MAY 08, 2013
Neuro-Ophthalmology/Orbit
This prospective study found a significant association between (spell out on first reference) RNFL loss and delayed multifocal visual evoked potential (mfVEP) in eyes with multiple sclerosis non-optic neuritis (MS-NON).
The authors analyzed the relationship between RNFL thickness and latency of the mfVEP in 45 patients with MS-NON and 25 age- and gender-matched controls. They assumed that RNFL thinning predominantly indicates retinal ganglion cell axonal loss, whereas mfVEP latency prolongation was interpreted as evidence of inflammatory demyelination along the visual pathway.
MS-NON eyes showed significant reduction of total and temporal RNFL thickness and significant latency delay, with both total and temporal RNFL thickness showing association with latency of the mfVEP. MS-NON eyes with normal latency showed no significant reduction of RNFL thickness compared with controls, whereas eyes with delayed latency demonstrated significantly thinner RNFL.
MS-NON eyes with delayed latency also had significantly thinner RNFL compared with MS-NON eyes with normal latencies. In patients with no previous optic neuritis in either eye, delayed latency and reduced RNFL were bilateral whenever present.
The authors note that a causal link between optic neuritis and subsequent RNFL thinning is well documented. Transection of optic nerve fibers during an acute attack is followed by retrograde degeneration, which results in RNFL thinning. Therefore, it is reasonable to assume that subclinical inflammatory demyelination may also cause RNFL loss, and the result of this study supports this assumption.
They also note that other factors, such as chronic demyelination or diffuse CNS inflammation, may potentially contribute to the axonal loss. A longitudinal study now underway may help answer the question of causality between subclinical inflammatory demyelination and RNFL loss in MS-NON eyes.