Abstract
Elevated serum neuron-specific enolase levels are correlated with brain cell damage. Low scores according to Glasgow Coma Scale are also considered as serious poor prognostic factor. The aims of the study were to investigate whether there is a correlation between the two measurements in patients with traumatic brain injury and whether serum neuron-specific enolase levels have potential as a screening test to predict outcome. A total of 169 consecutive patients with traumatic brain injury admitted to our clinic between 2002 and 2005 are included in this study. Those patients, who had any major health problem before trauma, were excluded from the study. However, patients with isolated head injury were included in the study. Serial serum neuron-specific enolase concentrations taken at the first 2, 24, and 48 h after traumatic brain injury were analyzed. A computed tomography was performed on each patient on admission. Their Glasgow Coma Scale scores were recorded serially. The relationship between Glasgow Coma Scale scores and the serum neuron-specific enolase levels were assessed by statistical methods. There was a significant negative correlation between the serum neuron-specific enolase levels and Glasgow Coma Scale scores. The levels of neuron-specific enolase were significantly higher in the patients who died in 30 days after trauma and whose scores were lower than or equal to 8 points in Glasgow Coma Scale. Although there are several serious limitations of the use of neuron-specific enolase as a biomarker in traumatic brain injury (i.e., hypoperfusion, extracranial trauma, bleeding, liver, or kidney damage also increase the level of neuron-specific enolase), its concentrations may be useful as a practical and helpful screening test to identify neurotrauma patients who are at increased risk and may provide supplementary estimation with radiological and clinical findings.
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Dietmar Krex, Dresden, Germany
Serum NSE levels are known to be a helpful marker in the determination of brain damage since more than 10 years. However, the meaning of this and comparable serum markers for patients’ outcome in various diseases like traumatic brain injury or stroke are still matters of debate. Guzel et al. performed a simple and straightforward study by determination of serum NSE levels 2, 24, and 48 h after traumatic brain injury in 169 patients in addition to clinical parameters like the GCS score. They found a strong correlation between elevated serum NSE levels and a poor short-term outcome, i.e., 24–48 h after the injury. The present study is thoroughly performed and inclusion criteria and blood sampling procedures are well defined, thus providing a solid basis for their data and avoiding sources of bias. Therefore, the present data are solid and substantially confirm other reports where a predictive value of that specific serum marker has been suggested. Nevertheless, the authors critically reflect their results in the light of the current literature, and limitations are clearly presented. However, the identification of prognostic serum markers in patients with traumatic brain injury is desirable, as radiological and clinical assessments of the degree of the brain damage and patients’ prognosis are invalid and insufficient in many cases.
Attila Schwarcz, Pecs, Hungary
The authors present a prospective study of 169 patients with TBI. They suggest that serum level of NSE may predict short-term outcome in TBI. It is generally accepted that biomarkers would provide substantial diagnostic tool to monitor TBI and also to determine the severity of TBI (i.e., possible prognosis). However, NSE is non-specific to the central nervous system, so the measurement of NSE would be useful only in brain monotrauma. Maybe other biomarkers withdrawn from cerebrospinal fluid would be better candidates.
Apart from the non-specificity of NSE, the study has two major pitfalls: (1) they do not present the measured ICP data and (2) GCS score cannot be an objective measure for short-term outcome in severe cases (i.e., GCS<8).
Regarding the ICP monitoring, the authors cite the recent paper of Shafi et al. who pointed out that ICP monitoring is associated with worsening the survival of patients with TBI. I am convinced that this is a wrong argument, since no monitoring technique would result in a better or poorer outcome. Only treatment triggered by adequate monitoring would have any effect on the outcome. I hope that people from Brain Trauma Foundation will also express their opinion regarding the misleading conclusion of Shafi et al., already cited by the authors.
The other pitfall of the study is that GCS measured on admission was assumed to be unaltered during the first 72 h in intubated, sedated patients. Hence, the deterioration of these patients could not be followed by GCS changes. Taking this pitfall into account, the study cannot provide reliable data in a patient group (i.e., GCS <8) which would mostly need a prognosis prediction. I think biomarkers withdrawn from cerebrospinal fluid together with CT findings and ICP changes would have a larger impact to predict short-term or even long-term outcome.
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Guzel, A., Er, U., Tatli, M. et al. Serum neuron-specific enolase as a predictor of short-term outcome and its correlation with Glasgow Coma Scale in traumatic brain injury. Neurosurg Rev 31, 439–445 (2008). https://doi.org/10.1007/s10143-008-0148-2
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DOI: https://doi.org/10.1007/s10143-008-0148-2