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The course of neuromyelitis optica is irregular in most font with more than 90 % of patients experience lapsing of ocular neuritis , myelitis or both . Rest 10 % of cases are associated with the coincident course of myelitis and optic neuritis . Other symptoms include hiccup , vomiting , encephalitis , seizures , posterior two-sided encephalopathy syndrome , myeloradiculitis , meningoencephalitis , try red ink , double vision , olfactive disfunction , endocrinological abnormalcy , pain syndromes , cognitive dysfunction , and other cranial nerve palsies . It is also colligate with other autoimmune diseases ( in 30 - 50 % case ) , includingSLE , Sjogren ’s syndrome , myasthenia gravis , autoimmune thyroid disease , and autoimmune - mediatedvitamin B12 deficiency.(1 )
Can Neuromyelitis Optica Be Cured?
Practically , neuromyelitis optica can not be cured ; however , the objective of the treatment is to forbid relapses and if they occur improve symptomatology of relapse , and restitute the neurologic purpose . Since 90 % of the patient receive relapses ; they are treated with mellow dose endovenous methylprednisolone . In cases where steroid treatment is not effectual , plasma exchange may be used . Plasma exchange can be consider as initial therapy if the patient role has responded well to it antecedently . In patients with the ineffective response from both steroid and plasma telephone exchange , endovenous immune gamma globulin or cyclophosphamide can be considered.(1 )
patient role with neuromyelitis optica have to undergo long term therapy for immunosuppression . Immunosuppressives let in therapy direct B prison cell , such as endovenous rituximab or oral Imuran and Deltasone . Other treatment options include mycophenolate mofetil , methotrexate , and mitoxantrone . It is important to remark that , interferon - beta that is wide used in the management ofmultiple sclerosis , is not indicated in the direction of neuromyelitis optica as it has been known to aggravate the symptom rendering it ineffective in its management.(1 )
Neuromyelitis optica , also hump as Devic ’s syndrome or neuromyelitis optica spectrum disorder , is an inflammatory disease affecting the central skittish system characterise by relapses of optical neuritis or myelitis . The humoral immune system has long been advise in the disease pathogenesis and after the detecting of disease - specific serum immunoglobulin G autoantibody that targets the astrocytic water channel aquaporin-4 ; it is exonerated that neuromyelitis optica is a distinctly separate entity from multiple sclerosis . NMO - IgG / AQP4 antibodies are present in about 80 % of the patients with neuromyelitis optica . Although there is lap in the symptoms and other paraclinical findings of neuromyelitis optica and multiple induration , neuromyelitis optica is considered an autoimmune experimental condition that has different pathogenesis from that of multiple sclerosis.(1 )
There are various clinical , morbid and immunologic evidence that signal the association of AQP4 antibodies in the pathogenesis of neuromyelitis optica . AQP4 is mostly expressed in the opticospinal tissues and an resistant reply involving optic nerve and spinal electric cord can explain high symptoms and tie-up of these land site . Similarly , disease - specific several studies have correlated the disease activeness of neuromyelitis optica and increase serum horizontal surface of the antibody before relapse and refuse stage at the clock time of retrieval . In patients with isolated optic neuritis or with isolated longwise extensive thwartwise myelitis , the comportment of AQP4 antibodies is relate to increase development of neuromyelitis optica . The comportment of this antibody also predicts the course of action of succeeding relapses . what is more , the seropositivity is also related to the severity of the disease and more extensive involvement of the spinal corduroy , ocular and motor disability along with rigour in the long term disablement course.(1 )
It is noteworthy , that most of the patient with AQP4 antibodies are females with a female to male proportion of 10:1 and it is often associate with the more relapsing course than seronegative patients . It is also noted that successful treatment is assort with a decrease in the serum floor of the AQP4 antibodies . Additionally , B cell or antibody - point treatment , such as plasma exchange , rituximab , and tocilizumab are effective in neuromyelitis optica and incomplete vitamin B cell depletion and recurrence of B cells have been connect with spartan attacks.(1 )
Apart from AQP4 antibodies , there are other immunologic mediators associate with neuromyelitis optica that includes macrophages , eosinophils , neutrophils , proinflammatory cytokine ( IL-6 , CXCL13 , BAFF ) , B cells , T cadre , glutamate - liaise excitotoxicity along with IgG and IgM deposits in neuromyelitis optica lesion .
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