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. 2013 Jun 21;8(6):e66151.
doi: 10.1371/journal.pone.0066151. Print 2013.

Optical Coherence Tomography Reveals Distinct Patterns of Retinal Damage in Neuromyelitis Optica and Multiple Sclerosis

Elisa Schneider  1 , Hanna Zimmermann, Timm Oberwahrenbrock, Falko Kaufhold, Ella Maria Kadas, Axel Petzold, Frieder Bilger, Nadja Borisow, Sven Jarius, Brigitte Wildemann, Klemens Ruprecht, Alexander U Brandt, Friedemann Paul
Affiliations

Optical Coherence Tomography Reveals Distinct Patterns of Retinal Damage in Neuromyelitis Optica and Multiple Sclerosis

Elisa Schneider et al. PLoS One. .

Abstract

Background: Neuromyelitis optica (NMO) and relapsing-remitting multiple sclerosis (RRMS) are difficult to differentiate solely on clinical grounds. Optical coherence tomography (OCT) studies investigating retinal changes in both diseases focused primarily on the retinal nerve fiber layer (RNFL) while rare data are available on deeper intra-retinal layers.

Objective: To detect different patterns of intra-retinal layer alterations in patients with NMO spectrum disorders (NMOSD) and RRMS with focus on the influence of a previous optic neuritis (ON).

Methods: We applied spectral-domain OCT in eyes of NMOSD patients and compared them to matched RRMS patients and healthy controls (HC). Semi-automatic intra-retinal layer segmentation was used to quantify intra-retinal layer thicknesses. In a subgroup low contrast visual acuity (LCVA) was assessed.

Results: NMOSD-, MS- and HC-groups, each comprising 17 subjects, were included in analysis. RNFL thickness was more severely reduced in NMOSD compared to MS following ON. In MS-ON eyes, RNFL thinning showed a clear temporal preponderance, whereas in NMOSD-ON eyes RNFL was more evenly reduced, resulting in a significantly lower ratio of the nasal versus temporal RNFL thickness. In comparison to HC, ganglion cell layer thickness was stronger reduced in NMOSD-ON than in MS-ON, accompanied by a more severe impairment of LCVA. The inner nuclear layer and the outer retinal layers were thicker in NMOSD-ON patients compared to NMOSD without ON and HC eyes while these differences were primarily driven by microcystic macular edema.

Conclusion: Our study supports previous findings that ON in NMOSD leads to more pronounced retinal thinning and visual function impairment than in RRMS. The different retinal damage patterns in NMOSD versus RRMS support the current notion of distinct pathomechanisms of both conditions. However, OCT is still insufficient to help with the clinically relevant differentiation of both conditions in an individual patient.

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Conflict of interest statement

Competing Interests: Friedemann Paul is a PLOS ONE Editorial Board member. This does not alter the authors’ adherence to all the PLOS ONE policies on sharing data and materials.

Figures

Figure 1
Figure 1. Sample OCT measurement and segmentation.
A) Sample scanning laser ophthalmoscopy image showing the peripapillary ring-scan for retinal nerve fiber layer analysis. Nasal and temporal quadrants were analyzed separately B) Sample scanning laser ophthalmoscopy image showing the B-scans included in the segmentation procedure (green and blue) and the area included into analysis (blue only). C) Sample macular scan showing the segmentation lines and intra-retinal layer layout. Red segmentation lines provided by the software define the macular retinal nerve fiber layer (mRNFL), the ganglion cell layer (GCL), the inner plexiform layer (IPL), the inner nuclear layer (INL), the outer plexiform layer (OPL), the outer nuclear layer (ONL), and inner segments of the photoreceptor layer (IS). OPL, ONL and IS were analyzed combined as outer retinal layers (ORL). D) Sample B-scan of an NMOSD patient with microcystic macular edema (MME).
Figure 2
Figure 2. Sample patient data from NMOSD and MS eyes.
A) Peripapillary retinal nerve fiber layer (pRNFL) thickness data (in µm) for average RNFL (G) and sectors (nasal-superior quadrant (NS), temporal-superior (TS), temporal, temporal-inferior (TI), nasal-inferior (NI) and nasal (N)) for a multiple sclerosis (MS) patient’s eye with a previous optic neuritis (ON) (left), a neuromyelitis optica spectrum disorder (NMOSD) patient’s eye with a previous ON without microcystic macular edema (MME) (center), and an NMOSD patient’s eye with previous ON and MME (right). Background colors describe the comparison to a healthy reference group from the device’s database. B) and C) Thickness maps of the retinal ganglion cell layer (GCL, B) and inner nuclear layer (INL, C) respective to the patients’ data from A).
Figure 3
Figure 3. Correlation between visual function and retinal morphology.
Scatterplots illustrating relations of ganglion cell thickness of neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS) patients’ eyes with a previous optic neuritis to A) high contrast visual acuity (determined by ETDRS charts) and B) low contrast visual acuity determined by functional acuity contrast testing.
Figure 4
Figure 4. Intra-retinal layer thickness in NMOSD-ON eyes with and without microcystic macular edema.
Layer thicknesses for the macular retinal nerve fiber layer (mRNFL), ganglion cell layer (GCL), inner plexiform layer (IPL), inner nuclear layer (INL) and the combined outer retinal layers for NMOSD-ON eyes with (MME+, in red) and without (MME-, in blue) microcystic macular edema and healthy controls eyes (HC, in green). Outer retinal layers include outer plexiform layer, outer nuclear layer and inner photoreceptor layer segments.
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This work was supported by the German Research Council (DFG Exc 257 to FP). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.