{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T18:02:18Z","timestamp":1770746538018,"version":"3.49.0"},"reference-count":20,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2003,9,24]],"date-time":"2003-09-24T00:00:00Z","timestamp":1064361600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2003,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We found voltage\u2010gated potassium channel (VGKC) antibodies in 4 of 15 patients with limbic encephalitis (LE). Two patients with idiopathic LE had high VGKC antibody levels (&gt;800pM; controls &lt;100pM), that fell in parallel with a clinical response to immunotherapy. Two patients with lower VGKC antibodies (170pM, 300pM) had lung cancer (radiological evidence only in one) and the LE improved with immunotherapy in one. The other 11 patients without VGKC antibodies had paraneoplastic LE and eight onconeural antibodies (Hu in 6; Ma2 in 2). VGKC antibodies do not unambiguously discriminate between idiopathic or paraneoplastic LE but probably indicate a good response to immunotherapy. 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