Commentary
Video
Navigating MOGAD Diagnosis: Clinical Insights and Key Considerations
Author(s):
In this segment, the duo of neurologists provided a number of informative considerations treating clinicians should take when diagnosing MOGAD, emphasizing careful testing and interpretation of data in this complex process. [WATCH TIME: 4 minutes]
WATCH TIME: 4 minutes
Over the last 2 decades, the understanding of inflammatory demyelinating disorders of the central nervous system has radically changed with the identification of specific autoantibody-associated conditions distinct from multiple sclerosis, namely aquaporin-4-IgG-positive neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein (MOG)-IgG-associated disease. In the most recently published diagnostic criteria of MOGAD, the identification of MOG-IgG was considered a core criterion, marking a major step in improving care and diagnosis rates.
That criterion, which was authored by Jeffrey Bennett, MD, PhD, and others, noted that MOGAD is typically associated with acute disseminated encephalomyelitis, optic neuritis, or transverse myelitis, and is less commonly associated with cerebral cortical encephalitis, brainstem presentations, or cerebellar presentations. In collaboration with the Siegel Rare Neuroimmune Association (SRNA), NeurologyLive® gathered Bennett and autoimmune expert Benjamin Greenberg, MD, for a Roundtable Discussion highlighting the latest updates in the diagnosis, treatment, and research of MOGAD.
In episode 1, the duo provide an overview of how MOGAD is currently diagnosed, including the neurological symptoms that clinicians should be aware of, and the presence of MOG-IgG antibody in either serum of cerebrospinal fluid. Bennett, who serves as a professor of neurology at the University of Colorado School of Medicine, and Greenberg, a pediatric neurologist at the University of Texas Southwestern Medical Center, describe the conditions to rule out during diagnosis, considerations for testing, and the need to be aware of false positives.
SRNA is also hosting the 2024 Rare Neuroimmune Disorders Symposium (RNDS) on October 18-20th. The RNDS was created to bring together individuals diagnosed with acute disseminated encephalomyelitis (ADEM), acute flaccid myelitis (AFM), MOG antibody disease (MOGAD), neuromyelitis optica spectrum disorder (NMOSD), optic neuritis (ON), and transverse myelitis (TM) and clinicians and researchers that focus on these disorders. Invite your patients who may benefit from attending either virtually or in person in Dallas, TX. Healthcare professionals are also welcome to join! Learn more here.
Transcript edited below for clarity.
Marco Meglio: The first topic we're going to talk about is the diagnosis of MOGAD. So, how is MOGAD diagnosed these days? And from a clinician’s perspective, what are the clinical pearls that treating physicians should understand about this process?
Benjamin Greenberg, MD: Well, happy to have Jeff go first.
Jeffrey Bennett, MD, PhD: MOGAD is diagnosed through a combination of a new clinical neurologic symptom—something that, upon evaluation, is consistent with an inflammatory attack on the central nervous system—and the presence of the MOG-IgG antibody. We’ve now published compendium criteria for this diagnosis, which can be found in The Lancet Neurology. Essentially, the first step is identifying such an event in a domain of the nervous system, which could be the optic nerve, brain, brainstem, or spinal cord. There’s also a caveat for more diffuse presentations like acute disseminated encephalomyelitis (ADEM), which can involve multiple areas of the nervous system at once, often with altered consciousness or behavior.
Once that’s identified, testing for the MOG-IgG antibody is prompted, and this can be done in the serum or cerebrospinal fluid (CSF), though there are some caveats. For instance, if the antibody is only present in the CSF, you need to see a definitively high positive titer for the MOG antibody to make the diagnosis, after ruling out neuromyelitis optica spectrum disorder (NMOSD). If the titer is equivocal, then additional MRI and clinical criteria are considered. The criteria vary slightly depending on whether the antibody is found in the CSF or serum. So, that’s the basic rundown for diagnosing MOGAD.
Benjamin Greenberg, MD: Yeah, I agree with Jeff. The only thing I’d add, just to raise awareness, is about when clinicians should consider sending the test. Basically, anytime you’re thinking about diagnosing multiple sclerosis (MS) or NMOSD, it should at least prompt you to consider the MOG test. There are different practice patterns out there—some clinicians say, “Before I make an MS or NMOSD diagnosis, I send the anti-MOG antibody test to rule it out as a mimic.” Others limit testing to certain presentations. I’m in the former camp—I tend to send it for everyone and then interpret the data. But it should definitely be on your radar if a patient has symptoms like loss of vision, numbness, or weakness, and you’re working them up for a demyelinating disease. At some point, testing for the anti-MOG antibody should come into consideration.
Jeffrey Bennett, MD, PhD: On the flip side, I would caution physicians to have a strong indication that the condition is inflammatory—whether it’s vision loss, weakness, or altered consciousness—before sending off the test. Most of the false positives I’ve seen happen when the test is sent without a firm belief that the condition in front of them is inflammatory, either based on MRI findings or spinal fluid criteria.
