Skip to main content

Advertisement

Log in

Serum neuron-specific enolase as a predictor of short-term outcome and its correlation with Glasgow Coma Scale in traumatic brain injury

  • Original Article
  • Published:
Neurosurgical Review Aims and scope Submit manuscript

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.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Fig. 1
Fig. 2

Similar content being viewed by others

References

  1. Bandyopadhyay S, Hennes H, Gorelick MH, Wells RG, Walsh-Kelly CM (2005) Serum neuron-specific enolase as a predictor of short-term outcome in children with closed traumatic brain injury. Acad Emerg Med 12(8):732–738

    Article  PubMed  Google Scholar 

  2. Beems T, Simons KS, Van Geel WJ, De Reus HP, Vos PE, Verbeek MM (2003) Serum- and CSF-concentrations of brain specific proteins in hydrocephalus. Acta Neurochir (Wien) 145(1):37–43

    Article  CAS  Google Scholar 

  3. Beers SR, Berger RP, Adelson PD (2007) Neurocognitive outcome and serum biomarkers in inflicted versus non-inflicted traumatic brain injury in young children. J Neurotrauma 24(1):97–105

    Article  PubMed  Google Scholar 

  4. Berger RP, Adelson PD, Pierce MC, Dulani T, Cassidy LD, Kochanek PM (2005) Serum neuron-specific enolase, S 100B, and myelin basic protein concentrations after inflicted and noninflicted traumatic brain injury in children. J Neurosurg (Pediatrics 1) 103:61–68

    Google Scholar 

  5. Berger RP, Dulani T, Adelson PD, Leventhal JM, Richichi R, Kochanek PM (2006) Identification of inflicted traumatic brain injury in well-appearing infants using serum and cerebrospinal markers: a possible screening tool. Pediatrics 117(2):325–332

    Article  PubMed  Google Scholar 

  6. Casmiro M, Maitan S, De Pasquale F, Cova V, Scarpa E, Vignatelli L (2005) Cerebrospinal fluid and serum neuron-specific enolase concentrations in a normal population. Eur J Neurol 12(5):369–374

    Article  PubMed  CAS  Google Scholar 

  7. Guan W, Yang YL, Xia WM, Li L, Gong DS (2003) Significance of serum neuron-specific enolase in patients with acute traumatic brain injury. Chin J Traumatol 6(4):218–221

    PubMed  CAS  Google Scholar 

  8. Hermann M, Curio N, Jost S, Wunderlich MT, Synowitz H, Wallesch CW (1999) Protein S-100B and neuron specific enolase as early neurobiochemical markers of severity of traumatic brain injury. Restor Neurol Neurosci 14:109–114

    Google Scholar 

  9. Hermann M, Curio N, Jost S, Grubich C, Ebert AD, Fork ML, Synowitz H (2001) Release of biochemical markers of damage to neuronal and glial brain tissue is associated with short and long term neuropsychological outcome after traumatic brain injury. J Neurol Neurosurg Psychiatry 70:95–100

    Article  Google Scholar 

  10. Kruijk JR, Leffers P, Menheere PPCA, Meerhoff S, Twijnstra A (2001) S-100B and neuron-specific enolase in serum of mild traumatic brain injury patients. Acta Neurol Scand 103:175–179

    Article  PubMed  Google Scholar 

  11. Li N, Shen JK, Zhao WG, Cai Y, Li YF, Zhan SK (2004) S-100B and neuron specific enolase in outcome prediction of severe head injury. Chin J Traumatol 7(3):156–158

    PubMed  Google Scholar 

  12. Loy DN, Sroufe AE, Pelt JL, Burke DA, Cao QL, Talbott JF, Whittemore SR (2005) Serum biomarkers for experimental acute spinal cord injury: rapid elevation of neuron-specific enolase and S-100b. Neurosurgery 56(2):391–397, discussion 391–397

    Article  PubMed  Google Scholar 

  13. Missler U, Wiesmann M, Friedrich C, Kaps M (1997) S-100 protein and neuron-specific enolase concentrations in blood as indicators of infarction volume and prognosis in acute ischemic stroke. Stroke 28(10):1956–1960

    PubMed  CAS  Google Scholar 

  14. Nguyen Dn, Spapen H, Su Fuhong, Schiettecatte J, Shi L, Idrissi SH, Huygens L (2006) Elevated serum levels of S-100b protein and neuron-specific enolase are associated with brain injury in patients with severe sepsis and septic shock. Crit Care Med 34(6):1–8

    Google Scholar 

  15. Ogata M, Tsuganezawa O (1999) Neuron-specific enolase as an effective immunohistochemical marker for injured axons after fatal brain injury. Int J Legal Med 113:19–25

    Article  PubMed  CAS  Google Scholar 

  16. Pelinka LE, Jafardamar M, Redl H, Bahrami S (2004) Neuron-specific enolase is increased in plasma after hemorrhagic shock and after bilateral femur fracture without traumatic brain injury in the rat. Shock 22(1):88–91

    Article  PubMed  CAS  Google Scholar 

  17. Pelinka LE, Hertz H, Mauritz W, Harada N, Jafarmadar M, Albrecht M, Redl H, Bahrami S (2005) Nonspecific increase of systemic neuron-specific enolase after trauma: clinical and experimental findings. Shock 24(2):119–123

    Article  PubMed  CAS  Google Scholar 

  18. Persson L, Hardemark HG, Gustafsson J, Rundstrom G, Mendel-Hartvig I, Esscher T, Pahlman S (1987) S-100 protein and neuron-specific enolase in cerebrospinal fluid and serum: markers of cell damage in human central nervous system. Stroke 18(5):911–918

    PubMed  CAS  Google Scholar 

  19. Raabe A, Grolms C, Seifert V (1999) Serum markers of brain damage and outcome prediction in patients after severe head injury. Br J Neurosurg 13(1):56–59

    Article  PubMed  CAS  Google Scholar 

  20. Ross SA, Cunningham RT, Johnston CF, Rowlands BJ (1996) Neuron-specific enolase as an aid to outcome prediction in head injury. Br J Neurosurg 10(5):471–476

    Article  PubMed  CAS  Google Scholar 

  21. Schaarschmidt H, Prange HW, Reiber H (1994) Neuron-specific enolase concentrations in blood as a prognostic parameter in cerebrovascular diseases. Stroke 25(3):558–565

    PubMed  CAS  Google Scholar 

  22. Shafi S, Diaz-Arrastia R, Madden C, Gentilello L (2008) Intracranial pressure monitoring in brain-injured patients is associated with worsening of survival. J Trauma 64:335–340

    PubMed  Google Scholar 

  23. Vos PE, Lamers KJB, Hendriks JCM, van Haaren M, Beems T, Zimmerman C, van Geel W, de Reus H, Biert J, Verbeek MM (2004) Glial and neuronal proteins in serum predict outcome after severe traumatic brain injury. Neurology 62:1303–1310

    PubMed  CAS  Google Scholar 

  24. Woertgen C, Rothoerl RD, Holzschuh M, Metz C, Brawanski A (1997) Comparison of serial S-100 and NSE serum measurements after severe head injury. Acta Neurochir (Wien) 139:1161–1165

    Article  CAS  Google Scholar 

  25. Woertgen C, Rothoerl RD, Metz C, Brawanski A (1999) Comparison of clinical, radiologic, and serum marker as prognostic factors after severe head injury. J Trauma 47(6):1126–1130, (erratum in J Trauma 2000 Sep; 49(3):570–571, Dec)

    Article  PubMed  CAS  Google Scholar 

  26. Wunderlich MT, Wallesch CW, Goertler M (2004) Release of neurobiochemical markers of brain damage is related to the neurovascular status on admission and the site of arterial occlusion in acute ischemic stroke. J Neurol Sci 227(1):49–53

    Article  PubMed  CAS  Google Scholar 

  27. Yamazaki Y, Yada K, Morii S, Kitahara T, Ohwada T (1995) Diagnostic significance of serum neuron-specific enolase and myelin basic protein assay in patients with acute head injury. Surg Neurol 43(3):267–270, discussion 270–271

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Uygur Er.

Additional information

Comments

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.

Rights and permissions

Reprints and permissions

About this article

Cite this article

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

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s10143-008-0148-2

Keywords

Navigation