Long-term recovery and fellow eye deterioration after optic neuritis, determined by serial visual evoked potentials
| Autor: | David Miller, Gordon T. Plant, Adriana Brusa, Raju Kapoor, Steve J. Jones |
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| Rok vydání: | 1999 |
| Předmět: |
Adult
Male medicine.medical_specialty Optic Neuritis Time Factors genetic structures media_common.quotation_subject Eye disease Audiology Functional Laterality Contrast Sensitivity Psychophysics medicine Humans Contrast (vision) Cranial nerve disease Optic neuritis Remyelination media_common Multiple sclerosis Middle Aged medicine.disease eye diseases Visual field Electrophysiology medicine.anatomical_structure Neurology Nerve Degeneration Optic nerve Evoked Potentials Visual Female sense organs Neurology (clinical) Visual Fields medicine.symptom Psychology |
| Zdroj: | Journal of Neurology. 246:776-782 |
| ISSN: | 1432-1459 0340-5354 |
| DOI: | 10.1007/s004150050454 |
| Popis: | 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 potentials (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 of mean latency (whole field, 131-123 ms; central field, 136-125 ms). Conversely, the responses of the previously unaffected eyes showed a contemporaneous latency prolongation (significant for the whole field, 110-113 ms) which 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 improvement or deterioration. If the strong tendency for VEP latencies to shorten is due to ongoing remyelination, the lack of significant improvement in visual function may be because the visual deficit at 6 months is due to irreversible axonal loss rather than demyelination. The absence of functional deterioration in the affected eye, while VEPs and contrast sensitivity deteriorated in the unaffected eye, suggests that long-term remyelination may for a while counteract the effects of insidious demyelination and axonal degeneration which affect the visual pathway during clinical remission. |
| Databáze: | OpenAIRE |
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