TY - JOUR
T1 - Quantitative spinal cord MRI in radiologically isolated syndrome
AU - Alcaide-Leon, Paula
AU - Cybulsky, Kateryna
AU - Sankar, Stephanie
AU - Casserly, Courtney
AU - Leung, General
AU - Hohol, Marika
AU - Selchen, Daniel
AU - Montalban, Xavier
AU - Bharatha, Aditya
AU - Oh, Jiwon
N1 - Funding Information:
Actelion, Bayer, Biogen, Merck, Novartis, Oryzon Genomics, Receptos, Roche, Sanofi-Genzyme, and Teva Pharmaceuticals; and received research support from the Foundation of Barcelona and Fundacio Cemcat. A. Bharatha received travel funding and/or speaker honoraria from EMD Serono, Biogen, and Novartis. J. Oh served on the scientific advisory board of EMD Serono, Genzyme, Novartis, Teva, and Roche; received travel funding and/or speaker honoraria from Roche, Novartis, EMD Serono, and Genzyme; and received research support from Biogen-Idec, the Multiple Sclerosis Society, and the National MS Society. Go to Neurology.org/nn for full disclosure forms.
Funding Information:
P. Alcaide-Leon received research support from Novartis. K. Cybulsky and S. Sankar report no disclosures. C. Casserly received travel funding from EMD Serono and Novartis. G. Leung holds patents for and receives fees from Wireless Transmission through Faraday Cage, uses of waveguide insert to deliver a wireless signal through the faraday cage, optical detection of multispectral tissue damage, and uses of near-infrared light source and reflectance spectroscopy to generate images of blood breakdown products using a cell phone; consulted with hospitals for MRI installations and acceptance testing; received research support from the Canadian Institute of Health, National Science & Engineering Research Council, and S. Michael’s Foundation Innovation Fund; and holds stock or stock options from MIMOSA Diagnostics. M. Hohol served on the scientific advisory board of Biogen, EMD Serono, Genzyme, Novartis, Pharmascience Inc, Roche, and Teva Canada Innovation and received travel funding and/or speaker honoraria from Biogen, EMD Serono, Genzyme, and Novartis. D. Selchen received travel funding and/or speaker honoraria from Biogen, Sanofi-GenYme, Teva, Roche, Novartis, and Merk-Serono. X. Montalban served on the scientific advisory board of Actelion, Bayer, Biogen, Merck, Novartis, Oryzon Genomics, Receptos, Roche, Sanofi-Genzyme, and Teva Pharmaceuticals; received travel funding from Biogen, Merck, Novartis, Receptos, Roche, Sanofi-Genzyme, and Teva Pharmaceuticals; served on the editorial board of Multiple Sclerosis Journal, Journal of Neurology, The International MS Journal, Revista de Neurologia, and
Publisher Copyright:
Copyright © 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.
PY - 2018/3/1
Y1 - 2018/3/1
N2 - Objectives To assess whether quantitative spinal cord MRI (SC-MRI) measures, including atrophy, and diffusion tensor imaging (DTI) and magnetization transfer imaging metrics were different in radiologically isolated syndrome (RIS) vs healthy controls (HCs). Methods Twenty-four participants with RIS and 14 HCs underwent cervical SC-MRI on a 3T magnet. Manually segmented regions of interest circumscribing the spinal cord cross-sectional area (SC-CSA) between C3 and C4 were used to extract SC-CSA, fractional anisotropy, mean, perpendicular, and parallel diffusivity (MD, λ, and ⊥ λ∥) and magnetization transfer ratio (MTR). Spinal cord (SC) lesions, SC gray matter (GM), and SC white matter (WM) areas were also manually segmented. Multivariable linear regression was performed to evaluate differences in SC-MRI measures in RIS vs HCs, while controlling for age and sex. Results In this cross-sectional study of participants with RIS, 71% had lesions in the cervical SC. Of quantitative SC-MRI metrics, spinal cord MTR showed a trend toward being lower in RIS vs HCs (p = 0.06), and there was already evidence of brain atrophy (p = 0.05). There were no significant differences in SC-DTI metrics, GM, WM, or CSA between RIS and HCs. Conclusion The SC demonstrates minimal microstructural changes suggestive of demyelination and inflammation in RIS. These findings are in contrast to established MS and raise the possibility that the SC may play an important role in triggering clinical symptomatology in MS. Prospective follow-up of this cohort will provide additional insights into the role the SC plays in the complex sequence of events related to MS disease initiation and progression.
AB - Objectives To assess whether quantitative spinal cord MRI (SC-MRI) measures, including atrophy, and diffusion tensor imaging (DTI) and magnetization transfer imaging metrics were different in radiologically isolated syndrome (RIS) vs healthy controls (HCs). Methods Twenty-four participants with RIS and 14 HCs underwent cervical SC-MRI on a 3T magnet. Manually segmented regions of interest circumscribing the spinal cord cross-sectional area (SC-CSA) between C3 and C4 were used to extract SC-CSA, fractional anisotropy, mean, perpendicular, and parallel diffusivity (MD, λ, and ⊥ λ∥) and magnetization transfer ratio (MTR). Spinal cord (SC) lesions, SC gray matter (GM), and SC white matter (WM) areas were also manually segmented. Multivariable linear regression was performed to evaluate differences in SC-MRI measures in RIS vs HCs, while controlling for age and sex. Results In this cross-sectional study of participants with RIS, 71% had lesions in the cervical SC. Of quantitative SC-MRI metrics, spinal cord MTR showed a trend toward being lower in RIS vs HCs (p = 0.06), and there was already evidence of brain atrophy (p = 0.05). There were no significant differences in SC-DTI metrics, GM, WM, or CSA between RIS and HCs. Conclusion The SC demonstrates minimal microstructural changes suggestive of demyelination and inflammation in RIS. These findings are in contrast to established MS and raise the possibility that the SC may play an important role in triggering clinical symptomatology in MS. Prospective follow-up of this cohort will provide additional insights into the role the SC plays in the complex sequence of events related to MS disease initiation and progression.
UR - http://www.scopus.com/inward/record.url?scp=85044286453&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85044286453&partnerID=8YFLogxK
U2 - 10.1212/NXI.0000000000000436
DO - 10.1212/NXI.0000000000000436
M3 - Article
C2 - 29359174
AN - SCOPUS:85044286453
SN - 2332-7812
VL - 5
JO - Neurology: Neuroimmunology and NeuroInflammation
JF - Neurology: Neuroimmunology and NeuroInflammation
IS - 2
M1 - e436
ER -