Painful Tonic Spasm in Neuromyelitis Optica Incidence, Diagnostic Utility, and Clinical Characteristics Sung-Min Kim, MD; Min Jin Go, MS; Jung-Joon Sung, MD, PhD; Kyung Seok Park, MD, PhD; Kwang-Woo Lee, MD, PhD Arch Neurol.
The prevalence of neuromyelitis optica in South East Wales.
Dujmovic I, Mader S, Schanda K, Deisenhammer F, Stojsavljevic N, Kostic J, Berger T, Drulovic J, Reindl M? Temporal dynamics of cerebrospinal fluid anti-aquaporin-4 antibodies in patients with neuromyelitis optica spectrum disorders. [JOURNAL ARTICLE] J Neuroimmunol 2011?Feb?10. Neuromyelitis optica spectrum disorders (NMOSD) are associated with anti-aquaporin-4 autoantibodies (AQP4-IgG).
Anti–Aquaporin-4 monoclonal antibody blocker therapy for neuromyelitis optica Lukmanee Tradtrantip PhD 1 , Hua Zhang PhD 1 , Samira Saadoun PhD 2 , Puay-Wah Phuan PhD 1 , Chiwah Lam BS 3 , Marios C.
Research Anti-CD20 B-cell depletion enhances monocyte reactivity in neuroimmunological disorders Klaus Lehmann-Horn , Eva Schleich , Deetje Hertzenberg , Alexander Hapfelmeier , Tania Kuempfel , Nikolas von Bubnoff , Reinhard Hohlfeld , Achim Berthele , Bernhard Hemmer and Martin S Weber ? For all author emails, please log on . Journal of Neuroinflammation 2011, 8 :146? doi:10.1186/1742-2094-8-146 Published: 26 October 2011 Abstract (provisional) Background Clinical trials evaluating anti-CD20-mediated B-cell depletion in multiple sclerosis (MS) and neuromyelitis optica (NMO) generated encouraging results.
The functional role of ELR-positive CXC chemokines in host defense during acute viral-induced encephalomyelitis was determined. Inoculation of the neurotropic JHM strain of mouse hepatitis virus (JHMV) into the central nervous system (CNS) of mice resulted in the rapid mobilization of PMNs expressing the chemokine receptor CXCR2 into the blood. Migration of PMNs to the CNS coincided with increased expression of transcripts specific for the CXCR2 ELR-positive chemokine ligands CXCL1, CXCL2, and CXCL5 within the brain.
Rituximab is increasingly used for prevention of relapses of neuromyelitis optica (NMO), a condition that is highly associated with serum anti-aquaporin-4 (AQP4) antibodies. However, B-cell depletion also induces systemic B-cell activating factor (BAFF), which may promote antibody production. We collected serial serum samples from a total of seven patients with NMO prior to, and following, treatment with rituximab
The autoantibody to aquaporin-4 (AQP4) is a marker and a pathogenetic factor in Neuromyelitis Optica (NMO) (Devic’s syndrome). Our aim was to identify B-cell antigenic linear epitopes of the AQP4 protein and investigate similarities with other molecules. To this end, we screened sera from 21 patients positive for anti-AQP4 antibodies (study group), from 23 SLE and 23 pSS patients without neurologic involvement (disease controls) and from 28 healthy individuals (normal controls)
We present a pediatric case of recurrent optic neuritis, celiac disease, partial IgA and IgG3 deficiency in the context of anti-aquaporin-4 auto-immunity and familial IgA deficiency with celiac disease. Treatment with tacrolimus was successful in preventing disease relapses
BACKGROUND: Antibodies targeting membrane proteins play an important role in various autoimmune diseases of the nervous system.
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) is an aggressive devastating autoimmune disorder affecting predominantly optic nerves and the spinal cord. We are able to assess the serum antibodies against aquaporin 4 (anti-AQP4 Ab, also known as NMO-IgG), which are highly sensitive and specific for NMO.