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Posts tagged: treatment

Mayo Clinic Researcher Receives AAN’s Dystel Prize for Multiple Sclerosis Research Released: 3/31/2011 8:00 PM EDT Source: American Academy of Neurology (AAN) ? Newswise — HONOLULU – The American Academy of Neurology (AAN) is awarding the 2011 John Dystel Prize for Multiple Sclerosis Research to Brian G. Weinshenker, MD, of the Mayo Clinic in Rochester, Minnesota and a Fellow with the AAN. Weinshenker will receive the award during the AAN’s 63rd Annual Meeting in in Honolulu, held April 9 through April 16, 2011


Neuromyelitis optica (NMO) is a severe demyelinating syndrome defined principally by its tendency to affect optic nerves and the spinal cord selectively. Asymptomatic brain lesions have recently become a common finding in NMO, and symptomatic brain lesions do not exclude the diagnosis of this entity. The authors describe the case of a 12-year-old girl suffering from an unusually atypical form of NMO in which a brainstem lesion was mistaken for a brainstem glioma


Fazio R et al. – Neuromyelitis optica (NMO) is a rare demyelinating disease, affecting selectively the optic nerve and the spinal cord. It was previously considered to be a severe variant of multiple sclerosis (MS) due to the similar pathological features and its resemblance to optico–spinal, or Japanese, MS, typical of Asian populations.


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.


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


OBJECTIVE: To investigate an association between serum B cell activating factor of TNF family (BAFF) levels and anti-aquaporin-4 (AQP4) antibody titers in patients with neuromyelitis optica (NMO) after rituximab treatment. BACKGROUND: Anti-AQP4 antibodies are present in approximately 70% of NMO patients. Such antibodies are probably pathogenic and the titers are elevated during relapse as compared with those in remission.


We evaluated 30 patients with clinically definite multiple sclerosis (MS) and 8 patients with neuromyelitis optica (NMO) to investigate correlations between Th1/Th2 balance, disease activity, effects of interferon (IFN)-beta treatment, and expressions of chemokine receptors CXCR3 and CCR4 on CD4+ and CD8+ T cells in peripheral blood. MS and NMO patients in the relapsing phase showed a significantly increased CD4+CXCR3+/CD4+CCR4+ ratio and CD8+CXCR3+/CD8+CCR4+ ratio compared with respective patients in the remission phase


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


Neuromyelitis optica (NMO) is a relapsing inflammatory condition characterized by selective involvement of the optic nerves and spinal cord. Humoral immune mechanisms play a role in the pathogenesis of NMO.


Interferon (IFN)-β is the treatment most often prescribed for relapsing–remitting multiple sclerosis (RRMS). 30–50% of MS patients, however, do not respond to IFN-β


Background: Neuromyelitis optica (NMO) is a severe demyelinating disease often leading to serious disability. Accumulating evidence now implicates humoral mechanisms in its pathogenesis.