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Objectives: The aim of this study was to determine the added value of the serum biomarkers S100 and neuron-specific enolase to clinical characteristics for predicting outcome after out-of-hospital cardiac arrest., Background: Serum S100 beta (S100B) and neuron-specific enolase concentrations rise after brain injury., Methods: A prolective observational study was conducted among all adult survivors of nontraumatic out-of-hospital cardiac arrest admitted to 1 hospital (April 3, 2008 to April 3, 2011). Three blood samples (on arrival and on days 1 and 3) were drawn for biomarkers, contingent on survival. Follow-up continued until in-hospital death or discharge. Outcomes were defined as good (Cerebral Performance Category score 1 or 2) or poor (Cerebral performance category score 3 to 5)., Results: A total of 195 patients were included (65.6% men, mean age 73 ± 16 years), with presenting rhythms of asystole in 61.5% and ventricular tachycardia or ventricular fibrillation in 24.1%. Only 43 patients (22.0%) survived to hospital discharge, 26 (13.3%) with good outcomes. Patients with good outcomes had significantly lower S100B levels at all time points and lower neuron-specific enolase levels on days 1 and 3 compared with those with poor outcomes. Independent predictors at admission of a good outcome were younger age, a presenting rhythm of ventricular tachycardia or ventricular fibrillation, and lower S100B level. Predictors on day 3 were younger age and lower day 3 S100B level. The area under the receiver-operating characteristic curve of the admission-day model was 0.932 with and 0.880 without biomarker data (p = 0.027 for the difference)., Conclusions: Risk stratification after out-of-hospital cardiac arrest using both clinical and biomarker data is feasible. The biomarkers, although adding an ostensibly modest 5.2% to the area under the receiver-operating characteristic curve, substantially reduced the level of uncertainty in decision making. Nevertheless, current biomarkers cannot replace societal considerations in determining acceptable levels of uncertainty. (Protein S100 Beta as a Predictor of Resuscitation Outcome; NCT00814814)., (Copyright © 2012 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Levels of antibodies AB (AB) to S100B and S100B protein were studied in the blood serum of children with different severity and outcomes of traumatic brain injury (TBI) from the 1st to 15-75th days after TBI. Severity and outcomes were assessed using the Glasgow Coma Scale (GCS). Patients were stratified by outcomes into the following groups: complete recovery (group 1), moderate disability (group 2), high disability (group 3), vegetative state (group 4) and fatal outcome (group 5). In patients of groups 1-3, the changes of S100B in the blood serum didn't depend on the severity of brain's damage; the significant increase of S100B protein levels in the 1st day was accompanied by the decrease to the normal range in the following 2-3 days. On the contrary, the levels of nAB in these groups increased starting from 3-5 days corresponding to the severity of brain's damage. The development of vegetative state was accompanied by low S100B and high AB to S100B levels in the blood serum. The maximal level of S100B protein and increased levels of AB were observed in patients with fatal outcome. In most patients with combined TBI, the levels of both parameters were higher compared to those with separate TBI.

Effects of caffeic acid phenethyl ester (CAPE) on the serum S-100B levels were studied as an index for brain damage after permanent middle cerebral artery (MCA) occlusion in rabbits. Twenty rabbits were divided into four groups (n=5): control, sham, non-treatment and CAPE. The right MCA was occluded using a microsurgical procedure with bipolar coagulation and was then transected in non-treatment and CAPE groups. The rabbits in the sham group underwent a surgical procedure but the MCA was not occluded. No surgery was performed in the control group. CAPE was administered after MCA occlusion at the dose of 10 microg/kg, once a day intraperitoneally for 7 days in the CAPE group. Serum S-100B levels were determined on days 1, 2, 4 and 7. Serum S-100B level was significantly increased following permanent MCA occlusion. Posttreatment of CAPE significantly reduced the serum S-100B level. This study demonstrated that CAPE is capable of attenuating increased serum S-100B level induced by MCA occlusion in rabbits. CAPE may be useful as a neuroprotective agent.

Objective: To investigate the prognostic value of serum neuron specific enolase (NSE) and S100 protein in evaluation of brain damage in patients resuscitated from cardiac arrest (CA)., Methods: According to whether the patients regained consciousness after 6 months or not, 25 patients after cardiopulmonary resuscitation (CPR) were divided into 2 groups, and blood samples were obtained for determination of NSE and S100 protein at 2, 12, 24, 48 and 72 hours after recovery of spontaneous circulation (ROSC), then the values at each time point were compared between 2 groups and also with that of 7 healthy volunteers. Receiver operator characteristic (ROC) curves of serum NSE and S100 protein were depicted and used area under curve (AUS) to scale the ability in evaluating the state of consciousness in patients after CPR., Results: (1)The levels of serum NSE at 12, 48 and 72 hours and S100 protein at 2, 12, 48 and 72 hours were significantly higher in patients who did not regain consciousness compared with patients who regained consciousness (all P<0.01). (2)Compared with healthy volunteers, the levels of NSE at 12 and 24 hours and S100 protein at 12 hours were higher in patients who regained consciousness (all P<0.05), the levels of NSE at all time points and S100 protein at 12, 48 and 72 hours were significantly higher in patients who did not regain consciousness (P<0.05 or P<0.01). (3)Area under curve AUC(NSE) =0.848 (P=0.000), AUC(S100) =0.896 (P=0.000), therefore both serum NSE and S100 protein had diagnostic value for predicting whether patients resuscitated from CA could regain consciousness or not. Serum S100 protein cut-off was 0.165 microg/L, with a sensitivity of 94.4%, a specificity of 100%, a positive predictive value of 100%, a negative predictive value of 80% and an accuracy of 95.5% at 2 hours after ROSC. Serum NSE cut-off was 45.6 microg/L, all values reached 100% 48 hours after ROSC., Conclusion: Measurement of serum NSE and S100 protein concentrations can help judge the degree of brain damage and whether patients can regain consciousness after CPR. It will be more valuable to prognosticate a serious and continuous brain damage with dynamic observation of the serum NSE together with S100 protein.

Objective: Studies have shown signs of brain damage caused by different mechanisms in cocaine users. The serum neuron specific enolase and S100B protein are considered specific biochemical markers of neuronal and glial cell injury. This study aimed at comparing blood levels of S100B and NSE in chronic cocaine users and in volunteers who did not use cocaine or other illicit drugs., Method: Twenty subjects dependent on cocaine but not on alcohol or marijuana, and 20 non-substance using controls were recruited. Subjects were selected by consecutive and non-probabilistic sampling. Neuron specific enolase and S100B levels were determined by luminescence assay., Results: Cocaine users had significantly higher scores than controls in all psychiatric dimensions of the SCL-90 and had cognitive deficits in the subtest cubes of WAIS and the word span. Mean serum S100B level was 0.09 +/- 0.04 microg/l among cocaine users and 0.08 +/- 0.04 microg/l among controls. Mean serum neuron specific enolase level was 9.7 +/- 3.5 ng/l among cocaine users and 8.3 +/- 2.6 ng/l among controls., Conclusions: In this first study using these specific brain damage markers in cocaine users, serum levels of S100B and neuron specific enolase were not statistically different between cocaine dependent subjects and controls.

Background and Purpose: Biochemical markers of acute neuronal injury may aid in the diagnosis and management of acute ischemic stroke. Serum samples from the National Institute for Neurological Disorders and Stroke (NINDS) recombinant tissue plasminogen activator Stroke Study were analyzed for the presence of 4 biochemical markers of neuronal, glial, and endothelial cell injury. These biochemical markers, myelin basic protein (MBP), neuron-specific enolase (NSE), S100beta, and soluble thrombomodulin, were studied for an association with initial stroke severity, infarct volume, and functional outcome., Methods: In the original NINDS study, serum samples were drawn from all patients on presentation to the Emergency Department and at approximately 2 and 24 hours after initiation of study therapy. In this analysis, stored serum samples were available for 359 patients; 107 patients had samples for all 3 time points. Serum marker concentrations were measured by ELISA techniques. We examined the relation between serum concentrations of each marker and the degree of baseline neurological deficit, functional outcome, and infarct size on computed tomography at 24 hours and the effect of fibrinolytic therapy., Results: Higher 24-hour peak concentrations of MBP, NSE, and S100beta were associated with higher National Institutes of Health Stroke Scale baseline scores (r=0.186, P<0.0001; r=0.117, P=0.032; and r=0.263, P<0.0001, respectively). Higher peak concentrations of MBP and S100beta (r=0.209, P<0.0001; r=0.239, P<0.0001) were associated with larger computed tomography lesion volumes. Patients with favorable outcomes had smaller changes in MBP and S100beta (P<0.05) concentrations in the first 24 hours. Soluble thrombomodulin was not associated with any severity or outcome measure., Conclusions: This study corroborates previous work demonstrating correlations of MBP, NSE, and S100beta with clinical and radiographic features in acute stroke. Despite significantly better outcomes in the tissue plasminogen activator-treated group, we found no difference in the early release of the 4 biomarkers between treatment groups. Further study will define the role of biomarkers in acute stroke management and prognostication.

Background and Purpose: Obstructive sleep apnea syndrome (OSAS) is a chronic disease ranging from innocuous to life-threatening and causes brain alterations manifested by neuropsychiatric symptoms. Neuron-specific enolase (NSE) and the astrocytic protein S100B are established sensitive peripheral biochemical markers of brain injury. In the present work we measured the serum levels of S100B and NSE in order to evaluate the deleterious effects of OSAS to the brain., Patients and Methods: We studied 29 male patients with OSAS and 17 male asymptomatic control subjects with an apnea-hypopnea index (AHI) less than five events per hour. Patients and control subjects were evaluated by full-night polysomnography (PSG) and by Mini International Neuropsychiatric Interview (MINI) for the presence of neuropsychiatric symptoms. In the morning following the PSG, blood was collected and serum levels of S100B and NSE were measured using standard techniques., Results: The AHI in the OSAS group was (mean+/-SD) 27+/-25 AH/h, ranging from 5 to 99 AH/h. S100B was higher in OSAS (0.15+/-0.09 microg/l) than in the control group (0.08+/-0.06 microg/l; P<0.01). Serum NSE was similar in both groups (17.5+/-12.2 vs. 15.8+/-6.8ng/ml)., Conclusions: We report elevated serum S100B levels in OSAS patients in this study.

Introduction: Elevated serum levels of S100beta, an astrocyte-derived protein, correlate with unfavourable neurological outcomes following cardiac surgery, neurotrauma, and resuscitation. This study evaluated whether pre-/postoperative serum S100beta levels correlate with unfavourable clinical and radiological findings in patients undergoing elective meningioma resection., Methods: In 52 consecutive patients admitted for meningioma surgery, serum S100beta levels were determined upon admission and immediately, 24 hours, and 48 hours after surgery. All patients underwent complete pre- and postoperative neurological examination and mini-mental state examination. Radiological evaluation included preoperative magnetic resonance imaging (MRI) and postoperative computed tomography. Tumour volume, brain edema, and bleeding volume were calculated using BrainSCAN software., Results: Preoperative S100beta levels did not correlate with the tumour characteristics demonstrated by preoperative MRI (for example, tumour volume, edema volume, ventricular asymmetry, and/or midline shift). Preoperative serum S100beta levels (0.065 +/- 0.040 microg/l) were significantly lower than the levels measured immediately (0.138 +/- 0.081 microg/l), 24 hours (0.142 +/- 0.084 microg/l), and 48 hours (0.155 +/- 0.119 microg/l) postoperatively (p < 0.0001). Significantly greater postcraniotomy S100beta levels were observed with prolonged surgery (p = 0.039), deterioration in the mini-mental state examination (p = 0.005, 0.011, and 0.036 for pre versus immediate, 24 hours, and 48 hours postsurgery, respectively), and with postoperative brain computed tomography evidence of brain injury; bleeding was associated with higher serum S100beta levels at 24 and 48 hours after surgery (p = 0.046, 95% confidence interval [CI] -0.095 to -0.001 and p = 0.034, 95% CI -0.142 to -0.006, respectively) as was the presence of midline shift (p = 0.005, 95% CI -0.136 to -0.025 and p = 0.006, 95% CI -0.186 to -0.032, respectively). Edema was associated with higher serum S100beta levels immediately (p = 0.022, 95% CI -0.092 to -0.007) and at 48 hours after surgery (p = 0.017, 95% CI -0.142 to -0.026). The degree of elevation in S100beta levels at 24 and 48 hours after surgery also correlated with the severity of midline shift and edema., Conclusion: In patients with meningioma, serum S100beta levels perform poorly as an indicator of tumour characteristics but may suggest ongoing postcraniotomy injury. Serum S100beta levels may serve as a potentially useful early marker of postcraniotomy brain damage in patients undergoing elective meningioma resection.

Background and Purpose: Patients resuscitated from cardiac arrest are at risk of subsequent death or poor neurological outcome up to a persistent vegetative state. We investigated the prognostic value of several epidemiological and clinical markers and two neuroproteins, neuron-specific enolase (NSE) and S-100 protein (S-100), in 97 patients undergoing cardiopulmonary resuscitation (CPR) after non-traumatic cardiac arrest between 1998 and 2002., Results: 52.6% of the patients died, 28.8% survived with severe, moderate or without neurological disorders, and 18.6% remained in a persistent vegetative state. Unconsciousness>48 h after CPR predicted a 60.6-fold (95% CI 14.3287-257.205, p=0.001) and a Glasgow Coma Scale (GCS)<6 points after 72 h a 11.2-fold (CI 95%, 3.55-36.44, p<0.001) risk of poor neurological outcome. Serum levels>or=65 ng/ml for NSE and >or=1.5 microg/l for S-100 increased the risk of death and persistent vegetative state 16.8 (95% CI 2.146-131.520)- and 12.6 (95% CI 1.1093-99.210)-fold, respectively. By combination of the GCS with elevated serum concentrations of both neuroproteins above the cut off levels on third day after CPR a poor neurological outcome was predicted with a specificity of 100%., Conclusion: The combination of GCS with the serum levels of both neuroproteins at 72 h after CPR permit a more reliable prediction of outcome in post arrest coma than the single markers alone, independent of the application of anaesthetic agents.

Background: We used serial measurements of serum S-100B protein to evaluate the time course of serum S-100B protein concentration after cardiovascular surgery and to determine the clinical relevance of its concentration and cerebral damage., Methods: We assessed neurologic function in 149 patients undergoing cardiovascular surgery with cardiopulmonary bypass. The patients were classified into three groups according to their early postoperative outcome: those without complications (group A), those having unconsciousness or convulsion or both but no hemiplegia (group B), and those having unconsciousness and hemiplegia either with or without convulsion (group C). Serum S-100B protein concentrations were measured with a commercially available immunoluminometric assay, Sangtec 100 LIA, at seven time-points: before cardiopulmonary bypass, at the end of cardiopulmonary bypass, and at 5, 12, 24, 48, and 72 hours after cardiopulmonary bypass., Results: At 5 hours after cardiopulmonary bypass, the S-100B values in groups B and C were significantly higher than the value in group A. Although the S-100B level decreased in group C during the first 5 hours after cardiopulmonary bypass, it increased thereafter (12 through 24 hours) and continued at a high level until the final measurement at 72 hours. At 12 hours after cardiopulmonary bypass, S-100B was significantly higher in group C than in group B. This late increase in S-100B was associated with radiologically detected abnormalities and cerebral damage., Conclusions: Serial measurement of serum S-100B protein in the initial 12 hours after cardiopulmonary bypass can be used to predict early postoperative brain injury.

This prospective clinical study was conducted to determine whether S 100 B is a reliable serum marker for traumatic brain injury (TBI) with and without multiple trauma. Fifty-five trauma patients (Injury Severity Score [ISS] > or = 24 and Glasgow Coma Score [GCS] < or = 8) were classified by radiography, computer tomography, ultrasound, and neurology as TBI without multiple trauma (n = 23), TBI with multiple trauma (n = 23), or multiple trauma without TBI (n = 9). S 100 B was measured initially after trauma and daily for a maximum of 21 days. Both survivors and nonsurvivors had markedly increased S 100 B initially. All survivors returned to normal or moderately increased S 100 B levels within the first 48 h after trauma. In contrast, all nonsurvivors of isolated TBI had S 100 B values that either increased consistently or dropped and then increased again 48 h after the initial increase after trauma. There was no relationship between localization, extent, or severity of TBI and S 100 B. According to receiver operating characteristic curve analysis and calculation of the area under the curve (AUC), S 100 B is equally accurate for mortality prediction at 24, 48, and 72 h after trauma and is most accurate >84 h after trauma. Sensitivity/specificity for mortality prediction are more accurate in TBI without multiple trauma (AUC 0.802-0.971) than in TBI with multiple trauma (AUC 0.693-0.783). Thus, though S 100 B may be a reliable marker of brain damage in TBI without multiple trauma 24 h after trauma and thereafter, it appears to be less reliable in TBI with multiple trauma.

Aim: S-100beta is a specific astroglial protein whose serum level increases after cerebral injury. The purpose of this study was to investigate the correlation between elevated levels of S-100beta and the neurocognitive outcome after cardiac surgery., Methods: Fifty consecutive patients undergoing elective coronary artery bypass grafting were studied. Serum S-100beta levels were measured on induction of anaesthesia, at the 15(th) minute, at skin closure and on the 1(st) postoperative day. Neurocognitive outcome was evaluated by STAI-T and Zung tests preoperatively and by Mini-mental state examination every postoperative day until discharge. Neurocognitive tests and S-100beta levels were correlated within the scope of risk factors by Pearson correlation., Results: Serum S-100beta was not detected preoperatively. Peak serum S-100beta levels were reached at skin closure in 36 of 50 patients (72%). In 24 hours, serum S-100beta disappeared in 25 patients but was still elevated in 11 (22%). A highly significant correlation was demonstrated between the duration of CPB and peak serum S-100beta levels (r=0.91). There was a weak correlation between age and peak S-100beta levels (r=0.62). Nine patients (18%) had a positive MMSE test which correlated well with persistent high serum S-100 levels (r=0.98)., Conclusions: Serum S-100beta is a promising early biochemical marker for cerebral injury following cardiac surgery within a good correlation with the CPB time, age and especially with neurocognitive tests.

Object: Hydrocephalus is characterised by elevated intracranial pressure (ICP) and gives rise to brain damage. The aim of this study was to investigate the significance of brain specific proteins as markers in the evaluation of brain damage in hydrocephalus. Therefore we determined the levels of four brain specific proteins in cerebrospinal fluid (CSF) and serum of symptomatic hydrocephalic patients., Methods: During 41 CSF shunt-operations (both primarily placed shunts and shunt-revisions) CSF and blood samples were obtained and analysed for neuron-specific enolase (NSE), S-100b, glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP). The results were compared with an age-matched control group. Patients with varying clinical symptoms, denoting different levels of increased intracranial pressure prior to surgery, were included in this study., Results: We observed significantly increased CSF-levels of S-100b and GFAP in the hydrocephalic patients, whereas NSE and MBP were markedly increased only in patients with very severe symptoms. Serum levels of all proteins were only minimally increased and did not correlate with CSF-levels. The slightly elevated levels of CSF-NSE in most of the patients suggest only subtle neuronal damage, which is not related to permanent neurological symptoms. The elevated levels of S-100b and GFAP are indicative of a reactive astrogliosis, which has also been demonstrated in histopathological studies. No demyelination seems to occur, according to the normal levels of MBP observed in this study., Conclusions: Although CSF levels of brain specific proteins are elevated in hydrocephalic patients, indicating brain damage due to hydrocephalus, neither CSF- nor serum-concentrations of brain specific proteins seem to be valuable tools in the clinical evaluation of the severity of hydrocephalus.

Unlabelled: The presence in blood of proteins normally confined to the cytoplasm of brain cells is considered peripheral evidence of brain damage. Only recently have these proteins been measured in the blood of children at risk of brain damage. To show the value and limitations of measuring these proteins, we review their biology and the adult literature that has correlated the blood concentrations of these proteins with lesion size and dysfunction., Conclusion: We conclude that brain damage markers will increasingly be measured in the blood of newborns and other children at risk of brain damage.

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.

Background: Astrocyte protein S100beta is a potential serum marker for neurologic injury. The goals of this study were to determine whether elevated serum S100beta correlates with neurologic complications in patients requiring hypothermic circulatory arrest (HCA) during thoracic aortic repair, and to determine the impact of retrograde cerebral perfusion (RCP) on S100beta release in this setting., Methods: Thirty-nine consecutive patients underwent thoracic aortic repairs during HCA; RCP was used in 25 patients. Serum S100beta was measured preoperatively, after cardiopulmonary bypass, and 24 hours postoperatively., Results: Neurologic complications occurred in 3 patients (8%). These patients had higher postbypass S100beta levels (7.17 +/- 1.01 microg/L) than those without neurologic complications (3.63 +/- 2.31 microg/L, p = 0.013). Patients with S100beta levels of 6.0 microg/L or more had a higher incidence of neurologic complications (3 of 7, 43%) compared with those who had levels less than 6.0 microg/L (0 of 30, p = 0.005). Retrograde cerebral perfusion did not affect S100beta release., Conclusions: Serum S100beta levels of 6.0 microg/L or higher after HCA correlates with postoperative neurologic complications. Using serum S100beta as a marker for brain injury, RCP does not provide improved cerebral protection over HCA alone.

S-100b is thought to be a screening marker of hypoxic brain damage in patients with cardiac arrest. However, the time-dependent occurrence and relevance of increased S-100b serum levels in out-of-hospital patients with cardiopulmonary resuscitation (CPR) is still discussed. The purpose of our study was to evaluate the diagnostic utility of S-100b measurements in comparison to that of adhesion molecules sE-selectin and sP-selectin in patients with CPR. Sixteen out-of-hospital patients (median age 69.6 years; range 59.2-82.2 years) suffering from cardiac arrest due to ventricular fibrillation, asystole, or electromechanical dissociation were recruited prospectively. Blood samples were drawn on scene after the return of spontaneous circulation (ROSC) and 12 hours after successful CPR. The reference group consisted of 10 patients with isolated severe head trauma (SHT) (Glasgow Coma Score

Severe neurological deficits are common characteristics of patients surviving cardiopulmonary resuscitation (CPR) or isolated severe head trauma (SHT). For comparative evaluation of underlying pathomechanisms, 22 patients with out-of-hospital cardiac arrest and successful CPR as well as 10 patients with SHT were included in our prospective study. Circulating S-100B was determined as an indicator of cellular brain damage. Interleukin-8 (IL-8), soluble E-selectin (sE-selectin) and polymorphonuclear (PMN-) elastase were measured as markers of systemic inflammation following whole body ischaemia and reperfusion injury. Venous blood samples were drawn on scene (median time 11.0 min after starting basic life support) and in the intensive care unit (median time 12.5 h thereafter) in CPR patients and at admission to hospital (median time 43.8 min after trauma) and approx. 12 h later in SHT patients. Biochemical parameters in these samples were compared with specimens taken from 20 healthy volunteers. Initial median S-100B levels of the CPR and SHT patients were both significantly increased compared with the controls. Twelve hours later, significant falls in S-100B revealed no differences between the two patient groups, but did not reach control values. Median IL-8 and sE-selectin levels entry to the study were elevated in both patient groups compared with controls and showed further rises within the following 12 h. Finally, increased initial median levels of PMN-elastase revealed significant differences between the patient groups and between patients and controls. Twelve hours later, median PMN-elastase values were equally elevated in the CPR and SHT subjects. Our preliminary data suggest similar pathomechanisms occurring after both CPR and SHT. Both clinical entities seem to be associated with early transient cellular brain damage as shown by prolonged rapidly increasing and subsequent fall in S-100B serum levels. In contrast, the prolonged elevation of circulating IL-8, sE-selectin and PMN-elastase may indicate a very similar systemic inflammatory response by endothelial cells and neutrophils initiated by ischaemia and reperfusion injury in both conditions. Further studies should be carried out to determine the cause and the prognostic value of these biochemical parameters in relation to long-term neurological outcome.

Objective: Serum S-100beta protein is suggested to be a neurobiochemical marker of brain injury after cardiac and aortic arch surgery. The aim of the present study was to investigate the predictive value of S-100beta protein with respect to histopathological analysis of the brain after a prolonged period of hypothermic circulatory arrest (HCA)., Methods: Eighteen pigs (21 to 31 kg) underwent a 75 min period of HCA at 20 degrees C. Serum concentrations of S-100beta were assayed in mixed venous blood before and 2, 4, 7 and 20 h after HCA. A semiquantitative post-mortem histopathological analysis scoring all main regions of the brain was carried out in every animal., Results: All animals were stable during and after cardiopulmonary bypass (CPB) and survived at least to the first postoperative day. Ten of the 18 animals survived 7 days after surgery and were electively sacrificed. Animals with severe histopathological injury showed higher serum S-100beta protein levels at every time point after HCA. The strongest correlation between the total histopathologic score and serum S-100beta levels was found at 7 h after HCA (tau = 0.422 and p = 0.023)., Conclusion: Serum S-100beta protein levels correlate with histopathological injury after a prolonged period of HCA in pigs. This finding supports the results of previous studies suggesting the potential accuracy of S-100beta in the prediction of brain injury after cardiac surgery.

Background: Newborns undergoing cardiac operation may acquire some extent of neuronal damage. An early diagnosis is especially hard regarding neonates. In the past years, S-100 has been widely discussed as a marker revealing perioperative damage to the brain., Methods: Sequential blood samples from 33 neonates undergoing repair of congenital heart disease were taken perioperatively. Samples of 12 healthy neonates were taken at birth as a control group. The newborns were divided into four groups: cyanotic and acyanotic disease operated on in deep hypothermic circulatory arrest, operation without deep hypothermic cardiac arrest, and operation without extracorporeal circulation., Results: Even in healthy neonates, serum S-100 levels were at 10-fold values compared with adults. On admission, S-100 values in the operative groups were similar. During extracorporeal circulation, levels rose to a certain degree. Cyanotic newborns operated on in deep hypothermic cardiac arrest had significantly higher S-100 levels compared with acyanotic newborns also operated on in deep hypothermic cardiac arrest (p < 0.001). Two newborns who experienced seizures postoperatively had the highest absolute S-100 levels. One child with a poor neurologic outcome but no seizures did not have different values when compared with her group., Conclusions: In this study, S-100 seemed to be a possible marker for a certain degree of neurologic deficit after cardiac operation in neonates, especially regarding postoperative seizures. The missing peaks of this protein in one newborn with poor neurologic outcome show that it is not possible to exclude damage to the brain with normal postoperative values. These results suggest that the mechanism of cerebral damage and S-100 release into the blood in neonates with a developing central nervous system and blood-brain barrier is not fully understood.

S-100B a protein of astroglial cells is described as a marker for neuronal damage. Reliable outcome prediction from severe head injury is still unresolved. Clinical scores like the Glasgow Coma Score (GCS) and diagnostic scores like the Marshall CT Classification (MCTC) are well established and investigated, but there are still some concerns about these tools. The aim of this study was to investigate the predictive value of the initial serum level of S-100B. 44 patients with severe head injury (GCS < 9) were included. Blood samples were drawn within 1 to 6 hours of injury. After a period of 11 months their outcome was correlated using the Glasgow Outcome Scale. Patients with good outcome had significantly lower serum concentrations of S-100 on admission (0.96 microgram/l versus 5.5 micrograms/l mean, p < 0.0001). In addition patients with a S-100 serum level below 2 micrograms/l showed a significant better rating on the GOS at follow-up (4 points versus 1.8 points mean, p < 0.0001). With this cut-off line it was possible to predict longterm outcome with a sensitivity of 75% and specitivity of 82%. The serum level of S-100B calculated with one to six hours of a severe head injury is a useful additional outcome predictor.

Background: Cerebral injury is the most important complication of cardiac operations with cardiopulmonary bypass. Prolonged total circulatory arrest (TCA) can expose patients to an even greater risk of cerebral injury. We sought to detect the degree of cerebral injury in adults who had thoracic aortic operations with TCA by measuring S100B protein, which is released into the circulation after cerebral injury., Methods: Serial measurements of S100B protein, a highly specific serum marker of astroglial damage, were performed in 26 patients who had complex aortic operations, of whom 13 required cardiopulmonary bypass alone (for aortic root replacement), and in 13 patients who required an additional period of TCA (for type A aortic dissections and arch aneurysms). Blood samples were taken preoperatively, at skin closure, and 5 and 24 hours postoperatively., Results: There were significant increases in serum S100B concentrations in all patients, and peak levels occurred at skin closure. The magnitude of the increase in S100B was significantly greater at all postoperative time points and persisted longer in the TCA group. There was a significant correlation between the duration of the TCA and S100B concentration at 5 hours (r = 0.66, p = 0.01) and 24 hours (r = 0.63, p = 0.02) postoperatively., Conclusions: S100B levels were higher in all patients who had complex aortic operations and were significantly greater in patients requiring a period of TCA. The duration of the TCA period correlated with S100B levels 5 hours and at 24 hours postoperatively. Circumstantial evidence, in accordance with other studies, suggests that S100B protein is a marker for cerebral injury during cardiac operations.

Background: Intraoperative thromboembolism and the systemic inflammatory reaction are thought to play a role in causing cerebral dysfunction following cardiopulmonary bypass (CPB). Increased levels of S100B, an astroglial protein, have been linked to neuropsychological deficits after CPB. The present study investigated whether S100B release correlates with intraoperative embolus formation, thrombin formation, or the release of inflammatory parameters., Methods: 40 patients undergoing coronary artery bypass grafting were included. Blood samples were taken before, during, and after CPB, and levels of S100B, thrombin-antithrombin complex (TAT), complement C5a, and interleukin 8 were analysed. Embolus formation was assessed by Doppler ultrasound at the arterial line of CPB., Results: The release of S100B correlated with embolus count (r = 0.42; p = 0.009) and TAT formation (r = 0.71; p = 0.0001). The correlation of S100B with interleukin 8 (r = 0.58; p = 0.0001) was due to the dependence of both parameters on bypass time (r = 0.29; p = 0.075, partial correlation). A correlation of S100B with C5a formation could not be observed., Conclusions: S100B release is related to embolus and thrombin formation during CPB, indicating that thrombofibrinous embolism is involved in perioperative brain damage. Inflammatory parameters (i.e. interleukin 8 and C5a) seem to have no influence on S100B release.

The objective of our study was to investigate the association between the initial levels of serum S-100B protein and neuron specific enolase and the severity of radiologically visible brain damage and outcome after severe head injury. Admission computed tomography (CT) scans of forty-four patients with severe head injury were analysed. Initial levels of S-100B protein and neuron specific enolase were compared between the different outcome groups at 6 month, the different categories of the Marshall classification, the presence of traumatic subarachnoid haemorrhage, the type of haematoma and the volume of contusion. Serum S-100B was significantly higher in patients with unfavourable outcome (1.1 micrograms/l versus 0.3 microgram/l, p < 0.005, Mann-Whitney U test). In diffuse injury, unfavourable outcome significantly increased with higher Marshall grades (p < 0.05). There was a significant correlation between the four grades of diffuse injury and initial serum S-100B protein (r = 0.48, p < 0.001). Patients with focal mass lesions and a favourable outcome after 6 month had significantly lower S-100B values than those who had an unfavourable outcome (0.51 microgram/l versus 1.3 micrograms/l, p < 0.05). A significant correlation was demonstrated between the volume of contusion visible on CT scans and serum S-100B (r = 0.58, p < 0.001). In our study, initial serum S-100B protein was a powerful predictor of outcome even within the same category of radiologically visible brain damage. Serum S-100B protein may provide independent information about the severity of primary brain damage after head injury.

Background and Purpose: Elevations of protein S-100 (S-100) in cerebrospinal fluid and serum have been reported after cerebral infarctions. The aim of our study was to evaluate the time course of serum S-100 concentrations after territorial middle cerebral artery (MCA) infarctions in correlation with clinical data and prognosis., Methods: S-100 serum levels were serially determined in 26 patients with an acute infarction in the territory of the MCA at day 0 (within 12 hours after onset of symptoms), day 1 (24 hours after stroke onset), and days 2, 3, 4, 5, 7 or 8, and 10 after stroke and in 26 age- and sex-matched control subjects. S-100 assays were performed using a two-site radioimmunoassay technique. The clinical status was documented using the Scandinavian Stroke Scale. The functional deficit 4 weeks after stroke onset was scored by use of the modified Rankin scale. A cranial computed tomography (CCT) was performed initially and at day 4 or 5., Results: Elevated concentrations of S-100 (> 0.2 microgram/L) were observed in 21 of 26 patients with MCA infarction but in none of the control subjects. S-100 levels peaked at days 2 and 3 after stroke. The S-100 concentrations in serum were significantly higher in patients with severe neurological deficits at admission, with extensive infarctions and a space-occupying effect of ischemic edema as compared with the rest of the population. S-100 values were not significantly correlated with the functional prognosis., Conclusions: Presence of S-100 in serum after ischemic stroke may be due to combined leakage out of necrotic glial cells and passage through an impaired brain-blood barrier, indicating severe ischemic cell injury. Therefore, S-100 in serum can be used as a peripheral marker of ischemic focal brain damage and may be helpful for therapeutic decisions in acute ischemic stroke.

Protein S-100 is a calcium binding protein, synthetized in astroglial cells in all parts of the central nervous system (CNS). We have previously reported high serum levels of protein S-100 in patients after minor head injury (MHI). A battery of conventional and computerized neuropsychological measures was administered to two groups of MHI patients. Neuropsychological outcome at 12 months postinjury was examined in a group of 7 patients with increased serum levels of protein S-100 after MHI and 7 age- and sex-matched controls without detectable S-100 in serum after MHI. Our results demonstrate no overall cognitive dysfunction in either of the two groups. Our findings indicate specific dysfunction on measures of reaction time, attention and speed of information processing for the S-100 group. Posttraumatic depression does not explain the neuropsychological differences between the groups. These findings support that increased serum levels of protein S-100 may be of predictive and prognostic value for longlasting neurocognitive abnormalities after minor head injury. Presence of S-100 in serum may indicate the presence of diffuse brain damage. Our results suggest that information processing measures in computerized neuropsychological assessment are more sensitive for detecting small signs of neurocognitive abnormalities after MHI than conventional test batteries.