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Comparative Study
. 2006 May;58(5):844-50; discussion 844-50.
doi: 10.1227/01.NEU.0000209638.62401.7E.

Predictors of neurocognitive decline after carotid endarterectomy

Affiliations
Comparative Study

Predictors of neurocognitive decline after carotid endarterectomy

J Mocco et al. Neurosurgery. 2006 May.

Expression of concern in

  • Editorial Expression of Concern.
    [No authors listed] [No authors listed] Neurosurgery. 2023 Aug 1;93(2):489. doi: 10.1227/neu.0000000000002565. Epub 2023 Jun 9. Neurosurgery. 2023. PMID: 37293834 No abstract available.

Abstract

Objective: Although the incidence of stroke after carotid endarterectomy (CEA) is low (1-3%), approximately 25% of patients experience subtle declines in postoperative neuropsychometric function. No studies have investigated the risk factors for this neurocognitive change. We sought to identify predictors of postoperative neurocognitive dysfunction.

Methods: We enrolled 186 CEA patients, with both symptomatic and asymptomatic stenosis, to undergo a battery of neuropsychometric tests preoperatively and on postoperative Days 1 and 30. Neurocognitive dysfunction was defined as a two standard deviation decline in performance compared with a similarly aged control group of lumbar laminectomy patients. Univariate logistic regression was performed for age, sex, obesity, smoking, symptomatology, diabetes mellitus, hypertension, hypercholesterolemia, use of statin medication, previous myocardial infarction, previous CEA, operative side, duration of surgery, duration of carotid cross-clamp, and weight-adjusted doses of midazolam and fentanyl. Variables achieving univariate P < 0.10 were included in a multivariate analysis. Data is presented as (odds ratio, 95% confidence interval, P-value).

Results: Eighteen and 9% of CEA patients were injured on postoperative Days 1 and 30, respectively. Advanced age predicted neurocognitive dysfunction on Days 1 and 30 (1.93 per decade, 1.15-3.25, 0.01; and 2.57 per decade, 1.01-6.51, 0.049, respectively). Additionally, diabetes independently predicted injury on Day 30 (4.26, 1.15-15.79, 0.03).

Conclusions: Advanced age and diabetes predispose to neurocognitive dysfunction after CEA. These results are consistent with risk factors for neurocognitive dysfunction after coronary bypass and major stroke after CEA, supporting an underlying ischemic pathophysiology. Further work is necessary to determine the role these neurocognitive deficits may play in appropriately selecting patients for CEA.

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Figures

FIGURE 1
FIGURE 1
Incidence of neurocognitive decline on postoperative Day 1 by age. The rates of neurocognitive decline on Day 1 for patients younger than 65 years, 65 to 74 years, and older than 74 years of age are 9.3, 14.9, and 28.6%, respectively (Kruskal-Wallis ANOVA P = 0.03).
FIGURE 2
FIGURE 2
Incidence of neurocognitive decline at Day 30 by diabetes status. On Day 30, 21.1% of diabetics and 5.3% of non-diabetics experienced significant declines in NPMT performance (Fisher P = 0.007). DM, diabetes mellitus.

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