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Review Inflammatory demyelinating events following treatment with anti-tumor necrosis factor. 2009
Fromont A, De Seze J, Fleury MC, Maillefert JF, Moreau T. · Department of Neurology, University Hospital of Dijon, 21000 Dijon, France. · Cytokine. · Pubmed #19109035 No free full text.
Abstract: BACKGROUND: Tumor necrosis factor alpha (TNF-alpha) is an inflammatory cytokine involved in certain inflammatory diseases including multiple sclerosis (MS), rheumatoid arthritis (RA), and Crohn's disease. The anti-TNF-alpha treatments used for RA may be associated with inflammatory demyelinating events affecting the central nervous system and may possibly aggravate known MS. OBJECTIVE: We report here three new cases of inflammatory demyelinating events of the central nervous system following treatment with anti-TNF-alpha. RESULTS: The neurological symptoms appeared on average 5 months after initiation of the treatment. For all patients, the inflammatory process was confirmed by brain magnetic resonance imaging. The symptoms totally or partially regressed as soon as anti-TNF-alpha treatment was stopped except for one patient who developed clinically defined MS. CONCLUSIONS: Inflammatory demyelination of the central nervous system may be associated with the use of anti-TNF-alpha. Patients with rheumatoid arthritis treated with these treatments should benefit from a follow-up which includes brain MRI.
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Article Bilateral optic neuropathy revealing Sjögren's syndrome. 2008
Béjot Y, Osseby GV, Ben Salem D, Beynat J, Muller G, Moreau T, Giroud M. · Service de neurologie, CHU de Dijon, 3, rue du Faubourg-Raines, 21000 Dijon, France. · Rev Neurol (Paris). · Pubmed #18808771 No free full text.
Abstract: INTRODUCTION: The central nervous system involvement has been reported in 20% of cases of primary Sjogrën's syndrome (SS), a chronic autoimmune disease characterized by a disorder of the exocrine glands secondary to progressive lymphocyte infiltration. Classically described neurological manifestations include sensorimotor deficits, aseptic meningitis or meningoencephalitis, multiple sclerosis-like syndromes and myeolopathies. OBSERVATION: We report here the case of a 53-year-old woman who exhibited rapidly progressive visual loss, disclosing bilateral optic neuropathy, as an uncommon initial symptom of primary SS. Examination of CSF revealed associated aseptic meningitis. Because of the lack of efficacy of the first treatment by intravenous corticosteroids, monthly intravenous cyclophosphamide was quickly introduced. After six months, significant visual recovery was observed. CONCLUSION: Optic neuropathies have been rarely reported as the initial symptom revealing primary Sjogrën syndrome, and bilateral simultaneous lesions remain exceptional.
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