ECTRIMS 2025 | Clinical presentation of MS, NMOSD, and MOGAD: differentiating between the three conditions
Marcello Moccia, MD, PhD, University of Naples Federico II, Naples, Italy, comments on the clinical presentations of multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). Dr Moccia notes that the three conditions often have similar presentations and differentiation relies on a combination of clinical presentation, imaging studies, and cerebrospinal fluid analysis. This interview took place at the 41st Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) in Barcelona, Spain.
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Transcript
MS, MOGAD and NMOSD share a lot of similarities in their clinical presentation. One of the most common clinical presentations of MS is optic neuritis, so an acute inflammatory disease of the optic nerve that causes blurred vision, painful eye movements and reduced color vision. We can have something very similar in NMOSD, but in NMOSD it’s quite often bilateral, so it affects the two eyes and it is much more severe...
MS, MOGAD and NMOSD share a lot of similarities in their clinical presentation. One of the most common clinical presentations of MS is optic neuritis, so an acute inflammatory disease of the optic nerve that causes blurred vision, painful eye movements and reduced color vision. We can have something very similar in NMOSD, but in NMOSD it’s quite often bilateral, so it affects the two eyes and it is much more severe. Another typical presentation is the involvement of the spinal cord. The involvement of the spinal cord can be with motor signs, reduced power, reduced power especially in the legs, can be with sensory symptoms, so pins and needles or tingling in the legs, or can be with acute onset bowel and bladder dysfunction. Generally speaking, the clinical presentations in NMOSD when there is an involvement of the spinal cord are much more severe than MS and MOGAD. In NMOSD we have quite often an involvement of the motor tract, so with very severe motor symptoms, and this is generally not the case in MS where sensory symptoms are much more common. Another key point is that based on the current evidence that we have, we don’t have really asymptomatic brain lesions or spinal cord lesions in NMO and in MOGAD. While in MS we can have asymptomatic brain and spinal cord lesions. So ideally a person with MS can present with isolated radiological presentation, so where there are only brain lesions in the absence of typical symptoms. Overall the differentiation is not entirely clinical. Of course the clinical picture has to guide investigations, but the diagnosis is made of different parts. So for instance, if there is an involvement of the optic nerve, we need to study the optic nerve using different modalities. And MRI and OCT can actually help detecting differences between MOGAD and NMOSD and MS. Brain MRI is extremely helpful and can show a lot of difference between the three diseases. And same is spinal cord MRI. Last but not least there is CSF analysis. CSF analysis, in my opinion, remains very important in confirming the diagnosis of MS but also in excluding other diagnoses. For instance, we have oligoclonal bands and the kappa-3 light chain index that can differentiate MS from NMOSD and MOGAD where the rate of positivity of these two tests is much lower. Last but not least there are cell-based assays for the detection of specific antibodies in aquaporin-4 for NMOSD and MOG antibodies for MOGAD. So actually the final diagnosis starts from the clinical presentation but is made of little paraclinical tools that need to be combined as needed.
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