Optical coherence tomography helps differentiate neuromyelitis optica and MS optic neuropathies. Neurology

Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Neurology (Impact Factor: 8.29). 07/2009; 73(4):302-8. DOI: 10.1212/WNL.0b013e3181af78b8
Source: PubMed


To evaluate the retinal nerve fiber layer (RNFL) thickness and macular volume in neuromyelitis optica (NMO) spectrum patients using optical coherence tomography (OCT).
OCT can quantify damage to retinal ganglion cell axons and can identify abnormalities in multiple sclerosis and optic neuritis (ON) eyes. OCT may also be useful in the evaluation of patients with NMO.
OCT and visual function testing were performed in 26 NMO spectrum patients with a history of ON, 17 patients with isolated longitudinally extensive transverse myelitis (LETM) without ON, 378 patients with relapsing-remitting multiple sclerosis (RRMS), and 77 healthy controls at 2 centers.
Substantial RNFL thinning was seen in NMO ON eyes (63.6 microm) relative to both RRMS ON eyes (88.3 microm, p < 0.0001) and control eyes (102.4 microm, p < 0.0001). A first episode of ON was estimated to cause 24 microm more loss of RNFL thickness in NMO than RRMS. Similar results were seen for macular volume. ON also was associated with more severe visual impairment in NMO spectrum patients than in RRMS patients. Eyes in the LETM group and unaffected NMO eyes were not significantly different from controls, though conclusions about these subgroups were limited by small sample sizes.
Optical coherence tomography (OCT) shows more severe retinal damage after optic neuritis (ON) episodes in neuromyelitis optica (NMO) than in relapsing-remitting multiple sclerosis. Identification of substantial retinal nerve fiber layer loss (>15 microm) after ON in a non-multiple sclerosis patient should prompt consideration of an NMO spectrum condition. OCT may be a useful tool for the evaluation of patients with NMO.

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Available from: Teresa C Frohman, Aug 28, 2015
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    • "Past studies using time domain OCT (TD-OCT) revealed that OCT findings are different between patients with MS and NMO (Naismith et al. 2009; Ratchford et al. 2009). Patients with NMO generally have thinner NFLs, suggesting more widespread axonal injury (Naismith et al. 2009; Ratchford et al. 2009; Nakamura et al. 2010). "
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    ABSTRACT: Purpose: To compare the retinal layer thickness of eyes with optic neuritis (ON) and that of control eyes and ON eyes with and without neuromyelitis optica (NMO) or multiple sclerosis (MS). Methods: Horizontal and vertical SD-OCT scans of the fovea were undertaken for 56 patients with ON with and without NMO or MS and for 24 healthy controls. Patients with ON were divided into three groups: NMO, MS and isolated ON without NMO or MS. The thickness of each retinal layer was compared between ON and healthy control eyes, and between ON eyes with and without NMO or MS. Results: Compared with healthy control eyes, ON eyes showed significant thinning of the ganglion cell layer plus the inner plexiform layer (GCL + IPL) at all eight inner and outer macular locations. Significant differences in thickness were observed for the retinal layers of NMO, MS and isolated ON without NMO or MS at several retinal locations. Conclusions: Our SD-OCT data revealed a notable difference in the GCL + IPL thickness between ON and healthy control eyes. It also showed differences in the thickness of several retinal layers for ON subgroups including NMO, MS and isolated ON. This may be helpful for distinguishing the aetiology of ON.
    Acta ophthalmologica 07/2013; 92(1). DOI:10.1111/aos.12215 · 2.84 Impact Factor
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    • "Half of NMOSD-ON eyes had pRNFL values below 46.6 µm versus none of the MS-ON eyes, and the mean pRNFL difference between both groups was 27 µm. This difference is in striking accordance with values reported by two previous seminal studies in NMO using the older time domain OCT technology [29], [30]. The stronger association between morphology and visual function in NMOSD-ON eyes that tend to have lower axonal and neuronal OCT measures may suggest that below a certain threshold of neuroaxonal loss retinal neurons and axons are no longer able to sufficiently maintain visual function. "
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    ABSTRACT: 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. 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). 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. 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. 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.
    PLoS ONE 06/2013; 8(6):e66151. DOI:10.1371/journal.pone.0066151 · 3.23 Impact Factor
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    • "Retinal segmentation of the neuromyelitis optica optical coherence tomography scans revealed neuronal layer changes not only in those with, but interestingly also in those without a history of optic neuritis. In keeping with earlier studies, neuromyelitis optica participants with a history of optic neuritis had greater retinal nerve fibre layer and macular thickness reductions compared with neuromyelitis optica participants without a history of optic neuritis, as well as participants with multiple sclerosis with and without a history of optic neuritis (Naismith et al., 2009a; Ratchford et al., 2009). While participants with neuromyelitis optica and a history of optic neuritis demonstrated significant ganglion cell layer plus inner plexiform layer thinning, they did not have significant inner or outer nuclear layer changes. "
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    ABSTRACT: Post-mortem ganglion cell dropout has been observed in multiple sclerosis; however, longitudinal in vivo assessment of retinal neuronal layers following acute optic neuritis remains largely unexplored. Peripapillary retinal nerve fibre layer thickness, measured by optical coherence tomography, has been proposed as an outcome measure in studies of neuroprotective agents in multiple sclerosis, yet potential swelling during the acute stages of optic neuritis may confound baseline measurements. The objective of this study was to ascertain whether patients with multiple sclerosis or neuromyelitis optica develop retinal neuronal layer pathology following acute optic neuritis, and to systematically characterize such changes in vivo over time. Spectral domain optical coherence tomography imaging, including automated retinal layer segmentation, was performed serially in 20 participants during the acute phase of optic neuritis, and again 3 and 6 months later. Imaging was performed cross-sectionally in 98 multiple sclerosis participants, 22 neuromyelitis optica participants and 72 healthy controls. Neuronal thinning was observed in the ganglion cell layer of eyes affected by acute optic neuritis 3 and 6 months after onset (P < 0.001). Baseline ganglion cell layer thicknesses did not demonstrate swelling when compared with contralateral unaffected eyes, whereas peripapillary retinal nerve fibre layer oedema was observed in affected eyes (P = 0.008) and subsequently thinned over the course of this study. Ganglion cell layer thickness was lower in both participants with multiple sclerosis and participants with neuromyelitis optica, with and without a history of optic neuritis, when compared with healthy controls (P < 0.001) and correlated with visual function. Of all patient groups investigated, those with neuromyelitis optica and a history of optic neuritis exhibited the greatest reduction in ganglion cell layer thickness. Results from our in vivo longitudinal study demonstrate retinal neuronal layer thinning following acute optic neuritis, corroborating the hypothesis that axonal injury may cause neuronal pathology in multiple sclerosis. Further, these data provide evidence of subclinical disease activity, in both participants with multiple sclerosis and with neuromyelitis optica without a history of optic neuritis, a disease in which subclinical disease activity has not been widely appreciated. No pathology was seen in the inner or outer nuclear layers of eyes with optic neuritis, suggesting that retrograde degeneration after optic neuritis may not extend into the deeper retinal layers. The subsequent thinning of the ganglion cell layer following acute optic neuritis, in the absence of evidence of baseline swelling, suggests the potential utility of quantitative optical coherence tomography retinal layer segmentation to monitor neuroprotective effects of novel agents in therapeutic trials.
    Brain 02/2012; 135(Pt 2):521-33. DOI:10.1093/brain/awr264 · 9.20 Impact Factor
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