Background: Neuromyelitis optica (NMO) is a CNS demyelinating disease characterized by relatively selective injury to the optic nerves and spinal cord. As the prognosis and treatment differ between NMO and multiple sclerosis (MS), distinguishing these two diseases in patients presenting optic neuritis (ON) is important
Background: Neuromyelitis optica is an autoimmune disease usually restricted to spinal cord and optic nerves. Recently, an immunological marker (NMO-IgG) directed against the aquaporin-4 (AQP4) has been found in this disease. Although it usefulness in NMO diagnosis was established, its correlation with disease activity and its interest for NMO follow up was not demonstrated yet
BACKGROUND: Neuromyelitis optica (NMO), a severe demyelinating disease, represents itself with optic neuritis and longitudinally extensive transverse myelitis. Serum NMO-IgG autoantibodies (Abs), a specific finding in NMO patients, target the water channel protein aquaporin-4 (AQP4), which is expressed as a long (M-1) or a short (M-23) isoform.
Primary loss and dysfunction of astrocytes may trigger demyelination, as seen in neuromyelitis optica, an inflammatory disease of the central nervous system. In most patients affected by this disease, injury to astrocytes is initiated by the action of autoantibodies targeting aquaporin 4 (AQP-4), a water channel on astrocytes.
Background: Detection of aquaporin-4–specific immunoglobulin G (IgG) has expanded the spectrum of neuromyelitis optica (NMO). Rare reports of familial aggregation have suggested a component of genetic susceptibility but these reports mostly antedated the discovery of the NMO-IgG biomarker and recently updated diagnostic criteria.
Objective: To study antibody-independent contributions of B cells to inflammatory disease activity, and the immune consequences of B-cell depletion with rituximab, in patients with multiple sclerosis (MS).Methods: B-Cell effector-cytokine responses were compared between MS patients and matched controls using a 3-signal model of activation. The effects of B-cell depletion on Th1/Th17 CD4 and CD8 T-cell responses in MS patients were assessed both ex vivo and in vivo, together with pharmacokinetic/pharmacodynamic studies as part of 2 rituximab clinical trials in relapsing–remitting MS.Results: B Cells of MS patients exhibited aberrant proinflammatory cytokine responses, including increased lymphotoxin (LT):interleukin-10 ratios and exaggerated LT and tumor necrosis factor (TNF) secretion, when activated in the context of the pathogen-associated TLR9-ligand CpG-DNA, or the Th1 cytokine interferon-y, respectively
OBJECTIVE: Severe inflammation and astrocyte loss with profound demyelination in spinal cord and optic nerves are typical pathological features of neuromyelitis optica (NMO).
Purpose. To report changes in retinal nerve fiber layer (RNFL) thickness in a patient with neuromyelitis optica (NMO).
Neuromyelitis optica (NMO) is an inflammatory disease mainly affecting the optic nerve and spinal cord.
BACKGROUND: Neuromyelitis optica (NMO) is a neurological inflammatory disease associated with autoimmunity to aquaporin 4, predominantly localised in astrocytic foot processes. Recent studies have revealed that loss of aquaporin 4 and glial fibrillar acidic protein (GFAP) is a prominent feature of NMO lesions, suggesting astrocytic impairment. OBJECTIVE: To reveal a useful clinical biomarker of NMO.
BACKGROUND: Antibodies to aquaporin-4 (AQP4) are found in a fraction of Japanese opticospinal multiple sclerosis (OSMS) patients. However, it remains unknown whether anti-AQP4 antibody-positive and negative OSMS patients possess an identical disease
Both general neurologists and neurologists with a broad spectrum of subspecialty interests are often asked to evaluate patients with disorders of the spinal cord. Over the past decade, there have been significant advances in our understanding of a wide spectrum of immune-mediated, infectious, metabolic, hereditary, paraneoplastic, and compressive myelopathies. Advances have been made in the classification and management of spinal vascular malformations.