@article{1e38407f5e924aee8be348e3edbdcd1e,
title = "Active MS is associated with accelerated retinal ganglion cell/inner plexiform layer thinning",
abstract = "Objective: To determine the effect of clinical and radiologic disease activity on the rate of thinning of the ganglion cell/inner plexiform (GCIP) layer and the retinal nerve fiber layer in patients with multiple sclerosis (MS) using optical coherence tomography (OCT). Methods: One hundred sixty-four patients with MS and 59 healthy controls underwent spectraldomain OCT scans every 6 months for a mean follow-up period of 21.1 months. Baseline and annual contrast-enhanced brain MRIs were performed. Patients who developed optic neuritis during follow-up were excluded from analysis. Results: Patients with the following features of disease activity during follow-up had faster rates of annualized GCIP thinning: relapses (42% faster, p = 0.007), new gadolinium-enhancing lesions (54% faster, p < 0.001), and new T2 lesions (36% faster, p = 0.02). Annual GCIP thinning was 37% faster in those with disability progression during follow-up, and 43% faster in those with disease duration <5 years vs >5 years (p = 0.003). Annual rates of GCIP thinning were highest in patients exhibiting combinations of new gadolinium-enhancing lesions, new T2 lesions, and disease duration <5 years (70% faster in patients with vs without all 3 characteristics, p < 0.001). Conclusions: MS patients with clinical and/or radiologic nonocular disease activity, particularly early in the disease course, exhibit accelerated GCIP thinning. Our findings suggest that retinal changes in MS reflect global CNS processes, and that OCT-derived GCIP thickness measures may have utility as an outcome measure for assessing neuroprotective agents, particularly in early, active MS.",
author = "Ratchford, {John N.} and Shiv Saidha and Sotirchos, {Elias S.} and Oh, {Jiwon A.} and Seigo, {Michaela A.} and Christopher Eckstein and Durbin, {Mary K.} and Oakley, {Jonathan D.} and Meyer, {Scott A.} and Amy Conger and Frohman, {Teresa C.} and Newsome, {Scott D.} and Balcer, {Laura J.} and Elliot Frohman and Calabresi, {Peter A.}",
note = "Funding Information: J. Ratchford consulted for Bristol-Myers Squibb and DioGenix, received a speaking honorarium from Teva, and receives research funding for clinical trials from Novartis and Biogen Idec. S. Saidha received consulting fees from Medical Logix for the development of continuing medical education programs in neurology, and has received educational grant support from Teva Neurosciences. E. Sotirchos, J. Oh, M. Seigo, and C. Eckstein report no disclosures. M. Durbin is employed by Carl Zeiss Meditec Inc. J. Oakley is a cofounder and employee of Voxeleron. He was previously employed by Carl Zeiss Meditec Inc. S. Meyer is employed by Carl Zeiss Meditec Inc. A. Conger and T. Frohman report no disclosures. S. Newsome received consulting fees from Biogen Idec, Teva, and Novartis and speaking honoraria from Biogen Idec and Teva. L. Balcer received speaking and consulting honoraria from Biogen Idec, Bayer, and Novartis. E. Frohman received speaking honoraria and consulting fees from Biogen Idec, Teva, and Athena. He received consulting fees from Abbott Laboratories. P. Calabresi has provided consultation services to Novartis, Teva, Biogen Idec, Vertex, Vaccinex, and Genentech, and has received grant support from EMD-Serono, Teva, Biogen Idec, Genentech, Bayer, Abbott, and Vertex. Go to Neurology.org for full disclosures.",
year = "2013",
month = jan,
day = "1",
doi = "10.1212/WNL.0b013e31827b1a1c",
language = "English (US)",
volume = "80",
pages = "47--54",
journal = "Neurology",
issn = "0028-3878",
publisher = "Lippincott Williams and Wilkins",
number = "1",
}