Abstract
Objective
To investigate posterior visual pathway damage in multiple sclerosis using ultrahigh-field magnetic resonance imaging (MRI) at 7 Tesla (7 T), and to determine its correlation with visual disability and retinal fibre layer (RNFL) damage detectable by optic coherence tomography (OCT).
Methods
We studied 7 T MRI, OCT, functional acuity contrast testing (FACT), and visually evoked potentials (VEP, n = 16) in 30 patients (including 26 relapsing-remitting MS and four clinically isolated syndrome patients) and 12 healthy controls to quantify RNFL thickness, optic radiation lesion volume, and optic radiation thickness.
Results
Optic radiation lesion volume was associated with thinning of the optic radiation (p < 0.001), delayed VEP (p = 0.031), and visual disability indicated by FACT (p = 0.020). Furthermore, we observed an inverse correlation between optic radiation lesion volume and RNFL thickness (p < 0.001), including patients without previous optic neuritis (p < 0.001).
Conclusions
Anterior visual pathway damage, but also (subclinical) optic radiation integrity loss detectable by 7 T MRI are common findings in MS that are mutually affected. Given the association between optic radiation damage, visual impairment, and increased VEP latency in this exploratory study of a limited sample size, clinicians should be aware of acute lesions within the optic radiation in patients with (bilateral) visual disturbances.
Key Points
• Focal destruction of the optic radiation is detectable by 7 T MRI.
• Focal optic radiation damage is common in MS.
• Optic radiation damage is associated with RNFL thinning, detectable by OCT.
• Optic radiation damage is associated with delayed VEP and visual dysfunction.
• RNFL thickness in non-optic neuritis eyes correlates with optic radiation demyelination.
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Acknowledgements
This work was supported by the German Research Foundation (DFG Exc 257). Our technicians and study nurses Antje Els, Susan Pikol, Cynthia Kraut, and Gritt Stoffels gave invaluable support.
The scientific guarantor of this publication is Jens Wuerfel.
The authors of this manuscript declare relationships with the following companies: TS received a travel grant from Bayer and Genzyme as well as speaker honoraria from Novartis. TO has nothing to disclose. IM received payments for lectures from Teva, Biogen Idec, and Sanofi as well as travel/accommodation/meeting expenses from Biogen Idec and Bayer. HZ has nothing to disclose. CFP has received travel grants from Teva. LH has received speaker honoraria from Biogen Idec, Bayer, Novartis, Merck-Serono, and Talecris. He serves on the advisory board for Biomarin and has received research support from Biogen and Bayer. KR has received travel grants and speaker honoraria from Merck-Serono, Biogen Idec, Bayer, and Novartis, and receives research support from Novartis. KH has nothing to disclose. WB received grants from Teva, Biogen Idec, Novartis, and Bayer. He also received honoraria for talks from Bayer, Biogen Idec, Merck-Serono, Teva, Genzyme, and Novartis and is member of the company advisory boards of Teva/Sanofi, Novartis, and Biogen Idec. TN is founder of MRI.TOOLS GmbH, Berlin, Germany and received speaker honoraria from Siemens Healthcare, Erlangen, Germany. AUB is cofounder and director of Motognosis UG (haftungsbeschränkt) and has received speaker honoraria, research grants and travel support from Bayer, Biogen Idec, Novartis Pharma, and Heidelberg Engineering. FP has received speaker honoraria, travel grants and research grants from Teva/Sanofi, Bayer, Merck-Serono, Biogen Idec, and Novartis. FP is supported by the German Research Foundation (Exc 257) and has received travel reimbursement from the Guthy Jackson Charitable Foundation. JD receives research grants from Novartis and Bayer, and has received travel support from Novartis, Teva, Bayer, and Merck-Serono, honoraria for consultancy from Bayer, Genzyme, and Teva, and speaker honoraria from Bayer, Teva, Genzyme, and Novartis. JW serves for a Novartis advisory board, received a Novartis research grant, and speaker honoraria from Novartis, Bayer, and Biogen Idec. He is supported by the German ministry for science and research (BMBF/KKNMS).
This study has received funding by the German Research Foundation (DFG Exc 257) and by a restricted research grant from TEVA Pharma, Germany.
One of the authors (Alexander U. Brandt) has significant statistical expertise.
Institutional review board approval was obtained.
Written informed consent was obtained from all subjects (patients) in this study.
Methodology: prospective cross sectional study performed at one institution.
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Jan Dörr and Jens Wuerfel are equally contributing senior authors
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Supplemental Fig. 1
Degeneration of the optic radiation. Patient A (male, 42 years, disease duration 14.6 years, EDSS 4.5) had extensive bilateral focal damage (white arrows) and atrophy of the optic radiation (black arrows). When looking at all patient data (B) including CIS (nON), RRMS (nON/ON), and early MS (nON/ON) patients, an association between the OR thickness and OR lesion volume was detectable. C shows seven consecutive T2*w FLASH MRI slices of patient C (female, 37 years old, disease duration 18.0 years, EDSS 2.5; this patient was excluded for technical reasons). A large lesion (white arrows) within the optic radiation (black arrows) is shown. The visibility of the optic radiation is dramatically diminished in the occipital part, indicative of anterograde degeneration. Sequence parameters: 7 T T2*w FLASH, TE = 25 ms, TR = 1,820 ms, spatial resolution = (0.5 × 0.5) mm2 (GIF 131 kb)
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Sinnecker, T., Oberwahrenbrock, T., Metz, I. et al. Optic radiation damage in multiple sclerosis is associated with visual dysfunction and retinal thinning – an ultrahigh-field MR pilot study. Eur Radiol 25, 122–131 (2015). https://doi.org/10.1007/s00330-014-3358-8
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DOI: https://doi.org/10.1007/s00330-014-3358-8