{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T22:17:10Z","timestamp":1790806630213,"version":"4.1.0"},"reference-count":88,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,10]]},"abstract":"<jats:sec>\n                    <jats:title>OBJECTIVE<\/jats:title>\n                    <jats:p>In the histopathological examination of treatment-resistant epilepsy, focal cortical dysplasia (FCD) is the most common diagnosis in the pediatric group. FCD is classified histopathologically according to the International League Against Epilepsy (ILAE) classification. In the last decade since the ILAE classification has been released, molecular genetic studies have revealed mTOR pathway\u2013related mutations as a major etiology. The objective of this study was to determine the incidence of FCD in treatment-resistant epilepsy patients, explore histomorphological and immunohistochemical features, examine clinicopathological correlation, demonstrate mTOR pathway activation using a pS6 antibody immunohistochemically, and try to introduce a candidate for possible targeted therapies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>Paraffin blocks and slides of tissue from patients with treatment-resistant epilepsy were reexamined retrospectively. Histopathological subtypes of FCD were determined according to the ILAE classification. NeuN and neurofilament H (NF-H) staining were performed, and additionally a pS6 antibody was used to demonstrate mTOR pathway activation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>In 32 cases diagnosed with FCD, or 17.5% of 183 surgical epilepsy materials, there were no significant differences in the statistical analysis of clinical variables between the ILAE FCD subtypes. Recommended antibody NeuN revealed microcolumnar alignment in the FCD type Ia and IIIa groups and the loss of lamination in the type Ib group. Another recommended antibody, NF-H, was not found to be useful in discriminating between normal and dysmorphic neurons. pS6 expression, showing mTOR pathway activation, was observed in dysmorphic neurons and balloon cells in all FCD type II cases.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS<\/jats:title>\n                    <jats:p>\n                      Significant pS6 expression in FCD type II represents the genomic nature of the disease noted in the literature. Nevertheless, the known\n                      <jats:italic>MTOR<\/jats:italic>\n                      gene and mTOR pathway\u2013related mutations remain behind proportionally to explain the mTOR pathway activation in all FCD type II cases. Clinicopathologically and genetically integrated classification and usage of mTOR pathway inhibitors in treatment are expected as a recent evolution.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3171\/2022.7.focus21731","type":"journal-article","created":{"date-parts":[[2022,10,1]],"date-time":"2022-10-01T10:22:18Z","timestamp":1664619738000},"page":"E6","source":"Crossref","is-referenced-by-count":8,"title":["Focal cortical dysplasia pathology: diagnostic difficulty, classification, and utility for pathogenesis"],"prefix":"10.3171","volume":"53","author":[{"given":"Ozge","family":"Kapar","sequence":"first","affiliation":[{"name":"Department of Pathology, Istanbul University;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zahide Mail","family":"Gurkan","sequence":"additional","affiliation":[{"name":"Department of Neurology and Clinical Neurophysiology, Istanbul University;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Muge","family":"Dolgun","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Sultangazi Haseki Training and Research Hospital;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Altay","family":"Sencer","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Istanbul Faculty of Medicine, Istanbul University; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Candan","family":"G\u00fcrses","sequence":"additional","affiliation":[{"name":"Department of Neurology, Koc University, Istanbul, Turkey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bilge","family":"Bilgic","sequence":"additional","affiliation":[{"name":"Department of Pathology, Istanbul University;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1754","reference":[{"issue":"17","key":"b1","series-title":"N Engl J Med","doi-asserted-by":"publisher","first-page":"1648","DOI":"10.1056\/NEJMoa1703784","article-title":"Histopathological findings in brain tissue obtained during epilepsy surgery","volume":"377","author":"Blumcke I","year":"2017","unstructured":"Blumcke I, Spreafico R, Haaker G,  Histopathological findings in brain tissue obtained during epilepsy surgery. 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