Abstract: Neuromyelitis optica (NMO), or Devic disease, has been distinguished from multiple sclerosis (MS) by the presence of optic neuritis that is usually bilateral, simultaneous, and often severe, myelopathic findings accompanied by longitudinally extensive spinal cord imaging abnormalities, no brain imaging abnormalities typical of MS, and often rapid progression to debility and even death. Researchers at the Mayo Clinic have identified an immunoglobulin marker of NMO (the NMO antibody) that binds selectively to the aquaphorin-4 water channel and may play a causative role
Background Neuromyelitis optica (NMO) is an inflammatory demyelinating disease that predominantly affects the optic nerves and the spinal cord, and is possibly mediated by an immune mechanism distinct from that of multiple sclerosis (MS).
Background and Objective: Our objective was to characterize the clinical and radiologic features of Korean pediatric patients with relapsing central nervous system (CNS) demyelination disease.
Neuromyelitis optica (NMO) is a neurologic disease characterized by severe optic neuritis, longitudinally extended, transverse myelitis and serum aquaporin-4 (AQP4) antibody. Our recent neuropathological study revealed the extensive loss of AQP4 and glial fibrillary acidic protein (GFAP), an astrocyte-specific protein, in NMO lesions, but not in MS lesions, suggesting that severe astrocytic damage or dysfunction may be related to the pathogenesis of NMO. Here we report a patient of NMO, in which the cerebrospinal fluid (CSF) levels of GFAP were measured both during relapse of myelitis and after high-dose intravenous methylprednisolone (HIMP).
Devic’s Neuromyelitis Optica (NMO) is an idiopathic, inflammatory, demyelinating disease specific to the spinal cord and optic nerves resulting in acute, severe myelitis and optic neuritis. Unlike “typical” Multiple Sclerosis (MS), the brain is characteristically spared and spinal cord involvement spans at least three vertebral segments. NMO is often misdiagnosed as MS; however, recent research has identified distinguishing pathophysiologic, clinical, neuroimaging, and autoantibody criteria favoring a distinct disease