Serum S100B Protein Levels Are Correlated with Subclinical Neurocognitive Declines after Carotid Endarterectomy

Abstract

OBJECTIVE-Carotid endarterectomy (CEA) is an effective means of stroke prevention among appropriately selected patients; however, neuropsychometric testing has revealed subtle cognitive injuries in the early postoperative period. The purpose of this study was to establish whether serum levels of two biochemical markers of cerebral injury were correlated with postoperative declines in neuropsychometric test performance after CEA. METHODS-Fifty-five consecutive patients underwent a battery of neuropsychometric tests 24hours before and 24 hours after elective CEA. Two patients were excluded because of postoperative strokes. The pre-and postoperative serum levels of S100B protein and neuronspecific enolase for injured patients, defined as those who exhibited significant declines in neuropsychometric test performance (n = 12), were compared with the levels for uninjured patients (n = 41).RESULTS-There were no significant differences in the baseline S100B levels for the two groups. Injured patients exhibited significantly higher S100B levels, compared with uninjured patients, at 24, 48, and 72 hours after surgery (P < 0.05). There were no significant differences in neuron-specific enolase levels for injured and uninjured patients at any time point.CONCLUSION-These data suggest that subtle cerebral injuries after CEA, even in the absence of overt strokes, are associated with significant increases in serum S100B but not neuron-specific enolase levels. Analyses of earlier time points in future studies of subtle cognitive injuries and biochemical markers of cerebral injury after CEA may be revealing. KeywordsCarotid endarterectomy; Cerebral ischemia; Neuron-specific enolase; Neuropsychological tests; S100B Carotid endarterectomy (CEA) is an effective means to prevent stroke among patients at high risk. Although the risk of major stroke after CEA is relatively low, the incidence of subtle cognitive injuries, as revealed by neuropsychometric tests (NPMTs), is quite high (4,6,11). NPMTs are sensitive measures of subtle neurological dysfunctions that are not revealed in routine neurological examinations. We recently demonstrated that as many as A variety of biochemical markers of severe neurological injury have been described. Neuron-specific enolase (NSE) is a glycolytic enzyme found in neurons and neuroendocrine cells (19). The calcium-binding protein S100B is an important participant in neuronal and glial cell-cell communication and intracellular signal transduction and exhibits its highest levels of expression in the nervous system (33). These molecules have been demonstrated to be markers of cerebral injury in animal models of stroke (1,9) and among human stroke patients (3,5,21,23,27).Among patients with cerebral infarctions, high S100B levels were correlated with mildly poorer performance on NPMTs, but these results did not reach significance (32). Another study demonstrated no correlation between increased NSE and S100B levels and a decline in performance on NPMTs after CEA (25). In that study, however, the au...

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

“…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.…”

“…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.…”

“…Age was dichotomized at 75 years and treated as a categorical variable (> 75 or ≤ 75 years). 3,21,31,32 All other factors were also treated categorically, and the results are presented as percentages of patients who satisfy the criteria for that variable. For univariate analyses, Student t-test, Wilcoxon rank-sum test, Fisher exact test, Pearson chi-square test, and simple logistic regression were used where appropriate.…”

“…8,9,11,12,21,27 The underlying pathophysiology of this early cognitive dysfunction (eCD) is not completely understood, but data from a number of studies suggest that ischemic injury is a contributing factor, 3,21,31,32 related to hypoperfusion during intraoperative CA cross-clamping and/or to dislodgment of atheroemboli during vessel dissection and plaque removal.…”

Brain injury markers (S100B and NSE) in chronic cocaine dependents

“…Some studies show a correlation between S100B levels and neuropsychological functions in patients with brain trauma and cardiac surgery. 24,[44][45] Other authors comment that there is no direct correlation between serum concentrations of S100B and cognitive function. 46 We could also think that maybe cocaine use did not elicit large damage in the subjects, and their chronic cocaine use did not cause neurobiological and physiological injuries that could explain the cognitive deficits.…”