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These autoantibodies target surface-exposed domains of LGI1 or CASPR2, and appear to be directly pathogenic. In contrast, voltage-gated potassium channel (VGKC) antibodies that lack LGI1 or CASPR2 reactivities (\u2018double-negative\u2019) are common in healthy controls and have no consistent associations with distinct syndromes. These antibodies target intracellular epitopes and lack pathogenic potential. Moreover, the clinically important LGI1 and CASPR2 antibodies comprise only ~15% of VGKC-positive results, meaning that most VGKC-antibody positive results mislead rather than help. Further, initial VGKC testing misses some cases that have LGI1 and CASPR2 antibodies. These collective observations confirm that laboratories should stop testing for VGKC antibodies and instead, test only for LGI1 and CASPR2 antibodies. This change in practice will lead to significant patient benefit.<\/jats:p>","DOI":"10.1136\/practneurol-2019-002494","type":"journal-article","created":{"date-parts":[[2020,6,28]],"date-time":"2020-06-28T17:17:20Z","timestamp":1593364640000},"page":"377-384","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":72,"title":["Stop testing for autoantibodies to the VGKC-complex: only request LGI1 and CASPR2"],"prefix":"10.1136","volume":"20","author":[{"given":"Sophia","family":"Michael","sequence":"first","affiliation":[{"name":"Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK"},{"name":"Department of Neurology, John Radcliffe Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4142-2667","authenticated-orcid":false,"given":"Patrick","family":"Waters","sequence":"additional","affiliation":[{"name":"Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7667-9748","authenticated-orcid":false,"given":"Sarosh R","family":"Irani","sequence":"additional","affiliation":[{"name":"Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK"},{"name":"Department of Neurology, John Radcliffe Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"239","published-online":{"date-parts":[[2020,6,28]]},"reference":[{"key":"2025090411121457000_20.5.377.1","doi-asserted-by":"crossref","first-page":"75","DOI":"10.1016\/0140-6736(91)90073-X","article-title":"Autoimmune aetiology for acquired neuromyotonia (Isaac\u2019s syndrome)","volume":"13","author":"Sinha","year":"1991","journal-title":"Lancet"},{"key":"2025090411121457000_20.5.377.2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410380505"},{"key":"2025090411121457000_20.5.377.3","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410410215"},{"key":"2025090411121457000_20.5.377.4","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/124.12.2417"},{"key":"2025090411121457000_20.5.377.5","doi-asserted-by":"publisher","DOI":"10.1002\/ana.10713"},{"key":"2025090411121457000_20.5.377.6","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/awh077"},{"key":"2025090411121457000_20.5.377.7","doi-asserted-by":"publisher","DOI":"10.1212\/01.WNL.0000122648.19196.02"},{"key":"2025090411121457000_20.5.377.8","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/awq213"},{"key":"2025090411121457000_20.5.377.9","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(10)70137-X"},{"key":"2025090411121457000_20.5.377.10","doi-asserted-by":"publisher","DOI":"10.1038\/ng832"},{"key":"2025090411121457000_20.5.377.11","first-page":"1","article-title":"Characterisation of CASPR2 deficiency disorder - a syndrome involving autism, epilepsy and language impairment. 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