Long-term recovery and fellow eye deterioration after optic neuritis, determined by serial visual evoked potentials

Citation
A. Brusa et al., Long-term recovery and fellow eye deterioration after optic neuritis, determined by serial visual evoked potentials, J NEUROL, 246(9), 1999, pp. 776-782
Citations number
16
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROLOGY
ISSN journal
03405354 → ACNP
Volume
246
Issue
9
Year of publication
1999
Pages
776 - 782
Database
ISI
SICI code
0340-5354(199909)246:9<776:LRAFED>2.0.ZU;2-O
Abstract
Twelve optic neuritis patients (part of a larger group in whom the effects of intravenous methylprednisolone treatment were previously reported), were followed-up 3 years from the onset of symptoms with visual evoked potentia ls (VEPs), contrast sensitivity and visual field examination. Findings from the previously "unaffected" eyes, none of which had had symptomatic optic neuritis, were also assessed. Between 6 months and 3 years after the onset of symptoms the VEPs of the affected eyes showed a significant shortening o f mean latency (whole field, 131-123 ms; central field, 136-125 ms). Conver sely, the responses of the previously unaffected eyes showed a contemporane ous latency prolongation (significant for the whole field, 110-113 ms) whic h exceeded the expected effect of aging. Contrast sensitivity tests showed no significant change in the affected eyes but a mild deterioration in the unaffected eyes, while the visual fields showed no overall pattern of impro vement or deterioration. If the strong tendency for VEP latencies to shorte n is due to ongoing remyelination, the lack of significant improvement in v isual function may be because the visual deficit at 6 months is due to irre versible axonal loss rather than demyelination. The absence of functional d eterioration in the affected eye, while VEPs and contrast sensitivity deter iorated in the unaffected eye, suggests that long-term remyelination may fo r a while counteract the effects of insidious demyelination and axonal dege neration which affect the visual pathway during clinical remission.