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NMOtion Blog

Discussing NMO Research and Advocacy

Source: Neurology Today Conference Reporter: ECTRIMS Congress

PARIS—Should myelin oligodendrocyte glycoprotein (MOG) antibody disease, which causes brain inflammation, be no longer considered a disorder in the neuromyelitis optica (NMO) spectrum? Experts debated the question here at the joint meeting of the European Committee for Treatment and Research in Multiple Sclerosis and the Americas Committee for Treatment and Research in Multiple Sclerosis. When the dust had settled, the co-moderators declared that the answer was “yes.”

Douglas Sato, MD, PhD, professor of neurology at the Brain Institute of the Rio Grande do Sul in Porte Allegre, Brazil, contended that there were enough differences between patients whose brain inflammatory disease is caused by MOG antibodies to make it a separate disorder.

He noted that 161 citations supported his thesis in reports from cohorts in the United Kingdom, Switzerland, Austria, Japan, South Korea, India, Australia, France, and other countries. The studies noted distinct differences between MOG antibody diseases and aquaporin-4 antibody diseases that are hallmarks of NMO spectrum disorders.

NMO spectrum disorder has recently been proposed as a unifying term for relapsing inflammatory demyelinating disease that most commonly affects optic nerves and the spinal cord, leading to sudden vision loss or weakness in one or both eyes and loss of sensation and bladder function.

Dr. Sato said that assays can determine if a patient experiencing a variety of ailments has MOG antibody disease. He proposed that instead of including MOG antibody disease into the neuromyelitis spectrum, it should be part of a new group: “anti-MOG associated optic neuritis, encephalitis and myelitis (MONEM).”

“MOG is clearly associated with a set of disorders with distinct clinical phenotypes, which include myelitis and encephalitis,” he said.

Dr. Sato has received a scholarship from the Ministry of Education, Culture, Sports, Science and Technology of Japan, grant-in-aid for scientific research from the Japan Society for the Promotion of Science, research support from CAPES/Brasil, and speaker honoraria from Novartis.

Taking the opposite position, Roman Marignier, MD, PhD, a neurologist and head of the European Network EDEN at the Hospital Pierre Wertheimer of Lyon University Hospital in France, argued that MOG antibody disease is NMO that occurs without the biomarker of aquaporin-4 autoantibodies. A diagnosis of NMO can be made if there is one core clinical characteristic and the presence of aquaporin-4 autoantibodies. If those antibodies are not present, Dr. Marignier said that proposed criteria call for at least two core clinical characteristics, usually including optic neuritis, dissemination in space, and with lesions seen on magnetic resonance imaging (MRI). Both diagnoses also require exclusion of other possible pathologies.

Dr. Marignier said that both MOG antibody-caused disease and NMO share similar cerebrospinal fluid characteristics such as pleocytosis, and clinical characteristics. Both NMO and MOG cause relapses that can yield significant disability, but neither turns into a gradual worsening condition the way progressive MS does. Both diseases also share MRI presentation of swelling and contrast enhancement. Both diseases have similar brainstem localization observed on imaging scans.

He also noted that treatment is the same as well: high-dose intravenous steroids in acute manifestations of symptoms and maintenance therapy with steroids, rituximab, and azathioprine-mycophenolate mofetil.

Dr. Marignier serves on the scientific advisory board for MedImmune and has received funding for travel and honoraria from Biogen Idec, Merck Serono, Novartis, Sanofi- Genzyme, Roche, and Teva.

When the debate ended, the session co-chairs Jerome de Seze, MD, PhD, professor of neurology and head of neuroimmunology at University Hospital in Strasbourg, France, and Anthony Traboulsee, MD, associate professor of medicine at the University of British Columbia in Vancouver, consulted and declared Dr. Sato the winner.

Dr. Trabousee explained his reasoning to the Neurology Today Conference Reporter thusly: “Neuromyelitis optica spectrum disorders, which can be misdiagnosed as MS, are a new classification of inflammatory disorders that has a different mechanism from MS.

“The body produces antibodies that attack the nervous system. Down the road it has the same effects as MS because it destroys myelin,” he said.

“With NMO diseases you get this big explosion of inflammation which destroys myelin. It is sort of like a forest fire: With NMO, the fire started on the astrocyte and in this thing called anti-MOG, the fire started on the myelin. But they look the same because the fire is spreading.

“I would concur that Dr. Sato’s theory that MOG antibody disease is different than NMO is valid,” he said. “The important thing is how do you treat these patients. If you misclassify them you might be exposing patients to unnecessary medicine – even exposing children to unnecessary prednisone.”

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