The staff neurologist at the Cleveland Clinic Mellen Center for Multiple Sclerosis outlined key findings from her talk at a recent Institutional Perspectives in Neurology: Multiple Sclerosis event. [WATCH TIME: 3 minutes]
WATCH TIME: 3 minutes
“In the talk, we discussed a little bit about the clinical phenotype of aquaporin-4 [IgG] NMOSD. We went through the clinical features and radiological features, and then compared also, the clinical and radiological features of MOGAD.”
At a recent Institutional Perspectives in Neurology: Multiple Sclerosis event, Amy Kunchok, MD, staff neurologist, Mellen Center for Multiple Sclerosis Treatment and Research, Cleveland Clinic, provided an overview of the clinical and radiological features of aquaporin-4 antibody (AQP4) neuromyelitis optica spectrum disorder (NMSOD) and myelin oligodendrocyte glycoprotein antibody disease (MOGAD), as well as diagnostic approaches. Discussing AQP4-IgG NMOSD with NeurologyLive®, Kunchok highlighted that it is mostly seen in adult females, and patients often have peri-ependymal lesions, ring enhancing, and spinal cord lesions. Compared to patients with MOGAD, these patients also had more severe attacks and greater disability.
In her talk, Kunchok also discussed the most common phenotype for MOGAD, optic neuritis, which is often a bilateral optic neuritis involving the anterior optic nerve. Additionally, patients with MOGAD are younger and lack systemic autoimmunity and area postrema syndrome. Discussing brain and brainstem lesions, Kunchok noted that they are often large, fluffy acute disseminated encephalomyelitis-type lesions or cerebellar peduncle lesions. Less commonly observed were cortical encephalitis lesions seen with cortical FLAIR lesions, she said.