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Neuromyelitis optica (NMO) is a particular disease within the NMOSD spectrum. It is characterised by optic neuritis and longitudinally extensive myelitis. In more than 80% of NMO cases, the cause is immunoglobulin G autoantibodies to aquaporin 4 , the most abundant water channel protein in the central nervous system. [5] [1] [4]
Tumefactive demyelination: Tumefactive lesions in NMO are not usual, but they have been reported to appear in several cases mistakenly treated with interferon beta. [9] Devic's disease is currently considered a syndrome more than a disease, presenting an overlapping with the wide spectrum of multiple sclerosis in the form of Optic-Spinal MS. [10]
Anti-MOG antibodies have been described in some patients with NMOSD [15] [16] who were negative for the aquaporin 4 (AQP-4) antibody. However, most NMOSD is an astrocytopathy, specifically an AQP4 antibody-associated disease, whereas MOG antibody-associated disease is an oligodendrocytopathy, suggesting that these are two separate pathologic entities. [2]
Clinically, the disease is manifested with attacks/relapses that result in neurological impairment such as blindness, paraplegia, sensory loss, bladder dysfunction, and peripheral pain. The disability from each attack is cumulative, making neuromyelitis optica spectrum disorder a chronically debilitating and potentially life-threatening disease ...
In neuromyelitis optica higher AQP4 autoantibody levels are associated with the occurrence of optic neuritis. [16] Less common causes are: papilledema, brain tumor or abscess in the occipital region, cerebral trauma or hemorrhage, meningitis, arachnoidal adhesions, sinus thrombosis, liver dysfunction, or late stage kidney disease.
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