Ganglion cells loss in non-optic neuritis eyes of MS patients

Prema Sriram, Nonna Saakova, Chenyu Wang, Hema Arvind, Stuart Graham, Con Yiannikus, Raymond Garrick, A. Klistorner

    Research output: Contribution to journalMeeting abstractpeer-review


    Objective: Loss of retinal ganglion cells (RGCs) in non-opticneuritis (non-ON) eyes of MS patients has recently been reported.Several factors such as anterograde degeneration initiated byabnormalities in the outer retinal layer (ORL) or inner nuclearlayer (INL), or primary degeneration of RGCs themselves maycontribute to this process. Alternatively, RGC loss can result fromretrograde degeneration caused by sub-clinical inflammationproximal to the RGC body. In the case of optic radiation lesionssuch neurodegeneration would require trans-synaptic transmission.Therefore, the purpose of the current study was to look forevidence of sub-clinical inflammation along the visual pathwayand/or structural and functional changes in outer retina to investigatetheir role in RGC loss in NON-ON eyes of MS patients.

    Methods: Forty NON-ON eyes of 40 RRMS patients and thirtycontrols were included. The thickness of the retinal layers wasmeasured by OCT (Spectralis, Heidelberg) and analysed usingcustom design segmentation software. RGCs were assessed usingthickness of the Ganglion Cell Complex (GCC). Structural andfunctional integrity of outer retina was analysed using thickness ofINL and ORL and full-field electroretinogram (ERG), while multifocalvisual evoked potentials (mfVEP) were performed to assessevidence of sub-clinical inflammation along the visual pathway.

    Results: The thickness of GCC was significantly reduced innon-ON eyes (80.4±7.9µ vs 87.0±5.5µ, p=0.0003). No significantchange in INL or ORL was detected (p=0.2 and 0.06).There was also no significant change in any of the ERG parameters.The latency of mfVEP, however, was significantly delayed(p=0.00001). GCC thickness correlated significantly with latencydelay of the mfVEP (r2 =0.34, p<0.001), but not with thickness ofouter retina layers or any ERG parameters. There was no significantthinning of GCC (84.0±3.6µ, p=0.08) in patients with normal(<99th percentile) mfVEP latency (17 patients). However inpatients with a delayed latency (>99th percentile, 23 patients) GCCreduction become even more apparent (78.0±8.9µ, p=0.00005).

    Conclusions: Our results demonstrate a significant association ofRGC loss with mfVEP latency delay, indicating that sub-clinicalinflammation along the visual pathway contributes significantlyto neuronal damage. No evidence of primary retinal degenerationwas found.
    Original languageEnglish
    Article numberP846
    Pages (from-to)382-382
    Number of pages1
    JournalMultiple Sclerosis
    Issue number4 supplement
    Publication statusPublished - Oct 2012
    Event28th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis - Lyon, France
    Duration: 10 Oct 201213 Oct 2012


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