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Biomedical subjects

E S Connolly

Publications and source records attributed to E S Connolly.

At least 19 recordsLinked to original sources
PubMed2006

Predictors of hemorrhage in patients with untreated brain arteriovenous malformation.

BACKGROUND: Intracranial hemorrhage is a serious possible complication in patients with brain arteriovenous malformation (AVM). Several morphologic factors associated with hemorrhagic AVM presentation have been established, but their relevance for the risk of subsequent AVM hemorrhage remains unclear. METHODS: The authors analyzed follow-up data on 622 consecutive patients from the prospective Columbia AVM database, limited to the period between initial AVM diagnosis and the start of treatment (i.e., any endovascular, surgical, or radiation therapy). Univariate and multivariate logistic regression and Cox proportional hazard models were applied to analyze the effect of patient age, gender, AVM size, anatomic location, venous drainage pattern, and associated arterial aneurysms on the risk of intracranial hemorrhage at initial presentation and during follow-up. RESULTS: The mean pretreatment follow-up was 829 days (median: 102 days), during which 39 (6%) patients experienced AVM hemorrhage. Increasing age (hazard ratio [HR] 1.05, 95% CI 1.03 to 1.08), initial hemorrhagic AVM presentation (HR 5.38, 95% CI 2.64 to 10.96), deep brain location (HR 3.25, 95% CI 1.30 to 8.16), and exclusive deep venous drainage (HR 3.25, 95% CI 1.01 to 5.67) were independent predictors of subsequent hemorrhage. Annual hemorrhage rates on follow-up ranged from 0.9% for patients without hemorrhagic AVM presentation, deep AVM location, or deep venous drainage to as high as 34.4% for those harboring all three risk factors. CONCLUSIONS: Hemorrhagic arteriovenous malformation (AVM) presentation, increasing age, deep brain location, and exclusive deep venous drainage appear to be independent predictors for AVM hemorrhage during natural history follow-up. The risk of spontaneous hemorrhage may be low in AVMs without these risk factors.

Adolescent↗
PubMed2006

Shunt failure in idiopathic intracranial hypertension presenting with spontaneous cerebrospinal fluid leak.

A case of spontaneous cerebrospinal (CSF) fluid leak after ventriculoperitoneal shunt (VPS) failure in a patient with idiopathic intracranial hypertension (IIH) is reported. This is the first report of spontaneous CSF leak in an IIH patient without a history of trauma, sinus surgery, or intracranial surgery. The diagnosis was confirmed using thin-sliced post-contrast computed tomography, which revealed a micro-dehiscence of the cribiform plate at the superior aspect of the ethmoid sinus. The patient underwent VPS revision without complication, resulting in complete amelioration of symptoms and cessation of CSF rhinorrhoea at 1 year follow up.

Cerebrospinal Fluid Rhinorrhea↗
PubMed2006

Correlation of cerebral metabolites with functional outcome in experimental primate stroke using in vivo 1H-magnetic resonance spectroscopy.

BACKGROUND AND PURPOSE: Ensuring the translatability of primate stroke models is critical for preclinical testing of cerebroprotective strategies, and such models would benefit from further characterization of the experimental ischemic tissue. Our purpose was to examine the cerebral metabolic response to stroke in baboons with MR spectroscopy and to correlate metabolite levels with functional neurologic outcomes. METHODS: Seven baboons underwent 1 hour of middle cerebral artery occlusion. At 3 and 10 days, each animal was imaged with traditional MR imaging and multivoxel proton (1)H-MR spectroscopy, and a neurologic examination was performed. Spectra obtained from the infarcted hemisphere of each animal were compared with the contralateral hemisphere, and metabolite levels were correlated with neurologic outcome scores. RESULTS: Spectra obtained at 3 days postischemia revealed prominent lactate (LAC) resonances and attenuated N-acetylaspartate (NAA) peaks in infarcted hemispheres. Ten-day spectra showed persistence of these findings in animals with large strokes (>30% of the hemisphere), with partial normalization of the spectra in animals with small strokes (<30% of the hemisphere). Mean area under the curve from LAC spectra had a negative correlation with functional outcome by 2 different scoring systems (r(2) = 0.72 and 0.73), whereas NAA showed a positive correlation (r(2) = 0.79 and 0.62). CONCLUSIONS: The metabolic alterations observed in our primate model of reperfused ischemia by (1)H-MR spectroscopy recapitulate those seen in clinical stroke. Furthermore, correlations between LAC and NAA peaks with functional outcome further suggest that MR spectroscopy may play a role in outcome prediction following cerebral infarction in higher primates.

Animals↗
PubMed2005

APOE-epsilon4 predisposes to cognitive dysfunction following uncomplicated carotid endarterectomy.

BACKGROUND: Between 9% and 23% of patients undergoing otherwise uncomplicated carotid endarterectomy (CEA) develop subtle cognitive decline 1 month postoperatively. The APOE-epsilon4 allele has been associated with worse outcome following stroke. OBJECTIVE: To investigate the ability of APOE-epsilon4 to predict post-CEA neurocognitive dysfunction. METHODS: Seventy-five patients with CEA undergoing elective CEA were prospectively recruited in this nested cohort study and demographic variables were recorded. Patients were evaluated before and 1 month after surgery with a standard battery of five neuropsychological tests. APOE genotyping was performed by restriction fragment length polymorphism analysis in all patients. Neuropsychological deficits were identified by comparing changes (before to 1 month post-operation) in individual performance on the test battery. Logistic regression was performed for APOE-epsilon4 and previously identified risk factors. RESULTS: Twelve of 75 (16%) CEA patients possessed the APOE-epsilon4 allele. Eight of 75 (11%) patients experienced neurocognitive dysfunction on postoperative day 30. One month post-CEA, APOE-epsilon4-positive patients were more likely to be cognitively injured (42%) than APOE-epsilon4-negative patients (5%) (p = 0.002). In multivariate analysis, the presence of the APOE-epsilon4 allele increased the risk of neurocognitive dysfunction at 1 month 62-fold (62.28, 3.15 to 1229, p = 0.007). Diabetes (51.42, 1.94 to 1363, p = 0.02), and obesity (24.43, 1.41 to 422.9, p = 0.03) also predisposed to injury. CONCLUSION: The APOE-epsilon4 allele is a robust independent predictor of neurocognitive decline 1 month following CEA.

Aged↗
PubMed2004

Anti-adhesion molecule strategies as potential neuroprotective agents in cerebral ischemia: a critical review of the literature.

Despite recent advances in the understanding of the pathophysiology of cerebral ischemia, current approaches attempting to prevent ischemic brain damage after an acute stroke remain quite inadequate. Today, ischemic stroke remains the third leading cause of death in industrialized nations, and the leading cause of disability requiring long term institutional care in the U.S and other industrialized nations. While one treatment, tissue plasminogen activator, has shown efficacy in clinical trials, safety concerns limit its role in clinical practice to a narrow time window of use. Acute cerebral ischemia has been shown to evoke a profound and deleterious upregulation of the inflammatory response, initiated within the cerebral microvasculature. Recently, research efforts have focused on targeting individual components of the inflammatory cascade, such as leukocyte activation and adhesion, in an attempt to develop potential neuroprotective agents. While these strategies have shown promise preclinically, clinical trials have yet to show clear benefit. Here, we review the current understanding of the pathophysiologic consequences of acute cerebral ischemic injury. Additionally, we discuss the role of the inflammatory cascade, with specific attention given to the deleterious role played by leukocyte activation and adhesion in stroke. Finally, relevant efforts to translate these basic science observations into clinical efficacy in acute stroke trials are critically reviewed.

Animals↗
PubMed2003

Laser Doppler flowmetry in non-human primate stroke studies: model refinement for pre-clinical development of cerebroprotective strategies.

BACKGROUND: Safety, feasibility, and efficacy trials in non-human primate stroke models are essential to the evaluation of experimental therapies and their translation to humans. Although Laser Doppler Flowmetry has been successfully employed in rodent stroke to continuously monitor cerebral blood flow, it has not been applied in primate studies. This investigation examined the utility of Laser Doppler Flowmetry in refining an existing baboon model of cerebral ischemia/reperfusion. METHOD: Continuous Laser Doppler Flowmetry monitoring was used, in non-human primates, to document local cerebral blood flow before, during, and after middle cerebral artery territory occlusion. In each baboon (n = 7) a single Doppler probe was placed into the left frontal cortex through a precoronal burr hole. Correlations between Laser Doppler Flowmetry values and latencies to Motor Evoked Potential dropout were compared using a linear regression model. FINDINGS: Placement of the Laser Doppler probe was easily accomplished in all animals. Laser Doppler Flowmetry tracings accurately documented blood flow changes that occurred with each technical manipulation during the procedure. Laser Doppler confirmed decreased perfusion that coincided both regionally and temporally with vessel occlusion. Depth of ischemia as measured by Laser Doppler Flowmetry was associated with Motor Evoked Potential dropout latencies for individual animals. CONCLUSIONS: Continuous, single probe Laser Doppler Flowmetry is a reliable method of documenting perfusion changes following middle cerebral artery territory occlusion in a baboon model of reperfused stroke. This advanced intraoperative monitoring technique may lead to more accurate evaluation of acute stroke therapies in pre-clinical trials.

Animals↗
PubMed2003

Predictors and clinical impact of epilepsy after subarachnoid hemorrhage.

OBJECTIVE: To determine the frequency, predictors, and impact on outcome of epilepsy developing during the first year after subarachnoid hemorrhage (SAH). METHODS: The authors prospectively analyzed 247 of 431 patients with SAH treated over a period of 5 years who were alive with follow-up at 12 months. Epilepsy was defined as two or more unprovoked seizures after hospital discharge. RESULTS: New-onset epilepsy occurred in 7% (n = 17) of patients; an additional 4% (n = 10) had only one seizure after discharge. Independent predictors of epilepsy included subdural hematoma (OR 9.9, 95% CI 1.9 to 52.8) and cerebral infarction (OR 3.9, 95% CI 1.4 to 11.3). Unlike those without seizures, patients who developed epilepsy failed to experience functional recovery on the modified Rankin Scale (mRS) between 3 and 12 months after SAH. At 12 months epilepsy was independently associated with severe disability (score >/= 3) on the mRS (OR 10.3, 95% CI 2.5 to 42.0), increased instrumental disability on the Lawton Instrumental Activities of Daily Living scale (OR 4.9; 95% CI 1.1 to 22.2), reduced quality of life on the Sickness Impact Profile (OR 4.5; 95% CI 1.1 to 18.0), and increased state anxiety on the Spielberger Anxiety Inventory (OR 4.8; 95% CI 1.1 to 20.4). Epilepsy was not associated with cognitive impairment, depression, or subjective life satisfaction. CONCLUSION: Epilepsy occurred in 7% of patients with SAH, was predicted by subdural hematoma and cerebral infarction, and was associated with poor functional recovery and quality of life. Our findings indicate that focal pathology, rather than diffuse injury from hemorrhage, is the principal cause of epilepsy after SAH.

Activities of Daily Living↗
PubMed2002

Global and domain-specific cognitive impairment and outcome after subarachnoid hemorrhage.

BACKGROUND: Cognitive dysfunction is the most common form of neurologic impairment after subarachnoid hemorrhage (SAH). OBJECTIVE: To evaluate the impact of global and domain-specific cognitive impairment on functional recovery and quality of life (QOL) after SAH. METHODS: One hundred thirteen patients (mean age 49 years; 68% women) were evaluated 3 months after SAH. Three simple tests of global mental status and neuropsychological tests to assess seven specific cognitive domains were administered. Four aspects of outcome (global handicap, disability, emotional status, and QOL) were compared between cognitively impaired and unimpaired patients with analysis-of-covariance models controlling for age, race/ethnicity, and education. Multiple linear regression was used to evaluate the relative contribution of global and domain-specific cognitive status for predicting concurrent modified Rankin Scale (mRS) and Sickness Impact Profile (SIP) scores. RESULTS: Impairment of global mental status on the Telephone Interview of Cognitive Status (TICS) was associated with poor performance in all seven cognitive domains (all p < 0.0005) and was the only cognitive measure associated with poor recovery in all four aspects of outcome (all p < or = 0.005). Cognitive impairment in four specific domains was also associated with functional disability or reduced QOL. After accounting for global cognitive impairment with the TICS, however, neuropsychological testing did not contribute additional predictive value for concurrent mRS or SIP total scores. CONCLUSIONS: Cognitive impairment impacts broadly on functional status, emotional health, and QOL after SAH. The TICS may be a useful alternative to more detailed neuropsychological testing for detecting clinically relevant global cognitive impairment after SAH.

Adult↗
PubMed2002

Dysplastic vessels after surgery for brain arteriovenous malformations.

BACKGROUND AND PURPOSE: The cause and clinical significance of residual dysplastic vessels after surgery for brain arteriovenous malformations (AVM) are unclear. We studied predictors and frequency of residual dysplastic vessels on cerebral angiography after AVM surgery. METHODS: The 240 prospectively enrolled surgical patients from the New York AVM Databank underwent 269 AVM-related surgical procedures. Reported postoperative brain angiographic findings were classified post hoc as showing (1) persistent dysplastic vessels, (2) a residual AVM, (3) focal hyperemia in the surgical bed, (4) other changes, or (5) a normal angiogram. Univariate and multivariate models were applied to test for an association between residual dysplastic vessels and patient age, sex, preoperative AVM size, anatomic AVM location, number of embolization procedures before surgery, and the time interval between AVM surgery and the postoperative angiogram. RESULTS: Of the 224 documented postoperative angiograms, 78 (35%) showed dysplastic vessels, 24 (11%) had evidence for a residual AVM, 16 (7%) showed focal hyperemia, 6 (2%) revealed other findings, and 100 (45%) were normal. The number of cases showing angiographic evidence for dysplastic vessels was significantly associated with increasing size of the AVM (in millimeter increments; P=0.0001); the mean diameter of AVMs in patients showing dysplastic vessels after surgery was significantly larger (41 mm, SD +/-14) than in those without residual dysplastic vessels (27 mm, SD +/-13; P<0.001). Symptomatic postoperative intracerebral hemorrhage occurred in 4 patients (1%), in 2 of whom dysplastic vessels were seen on the postoperative angiogram. CONCLUSIONS: The findings suggest that persistent dysplastic vessels may be found in approximately one third of angiograms after AVM surgery. Preoperative AVM size was found to be an independent predictor for the occurrence of dysplastic vessels on the postoperative angiogram.

Adult↗
PubMed2001

The baboon (Papio anubis) extracranial carotid artery: an anatomical guide for endovascular experimentation.

BACKGROUND: As novel endovascular strategies are developed for treating neurological disease, there is an increasing need to evaluate these techniques in relevant preclinical models. The use of non-human primates is especially critical given their structural and physiological homology with humans. In order to conduct primate endovascular studies, a comprehensive understanding of the carotid anatomy is necessary. We therefore performed a detailed examination of the vessel lengths, lumen diameters and angles of origin of the baboon extracranial carotid system. METHODS: We characterized the extracranial carotid system often male baboons (Papio anubis, range 15.1-28.4 kg) by early post-mortem dissection. Photographic documentation of vessel lengths, lumen diameters, and angles of origin were measured for each segment of the carotid bilaterally. RESULTS: The common carotid arteries averaged 94.7 +/- 1.7 mm (left) and 87.1 +/- 1.6 mm (right) in length. The average minimal common carotid lumen diameters were 3.0 +/- 0.3 mm (left) and 2.9 +/- 0.2 mm (right). Each animal had a common brachiocephalic artery arising from the aorta which bifurcated into the left common carotid artery and right braciocephalic artery after 21.5 +/- 1.6 mm. The vascular anatomy was found to be consistent among animals despite a wide range of animal weights. CONCLUSIONS: The consistency in the Papio anubis extracranial carotid system may promote the use of this species in the preclinical investigation of neuro-interventional therapies.

Animals↗
PubMed2001

Epidemiology and natural history of arteriovenous malformations.

The epidemiology and natural history of cerebral arteriovenous malformations (AVMs) remains incompletely elucidated. Several factors are responsible. With regard to the incidence and prevalence of AVMs, the results of prior studies have suffered because of the retrospective design, the use of nonspecific ICD-9 codes, and a focus on small genetically isolated populations. Recent data from the New York Islands AVM Hemorrhage Study, an ongoing, prospective, population-based survey determining the incidence of AVM-related hemorrhage and the associated rates of morbidity and mortality in a zip code-defined population of 10 million people, suggests that the AVM detection rate is 1.21/100,000 person-years (95% confidence interval [CI] 1.02-1.42) and the incidence of AVM-hemorrhage is 0.42/100,000 person-years (95% CI 0.32-0.55). Contemporaneous data from the Northern Manhattan Stroke Study, a prospective, longitudinal population-based study of nearly 150,000 patients in which the focus is to define the incidence of stroke, suggest the crude incidence for first-ever AVM-related hemorrhage to be 0.55/100,000 person-years (95% CI 0.11-1.61). Efforts are ongoing to study the natural history of both ruptured and unruptured AVMs in these datasets to examine the relevance of prior studies of patients selected for conservative follow up in Finland. In addition, data are being gathered to determine whether risk factors for future hemorrhage, which have previously been established in small case series, are valid when applied to whole populations. Together, these data should help inform therapeutic decisionmaking.

Adult↗
PubMed2001

Dehydroascorbic acid, a blood-brain barrier transportable form of vitamin C, mediates potent cerebroprotection in experimental stroke.

Neuronal injury in ischemic stroke is partly mediated by cytotoxic reactive oxygen species. Although the antioxidant ascorbic acid (AA) or vitamin C does not penetrate the blood-brain barrier (BBB), its oxidized form, dehydroascorbic acid (DHA), enters the brain by means of facilitative transport. We hypothesized that i.v. DHA would improve outcome after stroke because of its ability to cross the BBB and augment brain antioxidant levels. Reversible or permanent focal cerebral ischemia was created by intraluminal middle cerebral artery occlusion in mice treated with vehicle, AA, or DHA (40, 250, or 500 mg/kg), either before or after ischemia. Given before ischemia, DHA caused dose-dependent increases in postreperfusion cerebral blood flow, with reductions in neurological deficit and mortality. In reperfused cerebral ischemia, mean infarct volume was reduced from 53% and 59% in vehicle- and AA-treated animals, respectively, to 15% in 250 mg/kg DHA-treated animals (P < 0.05). Similar significant reductions occurred in nonreperfused cerebral ischemia. Delayed postischemic DHA administration after 15 min or 3 h also mediated improved outcomes. DHA (250 mg/kg or 500 mg/kg) administered at 3 h postischemia reduced infarct volume by 6- to 9-fold, to only 5% with the highest DHA dose (P < 0.05). In contrast, AA had no effect on infarct volumes, mortality, or neurological deficits. No differences in the incidence of intracerebral hemorrhage occurred. Unlike exogenous AA, DHA confers in vivo, dose-dependent neuroprotection in reperfused and nonreperfused cerebral ischemia at clinically relevant times. As a naturally occurring interconvertible form of AA with BBB permeability, DHA represents a promising pharmacological therapy for stroke based on its effects in this model of cerebral ischemia.

Animals↗
PubMed2001

Molecular analysis of the prostate-specific antigen upstream gene enhancer.

BACKGROUND: Our objective was to identify factors other than androgen receptor that bind to and regulate the prostate-specific antigen (PSA) upstream gene enhancer (PSE). METHODS: DNAse I footprinting and electromobility shift assays (EMSA) were performed over the PSE using lysates from PSA-producing cell lines, LNCaP and LAPC4, and nonproducing PSA cell lines, PC-3 cells, U937 monocytes, and Namalwa B cells. Mutational analysis and transient transfection assays were used to determine the contributions made by different elements towards the regulation of the enhancer. RESULTS: Three distinct regions surrounding androgen response elements of the PSE were found to bind unknown ubiquitous and cell type-specific proteins. These regions, when mutated in a PSE reporter construct, were shown to be required for maximal activation in LNCaP cells. CONCLUSIONS: These results correlate unknown sequence-specific DNA binding proteins with androgen-mediated regulation of a prostate-specific gene, thus providing further insight into the mechanism of PSA gene expression.

Base Sequence↗
PubMed2001

Influence of smoking, hypertension, and sex on the phenotypic expression of familial intracranial aneurysms in siblings.

OBJECTIVE: To investigate the effects of smoking, hypertension, and sex on the phenotypic expression of familial intracranial aneurysms (FIAs). METHODS: We retrospectively reviewed the case records of 806 consecutive patients undergoing aneurysm surgery at our institution (1986-1995) and discovered 24 families with at least two affected siblings. Prevalence rates for the smoking, hypertension, and sex risk factors in these nuclear families were compared with those of patients with sporadic intracranial aneurysms (SIAs) and population-based control patients. RESULTS: Affected family members with FIAs exhibited prevalence rates of smoking and hypertension (74% and 43%, respectively) that tended to be higher than those of population-based control patients (52% [P < 0.005] and 36% [P = not significant (NS)], respectively) and comparable to those of patients with SIAs (64% [P = NS] and 40% [P = NS], respectively). A positive association existed between FIA formation and female sex but was somewhat less strong than that observed in the SIAs (59% FIAs, 71% SIAs, 50% control patients). In addition, the prevalence rates of smoking, hypertension, and female sex were higher in affected family members with FIAs than in their unaffected siblings (58% [P < 0.05], 28% [P = 0.06], and 39% [P < 0.05], respectively). Individuals in families with expressed FIAs who had high aneurysmal penetrance had a greater tendency to be smokers, hypertensive, and female (74%, 59%, and 55%, respectively) than did their low-penetrance counterparts (61% [P = 0.1], 27% [P < 0.05], and 45% [P = NS], respectively). CONCLUSION: Together these data suggest that hypertension, smoking, and female sex increase the likelihood that a member of a family with an expressed FIA will have an aneurysm. These observations may prove helpful in guiding the use of screening studies and encouraging education about the potential risks of continued tobacco use and untreated hypertension in this patient cohort.

Cohort Studies↗
PubMed2001

Elevation of soluble intercellular adhesion molecule-1 levels in symptomatic and asymptomatic carotid atherosclerosis.

OBJECTIVE: Recent data suggest that the increased expression of intercellular adhesion molecule-1 (ICAM-1) in atherosclerotic plaque taken from the carotid bifurcation correlates with the development of neurological symptoms. As a result, the authors sought to compare the serum levels of soluble forms of ICAM-1 (sICAM-1) in patients who were asymptomatic with those who were symptomatic for carotid artery stenosis as well as in patients who were matched in terms of sex, age, and risk factors who did not have carotid artery disease. METHODS: Using enzyme-linked immunosorbent assay, serum sICAM-1 levels were prospectively determined in 54 patients scheduled to undergo carotid endarterectomy for either symptomatic or asymptomatic high-grade stenosis (> or =60%) and in 5 additional patient controls. Data are expressed as mean +/- standard error of the mean, with significance defined as P < 0.05 using the Mann-Whitney two-tailed test for two-column comparison or analysis of variance and Fisher protected least significant difference test. RESULTS: Using a univariate model, serum sICAM-1 levels were significantly elevated in patients with carotid artery stenosis as compared with control patients without stenosis (347 +/- 15 ng/ml versus 216 +/- 8.2 ng/ml) (P < 0.01). When the asymptomatic and symptomatic patients with carotid artery stenosis were considered separately, these levels were still elevated relative to those of control patients (asymptomatic [312 +/- 18 ng/ml] and symptomatic [376 +/- 22 ng/ml] patients; P = 0.06 for asymptomatic versus control patients, P < 0.01 for symptomatic versus control patients). Symptomatic patients also had significantly elevated sICAM-1 levels as compared with asymptomatic patients (P < 0.05). Despite the fact that female patients demonstrated higher ICAM-1 levels than male patients (P < 0.05), sex, age, and risk factors such as the presence of hypercholesterolemia, diabetes, hypertension, or a history of smoking did not confound these findings. CONCLUSION: Levels of sICAM-1 are higher in patients with carotid stenosis than in control patients. Symptomatic patients demonstrate significantly elevated levels as compared with asymptomatic patients. These data support the contention that ICAM-1 is a reliable marker of carotid disease progression and suggest that serum levels may be useful in following certain asymptomatic patients.

Aged↗
PubMed2001

Serum S100B protein levels are correlated with subclinical neurocognitive declines after carotid endarterectomy.

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 24 hours 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 neuron-specific 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.

Aged↗