Retinal optical coherence tomography and magnetic resonance imaging in neuromyelitis optica spectrum disorders and MOG-antibody associated disorders: an updated review

ABSTRACT

Introduction

Neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein IgG antibody-associated disorders (MOGAD) comprise two groups of rare neuroinflammatory diseases that cause attack-related damage to the central nervous system (CNS). Clinical attacks are often characterized by optic neuritis, transverse myelitis, and to a lesser extent, brainstem encephalitis/area postrema syndrome. Retinal optical coherence tomography (OCT) is a non-invasive technique that allows for in vivo thickness quantification of the retinal layers. Apart from OCT, magnetic resonance imaging (MRI) plays an increasingly important role in NMOSD and MOGAD diagnosis based on the current international diagnostic criteria. Retinal OCT and brain/spinal cord/optic nerve MRI can help to distinguish NMOSD and MOGAD from other neuroinflammatory diseases, particularly from multiple sclerosis, and to monitor disease-associated CNS-damage.

Areas covered

This article summarizes the current status of imaging research in NMOSD and MOGAD, and reviews the clinical relevance of OCT, MRI and other relevant imaging techniques for differential diagnosis, screening and monitoring of the disease course.

Expert opinion

Retinal OCT and MRI can visualize and quantify CNS damage in vivo, improving our understanding of NMOSD and MOGAD pathology. Further efforts on the standardization of these imaging techniques are essential for implementation into clinical practice and as outcome parameters in clinical trials.

KEYWORDS:

• Aquaporin-4
• magnetic resonance imaging
• MOG-antibody associated disorders
• myelin oligodendrocytic glycoprotein
• neuroimmunology
• neuromyelitis optica spectrum disorders
• neuro-ophthalmology
• optical coherence tomography
• optic neuritis

Article highlights

• Neuromyelitis optica spectrum disorder (NMOSD) is mainly characterized by recurrent optic neuritis (ON) and longitudinally extensive transverse myelitis. In addition, a subset of NMOSD patients also have brain abnormalities.

• Myelin oligodendrocyte glycoprotein antibody associated disorders (MOGAD) feature a clinical NMOSD phenotype and/or recurrent ON episodes.

• Retinal structural damage and degeneration in NMOSD and MOGAD can be measured by optical coherence tomography (OCT), a non-invasive technique that allows for in vivo quantification of neuroaxonal loss by measuring the change in intraretinal layer thickness or volume.

• Apart from ON related damage in the afferent visual system, OCT also has the potential to identify subclinical primary retinal pathology in NMOSD.

• In comparison with multiple sclerosis, optic nerve injury in NMOSD and MOGAD is more likely to have bilateral involvement, and affect the optic chiasm, optic tract and posterior visual pathway.

• Brain and spinal cord magnetic resonance imaging (MRI) have essential roles for detecting CNS lesions or atrophy in NMOSD and MOGAD. Distinct MRI characteristics enables the differential diagnosis among NMOSD, MOGAD and other neuroinflammatory disorders.

• Advanced MRI techniques, such as diffusion tensor imaging and resting state functional MRI, advance the exploration of pathological responses of the visual system in NMOSD and MOGAD.

• The combination of MRI and OCT will facilitate the comprehension of trans-synaptic neuropathological processes between posterior visual pathway and retinal pathology.

• OCT and other recently explored MRI parameters have the potential to monitor disease activity and be used as study outcome measures in clinical trials evaluating treatment response.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Acknowledgments

The authors thank Hadas Kalish for providing the OCT images of a MOGAD patient in Figure 3.

Declaration of interests

C Chien has received research support from Novartis and speaking honoraria from Bayer Healthcare. F Paul reports research grants and speaker honoraria from Bayer, Teva, Genzyme, Merck, Novartis, MedImmune and is member of the steering committee of the OCTIMS study (Novartis). HG Zimmermann received research grants from Novartis and speaking honoraria from Bayer Healthcare. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or conflict with the subject matter or materials discussed in this manuscript apart from those disclosed.

Additional information

Funding

This work was supported by the Research Grant ‘CC-Neuro’ from the German Federal Ministry of Education and Research.