Johann Malte Enno Jende1, Felix Tobias Kurz1, Mirjam Korporal-Kuhnke2, Markus Weiler2, Brigitte Wildemann2, Andrea Viehöver2, Sabine Heiland1, Wolfgang Wick2, Martin Bendszus1, and Jennifer Kollmer1
1Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany, 2Neurology, Heidelberg University Hospital, Heidelberg, Germany
Synopsis
This study investigated the correlation between T2w-hyperintense lesions to the peripheral nervous system (PNS) and the central nervous system (CNS) in multiple sclerosis (MS) by combining 3 Tesla magnetic resonance neurography (MRN) and 3 Tesla CNS MRI. It was found that CNS lesions and PNS lesions were inversely correlated (r=-0.432; p=0.0002). This finding might help to elucidate the underlying pathomechanism of PNS involvement in MS by indicating that PNS demyelination in MS does not occur secondary to CNS lesions in the sense of Wallerian degeneration.
Introduction
Recent studies have found an involvement of the peripheral nervous system (PNS) in multiple sclerosis.1 The aim of this study was to investigate potential correlations between T2w-hyperintense lesions of the central nervous system (CNS) and lesions to the PNS in clinically and electrophysiologically characterized patients with multiple sclerosis (MS) in order to elucidate whether PNS lesions occur as a consequence of CNS lesions in the sense of a Wallerian degeneration. Methods
Seventy MS patients prospectively underwent detailed neurologic and assessments including the Expanded Disability Status Scale (EDSS) and electrophysiologic examinations of the lower limbs. High-resolution magnetic resonance neurography (MRN) of the left middle thigh was performed in a 3.0 Tesla MRI scanner (Magnetom TIM Trio, Siemens, Erlangen, Germany) by using a 15-channel Transmit-Receive extremity-coil (INVIVO, Gainesville, FL, USA), and two-dimensional, axial T2-weighted turbo spin echo sequences with spectral fat-saturation (Repetition time = 5970 ms, echo time = ms 55 ms, field of view 150 x 150 2, matrix size 512 x 512, slice thickness 3.5 mm, interslice gap 0.35 mm, voxel size 0.4 x 0.3 x 3.5mm3, 35 slices, acquisition time 4:42 min). T2-weighted MRI of the CNS (brain and spinal cord) was available or additionally acquired in all patients. T2w lesion count of the CNS as well as T2w-hyperintense fascicular lesions of the sciatic nerve were assessed by two independent neuroradiologists blinded to clinical data.Results
Sciatic nerve T2w lesions and total CNS T2w lesions were inversely correlated (r=-0.432; p=0.0002). With regards to different CNS regions, an inverse correlation between sciatic nerve T2w lesions and supratentorial (r=-0.411; p=0.0005), infratentorial (r=-0.300; p=0.0129), and total (supratentorial and infratentorial) brain T2w lesions (r=-0.417; p=0.0004) was identified. No correlation was found between PNS T2w lesion numbers and electrophysiologic parameters. No correlations were found of PNS lesions with any previous or ongoing MS-specific disease modifying therapy (DMT).Discussion
The finding that CNS and PNS lesions are inversely correlated in MS indicates that PNS involvement in MS is not a consequence of valerian degeneration. Instead, the results of this study suggest that different pathophysiological processes, or, more specifically, that different antibodies predominate in MS with either stronger CNS or PNS involvement. The finding that PNS involvement is not associated with MS specific DMTs indicates that PNS involvement in MS is not a DMT related side effect. Conclusion
Our results might help to elucidate the underlying pathomechanism of PNS involvement in relapsing remitting MS by indicating that PNS lesions in MS do not occur as a consequence of Wallerian degeneration and that the pathologic pathway causing PNS damage in MS is different from the pathway leading to demyelination in the CNS.Acknowledgements
References
Jende JME, Hauck GHGH, Diem R, et al.Peripheral nerve involvement in multiple sclerosis: Demonstration by magnetic resonance neurography. Ann Neurol2017; 82: 676–85.