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Pathophysiological basis of low contrast visual acuity loss in multiple sclerosis
James D Triplett1, Con Yiannikas1, Michael H Barnett2,3
1Concord Hospital Sydney New South Wales Australia.
Annals of Clinical and Translational Neurology
|December 20, 2018
Summary
Low contrast visual acuity (LCVA) loss in MS patients is primarily predicted by axonal loss. Demyelination also significantly impacts LCVA, especially in patients without severe axonal loss, supporting LCVA
Area of Science:
- Neuroscience
- Ophthalmology
- Clinical Biomarkers
Background:
- Multiple Sclerosis (MS) requires reliable biomarkers for remyelination trials.
- Low Contrast Visual Acuity (LCVA) is a potential functional measure of visual pathway integrity.
Purpose of the Study:
- To determine the roles of axonal loss and demyelination in MS patients' LCVA loss.
- To evaluate LCVA as a biomarker for remyelination therapies.
Main Methods:
- 50 relapsing-remitting MS patients with prior optic neuritis were studied.
- Linear regression analyzed multifocal Visual Evoked Potential (mfVEP) latency and Retinal Nerve Fiber Layer (RNFL) thickness in relation to LCVA.
Main Results:
- Intereye asymmetry in mfVEP latency and RNFL thickness correlated with LCVA asymmetry (P < 0.001).
- Combined mfVEP latency and RNFL thinning predicted LCVA (R² = 0.67), with RNFL thinning being a stronger predictor.
- Excluding severe axonal loss increased mfVEP latency's contribution, diminishing RNFL's significance.
Conclusions:
- Retinal ganglion cell axonal loss is the primary LCVA predictor.
- Demyelination significantly contributes to LCVA reduction, particularly in milder cases.
- LCVA is a feasible biomarker for remyelination trials with careful patient selection.
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