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dc.contributor.authorSaraya, Abhinbhenen_US
dc.contributor.authorMahavihakanont, Aekkapolen_US
dc.contributor.authorShuangshoti, Shanopen_US
dc.contributor.authorSittidetboripat, Nuntapornen_US
dc.contributor.authorDeesudchit, Tayarden_US
dc.contributor.authorCallahan, Michaelen_US
dc.contributor.authorWacharapluesadee, Supapornen_US
dc.contributor.authorWilde, Henryen_US
dc.contributor.authorHemachudha, Thiravaten_US
dc.date.accessioned2014-03-11T10:16:56Z
dc.date.issued2013en_US
dc.identifier.citationSaraya, Abhinbhen, Aekkapol Mahavihakanont, Shanop Shuangshoti, Nuntaporn Sittidetboripat, Tayard Deesudchit, Michael Callahan, Supaporn Wacharapluesadee, Henry Wilde, and Thiravat Hemachudha. 2013. “Autoimmune causes of encephalitis syndrome in Thailand: prospective study of 103 patients.” BMC Neurology 13 (1): 150. doi:10.1186/1471-2377-13-150. http://dx.doi.org/10.1186/1471-2377-13-150.en
dc.identifier.issn1471-2377en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:11879324
dc.description.abstractBackground: Data on encephalitis in Thailand have not been completely described. Etiologies remain largely unknown. We prospectively analyzed 103 Thai patients from 27 provinces for the causes of encephalitis using clinical, microbiological and neuroimaging indices; caseswithout a diagnosis were evaluated for autoimmune causes of encephalitis. Methods: Patients with encephalitis and/or myelitis were prospectively studied between October 2010 and August 2012. Cases associated with bacterial, rickettsial and mycobacterial diseases were excluded. Herpes viruses 1-6 and enteroviruses infection was diagnosed using PCR evaluation of CSF; dengue and JE viruses infection, by serology. The serum of test-negative patients was evaluated for the presence of autoantibodies. Results: 103 patients were recruited. Fifty-three patients (52%) had no etiologies identified. Twenty-five patients (24%) were associated with infections. Immune encephalitis was found in 25 (24%); neuropsychiatric lupus erythematosus (4), demyelinating diseases (3), Behcet’s disease (1) and the remaining had antibodies to NMDAR (5), ANNA-2 (6), Yo (2), AMPA (1), GABA (1), VGKC (1) and NMDA coexisting with ANNA-2 (1). Presenting symptoms in the autoimmune group included behavioral changes in 6/25 (versus 12/25 in infectious and 13/53 in unknown group) and as psychosis in 6/25 (versus 0/25 infectious and 2/53 unknown). Seizures were found in 6/25 autoimmune, 4/25 infectious and 19/53 unknown group. Two patients with anti-ANNA-2 and one anti-Yo had temporal lobe involvement by magnetic resonance imaging. Two immune encephalitis patients with antibodies to NMDAR and ANNA-2 had ovarian tumors. Conclusions: Autoantibody-associated encephalitis should be considered in the differential diagnosis and management algorithm regardless of clinical and neuroimaging features.en
dc.language.isoen_USen
dc.publisherBioMed Centralen
dc.relation.isversionofdoi:10.1186/1471-2377-13-150en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3853593/pdf/en
dash.licenseLAAen_US
dc.subjectEncephalitisen
dc.subjectAutoimmune encephalitisen
dc.subjectParaneoplastic encephalitisen
dc.subjectLimbic encephalitisen
dc.titleAutoimmune causes of encephalitis syndrome in Thailand: prospective study of 103 patientsen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalBMC Neurologyen
dc.date.available2014-03-11T10:16:56Z
dc.identifier.doi10.1186/1471-2377-13-150*


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