{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T14:58:46Z","timestamp":1791212326401,"version":"4.1.0"},"reference-count":40,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2014,1,21]],"date-time":"2014-01-21T00:00:00Z","timestamp":1390262400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Epilepsia"],"published-print":{"date-parts":[[2014,2]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      Thalamic abnormality in temporal lobe epilepsy (\n                      <jats:styled-content style=\"fixed-case\">TLE<\/jats:styled-content>\n                      ) is well known from imaging studies, but evidence is lacking regarding connectivity profiles of the thalamus and their involvement in the disease process. We used a novel multisequence magnetic resonance imaging (\n                      <jats:styled-content style=\"fixed-case\">MRI<\/jats:styled-content>\n                      ) protocol to elucidate the relationship between mesial temporal and thalamic pathology in\n                      <jats:styled-content style=\"fixed-case\">TLE<\/jats:styled-content>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      For 23 patients with\n                      <jats:styled-content style=\"fixed-case\">TLE<\/jats:styled-content>\n                      and 23 healthy controls, we performed\n                      <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                      <jats:sub>1<\/jats:sub>\n                      \u2010weighted (for analysis of tissue structure), diffusion tensor imaging (tissue connectivity), and\n                      <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                      <jats:sub>1<\/jats:sub>\n                      and\n                      <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                      <jats:sub>2<\/jats:sub>\n                      relaxation (tissue integrity)\n                      <jats:styled-content style=\"fixed-case\">MRI<\/jats:styled-content>\n                      across the whole brain. We used connectivity\u2010based segmentation to determine connectivity patterns of thalamus to ipsilateral cortical regions (occipital, parietal, prefrontal, postcentral, precentral, and temporal). We subsequently determined volumes, mean tractography streamlines, and mean\n                      <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                      <jats:sub>1<\/jats:sub>\n                      and\n                      <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                      <jats:sub>2<\/jats:sub>\n                      relaxometry values for each thalamic segment preferentially connecting to a given cortical region, and of the hippocampus and entorhinal cortex.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      As expected, patients had significant volume reduction and increased\n                      <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                      <jats:sub>2<\/jats:sub>\n                      relaxation time in ipsilateral hippocampus and entorhinal cortex. There was bilateral volume loss, mean streamline reduction, and\n                      <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                      <jats:sub>2<\/jats:sub>\n                      increase of the thalamic segment preferentially connected to temporal lobe, corresponding to anterior, dorsomedial, and pulvinar thalamic regions, with no evidence of significant change in any other thalamic segments. Left and right thalamotemporal segment volume and\n                      <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                      <jats:sub>2<\/jats:sub>\n                      were significantly correlated with volume and\n                      <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                      <jats:sub>2<\/jats:sub>\n                      of ipsilateral (epileptogenic), but not contralateral (nonepileptogenic), mesial temporal structures.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance<\/jats:title>\n                    <jats:p>\n                      These convergent and robust data indicate that thalamic abnormality in\n                      <jats:styled-content style=\"fixed-case\">TLE<\/jats:styled-content>\n                      is restricted to the area of the thalamus that is preferentially connected to the epileptogenic temporal lobe. The degree of thalamic pathology is related to the extent of mesial temporal lobe damage in\n                      <jats:styled-content style=\"fixed-case\">TLE<\/jats:styled-content>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/epi.12520","type":"journal-article","created":{"date-parts":[[2014,1,21]],"date-time":"2014-01-21T14:46:58Z","timestamp":1390315618000},"page":"306-315","source":"Crossref","is-referenced-by-count":78,"title":["Thalamotemporal impairment in temporal lobe epilepsy: A combined\n                    <scp>MRI<\/scp>\n                    analysis of structure, integrity, and connectivity"],"prefix":"10.1111","volume":"55","author":[{"given":"Simon S.","family":"Keller","sequence":"first","affiliation":[{"name":"The Department of Clinical Neuroscience Institute of Psychiatry King's College London London United Kingdom"},{"name":"The Department of Molecular and Clinical Pharmacology Institute of Translational Medicine University of Liverpool Liverpool United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan","family":"O'Muircheartaigh","sequence":"additional","affiliation":[{"name":"The Department of Neuroimaging Institute of Psychiatry King's College London London United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine","family":"Traynor","sequence":"additional","affiliation":[{"name":"The Department of Clinical Neuroscience Institute of Psychiatry King's College London London United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karren","family":"Towgood","sequence":"additional","affiliation":[{"name":"The Department of Clinical Neuroscience Institute of Psychiatry King's College London London United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gareth J.","family":"Barker","sequence":"additional","affiliation":[{"name":"The Department of Neuroimaging Institute of Psychiatry King's College London London United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark P.","family":"Richardson","sequence":"additional","affiliation":[{"name":"The Department of Clinical Neuroscience Institute of Psychiatry King's College London London United 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