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 spectral-domain 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.
authors.affiliation: Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
authors.forename: John N
authors.initials: JN
authors.lastname: Ratchford
authors.forename: Shiv
authors.initials: S
authors.lastname: Saidha
authors.forename: Elias S
authors.initials: ES
authors.lastname: Sotirchos
authors.forename: Jiwon A
authors.initials: JA
authors.lastname: Oh
authors.forename: Michaela A
authors.initials: MA
authors.lastname: Seigo
authors.forename: Christopher
authors.initials: C
authors.lastname: Eckstein
authors.forename: Mary K
authors.initials: MK
authors.lastname: Durbin
authors.forename: Jonathan D
authors.initials: JD
authors.lastname: Oakley
authors.forename: Scott A
authors.initials: SA
authors.lastname: Meyer
authors.forename: Amy
authors.initials: A
authors.lastname: Conger
authors.forename: Teresa C
authors.initials: TC
authors.lastname: Frohman
authors.forename: Scott D
authors.initials: SD
authors.lastname: Newsome
authors.forename: Laura J
authors.initials: LJ
authors.lastname: Balcer
authors.forename: Elliot M
authors.initials: EM
authors.lastname: Frohman
authors.forename: Peter A
authors.initials: PA
authors.lastname: Calabresi
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000473:pathology*; D009410:Nerve Degeneration / Q000473:pathology*; D009412:Nerve Fibers / Q000473:pathology; D059906:Neuroimaging / Q000379:methods / Q000706:statistics & numerical data; D012165:Retinal Ganglion Cells / Q000473:pathology*; D055351:Retinal Neurons / Q000473:pathology*; D041623:Tomography, Optical Coherence / Q000379:methods* / Q000706:statistics & numerical data