Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

Epilepsy is one of the most common neurological disorders, but in the majority of cases the cause of the seizures is unknown. There is increasing evidence of an autoimmune aetiology in some syndromes. Although a number of different antibodies have been detected in the sera of patients with epilepsy, it is probably only those antibodies directed against membrane proteins, such as ion channels and receptor proteins, that have the potential to be pathogenic. Antibodies to subtypes of the Shaker family of voltage-gated potassium channels (VGKC) have been detected in patients with a variety of seizure-associated conditions. Antibodies to GAD have also been found in patients with drug-resistant temporal lobe epilepsy, as well as in other neurological disorders, such as stiff person syndrome and cerebellar ataxia, but the relevance of these antibodies is still to be determined. Antibodies to other antigens, such as glutamate receptor type 3 (GluR3), gangliosides, thyroid antigens or phospholipids, have been measured in epilepsies but their significance is unknown. The VGKC antibodies denote patients responsive to therapy and for that reason their detection is clinically useful. The relevance of GAD antibodies is still being investigated and use of diagnostic tests for GAD in patients with epilepsy is uncertain. Additionally, there is no evidence that the detection of antibodies to gangliosides, phospholipids or nuclear proteins is useful in the diagnosis of epilepsy. © 2007 Elsevier Inc. All rights reserved.

Original publication

DOI

10.1016/B978-044452763-9/50085-8

Type

Journal article

Publication Date

01/12/2007

Pages

659 - 665