structure, whereas lowered AD values suggest axonal dysfunction. These findings suggest that myelin and axons are diffusely involved in MMN pathogenesis.Key Points• Diffusion magnetic resonance imaging provides quantitative information about multifocal motor neuropathy (MMN).• Diffusion tensor imaging allows non-invasive evaluation of the forearm nerves in MMN.• Nerve thickening and lowered diffusion parameters suggests myelin and axonal changes.• This study can help to provide insight into pathological mechanisms of MMN.

Highlights

Multifocal motor neuropathy (MMN) is a rare disorder characterized by progressive, asymmetric and predominantly distal limb weakness without any sensory involvement [1]
diffusion tensor imaging (DTI) images of 15 out of 60 arms had to be excluded due to motion distortion or other MR-related problems resulting in a total of 45 scans of arms that were available for analysis
T2-weighted scans of nine out of 60 arms had to be excluded, resulting in a total of 51 arms that were used for analysis

Summary

Introduction

Multifocal motor neuropathy (MMN) is a rare disorder characterized by progressive, asymmetric and predominantly distal limb weakness without any sensory involvement [1]. The presence of anti-GM1 IgM antibodies in more than half of the patients may suggest that MMN is caused by anti-GM1 antibody-mediated damage at or in the proximity of the nodes of Ranvier. This likely plays a role in the phenomenon of conduction block and in the demyelination or disruption of the compact myelin structure [2, 6]. Demyelination or disruption of the compact myelin structure represents an alternative pathogenic mechanism that causes MMN [6]. There is a need for new methodology to elucidate MMN pathogenesis and to eventually improve treatment strategies

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