S-100B and neuron specific enolase are poor outcome predictors in severe traumatic brain injury treated by an intracranial pressure targeted therapy

Abstract

Objective: To prospectively study S-100B and neuron specific enolase (NSE) levels in subjects treated for severe head injury (sTBI), and investigate the prognostic value of these biomarkers. Methods: Subjects included in a prospective double blind randomised study for sTBI. Inclusion criteria: Glasgow Coma Score (GCS) (8, age 15-70 years, first recorded cerebral perfusion pressure of .10 mm Hg and arrival ,24 h after trauma. Subjects were treated with an intracranial pressure (ICP) targeted therapy. Blood samples for S-100B and NSE were drawn immediately after arrival and every 12 h for 5 days. Outcome was evaluated as Glasgow Outcome Scale (GOS) by independent staff at 3 and 12 months. Results: 48 subjects, mean age 35.5 years, and median GCS 6 were included. The first blood sample was drawn at 15.6 (1.4) h after injury. Initial concentration of S-100B was 1.04 (0.21) mg/l and for NSE 18.94 (2.32) mg/l. The biomarkers were significantly higher in subjects with GCS 3 and in those who died compared with those with GCS 4-8 and GOS 2-5, respectively. Receiver operated characteristic curve analyses of the initial S-100B and NSE levels to GOS dichotomised as unfavourable (GOS 1-3) and favourable (GOS 4-5) showed a weak correlation: AUC 0.585 and 0.555, respectively. Using the dichotomisation dead (GOS 1)/alive (GOS 2-5), the AUC values were 0.687 and 0.734, respectively. Furthermore, a correlation was found between the biomarkers themselves and the biomarkers and ICP. Conclusion: At 3 and 12 months after trauma, no differences in prognostic values between the markers were apparent nor was there any clinical significant value of the markers as predictors of clinical outcome.Over the past decades there has been a rising interest in biochemical markers. They are used for diagnosis of many disorders, including: myocardial infarction (troponin), renal failure (creatinine), acute pancreatitis (amylase) and malignant diseases (prostate specific antigen, a-phoeto protein). One of the first substances studied as a biochemical marker of cerebral injury in the clinical setting was CK-BB.1 2 Today, several biochemical markers for brain injury have been evaluated for clinical use. The studies have mostly aimed at finding reliable biochemical markers for brain injury which would allow for discrimination between potentially serious and potentially non-serious head injury, mostly defined as findings on CT scan.3-5 Other studies have focused on the prediction of outcome after head injury. 7Among the recent most intensely studied biochemical markers are S-100B and neuron specific enolase (NSE).S-100B is a small calcium binding protein found in the astroglial cells and in Schwann cells. 8 9 It has been shown that the concentration of this protein increases in CSF and serum after cerebral injuries such as: head injury, meningitis, subarachnoid haemorrhage and stroke.10 11 However, increased levels of S-100B can also be detected after extracranial injuries (eg, coronary bypass surgery and fractures of long bones).12-14 S-100B i...

Utility of neuron-specific enolase in traumatic brain injury; relations to S100B levels, outcome, and extracranial injury severity

“…When compared to NSE, S100B has a higher overall predictive power, in accordance with other groups analyzing and comparing both biomarkers [59–61], where the predictive capability of NSE was found limited in the presence of S100B in multivariate outcome models [39, 62]. An explanation is, again, the notable covariance between serum S100B and NSE, which has been shown to be 0.50–0.78 (correlation coefficient) in previous studies [39, 58, 63, 64], similar to ours of 0.67. However, in our study this correlation decreases over time, highlighting the need for more granular temporal considerations when assessing biomarkers [65].…”

Dynamics of brain tissue changes induced by traumatic brain injury assessed with the Marshall, Morris–Marshall, and the Rotterdam classifications and its impact on outcome in a prostacyclin placebo-controlled study

“…There was no statistically significant difference between the control and prostacyclin groups in regard to age (un-paired Student's t test), gender (χ 2 test), GCS, GOS at 3, 6, and 12 months, Marshall, Rotterdam, and Morris-Marshall classifications (Wilcoxon rank-sum test). As previously reported, there was no difference in ISS, Sum score a +1 a Add plus 1 to make the grading numerically consistent with the grading of the motor score of the GCS and with the Marshall CT classification APACHII, S-100B, NSE, APOE, and microdialysis showed no significant differences in intracerebral lactat/pyruvate ratio or glucose between the placebo and prostacyclin group [31][32][33][34]. Thus, for further analysis of the results, the enrolled subjects are treated as one group.…”

Development of a simple score to predict outcome for unresponsive wakefulness syndrome

“…Previous studies have demonstrated that serum NSE levels often reflect the extent of brain injury, and that increased serum NSE within the first three days after cardiac arrest is associated with poor outcome [33–35]. However, serum NSE levels after brain injury displayed a gradual decline over time [36], which indicates that NSE collected from patients in the late phase of brain injury cannot be used as a prognostic factor to predict the outcome of patients with UWS.…”