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Disseminated Encephalomyelitis (disseminated + encephalomyelitis)
Kinds of Disseminated Encephalomyelitis Selected AbstractsDiagnosing paediatric multiple sclerosis versus acute disseminated encephalomyelitisDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 12 2007Daniela Pohl No abstract is available for this article. [source] Neurologic manifestations of ulcerative colitisEUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2007R. Scheid Ulcerative colitis (UC) has traditionally been considered to be an inflammatory disease limited to the colonic mucosa. However, since it has been shown that UC is frequently accompanied by various extraintestinal disorders, there is increasing evidence that UC may also manifest in the nervous system. The following review focuses particularly on these possible manifestations of UC, both in the peripheral (PNS), and in the central nervous system (CNS). A systematic literature search according to the MEDLINE database was performed for this purpose. Although a reliable differentiation may clinically not always be possible, three major pathogenic entities can be differentiated: (i) cerebrovascular disease as a consequence of thrombosis and thromboembolism; (ii) systemic and cerebral vasculitis; (iii) probably immune mediated neuropathy and cerebral demyelination. With the exception of thromboembolism and sensorineural hearing loss, evidence for a causal relationship relies merely on single case reports or retrospective case series. Considering the CNS-manifestations, similarities between UC-associated disorders of the white matter and acute disseminated encephalomyelitis (ADEM) are obvious. Epileptic seizures, unspecified encephalopathies and confusional states are most likely epiphenomena that have to be regarded symptomatic rather than as own entities. A prospective study on the neurologic aspects of UC would be very welcome. [source] Mycoplasma pneumoniae -associated myelitis: a comprehensive reviewEUROPEAN JOURNAL OF NEUROLOGY, Issue 2 2006S. Tsiodras Myelitis is one of the most severe central nervous system complications seen in association with Mycoplasma pneumoniae infections and both acute transverse myelitis (ATM) as well as acute disseminated encephalomyelitis (ADEM) have been observed. We reviewed all available literature on cases of Mycoplasma spp. associated ATM as well as ADEM with dominant spinal cord pathology and classified those cases according to the strength of evidence implicating M. pneumoniae as the cause. A wide range of data on diagnosis, epidemiology, immunopathogenesis, clinical picture, laboratory diagnosis, neuroimaging and treatment for this rare entity is presented. The use of highly sensitive and specific molecular diagnostic techniques may assist in clearly elucidating the role of M. pneumoniae in ATM/ADEM syndromes in the near future. Immunomodulating therapies may have a role in treating such cases. [source] Fulminant acute disseminated encephalomyelitis mimicking acute bacterial menigoencephalitisEUROPEAN JOURNAL OF NEUROLOGY, Issue 1 2005A. Harloff Most patients with acute disseminated encephalomyelitis (ADEM) recover quickly under corticosteroid treatment and have a favourable long-term prognosis. We report on a young woman with acute onset of an extensive and solitary white-matter lesion in the left hemisphere. Fever, high pleocytosis and elevated protein in cerebrospinal fluid initially suggested bacterial meningoencephalitis. The patient died from brain herniation despite maximal conservative therapy. Histological changes in necropsy were consistent with the diagnosis ADEM. Treatment options of fulminant ADEM are discussed. [source] Rapid clinical and CSF response to intravenous gamma globulin in acute disseminated encephalomyelitisEUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2001S. J. Pittock [source] Combination regimen of methylprednisolone, IV immunoglobulin, and plasmapheresis early in the treatment of acute disseminated encephalomyelitisJOURNAL OF CLINICAL APHERESIS, Issue 4 2006Rommel P. Lu Abstract Acute disseminated encephalomyelitis (ADEM) is a demyelinating disease of the central nervous system that is associated with significant morbidity and mortality. Early recognition of the disease is of paramount importance; however, treatment options are limited because only case reports and small series are available in the literature. We report a case of a 42 year-old previously healthy man, whom we treated successfully with a combination regimen of methyprednisolone, IV immunoglobulin, and plasmapheresis early in the course of the disease. J. Clin. Apheresis 21: 2006. © 2006 Wiley-Liss, Inc. [source] Intravenous immunoglobulin therapy in acute disseminated encephalomyelitis associated with hepatitis A infectionPEDIATRICS INTERNATIONAL, Issue 2 2004Bülent Ünay No abstract is available for this article. [source] Acute disseminated encephalomyelitis in a boy with elevated plasma levels of thrombin,antithrombin III complexPEDIATRICS INTERNATIONAL, Issue 2 2001Tatsuro Nobutoki No abstract is available for this article. [source] Antibodies to native myelin oligodendrocyte glycoprotein in children with inflammatory demyelinating central nervous system disease,ANNALS OF NEUROLOGY, Issue 6 2009Fabienne Brilot PhD Objective Myelin oligodendrocyte glycoprotein (MOG) is a candidate target antigen in demyelinating diseases of the central nervous system (CNS). Although MOG is encephalitogenic in different animal models, the relevance of this antigen in human autoimmune diseases of the CNS is still controversial. Methods We investigated the occurrence and biological activity of antibodies to native MOG (nMOG) in 47 children during a first episode of CNS demyelination (acute disseminated encephalomyelitis [ADEM], n = 19 and clinical isolated syndrome [CIS], n = 28) by a cell-based bioassay. Results High serum immunoglobulin G (IgG) titers to nMOG were detected in 40% of children with CIS/ADEM but 0% of the control children affected by other neurological diseases, healthy children, or adults with inflammatory demyelinating diseases, respectively. By contrast, IgM antibodies to nMOG occurred in only 3 children affected by ADEM. Children with high anti-nMOG IgG titer were significantly younger than those with low IgG titer. Anti-nMOG IgG titers did not differ between the ADEM and CIS group, and did not predict conversion from CIS to MS during a mean 2-year follow-up. However, intrathecal IgG anti-MOG antibody synthesis was only seen in CIS children. IgG antibodies to nMOG not only bound to the extracellular domain of nMOG, but also induced natural killer cell-mediated killing of nMOG-expressing cells in vitro. Interpretation Overall, these findings suggest nMOG as a major target of the humoral immune response in a subgroup of children affected by inflammatory demyelinating diseases of the CNS. Children may provide valuable insight into the earliest immune mechanisms of CNS demyelination. Ann Neurol 2009;66:833,842 [source] |