title: Early factors associated with axonal loss after optic neuritis.
abstract: OBJECTIVE
  Acute optic neuritis due to an inflammatory demyelinating lesion of the optic nerve is often seen in association with multiple sclerosis. Although functional recovery usually follows the acute episode of visual loss, persistent visual deficits are common and are probably due to axonal loss. The mechanisms of axonal loss and early features that predict it are not well defined. We investigated clinical, electrophysiological, and imaging measures at presentation and after 3 months as potential markers of axonal loss following optic neuritis.
  
  
  METHODS
  We followed 21 patients after their first attack of acute unilateral optic neuritis for up to 18 months. Axonal loss was inferred from optical coherence tomography measures of retinal nerve fiber layer (RNFL) thickness at least 6 months following the episode. Visual function, visual evoked potential, and optic nerve magnetic resonance imaging measures obtained during the acute episode and 3 months later were investigated for their association with later axonal loss.
  
  
  RESULTS
  After multivariate analysis, prolonged visual evoked potential latency and impaired color vision, at baseline and after 3 months, were significantly and independently associated with RNFL thinning. Low-contrast acuity measures exhibited significant univariate associations with RNFL thinning.
  
  
  CONCLUSIONS
  The association of RNFL loss with a prolonged visual evoked potential (VEP) latency suggests that acute and persistent demyelination is associated with increased vulnerability of axons. VEP latency and visual function tests that capture optic nerve function, such as color and contrast, may help identify subjects with a higher risk for axonal loss who are thus more suitable for experimental neuroprotection trials.
authors.affiliation: NMR Research Unit, University College London, Institute of Neurology, London, United Kingdom. a.henderson@ucl.ac.uk
authors.forename: Andrew P D
authors.initials: AP
authors.lastname: Henderson
authors.forename: Daniel R
authors.initials: DR
authors.lastname: Altmann
authors.forename: S Anand
authors.initials: SA
authors.lastname: Trip
authors.forename: Katherine A
authors.initials: KA
authors.lastname: Miszkiel
authors.forename: Patricio G
authors.initials: PG
authors.lastname: Schlottmann
authors.forename: Steve J
authors.initials: SJ
authors.lastname: Jones
authors.forename: David F
authors.initials: DF
authors.lastname: Garway-Heath
authors.forename: Gordon T
authors.initials: GT
authors.lastname: Plant
authors.forename: David H
authors.initials: DH
authors.lastname: Miller
mesh_terms: D000328:Adult; D001369:Axons / Q000473:pathology* / Q000502:physiology*; D003118:Color Perception / Q000502:physiology; D004569:Electroencephalography; D005074:Evoked Potentials, Visual / Q000502:physiology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D009900:Optic Nerve / Q000473:pathology*; D009902:Optic Neuritis / Q000473:pathology* / Q000503:physiopathology*; D010468:Perceptual Disorders / Q000175:diagnosis / Q000209:etiology; D010775:Photic Stimulation; D011930:Reaction Time / Q000502:physiology; D013997:Time Factors; D041623:Tomography, Optical Coherence / Q000379:methods