Clinical features of neuromyelitis optica in a large Japanese cohort: comparison between phenotypes. J Neurol Neurosurg Psychiatry
Keywords: Neuromyelitis optica; Systemic lupus erythematosus; Systemic Sjogren’s; Myelitis; Autoantibody Abstract Objective: To identify the presence of neuromyelitis optica spectrum disorders (NMOSD) in patients with acute myelitis and suspected connective tissue disease (CTD), and to discuss the utility of this distinction in establishing a diagnostic and therapeutic plan. Methods: Seventeen patients with myelitis were identified from a single university-based rheumatology clinic and prospectively followed. Clinical data and serologic profile were used to determine the presence of neuromyelitis optica (NMO) or NMOSD according to established criteria
Abstract Autologous peripheral hematopoietic stem cell transplantation (APHSCT) was performed to treat a patient with neuromyelitis optica. We observed that the patient achieved clinical remission after APHSCT during 12 months of follow-up. The patient improved on the expanded disability status scale neurologic assessment and the Scripps neurologic rating scale worksheet scores on follow-up examination compared with baseline.
NMDA RECEPTOR ENCEPHALITIS MIMICKING SERONEGATIVE NEUROMYELITIS OPTICA Data Supplement Two tables; two PDF documents.
Naznin A.
Long-term follow-up of patients with neuromyelitis optica after repeated therapy with rituximab. Pellkofer HL , Krumbholz M , Berthele A , Hemmer B , Gerdes LA , Havla J , Bittner R , Canis M , Meinl E , Hohlfeld R , Kuempfel T
? NARCOMS Report-2007 Registry Update Optic Neuritis in Multiple Sclerosis ? Neuromyelitis Optica Dean M. Wingerchuk, MD, MSc, FRCP(C) A Historical Perspective on NMO Neuromyelitis optica (NMO), also known as Devic’s disease, was identified more than one hundred years ago as a severe disorder affecting the spinal cord (causing paralysis) and both optic nerves (causing blindness).
Neuromyelitis optica is an inflammatory demyelinating disease of the central nervous system associated with autoantibodies against the glial water channel protein aquaporin-4. It has recently been reported that immunoglobulin from neuromyelitis optica patients injected peripherally does not cause lesions in naive rats, but only when pre-existing central nervous system inflammation is present
The focus of this paper is to summarize the current knowledge on visual pathway damage in neuromyelitis optica (NMO) assessed by magnetic resonance imaging (MRI) and optical coherence tomography (OCT).
OBJECTIVE:To describe the clinical, molecular, and neuropathological findings of a patient with aquaporin 4-positive relapsing myelitis who developed extensive brain involvement followed by death. DESIGN: Case report.
Inflammatory lesions in the central nervous system of patients with neuromyelitis optica are characterized by infiltration of T cells and deposition of aquaporin-4-specific antibodies and complement on astrocytes at the glia limitans. Although the contribution of aquaporin-4-specific autoantibodies to the disease process has been recently elucidated, a potential role of aquaporin- 4-specific T cells in lesion formation is unresolved. To address this issue, we raised aquaporin-4-specific T cell lines in Lewis rats and characterized their pathogenic potential in the presence and absence of aquaporin-4-specific autoantibodies of neuromyelitis optica patients
Devic’s neuromyelitis optica is an inflammatory demyelinating disorder normally restricted to the optic nerves and spinal cord. Since the identification of a specific autoantibody directed against aquaporin 4, neuromyelitis optica-immunoglobulin G/aquaporin 4 antibody, neuromyelitis optica has been considered an entity distinct from multiple sclerosis