Posts tagged: neuromyelitis

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.


Devic’s syndrome was first described in 1870 by Sir Thomas Allbutt (what a name to have had as a kid!) who pointed out an association between myelitis and optic nerve disorder.? In 1894, Eugene Devic and his student Fernand Gault described 16 patients who had lost vision in one or both eyes and developed spastic weakness, sensory loss, and incontinence.? The other name of the condition was neuromyelitis optica (NMO). A major breakthrough came in 2004 when a specific marker NMO-IgG was found for the disorder [1].? IgG stands for immunoglobulin (a kind of antibody).

My notes of reading/lectures/thoughts about neuromyelitis optica (Devic’s disease).

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

Quantification and Functional Characterization of Antibodies to Native Aquaporin 4 in Neuromyelitis Optica Sudhakar Reddy Kalluri, MSc; Zsolt Illes, MD; Rajneesh Srivastava, MSc; Bruce Cree, MD; Til Menge, MD; Jeffrey L. Bennett, MD, PhD; Achim Berthele, MD; Bernhard Hemmer, MD Arch Neurol.

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).

Neuromyelitis optica (NMO) is an inflammatory demyelinating disease of spinal cord and optic nerve caused by pathogenic autoantibodies (NMO-IgG) against astrocyte aquaporin-4 (AQP4). We developed a high-throughput screen to identify blockers of NMO-IgG binding to human AQP4 using a human recombinant monoclonal NMO-IgG and transfected Fisher rat thyroid cells stably expressing human M23-AQP4

Background and Objective: Neuromyelitis optica (NMO) shows various brain MRI abnormalities with recurrent CNS attacks, although NMO predominantly affects the spinal cord and optic nerve. The features and pathomechanisms of acute brain lesions associated with edema have not been clarified in NMO. We investigated diffusion weighted imaging (DWI) of brain MRI lesions with the enhancement patterns in patients with neuromyelitis optica spectrum disorder (NMOSD).

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

Neuromyelitis optica (NMO or Devic’s syndrome) is a rare autoimmune disease, previously considered a multiple sclerosis variant. The most important laboratory and clinical features are optic myelitis and transverse myelitis, associated with neuromyelitis optica-IgG antibody (NMO-IgG) positivity. Subsequent to this immunological test being available, different groups have described the not-so-rare comorbidity of neuromyelitis optica with other systemic autoimmune diseases, systemic lupus erythematosus with secondary anti-phospholipid syndrome (APS) in particular.