{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T06:03:35Z","timestamp":1789625015518,"version":"build-2803163510"},"reference-count":35,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T00:00:00Z","timestamp":1789603200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Neurol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Systemic inflammation after acute ischemic stroke is usually assessed using admission biomarkers, which may not distinguish transient stress from sustained immune-inflammatory activation. We examined whether serial immune-inflammatory recovery trajectories were associated with early neurological deterioration (END) and 90-day functional outcome.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>This single-center retrospective cohort included 760 adults with acute ischemic stroke identified from a hospital stroke database. NLR, SII, SIRI, and hs-CRP measured at admission, 24\u202fh, 72\u202fh, and day 7 were log-transformed and standardized, and equally weighted values were averaged at each observed time point. Latent class mixed models with 2\u20135 classes were compared without using outcome information, and a five-class solution was selected before association and prediction analyses. The primary outcome was 90-day mRS 3\u20136. END was defined as an NIHSS increase of \u22652 points within 72\u202fh; the landmark END analysis excluded END within 24\u202fh and tested 0\u201324\u202fh immune change for END from 24 to 72\u202fh.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The five LCMM classes comprised 182 low-stable, 223 transient moderate, 161 delayed recovery, 122 persistent high, and 72 extreme persistent high patients. Among 751 patients with 90-day outcome data, the observed rate of mRS 3\u20136 increased from 21.5 to 30.6%, 44.2, 71.9, and 98.6% across these classes. After adjustment, persistent high (OR 2.46, 95% CI 1.31\u20134.61;\n                      <jats:italic>p<\/jats:italic>\n                      \u202f=\u202f0.005) and extreme persistent high inflammation (OR 20.24, 95% CI 2.48\u2013165.26;\n                      <jats:italic>p<\/jats:italic>\n                      \u202f=\u202f0.005) were associated with mRS 3\u20136; a bias-reduced sensitivity estimate for the extreme class remained large (OR 13.61, 95% CI 2.34\u201379.26). Ordinal analysis showed progressively worse mRS for delayed recovery (common OR 2.73), persistent high (4.18), and extreme persistent high (6.72). The 0\u201324\u202fh composite immune-change metric was not associated with landmark END (OR 1.12, 95% CI 0.92\u20131.36;\n                      <jats:italic>p<\/jats:italic>\n                      \u202f=\u202f0.265). Adding LCMM-5 to the clinical model increased AUC from 0.828 to 0.841, but did not clearly outperform adding admission NLR\/SII.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Longitudinal classification identified five immune-inflammatory recovery trajectories with a marked gradient in 90-day disability. Persistent-high and extreme persistent-high classes retained independent associations with poor functional outcome.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fneur.2026.1913111","type":"journal-article","created":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T05:31:12Z","timestamp":1789623072000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Serial immune-inflammatory recovery trajectories after acute ischemic stroke: associations with early neurological deterioration and 90-day functional outcome in a retrospective cohort"],"prefix":"10.3389","volume":"17","author":[{"given":"Ruihan","family":"Ni","sequence":"first","affiliation":[{"name":"Suzhou Medical College, Soochow University","place":["Suzhou, Jiangsu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lan","family":"Chu","sequence":"additional","affiliation":[{"name":"Suzhou Medical College, Soochow University","place":["Suzhou, Jiangsu, China"]},{"name":"Department of Neurology, Affiliated Hospital of Guizhou Medical University","place":["Guiyang, Guizhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,17]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","first-page":"401","DOI":"10.1038\/nrneurol.2012.98","article-title":"The immunology of acute stroke","volume":"8","author":"Chamorro","year":"2012","journal-title":"Nat Rev Neurol"},{"key":"ref2","doi-asserted-by":"publisher","first-page":"661","DOI":"10.1007\/s13311-016-0483-x","article-title":"Inflammation and stroke: an overview","volume":"13","author":"Anrather","year":"2016","journal-title":"Neurotherapeutics"},{"key":"ref3","doi-asserted-by":"publisher","first-page":"779","DOI":"10.1189\/jlb.1109766","article-title":"Inflammatory mechanisms in ischemic stroke: role of inflammatory 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