![]() ![]() Ĭlassically, NMO included only symptoms of myelitis and ON. Compared to idiopathic ON and ON due to multiple sclerosis (MS), ON due to NMOSD more often results in severe visual loss at onset, with bilateral involvement, and permanent visual deficits. ON may lead to varying degrees of visual impairment with decreased visual acuity, although visual field defects, or loss of color vision, may occur in isolation or prior to formal loss of visual acuity. The second most common initial manifestation of the disease is inflammation of the optic nerve and/or optic chiasm ( optic neuritis, ON). The myelitis can be transverse, affecting an entire cross-section of the spinal cord, and showing bilateral symptoms. Myelitis causes spinal cord dysfunction, which can result in muscle weakness, paralysis in the limbs, lost or reduced sensation, spasms, loss of bladder and bowel control, or erectile dysfunction. The most common initial manifestation of the disease is inflammation of the spinal cord (myelitis). Deficits can be temporary or permanent, the latter especially in the absence of treatment. Signs and symptoms usually follow a relapsing and remitting course, but occasionally can be progressive (monophasic). The signs and symptoms of NMOSD depend on the neurologic structures the disease affects, and, to some extent, the antibodies involved. However, NMO is not related to MS in the vast majority of cases and differs from MS substantially in terms of pathogenesis, clinical presentation, magnetic resonance imaging, cerebrospinal fluid findings, disease course, and prognosis. In consequence, NMO was in the past wrongly considered a clinical variant of MS. in patients with long-standing MS resulting in confluent spinal cord lesions mimicking the longitudinally extensive spinal cord lesions typically seen in NMO). Multiple sclerosis (MS) and NMO can be similar in clinical and radiological presentation, and MS may very rarely present with an NMO-like phenotype (e.g. In some cases, the etiology remains unknown ( idiopathic NMO). connective tissue disorders, paraneoplastic syndromes) or infectious diseases. Rarely, NMO may occur in the context of other autoimmune diseases (e.g. A subset of anti-AQP4-negative cases is associated with antibodies against myelin oligodendrocyte glycoprotein ( anti-MOG). In more than 80% of cases, NMO is caused by immunoglobulin G autoantibodies to aquaporin 4 ( anti-AQP4), the most abundant water channel protein in the central nervous system. A relapsing disease course is common, especially in untreated patients. Episodes of ON and myelitis can be simultaneous or successive. Neuromyelitis optica spectrum disorders ( NMOSD), including neuromyelitis optica (NMO), are autoimmune diseases characterized by acute inflammation of the optic nerve ( optic neuritis, ON) and the spinal cord ( myelitis). Multiple sclerosis, various autoimmune disordersĮculizumab, inebilizumab, satralizumab, rituximab, methylprednisolone, azathioprine, cellCept, mitoxantrone, methotrexate, intravenous immunoglobulin, cyclophosphamide Median: age 40 for AQP4-IgG, age 31 for MOG-IgG ĪQP4-IgG-positive, MOG-IgG-positive (recurrent, monophasic) Vision loss, sensory loss, weakness, bladder dysfunction Neuromyelitis optica (NMO), Devic's disease, Devic's syndrome 4 Furthermore, MOGAD lesions in the brain can look like lesions seen in those with ADEM.Medical condition Neuromyelitis optica spectrum disorders 4 MOG antibody disease optic neuritis seems to predominantly affect the retrobulbar region, while AQP-4-associated optic neuritis is found intracranially. MRI findings are similar to those with MS and NMOSD, but there may be some differences. There appears to be no overlap between individuals with anti-MOG positivity and AQP-4 positivity, although there have been some isolated cases reported using the older ELISA assay. 2 Those with persistent detection of anti-MOG may be more likely to have a relapsing rather than monophasic disease course. Unlike anti-AQP4 antibodies, anti-MOG antibodies may decrease over time, and may not be detectable early in the disease process or during remission, and this is especially the case for MOG antibody disease associated ADEM. 2 CSF analysis from a lumbar puncture may show increased white blood cell counts in some patients during a relapse, and oligoclonal bands are not usually found. Only cell-based assays are considered reliable for the diagnosis of MOGAD because of the improved specificity over older ELISA tests. There are blood tests that can test for MOG antibodies. Coaching Series on Relationships and Communication. ![]()
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