A 21-year-old right-handed woman suffered cervical myelitis in 1971, followed by two episodes of bilateral optic neuritis and four relapses of thoracic or lumbar myelitis through 1998. Her initial brain MRI in 1989 revealed no abnormality, which met the MRI criteria for multiple sclerosis. In 2009, her serum anti-aquaporin-4 antibody was found to be positive, and a diagnosis of relapsing neuromyelitis optica (NMO) was made on the basis of current diagnostic criteria
Background: Although it has been well established that vaccination does not increase the risk of relapse in patients with multiple sclerosis (MS), no study on the influence of immunization on neuromyelitis optica spectrum disorder (NMOsd) has been conducted. As NMO differs from MS in a number of aspects, including its immunopathogenetic mechanisms, vaccination may have some influence on the occurrence of new relapses
Background: Based on case series and anecdotal evidence, immunosuppression has been shown to reduce relapse rates and delay disability in Neuromyelitis Optica spectrum disorders (NMOSD) and is currently the mainstay of disease modifying treatment.
Background: Neuromyelitis optica (NMO) is an autoimmune disease of the central nervous system (CNS) associated with a specific autoantibody, anti-aquaporin-4 antibody (AQP4-Ab). Although low-dose corticosteroids and immunosuppressants are widely used for prevention in NMO, the efficacy is not yet confirmed by large controlled studies. Objective: To evaluate the benefit of low-dose prednisolone therapy in patients with relapsing NMO.
Background: There are limited number of studies investigating efficacy and safety of plasma exchange (PLEX) in treating acute demyelinating diseases like Multiple Sclerosis (MS) and Neuromyelitis Optica (NMO). In a randomised double-blind trial of PLEX in treating acute demyelinating attacks,42% of patients on active treatment had significant improvement compared to 5.9% on sham.
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).
Neuromyelitis optica (NMO, Devic’s syndrorne.l is characterized by concurrence of optic neuritis and transverse myelitis, typically associated with a lesion in the spinal cord extending over three or more vertebral segments. It is an inflammatory, demyelinating central nervous system disorder, and although it is most commonly relapsing, it is distinct from multiple sclerosis in that it is more severe, tends to spare the brain, and is associated with a longitudinally extensive lesion on spinal cord MRI. Furthermore, NMO is associated with a highly specific serum autoantibody m,1rker, NMO-lgG, which targets the water channel aquaporin-4.
Neuromyelitis optica (NMO) is an uncommon, life-threatening inflammatory demyelinating disorder.
BACKGROUND: Antibodies to aquaporin-4 (AQP4-Ab) are found in 60-80% of patients with neuromyelitis optica (NMO), a severely disabling inflammatory CNS disorder of putative autoimmune aetiology, which predominantly affects the optic nerves and spinal cord.OBJECTIVE: To assess the frequency of AQP4-Ab in patients with optic neuritis (ON), and to investigate the prognostic implications of AQP4-Ab seropositivity in such patients.
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).
There are no specific treatments for patients with acute, severe neurological deficits caused by neuromyelitis optica (NMO) who fail to recover after treatment with high-dose corticosteroids. We evaluated the clinical response of anti-tuberculosis treatment (ATT) in patients suffering from steroid-refractory NMO, and investigated the correlation between NMO and tuberculous infection of the central nervous system (CNS)
OBJECTIVE: To describe a patient with neuromyelitis optica (NMO) whose aquaporin 4 (AQP4) antibody levels increased following treatment with interferon beta. DESIGN: Prospective clinical and laboratory case report. SETTING: Institutional referral center for multiple sclerosis (MS)