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

Mack, William J.; Ducruet, Andrew F; Hickman, Zachary L.; Zurica, Joseph; Starke, Robert M.; Garrett, Maria Carolina; Komotar, Ricardo J.; Quest, Donald O.; Solomon, Robert A.; Heyer, Éric; Connolly, E. Sander

doi:10.1007/s00701-008-1618-6

Cited by 9 publications

(10 citation statements)

References 25 publications

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“…Endothelial cells, macrophage-like cells, and neurons all express MCP-1 in the ischemic brain. Animal models studies suggest that MCP-1 contributes to exaggerate responses to ischaemia/reperfusion injury, and immunoneutralization of MCP-1 results in decreased infarct size (Mack et al 2008). Furthermore, elevated MCP-1 protein levels have been demonstrated in human cerebrospinal fluid 24 h after stroke.…”

Section: Discussionmentioning

confidence: 95%

Pretreatment with Lornoxicam, a Cyclooxygenase Inhibitor, Relieves Postoperative Immuno-Suppression after Total Abdominal Hysterectomy

Jiao

Ren

2009

Tohoku J. Exp. Med.

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Section: Discussionmentioning

confidence: 95%

Pretreatment with Lornoxicam, a Cyclooxygenase Inhibitor, Relieves Postoperative Immuno-Suppression after Total Abdominal Hysterectomy

Jiao

Ren

2009

Tohoku J. Exp. Med.

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“…MCP-1 has also been shown to attract monocytes to the brain during stress and has exhibited increased expression in the brains of suicide victims (Torres-Platas et al, 2014). Although no study has reported a significant relationship between MCP-1 and psychomotor slowing, it has been associated with cognitive impairment in multiple clinical populations including first episode psychosis (Martinez-Cengotitabengoa et al, 2012), mild cognitive impairment and early stage Alzheimer’s Disease (Galimberti et al, 2006; Westin et al, 2012), HIV-associated cognitive deficits (Yuan et al, 2015), and neurocognitive deficits post carotid endarterectomy (Mack et al, 2008). …”

Section: Discussionmentioning

confidence: 99%

Inflammatory markers are associated with decreased psychomotor speed in patients with major depressive disorder

Goldsmith

Haroon

Woolwine

et al. 2016

Brain, Behavior, and Immunity

109

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Previous data have demonstrated that administration of inflammatory cytokines or their inducers leads to altered basal ganglia function associated with reduced psychomotor speed. Decreased psychomotor speed, referred to clinically as psychomotor retardation, is a cardinal symptom of major depressive disorder (MDD) and has been associated with poor antidepressant treatment response. We therefore examined the association between plasma inflammatory markers and psychomotor speed in ninety-three un-medicated patients with MDD. Psychomotor speed was assessed by a range of neuropsychological tests from purely motor tasks (e.g. movement latency and finger tapping) to those that involved motor activity with increasing cognitive demand and cortical participation (e.g. Trails A and Digit Symbol Substitution Task (DSST)). Linear regression analyses were performed to determine the relationship of inflammatory markers and psychomotor task performance controlling for age, race, sex, education, body mass index, and severity of depression. MDD patients exhibited decreased psychomotor speed on all tasks relative to normative standards. Increased IL-6 was associated with decreased performance on simple and choice movement time tasks, whereas MCP-1 was associated with decreased performance on the finger tapping task and DSST. IL-10 was associated with increased performance on the DSST. In an exploratory principle component analysis including all psychomotor tasks, IL-6 was associated with the psychomotor speed factor. Taken together, the data indicate that a peripheral inflammatory profile including increased IL-6 and MCP-1 is consistently associated with psychomotor speed in MDD. These data are consistent with data demonstrating that inflammation can affect basal ganglia function, and indicate that psychomotor speed may be a viable outcome variable for anti-inflammatory therapies in depression and other neuropsychiatric disorders with increased inflammation.

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“…Because the incidence of perioperative stroke is exceedingly rare, investigators are studying subtler forms of neurological injury, such as eCD, to increase the neurological safety of this commonly performed procedure. A number of studies have attempted to elucidate the underlying pathophysiology of this eCD, 3,12,13,18,20,21,31 because it is exhibited by approximately 25% of patients after CEA. This is the first study to evaluate the adequacy of cerebral collateral circulation as a predictor of eCD after CEA.…”

Section: Discussionmentioning

confidence: 99%

“…All CEA procedures were performed under general anesthesia with routine monitoring as well as continuous electroencephalographic monitoring to detect cerebral ischemia, as previously described. 3,12,13,18,20,21,31 An intraoperative CA shunt was placed in 4 patients with significant electroencephalographic changes consistent with cerebral ischemia, and these patients were subsequently excluded from this study. The remaining 38 patients were included in the statistical analysis.…”

Section: Study Subjectsmentioning

confidence: 99%

Radiographic absence of the posterior communicating arteries and the prediction of cognitive dysfunction after carotid endarterectomy

Sussman¹,

Kellner

Mergeche³

et al. 2014

JNS

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Object Approximately 25% of patients exhibit cognitive dysfunction 24 hours after carotid endarterectomy (CEA). One of the purported mechanisms of early cognitive dysfunction (eCD) is hypoperfusion due to inadequate collateral circulation during cross-clamping of the carotid artery. The authors assessed whether poor collateral circulation within the circle of Willis, as determined by preoperative CT angiography (CTA) or MR angiography (MRA), could predict eCD. Methods Patients who underwent CEA after preoperative MRA or CTA imaging and full neuropsychometric evaluation were included in this study (n = 42); 4 patients were excluded due to intraoperative electroencephalographic changes and subsequent shunt placement. Thirty-eight patients were included in the statistical analyses. Patients were stratified according to posterior communicating artery (PCoA) status (radiographic visualization of at least 1 PCoA vs of no PCoAs). Variables with p < 0.20 in univariate analyses were included in a stepwise multivariate logistic regression model to identify predictors of eCD after CEA. Results Overall, 23.7% of patients exhibited eCD. In the final multivariate logistic regression model, radiographic absence of both PCoAs was the only independent predictor of eCD (OR 9.64, 95% CI 1.43–64.92, p = 0.02). Conclusions The absence of both PCoAs on preoperative radiographic imaging is predictive of eCD after CEA. This finding supports the evidence for an underlying ischemic etiology of eCD. Larger studies are justified to verify the findings of this study. Clinical trial registration no.: NCT00597883 (http://www.clinicaltrials.gov).

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

Cited by 9 publications

References 25 publications

Pretreatment with Lornoxicam, a Cyclooxygenase Inhibitor, Relieves Postoperative Immuno-Suppression after Total Abdominal Hysterectomy

Pretreatment with Lornoxicam, a Cyclooxygenase Inhibitor, Relieves Postoperative Immuno-Suppression after Total Abdominal Hysterectomy

Inflammatory markers are associated with decreased psychomotor speed in patients with major depressive disorder

Radiographic absence of the posterior communicating arteries and the prediction of cognitive dysfunction after carotid endarterectomy

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