{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,5]],"date-time":"2026-05-05T01:05:17Z","timestamp":1777943117713,"version":"3.51.4"},"reference-count":17,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2018,9,13]],"date-time":"2018-09-13T00:00:00Z","timestamp":1536796800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["International Journal of Stroke"],"published-print":{"date-parts":[[2019,2]]},"abstract":"<jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>To determine the role of inflammation in pediatric transient focal cerebral arteriopathy using cerebrospinal fluid cytokine\/chemokines as biomarkers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We measured 32 cytokine\/chemokines in acute cerebrospinal fluid collected from children with stroke due to focal cerebral arteriopathy (n\u2009=\u20095) using multiplex immunoassay and compared with two patients with arterial ischemic stroke due to other causes (non-focal cerebral arteriopathy group, vertebral dissection, n\u2009=\u20091; cryptogenic, n\u2009=\u20091), pediatric encephalitis (n\u2009=\u200943), and non-inflammatory neurological disease controls (n\u2009=\u200920).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Median age in the focal cerebral arteriopathy group was 9.3 years (range, 2.8\u201313 years). In the focal cerebral arteriopathy group (n\u2009=\u20095), four patients had middle cerebral\u2009\u00b1\u2009distal carotid arteriopathy; one patient had posterior circulation arteriopathy. The median time from symptom onset to cerebrospinal fluid sampling was four days (range, 0.6\u20137 days). Only IL-6, IL-8, CXCL1, and CXCL10 levels were significantly higher in the acute cerebrospinal fluid of focal cerebral arteriopathy patients compared to non-inflammatory neurological disease controls and non-focal cerebral arteriopathy stroke. In contrast to focal cerebral arteriopathy, a broad array of Th1, Th2, Treg, Th17, B-cell related, and other broad spectrum cytokine\/chemokines were elevated in encephalitis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>The elevated cerebrospinal fluid cytokine\/chemokines support innate, T cell, and granulocyte inflammatory mechanisms in children with focal cerebral arteriopathy. This warrants larger cohort studies to discriminate primary inflammatory signals of the arteriopathy from secondary inflammation due to the stroke itself.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/1747493018799975","type":"journal-article","created":{"date-parts":[[2018,9,13]],"date-time":"2018-09-13T07:21:14Z","timestamp":1536823274000},"page":"154-158","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":10,"title":["Elevation of cerebrospinal fluid cytokine\/chemokines involved in innate, T cell, and granulocyte inflammation in pediatric focal cerebral arteriopathy"],"prefix":"10.1177","volume":"14","author":[{"given":"Kavitha","family":"Kothur","sequence":"first","affiliation":[{"name":"Neuroimmunology Group, Institute for Neuroscience and Muscle Research, The University of Sydney, Sydney, Australia"},{"name":"TY Nelson Department of Neurology and Neurosurgery, The Children\u2019s Hospital at Westmead, Sydney, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christopher","family":"Troedson","sequence":"additional","affiliation":[{"name":"TY Nelson Department of Neurology and Neurosurgery, The Children\u2019s Hospital at Westmead, Sydney, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard","family":"Webster","sequence":"additional","affiliation":[{"name":"TY Nelson Department of Neurology and Neurosurgery, The Children\u2019s Hospital at Westmead, Sydney, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sushil","family":"Bandodkar","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, The Children\u2019s Hospital at Westmead, Sydney, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stephanie","family":"Chu","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology, Royal Prince Alfred Hospital, Sydney, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Louise","family":"Wienholt","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology, Royal Prince Alfred Hospital, Sydney, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alun","family":"Pope","sequence":"additional","affiliation":[{"name":"Statistical Consulting, The University of Sydney, Sydney, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark T","family":"Mackay","sequence":"additional","affiliation":[{"name":"Department of Neurology, Royal Children\u2019s Hospital, and University of Melbourne, Victoria, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0109-8877","authenticated-orcid":false,"given":"Russell C","family":"Dale","sequence":"additional","affiliation":[{"name":"Neuroimmunology Group, Institute for Neuroscience and Muscle Research, The University of Sydney, Sydney, Australia"},{"name":"TY Nelson Department of Neurology and Neurosurgery, The Children\u2019s Hospital at Westmead, Sydney, 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