{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:49:18Z","timestamp":1787014158639,"version":"build-2736575974"},"reference-count":49,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2022,5,29]],"date-time":"2022-05-29T00:00:00Z","timestamp":1653782400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82071457"],"award-info":[{"award-number":["82071457"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Euro J of Neurology"],"published-print":{"date-parts":[[2022,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and purpose<\/jats:title>\n                    <jats:p>Faciobrachial dystonic seizures (FBDS) and hyponatremia are the distinct clinical features of autoimmune encephalitis (AE) caused by antibodies against leucine\u2010rich glioma\u2010inactivated 1 (LGI1). The present study aims to explore the pathophysiological patterns and neural mechanisms underlying these symptoms.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We included 30 patients with anti\u2010LGI1 AE and 30 controls from a retrospective observational cohort. Whole\u2010brain metabolic pattern analysis was performed to assess the pathological network of anti\u2010LGI1 AE, as well as the symptom networks associated with FBDS. Logistic regression was applied to explore independent predictors of FBDS. Finally, we used a multiple regression model to investigate the hyponatremia\u2010associated brain network and its effect on serum sodium levels.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The pathological network of anti\u2010LGI1 AE involved hypermetabolism in the cerebellum, subcortical structures and Rolandic area, as well as hypometabolism in the medial prefrontal cortex. The symptom network of FBDS included hypometabolism in the cerebellum and Rolandic area (\n                      <jats:italic>p<\/jats:italic>\n                      <jats:sub>FDR<\/jats:sub>\n                      \u2009&lt;0.05). Hypometabolism in the cerebellum was an independent predictor of FBDS (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001). Hyponatremia\u2010associated network highlighted a negative effect on the caudate nucleus, frontal and temporal white matter. The metabolism of the hypothalamus was negatively associated with (Pearson's\n                      <jats:italic>R<\/jats:italic>\n                      = \u22120.180,\n                      <jats:italic>p<\/jats:italic>\n                      = 0.342),\u00a0while\u00a0not\u00a0the\u00a0independent\u00a0predictor\u00a0for\u00a0serum\u00a0sodium\u00a0level (path\n                      <jats:italic>c\u2019<\/jats:italic>\n                      = \u22127.238, 95% confidence interval\u2009= \u221230.947 to 16.472).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our results provide insights into the whole\u2010brain metabolic patterns of patients with anti\u2010LGI1 AE, including the symptom network associated with FBDS and the hyponatremia\u2010associated brain network. The findings help us to understand the neural mechanisms underlying anti\u2010LGI1 AE and to evaluate the progress of this disease.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/ene.15384","type":"journal-article","created":{"date-parts":[[2022,5,6]],"date-time":"2022-05-06T01:11:11Z","timestamp":1651799471000},"page":"2376-2385","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Whole\u2010brain metabolic pattern analysis in patients with\n                    <scp>anti\u2010<\/scp>\n                    leucine\u2010rich glioma\u2010inactivated 1 (\n                    <scp>LGI1)<\/scp>\n                    encephalitis"],"prefix":"10.1111","volume":"29","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9721-1378","authenticated-orcid":false,"given":"Jiajie","family":"Mo","sequence":"first","affiliation":[{"name":"Department of Neurosurgery, Beijing Tiantan Hospital Capital Medical University  Beijing 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