Other Articles published in this series Paraneoplastic neurological syndromes. Clinical and Experimental Immunology 2014, 175: 336–48.

Disease-modifying therapy in multiple sclerosis and chronic inflammatory demyelinating polyradiculoneuropathy: common and divergent current and future strategies. Clinical and Experimental Immunology 2014, 175: 359–72. Monoclonal antibodies in treatment of multiple sclerosis. Clinical and Experimental Immunology 2014, 175: 373–84. CLIPPERS: chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids. Review of an increasingly recognized entity within the spectrum Selleckchem Torin 1 of inflammatory central nervous system disorders. Clinical and Experimental Immunology 2014, 175: 385–96. Requirement for safety monitoring for approved multiple sclerosis therapies: an overview. Clinical and Experimental Immunology 2014, 175: 397–407. Myasthenia gravis: an update for the clinician. Clinical and Experimental Immunology 2014, 175: 408–18. Cerebral vasculitis in adults: what are the steps in order to establish the diagnosis? Red flags and pitfalls. Clinical and Experimental Immunology 2014, 175: 419–24. Multiple sclerosis treatment and infectious issues: update 2013.

Clinical and Experimental Immunology 2014, 175: 425–38. Diagnosis, pathogenesis and treatment of myositis: recent advances 2014, 175: 349–58. Management of disease-modifying treatments in neurological autoimmune diseases of the central nervous system 2014, 176: 135–48. Neuromyelitis GDC-0199 clinical trial optica (NMO, Devic’s syndrome) is an inflammatory disorder of the central nervous system (CNS) that presents typically with relapses of optic neuritis (ON) or myelitis [1-4]. In recent years, the condition has raised enormous interest among scientists and clinical neurologists, fuelled by the detection of a highly specific serum immunoglobulin (Ig)G autoantibody Celecoxib (NMO-IgG) targeting the most abundant astrocytic water channel aquaporin-4 (AQP4) [5-8]. NMO-IgG/AQP4-antibodies are

present in up to 80% of patients with NMO [8-11]. This seminal discovery has – together with previous neuropathological work that had already suggested humoral mechanisms to be relevant in the disease pathogenesis [12] – made clear that in most cases NMO is not a subform of multiple sclerosis (MS), as had been assumed for decades, but rather an autoimmune condition with an immunopathogenesis distinct from that of MS despite considerable overlap in clinical presentation and paraclinical findings. AQP4-antibody-positive NMO is part of an expanding spectrum of humorally mediated autoimmune diseases of the CNS that have been identified over the last few years [13, 14]. Several studies suggest that optimum treatment options may differ between NMO and MS, which underscores the necessity for a timely and accurate diagnosis.