Elevation of monocyte chemoattractant protein-1 in patients experiencing neurocognitive decline following carotid endarterectomy

W. J. Mack, A. F. Ducruet, Z. L. Hickman, J. Zurica, R. M. Starke, M. C. Garrett, R. J. Komotar, D. O. Quest, R. A. Solomon, E. J. Heyer, E. Sander Connolly

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)779-784
Number of pages6
JournalActa Neurochirurgica
Issue number8
StatePublished - Aug 2008
Externally publishedYes


  • Arteriolosclerosis
  • Brain ischemia
  • Carotid endarterectomy
  • Monocyte chemoattractant protein-1
  • Neuropsychological tests

ASJC Scopus subject areas

  • Clinical Neurology
  • Surgery


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