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dc.contributor.authorGurvit, Hakan
dc.contributor.authorBaykan, BETÜL
dc.contributor.authorHanagasi, Haşmet Ayhan
dc.contributor.authorBilgic, Basar
dc.contributor.authorUlusoy, CANAN AYSEL
dc.contributor.authorTuran, Selin
dc.contributor.authorYildiz, Senay
dc.contributor.authorCikrikcili, Ugur
dc.contributor.authorTuzun, Erdem
dc.date.accessioned2021-03-04T14:17:01Z
dc.date.available2021-03-04T14:17:01Z
dc.date.issued2013
dc.identifier.citationCikrikcili U., Ulusoy C. A. , Turan S., Yildiz S., Bilgic B., Hanagasi H. A. , Baykan B., Tuzun E., Gurvit H., "Non-Convulsive Status Epilepticus Associated With Glutamic Acid Decarboxylase Antibody", CLINICAL EEG AND NEUROSCIENCE, cilt.44, sa.3, ss.232-236, 2013
dc.identifier.issn1550-0594
dc.identifier.otherav_80bc15e2-3a74-4814-8c6f-983507fbe8bf
dc.identifier.othervv_1032021
dc.identifier.urihttp://hdl.handle.net/20.500.12627/87798
dc.identifier.urihttps://doi.org/10.1177/1550059412459330
dc.description.abstractAutoimmune encephalitis associated with glutamic acid decarboxylase antibodies (GAD-Ab) often presents with treatment-resistant partial seizures, as well as other central nervous system symptoms. In contrast to several other well-characterized autoantibodies, GAD-Ab has very rarely been associated with status epilepticus. We report a 63-year-old woman initially admitted with somnolence and psychiatric findings. The EEG findings, of generalized and rhythmical slow spike-wave activity over the posterior regions of both hemispheres, together with the clinical deterioration in responsiveness, led to the diagnosis of non-convulsive status epilepticus. Investigation of a broad panel of autoantibodies, revealed only increased serum GAD-Ab levels. Following methylprednisolone and intravenous immunoglobulin treatments, the patient's neurological symptoms improved, EEG findings disappeared and GAD-Ab levels significantly decreased. GAD-Ab should be added to the list of anti-neuronal antibodies associated with non-convulsive status epilepticus. Disappearance of clinical findings and seroreversion after immunotherapy suggest that GAD-Ab might be involved in seizure pathogenesis.
dc.language.isoeng
dc.subjectTemel Bilimler
dc.subjectKLİNİK NEUROLOJİ
dc.subjectKlinik Tıp
dc.subjectKlinik Tıp (MED)
dc.subjectNEUROSCIENCES
dc.subjectSinirbilim ve Davranış
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectNÖRO-GÖRÜNTÜLEME
dc.subjectPsikiyatri
dc.subjectPsikoloji
dc.subjectTemel Bilimler (SCI)
dc.subjectTıp
dc.subjectSağlık Bilimleri
dc.subjectDahili Tıp Bilimleri
dc.subjectNöroloji
dc.subjectSosyal ve Beşeri Bilimler
dc.subjectYaşam Bilimleri
dc.titleNon-Convulsive Status Epilepticus Associated With Glutamic Acid Decarboxylase Antibody
dc.typeMakale
dc.relation.journalCLINICAL EEG AND NEUROSCIENCE
dc.contributor.departmentİstanbul Üniversitesi , ,
dc.identifier.volume44
dc.identifier.issue3
dc.identifier.startpage232
dc.identifier.endpage236
dc.contributor.firstauthorID46452


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