کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3052123 | 1186080 | 2014 | 5 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Lack of antibodies to NMDAR or VGKC-complex in GAD and cardiolipin antibody-positive refractory epilepsy Lack of antibodies to NMDAR or VGKC-complex in GAD and cardiolipin antibody-positive refractory epilepsy](/preview/png/3052123.png)
• Different neuronal autoantibodies have been associated with seizure disorders.
• We analyzed the presence of NMDAR and VGKC-complex antibodies in patients with GAD or anticardiolipin antibodies.
• There were no positive titers of NMDAR or VGKC-complex antibodies.
• The negative results suggest that different neuronal antibodies have different significance and pathophysiological mechanisms in acute and chronic seizure disorders.
SummaryBackgroundOver the last few years autoantibodies against neuronal proteins have been identified in several forms of autoimmune encephalitis and epilepsy. NMDA receptor (NMDAR) and voltage gated potassium channel (VGKC) complex antibodies are mainly associated with limbic encephalitis (LE) whereas glutamic acid decarboxylase antibodies (GADA) and anticardiolipin (ACL) antibodies are more commonly detected in patients with chronic epilepsy. Clinical features vary between these antibodies suggesting the specificity of different neuronal antibodies in seizures.MethodsSerum samples of 14 GADA positive and 24 ACL positive patients with refractory epilepsy were analyzed for the presence of VGKC or NMDAR antibodies.ResultsNo positive VGKC or NMDAR antibodies were found in these patients.ConclusionsThe results confirm the different significance of these neuronal antibodies in seizure disorders. Different autoantibodies have different significance in seizures and probably have different pathophysiological mechanisms of actions.
Journal: Epilepsy Research - Volume 108, Issue 3, March 2014, Pages 592–596