PMID- 18574546 OWN - NLM STAT- MEDLINE DCOM- 20080925 LR - 20230612 IS - 0942-0940 (Electronic) IS - 0001-6268 (Print) IS - 0001-6268 (Linking) VI - 150 IP - 8 DP - 2008 Aug TI - Elevation of monocyte chemoattractant protein-1 in patients experiencing neurocognitive decline following carotid endarterectomy. PG - 779-84; discussion 784 LID - 10.1007/s00701-008-1618-6 [doi] AB - BACKGROUND: Previous studies have demonstrated that elevated pre-operative monocyte count is an independent predictor of acute neurocognitive decline following carotid endarterectomy (CEA). Monocyte chemoattractant protein-1 (MCP-1), secreted by human endothelial and monocyte-like cells, is a potent mediator of inflammation and mononuclear cell trafficking. This study examines the relationship between peri-operative serum MCP-1 elevation and post-operative neurocognitive injury following CEA. METHODS: Fifty-two patients undergoing CEA and 67 lumbar laminectomy (LL) controls were administered a battery of five neuropsychological tests pre-operatively and on post-operative day 1 (POD 1). Change in individual test scores from baseline to POD 1 were converted into Z-score and used to develop a point system quantifying the degree of neurocognitive dysfunction relative to change within the LL group. Neurocognitive injury following CEA was defined as a score greater than 2 standard deviations above mean total deficit scores of LL controls. Serum MCP-1 levels were measured pre-operatively and on POD 1 by enzyme-linked immunosorbent assay. FINDINGS: Mean percent MCP-1 elevation was higher for the 13 injured CEA patients (147.7 +/- 32.4%) in our cohort compared to 39 age- and sex-matched uninjured CEA patients (76.0 +/- 16.5%). In unconditional multivariate logistic regression analysis, percent elevation in serum MCP-1 level was associated with neurocognitive injury one day after CEA (OR = 2.19, 95% CI = 1.13-4.26, P = 0.021, for a 100% elevation from pre-operative levels). CONCLUSIONS: Peri-operative elevations in serum MCP-1 levels correlate with acute neurocognitive dysfunction following CEA. These data implicate an inflammatory mechanism in the pathogenesis of Ischaemic neurocognitive decline. FAU - Mack, W J AU - Mack WJ AD - Department of Neurological Surgery, Columbia University Medical Center, New York, NY 10032, USA. FAU - Ducruet, A F AU - Ducruet AF FAU - Hickman, Z L AU - Hickman ZL FAU - Zurica, J AU - Zurica J FAU - Starke, R M AU - Starke RM FAU - Garrett, M C AU - Garrett MC FAU - Komotar, R J AU - Komotar RJ FAU - Quest, D O AU - Quest DO FAU - Solomon, R A AU - Solomon RA FAU - Heyer, E J AU - Heyer EJ FAU - Sander Connolly, E AU - Sander Connolly E LA - eng GR - M01 RR000645/RR/NCRR NIH HHS/United States GR - RR00645/RR/NCRR NIH HHS/United States GR - R01 AG017604/AG/NIA NIH HHS/United States GR - R01 AG017604-05A2/AG/NIA NIH HHS/United States GR - R01AG17604/AG/NIA NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural DEP - 20080623 PL - Austria TA - Acta Neurochir (Wien) JT - Acta neurochirurgica JID - 0151000 RN - 0 (Chemokine CCL2) SB - IM MH - Aged MH - Chemokine CCL2/*blood MH - Cognition Disorders/diagnosis/*immunology MH - *Endarterectomy, Carotid MH - Female MH - Follow-Up Studies MH - Humans MH - Laminectomy MH - Lumbar Vertebrae/surgery MH - Male MH - Neuropsychological Tests MH - Postoperative Complications/diagnosis/*immunology MH - Prospective Studies MH - Reference Values PMC - PMC2698290 MID - NIHMS114030 EDAT- 2008/06/25 09:00 MHDA- 2008/09/26 09:00 PMCR- 2009/06/18 CRDT- 2008/06/25 09:00 PHST- 2007/12/20 00:00 [received] PHST- 2008/05/28 00:00 [accepted] PHST- 2008/06/25 09:00 [pubmed] PHST- 2008/09/26 09:00 [medline] PHST- 2008/06/25 09:00 [entrez] PHST- 2009/06/18 00:00 [pmc-release] AID - 10.1007/s00701-008-1618-6 [doi] PST - ppublish SO - Acta Neurochir (Wien). 2008 Aug;150(8):779-84; discussion 784. doi: 10.1007/s00701-008-1618-6. Epub 2008 Jun 23.