May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Acute Optic Neuritis From Presentation to One Year Post Diagnosis: A Multifocal Visual Evoked Potential Study
Author Affiliations & Notes
  • C.L. Fraser
    Electrophysiology, Save Sight Institute, Sydney, Australia
  • A. Klistorner
    Electrophysiology, Save Sight Institute, Sydney, Australia
  • S. Graham
    Electrophysiology, Save Sight Institute, Sydney, Australia
  • J. Grigg
    Electrophysiology, Save Sight Institute, Sydney, Australia
  • R. Garrick
    Neurology, St Vincents Hospital, Sydney, Australia
  • Footnotes
    Commercial Relationships  C.L. Fraser, None; A. Klistorner, ObjectiVision C, P; S. Graham, ObjectiVision C, P; J. Grigg, None; R. Garrick, None.
  • Footnotes
    Support  University of Sydney, UPA scholarship
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 5671. doi:
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      C.L. Fraser, A. Klistorner, S. Graham, J. Grigg, R. Garrick; Acute Optic Neuritis From Presentation to One Year Post Diagnosis: A Multifocal Visual Evoked Potential Study . Invest. Ophthalmol. Vis. Sci. 2005;46(13):5671.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: We follow 5 patients with a diagnosis of acute optic neuritis with serial multifocal visual evoked potentials (mVEP) for a year to track the changes seen in amplitude, latency and topography of their disease. Methods: Diagnosis of acute optic neuritis was made by a consultant neuro–ophthalmologist, with all other ocular and neurological pathology excluded. At each visit patients had visual acuity, colour vision, brightness perception, afferent pupillary defect test, Humphrey visual field 24–2 SITA fast and Accumap mVEP performed. All patients had at least two cranial MRI scans over the year. One patient developed optic atrophy, had a normal cranial MRI and was classified as very low risk of MS. The other 4 patients all had evidence of demyelination on cranial MRI, with 2 being given a diagnosis of multiple sclerosis (MS) based on clinical history. Patients were reviewed within the first three months since diagnosis, and again at 3, 6 and 12 months post diagnosis. Results: The patient with normal cranial MRI and a pale optic disc consistent with optic atrophy did not have significant latency delays. However, central amplitudes in the affected eye were decreased and the area involved enlarged during the year. Visual acuity has remained at 6/60. All of the 4 patients with demyelination on cranial MRI had initial amplitude loss, which recovered to near normal over the one year period. Improvement in visual acuity paralleled increasing amplitudes. Each of these patients had significant latency delays which persisted over the year, with z–scores of >2.5 at each test in the affected eye. In the fellow eyes, the latency z–scores remained <0.5 in 3 patients. The other patient had an episode of optic neuritis in his fellow eye, latency delays were seen to worsen in this eye to z–score of 3.0. Humphrey visual field testing was only abnormal in 3/5 patients and remained abnormal in the same 3 patients. Conclusions: The mVEP can detect changes of acute optic neuritis with greater sensitivity than Humphrey visual field testing. By analyzing the latency data we can distinguish between patients with demyelination and those with optic atrophy. We were also able to detect the onset of optic neuritis in a fellow eye.

Keywords: neuro-ophthalmology: optic nerve • electrophysiology: clinical • visual impairment: neuro-ophthalmological disease 
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