Multifocal Visual Evoked Potentials (mfVEP) and Ganglion Cell Inner Plexiform Thickness (GCIPT) in Relapsing Remitting Multiple Sclerosis (RRMS)

Friday, May 30, 2014: 11:40 AM
Divya Narayanan, B.S.Optometry , College of Optometry, University of Houston, Houston, TX
Han Cheng, Ph.D., O.D. , College of Optometry, University of Houston, Houston, TX
Rosa Tang, M.D. , MS Eye CARE clinic, University of Houston, Houston, TX
Laura Frishman, Ph.D. , College of Optometry, University of Houston, Houston, TX

Background: The primary visual pathway is a good model for studying demyelination and neurodegeneration in MS.

Objectives: To detect structural and functional damage using optical coherence tomography (OCT), mfVEP, and contrast sensitivity (CS) in RRMS eyes without active optic neuritis (ON).

Methods: SD-OCT, mfVEP, Pelli-Robson CS were obtained in 90 RRMS patients. There were 105 eyes (no-ON) without a history of ON and 58 eyes (ON) with last ON ≥6 months. 40 age matched normals had mfVEP and CS. MfVEP recorded with a 60-sector cortically-scaled stimulus (22° radius, VERIS 5.1), provided local response amplitude (AMP) (logSNR) and relative latency (LAT) (ms). Global mfVEP AMP and LAT were calculated as mean logSNR and median LAT from 60 sectors. Mean GCIPT, average retinal nerve fiber layer thickness (ARNFLT) and temporal RNFLT (TRNFLT) from OCT were analyzed. Traditional pattern-reversal VEP (tVEP) was recorded (22° radius) in 30 patients and 34 normals; p100 AMP and LAT were calculated for 15’, 60’ and 120’ checks. For mfVEP, CS and tVEP, responses worse than 5% of norms were classified as abnormal. For OCT, values below 5% of age matched machine norms were abnormal. Statistical analyses used proc Genmod (SAS 9.2) to account for age and intra-subject inter-eye correlation.

Results: MfVEP showed lower AMP and longer LAT in no-ON (p<0.01) and ON (p<0.0001) than normal (mean±SE logSNR: 0.61±0.02, 0.56±0.01, 0.42±0.02; relative LAT: 0.7±0.5, 3.2±0.7, 9.0±1.6 in normal, no-ON and ON). Compared to normal (1.61±0.01), mean CS was reduced in ON (1.40±0.04, p<0.001) but similar in no-ON (1.60±0.01, p=0.90). Mean GCIPT (µm) was 77.9±0.9 in no-ON and 69.7±1.7 in ON (p<0.001). For no-ON, 23% had abnormal mfVEP in AMP, 25% in LAT and 47% in AMP or LAT. Among those with abnormal LAT, 65% had significant delay within the central 5.6°, the mfVEP region that corresponds best with the region measured by GCIPT. More no-ON eyes had abnormal GCIPT (20%) than ARNFLT (12%) or TRNFLT (13%) (p=0.03 for both). 8% of no-ON had abnormal CS. For tVEP (120’), 3% of no-ON had abnormal AMP, 17% abnormal LAT, 23% abnormal AMP or LAT. Results of 15’ and 60’ were similar. For ON, percents of abnormal eyes were: 80% for mfVEP AMP/LAT, 60% for GCIPT, 51% for ARNFLT, 44% for TRNFLT, 38% for CS and 74% for tVEP 120’ AMP/LAT. 

Conclusions: GCIPT and mfVEP offer complementary information on the integrity of the visual pathway and are useful for detecting subclinical neuronal defects in MS.