Eye scans may distinguish NMOSD from MOGAD

Noninvasive imaging techniques reveal differences between the diseases

Margarida Maia, PhD avatar

by Margarida Maia, PhD |

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Eye scans of people with neuromyelitis optica spectrum disorder (NMOSD) revealed they may have a thicker retina — the eye’s light-detector — and more blood vessels than people with myelin oligodendrocyte glycoprotein antibody disease (MOGAD).

That’s according to a study in which researchers used two noninvasive imaging techniques, optical coherence tomography (OCT) and optical coherence tomography angiography (OCTA), to watch for differences between the two related diseases.

“Our study suggests that the OCT/OCTA tool can help facilitate the differentiation of MOGAD from NMOSD in settings with overlapping clinical features,” the researchers wrote.

The study, “Retinal structural and microvascular changes in myelin oligodendrocyte glycoprotein antibody disease and neuromyelitis optica spectrum disorder: An OCT/OCTA study,” was published in Frontiers in Immunology.

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In NMOSD and MOGAD, the immune system produces antibodies that wrongly attack nervous system cells, causing inflammation in the optic nerve, which sends signals between the eye and the brain, and the spinal cord.

The only way to accurately tell NMOSD from MOGAD is by checking for the presence of specific disease-driving antibodies.

In NMOSD, these abnormal antibodies most often target aquaporin-4, a protein that carries water across the membranes of neuron-supporting cells. In turn, MOGAD-driving antibodies target myelin oligodendrocyte glycoprotein (MOG), part of the myelin sheath that surrounds nerve fibers.

“Even though testing for MOG antibodies can help differentiate these disorders, MOG testing is time-consuming and not available in most countries,” the researchers wrote.

Previous studies showed that using OCT to analyze the thickness of certain retinal layers in the eye, and OCTA to examine the eye’s blood vessel structure, could help distinguish NMOSD from multiple sclerosis, another autoimmune disease with certain similar features. The retina is the back part of the eyeball that contains a layer of light-sensing cells.

Looking for a ‘reliable tool’

Now, a team of researchers at Sichuan University in China assessed whether OCT/OCTA also could “serve as a reliable tool to differentiate MOGAD from NMOSD.”

They compared OCT/OCTA data of 42 eyes from 21 NMOSD patients (mean age, 33.8 years), 40 eyes from 21 MOGAD patients (mean age, 33.7 years), and 44 eyes from 22 healthy people (mean age, 34.2 years).

Patients with optic neuritis, or optic nerve inflammation, sudden vision loss, or eyeball pain in the past six months were excluded from the study. An older history of optic neuritis was reported in 11 people with NMOSD (52.4%) and 13 MOGAD patients (61.9%).

Regarding differences in retinal layer thickness, the ganglion cell inner plexiform layer (GCIPL) was significantly thicker in people with NMOSD than in those with MOGAD. Both patient groups had a significantly thinner GCIPL relative to healthy controls.

The GCIPL is a layer of cells in the retina where the ganglion cells, which are responsible for relaying information from the eyes to the brain, and the cells they communicate with, called bipolar cells, come together to process visual information.

The superficial vascular plexus

In terms of blood vessel structure, the superficial vascular plexus (SVP), a network of tiny blood vessels located in the GCIPL, was significantly denser in NMOSD patients than in those with MOGAD. The SVP’s blood vessels feed the GCIPL nerve cells with oxygen and nutrients.

The foveal avascular zone (FAZ), an area in the center of the retina where there are no blood vessels, was significantly larger in people with NMOSD than in MOGAD patients. This difference remained true when comparing between patients with a history of optic neuritis.

Reduced small blood vessel, or microvascular, densities were also detected in NMOSD patients’ eyes without a history of optic neuritis relative to healthy controls.

Together with the presence of an enlarged FAZ area, this suggests that “some activities occur during the subclinical phase in NMOSD and may initiate relapse-independent disease progression,” the researchers wrote.

“We showed that enlarged FAZ area and reduced microvascular densities occur as unique features during the subclinical phase of NMOSD but not during MOGAD,” they added.

Further analyses showed that, in NMOSD patients, GCIPL thinning and reduced SVP density each were associated significantly with longer disease duration, more episodes of optic neuritis, and greater disability — as assessed with the Expanded Disability Status Scale.

A larger FAZ also was linked significantly to these clinical features, except for disability severity. A less-dense SVP also was associated significantly with worse visual acuity.

“These findings were different from those in MOGAD, where clinical correlations were most identified with the SVP … suggesting the [disease-associated] mechanisms are different in NMOSD and MOGAD,” the researchers wrote. “Retinal imaging via the [OCT/OCTA] might have the potential to be used as a clinical tool to evaluate the clinical features associated with NMOSD and MOGAD.”