Brusa, Adriana; (1999) Long-term recovery following optic neuritis: Evidence from serial electrophysiological and psychophysical investigations. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

Neuropathological studies have shown that remyelination occurs after experimental demyelination in the central nervous system and in patients affected by multiple sclerosis (MS). Previous neurophysiological studies of patients affected by optic neuritis (ON), used as a model for demyelinating lesions in MS, showed a shortening of the Visual evoked potential (VEP) latency delay which suggests a remyelinating process. Two groups of patients were studied after recovery from the acute stage of ON by means of clinical ocular examination, VEPs, Visual fields and Contrast sensitivity. The aim was to attempt to establish the extent and time course of VEP latency recovery, whether it is possible to identify any factor which could influence it and to evaluate its clinical consequences. Fourteen subjects were studied at 6 months and at 3 years after the attack of ON. The VEP from the affected eye showed a significant shortening of latency, which was not accompanied by visual function improvement. In the clinically unaffected eye a significant increase in VEP latency was associated with deterioration of contrast sensitivity. Thirty-one subjects were studied at 3 and 6 month intervals for two years after the onset of symptoms. In the affected eye the VEP latency shortened progressively throughout the follow-up period and functional improvement was seen for the first year. In the fellow eye there was no evidence of VEP latency increase or visual function deterioration. No other factors were discovered to influence the rate or extent of VEP latency and visual function recovery. The findings suggest that remyelination and insidious demyelination are both present over a 3 year follow-up. In the affected eye, although remyelination appears to assist visual function recovery only for the first year (possibly due to concurrent insidious demyelination and/or axonal loss), it is possible that serves to protect demyelinated axons against further inflammation which might result in permanent degeneration. In the fellow eye insidious demyelination is possibly continuously active but its effects become measurable only after more than 2 years. It is possible that a progressive phase of functional deterioration starts when insidious demyelination and/or axonal loss prevail over remyelination.

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