Of note, the development of MG occurred after a 2-year period of interferon -1b (IFN -1b) administration. whether in our case MG is usually induced by the administration of interferon, instead of an original pathogenic link between MG and NMO. In other words, immunomodulatory treatments can slip the immunity towards T-helper II predominant pathways that can trigger MG. However, if we assume that such an explanation (i.e. increased susceptibility to autoantibody-mediated disorders) is true, our case can be considered the first case of NMO who developed MG following IFN -1b treatment. strong class=”kwd-title” Key words: Neuromyelitis optica, Devic’s syndrome, Myasthenia gravis, Multiple sclerosis, Aquaporin-4, Interferon, Thymectomy Introduction Neuromyelitis optica (NMO or Devic’s syndrome) is an inflammatory demyelinating disorder of the central nervous system (CNS) that has been thought to be a severe subtype of multiple sclerosis (MS) for a long time. However, evidences emerging from clinical status, neuroimaging, and, laboratory findings would aid in distinguishing these two immune-mediated conditions at their developed stages [1, 2, 3, 4]. NMO predominantly affects optic nerve(s) and spinal cord; although, involvement of other parts of the CNS, for example, SF1670 brain is possible. Indeed, NMO-related brain lesions are sometimes undistinguishable from those pertaining to MS and, in some instances, this makes the diagnosis very difficult [4, 5]. During the recent decade, the discovery of aquaporin-4 (AQP4) antibody as a highly specific marker responsible for the pathogenesis of NMO, not only has made a revolutionary pace in establishing serologic distinction between the two diseases, but it has also classified NMO as an antibody-mediated disorder [6, 7]. Moreover, since this discovery, the concurrence of NMO with other types of B-cell autoimmunities has been focused by many authors [8, 9]. On the other hand, myasthenia gravis (MG) is usually a well-known antibody-mediated disorder that specifically affects nicotinic acetylcholine receptors (AChR) of the muscle tissue. The clinical picture of MG mostly reflects muscular fatigability caused by the disruption of AChR functions and motor-end-plate transmissions [10]. Notwithstanding the fact SF1670 that this pathophysiology of NMO and MG are both immune and antibody mediated, the concomitancy of these two disorders is usually uncommon whereby, to date, approximately 16 cases of this condition are reported. In all of such reported cases, MG preceded the development of NMO and, in the majority of them, NMO onset was induced by the procedure of thymectomy which is a routine therapy for MG [11, 12]. As far as we are aware, to date, there are no reports describing the development of MG after SF1670 initial symptoms of the chronic course of NMO. The purpose of this report was to illustrate the clinical and paraclinical features of a patient who manifested the above-mentioned condition and discuss on possible pathogenic mechanisms. Case Report A 40-year-old Persian woman was admitted to our department in October 2005. Her initial neurologic symptoms occurred at age 33, when she was diagnosed with optic neuritis (ON) of the right vision and paraparesia. Over the ensuing 7 years since her first symptoms, she experienced another relapse of ON in the left vision and also SF1670 several Rabbit polyclonal to AKAP13 episodes of paresthesia and paraparesia. Neurologic examination revealed moderate spastic paraplegia and bilateral optic atrophy. Her 48-year-old sister has definite NMO since 8 years (several ON and myelitis episodes, spinal lesion extending from C3 to C6, and normal brain MRI) with a negative AQP4 antibody test. She is currently taking immunosuppressant drugs. Furthermore, her nephew, a 26-year-old male, was diagnosed with definite MS since.