Clinical and neuroimaging findings in MOGAD-MRI and OCT

Abstract

Myelin oligodendrocyte glycoprotein antibody-associated disorders (MOGAD) are rare in both children and adults, and have been recently suggested to be an autoimmune neuroinflammatory group of disorders that are different from aquaporin-4 autoantibody-associated neuromyelitis optica spectrum disorder and from classic multiple sclerosis. In-vivo imaging of the MOGAD patient central nervous system has shown some distinguishing features when evaluating magnetic resonance imaging of the brain, spinal cord and optic nerves, as well as retinal imaging using optical coherence tomography. In this review, we discuss key clinical and neuroimaging characteristics of paediatric and adult MOGAD. We describe how these imaging techniques may be used to study this group of disorders and discuss how image analysis methods have led to recent insights for consideration in future studies.

Keywords: magnetic resonance imaging; myelin oligodendrocyte glycoprotein associated disorders; optical coherence tomography.

FIGURE 1

Cerebral magnetic resonance imaging (MRI) in paediatric myelin oligodendrocyte glycoprotein‐associated disorders (MOGAD). (a,b) Axial T2‐weighted fluid‐attenuated inversion recovery (FLAIR) MRI sequences of a 3‐year‐old female MOG‐immunoglobulin (Ig)G‐positive acute disseminated encephalomyelitis (ADEM) patient showing bilateral white matter and deep grey matter thalamic lesions. (c) Axial T2‐weighted MRI sequence of a 12‐year‐old female patient with MOG‐immunoglobulin (Ig)G‐positive ADEM and bilateral optic neuritis (ON) showing optic nerve swelling and hyperintensity

FIGURE 2

Spinal cord magnetic resonance imaging (MRI) in paediatric myelin oligodendrocyte glycoprotein associated disorders (MOGAD). Sagittal (a) and transversal (b) T2‐weighted spinal cord MRI of a 12‐year‐old female patient with MOG‐immunoglobulin (Ig)G‐positive acute disseminated encephalomyelitis (ADEM). (b) Longitudinally extensive transverse myelitis (LETM) with grey matter spinal cord affection presenting with the ‘H‐sign’ and (a) as longitudinal hyperintense line. (c) Sagittal T2‐weighted cervical cord MRI in a 3‐year‐old female patient with MOG‐IgG‐seropositive ADEM (the same patient shown in Figure 1a,b)

FIGURE 3

Adult myelin oligodendrocyte glycoprotein‐associated disorders (MOGAD) patient cerebral and spinal cord affection. (a) T2‐weighted fluid‐attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI) sequence in the axial orientation showing large, confluent hyperintense lesions in the white matter. (b) In the coronal view of the same cerebral scan as in (a), it can be seen that the lesions extend toward the cortex. (c) The T2‐weighted spinal cord MRI shows short segment lesions, appearing to be located centrally in the cord

FIGURE 4

Retinal anatomy and optical coherence tomography. (a) Anatomical representation of the human retina and (b) the human retina as imaged using optical coherence tomography (OCT). These images have been kindly reproduced and modified under a Creative Common Licence from www.neurodial.de. RNFL = retinal nerve fibre layer; GCL = ganglion cell layer; IPL = inner plexiform layer; GCIP = ganglion cell and inner plexiform layer

FIGURE 5

Macular scans from optical coherence tomography (OCT). Macular scans of various retinas with corresponding thickness scale (0–150 µm) with heat‐maps highlighting the thickness variations across the macular ganglion cell and inner plexiform (GCIP) layer. (a) Variations in the thickness across various pathologies in different patients. (b) Right eye of the same myelin oligodendrocyte glycoprotein‐associated disorders (MOGAD) patient prior to optic neuritis (ON) after two and four ONs. Thinner areas are depicted with cooler colours (purple/blue) and thicker areas depicted with warmer colours (red/yellow). HC = healthy control; MOGAD‐NON: MOGAD with no history of ON; AQP‐4‐IgG: aquaporin‐4 immunoglobulin G