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Neuromyelitis Optica  [PDF]
Goyal V,Rooru S,Gafoor AS,Sreekala VK
Indian Journal of Physical Medicine and Rehabilitation , 2009,
Abstract: Neuromyelitis optica (NMO) is a rare, idiopathic,inflammatory disease affecting the spine andcharacteristically sparing the brain. It mimics multiplesclerosis (MS) in many aspects. A case report of 55 yearold house-maker, with recurrent attacks of flaccidweakness with visual and bladder disturbances who wasadmitted in the Physical Medicine and Rehabilitation(PMR) ward for neuro-rehabilitation is presented. Herserological studies and magnetic resonance imaging ofthe spine and brain revealed a diagnosis of idiopathicdemyelinating disease affecting the spine – Devic’sdisease.
Neuromyelitis optica
Jacob Anu,Boggild Mike
Annals of Indian Academy of Neurology , 2007,
Abstract: Neuromyelitis optica (NMO) or Devic′s disease was until recently regarded as an unusual or severe variant of multiple sclerosis. However the last decade has seen major advances in our understanding of the etiopathogenesis of NMO. Though unsettled, there seems to be increasing evidence that NMO is a distinct immune mediated, largely relapsing, inflammatory, demyelinating disease of the central nervous system that most commonly targets the optic nerves and spinal cord. Longitudinally extensive spinal cord lesions on MRI, a serum antibody (NMO-IgG) which reacts specifically with water channel aquaporin 4 (AQP-4), response to immunosuppressive therapies (rather than immunomodulation like in MS) seem to be distinguish it from MS. We review the evolving epidemiological, clinical, imaging and immunological features of NMO and discuss the therapeutic options available. We also review the longstanding debate on whether NMO and Asian optico-spinal multiple sclerosis are two distinct entities or one. We have reviewed the all the published literature on NMO from India and there seems to be a higher proportion of NMO in India than reported in the West. An early accurate diagnosis and treatment with widely available drugs could alter the prognosis of NMO. A fuller understanding NMO may be the doorway to insights into MS and other demyelinating disorders. The information presented in this review has been obtained from peer reviewed publications, conference abstracts and personal experience. The data on Indian patients has been obtained by a literature search using the national library of medicine search engine with the search terms: "neuromyelitis optica or multiple sclerosis or transverse myelitis or optic neuritis or demyelination and India".
Neuromyelitis Optica. Case Report
Patricia Quintero Cusguen,ángela María Gutiérrez álvarez
Revista Ciencias de la Salud , 2009,
Abstract: Neuromyelitis Optica, also known as Devic’sSyndrome, is a disease which combines opticneuritis and transverse myelitis. Some years ago it was considered as a form of multiple sclerosis.Actually, it is consider as a different disease, onthe basis of the clinical, imaging, serology andimmunopatholoy profile.A case of 29 years old female patient is reported,based on her clinical findings which beganin the fifth postpartum month, with progressivelower limb paresis, associated with bilateralvision loss.This paper attempts giving a synoptic overviewof this uncommon immune mediateddemyelinating condition; it summarises themost important epidemiological parameters andpresents the diagnostic and therapeutic possibilitiesavailable today.
Immunotherapy of Neuromyelitis Optica  [PDF]
Benjamin Bienia,Roumen Balabanov
Autoimmune Diseases , 2013, DOI: 10.1155/2013/741490
Abstract: Neuromyelitis optica (NMO) is a chronic inflammatory disease of the central nervous system that affects the optic nerves and spinal cord resulting in visual impairment and myelopathy. There is a growing body of evidence that immunotherapeutic agents targeting T and B cell functions, as well as active elimination of proinflammatory molecules from the peripheral blood circulation, can attenuate disease progression. In this review, we discuss the immunotherapeutic options and the treatment strategies in NMO. We also analyze the pathogenic mechanisms of the disease in order to provide recommendations regarding treatments. 1. Introduction Neuromyelitis optica (NMO), also known as Devic’s disease, is a chronic inflammatory disease of the central nervous system (CNS) that preferentially targets the optic nerves and spinal cord [1]. The overall disease incidence has been estimated at 1?:?100,000 and that it has a predilection for middle-aged, non-Caucasian females [2]. NMO spectrum disorders (NMOSD) encompass a variation of this classical picture in that patients may have brain involvement or a more limited presentation such as isolated transverse myelitis or an optic neuritis [3]. Historically, many thought of NMO as a rare variant of multiple sclerosis (MS). Given the identification of unique clinical and radiological differences and the discovery of the NMO-IgG, an autoantibody against aquaporin-4 (aqp4), it is now understood to be its own entity with distinct pathogenesis, diagnostic criteria, prognosis, and treatment [1–5]. Until recently, NMO was considered a disease of limited therapeutic options and poor prognosis. Research over the last decade brought new understanding of the disease pathogenesis that translated into immunotherapy directed against this disease. Moreover, there is a growing body of evidence that NMO can be controlled by immunotherapeutics targeting its cellular and humoral immune mechanisms. We review the immunotherapy of NMO, the various treatment options, and the clinical strategies that are typically encountered in practice. 2. Neuromyelitis Optica: An Overview NMO is a neurological disorder that classically presents as a case of severe bilateral optic neuritis associated with a transverse myelitis [1–5]. The typical disease onset is either acute or subacute, and the symptoms are likely to persist without treatment. Optic neuritis results in decreased or a complete loss of vision. Transverse myelitis is usually extensive and spans more than 3 consecutive vertebral segments. Deficits related to myelitis include paralysis and sensory
Molecular Pathogenesis of Neuromyelitis Optica  [PDF]
Wajih Bukhari,Michael H Barnett,Kerri Prain,Simon A Broadley
International Journal of Molecular Sciences , 2012, DOI: 10.3390/ijms131012970
Abstract: Neuromyelitis optica (NMO) is a rare autoimmune disorder, distinct from multiple sclerosis, causing inflammatory lesions in the optic nerves and spinal cord. An autoantibody (NMO IgG) against aquaporin-4 (AQP4), a water channel expressed on astrocytes is thought to be causative. Peripheral production of the antibody is triggered by an unknown process in genetically susceptible individuals. Anti-AQP4 antibody enters the central nervous system (CNS) when the blood brain barrier is made permeable and has high affinity for orthogonal array particles of AQP4. Like other autoimmune diseases, Th17 cells and their effector cytokines (such as interleukin 6) have been implicated in pathogenesis. AQP4 expressing peripheral organs are not affected by NMO IgG, but the antibody causes extensive astrocytic loss in specific regions of the CNS through complement mediated cytotoxicity. Demyelination occurs during the inflammatory process and is probably secondary to oligodendrocyte apoptosis subsequent to loss of trophic support from astrocytes. Ultimately, extensive axonal injury leads to severe disability. Despite rapid advances in the understanding of NMO pathogenesis, unanswered questions remain, particularly with regards to disease mechanisms in NMO IgG seronegative cases. Increasing knowledge of the molecular pathology is leading to improved treatment strategies.
Atypical presentations of neuromyelitis optica
Sato, Douglas;Fujihara, Kazuo;
Arquivos de Neuro-Psiquiatria , 2011, DOI: 10.1590/S0004-282X2011000600019
Abstract: neuromyelitis optica (nmo) is an inflammatory disease of central nervous system classically characterized by acute, severe episodes of optic neuritis and longitudinally extensive transverse myelitis, usually with a relapsing course. the identification of an autoantibody exclusively detected in nmo patients against aquaporin-4 (aqp-4) has allowed identification of cases beyond the classical phenotype. brain lesions, once thought as infrequent, can be observed in nmo patients, but lesions have different characteristics from the ones seen in multiple sclerosis. additionally, some aqp-4 antibody positive patients may present with a variety of symptoms not being restricted to optic neuritis and acute myelitis during the first attack or in a relapse. examples are not limited to, but may include patients only with brain and/or brainstem lesions, narcolepsy with hypothalamic lesions or patients with intractable hiccups, nausea and vomiting. the prompt identification of nmo patients with atypical presentations may benefit these patients with institution of early treatment to reduce disability and prevent further attacks.
Altered Topological Organization of White Matter Structural Networks in Patients with Neuromyelitis Optica  [PDF]
Yaou Liu,Yunyun Duan,Yong He,Jun Wang,Mingrui Xia,Chunshui Yu,Huiqing Dong,Jing Ye,Helmut Butzkueven,Kuncheng Li,Ni Shu
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0048846
Abstract: To investigate the topological alterations of the whole-brain white-matter (WM) structural networks in patients with neuromyelitis optica (NMO).
Olfactory Dysfunction in Patients with Neuromyelitis Optica  [PDF]
Felix Schmidt,?nder G?ktas,Sven Jarius,Brigitte Wildemann,Klemens Ruprecht,Friedemann Paul,Lutz Harms
Multiple Sclerosis International , 2013, DOI: 10.1155/2013/654501
Abstract: Background. Neuromyelitis optica (NMO) is a severely disabling autoimmune disorder of the CNS, which mainly affects the optic nerves and spinal cord. However, recent studies have shown that extra-opticospinal are more common in NMO than previously thought. Objective. To investigate olfactory function (OF) in patients with neuromyelitis optica (NMO) versus healthy controls (HC). Methods. Psychophysical testing of the orthonasal OF was performed using the Threshold-Discrimination-Identification test (TDI), measuring different qualities of olfaction, in 10 unselected NMO patients and 10?HC. Results. Five of 10?NMO patients (50%) showed hyposmia, while all 10?HC were normosmic. Moreover, NMO patients had significantly lower mean TDI-scores compared to HC, based on a poorer performance in both the Discrimination and the Identification subtests. Conclusions. Our results suggest that hyposmia might be part of the expanding clinical spectrum of NMO. 1. Introduction Neuromyelitis optica (NMO, Devic’s syndrome) is an autoimmune central nervous system disorder that predominantly affects the optic nerves and the spinal cord [1, 2]. Impaired olfaction is increasingly recognized in neurodegenerative diseases such as Parkinson’s and Alzheimer’s diseases and has been reported in patients with multiple sclerosis (MS) [3, 4]. As the clinical presentation of NMO may extend beyond relapses of optic neuritis and myelitis [2, 5], we here investigated whether olfactory function (OF) is altered in NMO. 2. Patients and Methods This pilot study was performed from July 2011 to October 2012. Ten patients with NMO according to the 2006 diagnostic criteria [1] were prospectively recruited from the Charité outpatient clinics. Aquaporin-4 antibodies were tested using a commercially available cell-based assay employing recombinant human target antigen (EUROIMMUN, Luebeck, Germany) [6]. A healthy control group (HC) of 10 individuals closely matched for gender and age (±3 years) was recruited among the hospital staff. Exclusion criteria for both groups were olfactory disorders (postinfectious, posttraumatic, and sinunasal), infections of the upper respiratory tract, tumours treated with radiation or chemotherapy, allergies, major depression, and Parkinson’s or Alzheimer’s disease. All study participants declared to be nonsmokers. Patients taking drugs that could cause olfactory dysfunction as for example amitriptyline and D-penicillamine were excluded from the study. Furthermore, patients receiving corticosteroid treatment during the testing period were excluded because corticosteroids
Relapse of Neuromyelitis Optica Spectrum Disorder Associated with Intravenous Lidocaine
Akiyuki Uzawa,Masahiro Mori,Saeko Masuda,Kazuhiko Aoe,Satoshi Kuwabara
Case Reports in Medicine , 2011, DOI: 10.1155/2011/405837
Abstract: Lidocaine unmasks silent symptoms and eases neuropathic pain in multiple sclerosis patients; however, the effects of lidocaine in neuromyelitis optica have never been reported. We describe the case of a 59-year-old Japanese woman with neuromyelitis optica spectrum disorder who developed optic neuritis 1 day after intravenous lidocaine injection for treating allodynia. Her symptom seemed to result from a relapse of neuromyelitis optica induced by lidocaine administration, and not because of the transient effects of intravenous lidocaine administration. The possibility that lidocaine administration results in relapse of neuromyelitis optica due to its immunomodulating effects cannot be ruled out.
Interferon Alpha Association with Neuromyelitis Optica  [PDF]
Nasrin Asgari,Anne Voss,Troels Steenstrup,Kirsten Ohm Kyvik,Egon Stenager,Soeren Thue Lillevang
Journal of Immunology Research , 2013, DOI: 10.1155/2013/713519
Abstract: Interferon-alpha (IFN-α) has immunoregulatory functions in autoimmune inflammatory diseases. The goal of this study was to determine occurrence and clinical consequences of IFN-α in neuromyelitis optica (NMO) patients. Thirty-six NMO and 41 multiple sclerosis (MS) patients from a population-based retrospective case series were included. Expanded Disability Status Scale (EDSS) score and MRI findings determined disease activity. Linear regression was used to assess the effects of the level of IFN-α on disability (EDSS). IFN-α was determined by sensitive ELISA assays. IFN-α was detectable in sera from 9/36 NMO patients, significantly more often than in the MS group (2/41) ( ). A higher frequency of IFN-α was observed in NMO patients with acute relapse compared to NMO patients in remission ( ) and compared to the MS patients with relapse ( ). In NMO patients, the levels of IFN-α were significantly associated with EDSS ( ). It may be concluded that IFN-α was detectable in a subgroup of NMO patients. Association of IFN-α levels with clinical disease activity and severity suggests a role for IFN-α in disease perpetuation and may provide a plausible explanation for a negative effect of IFN-1 treatment in NMO patients.
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