title: Temporal profile of release of neurobiochemical markers of brain damage after traumatic brain injury is associated with intracranial pathology as demonstrated in cranial computerized tomography.
abstract: This study aimed at the investigation of release patterns of neuron specific enolase (NSE) and protein S-100B after traumatic brain injury (TBI) and their association with intracranial pathologic changes as demonstrated in computerized tomography (CT). We analyzed NSE and S-100B concentrations in serial venous blood samples taken one to three days after TBI in 66 patients by the use of immunoluminometric assays. These markers are considered to be specific neurobiochemical indicators of damage to glial (S-100B) or neuronal (NSE) brain tissue. Standardized neurological examination and plani- and volumetric evaluation of computerized tomography scans were performed in all patients. Patients with medium severe to severe TBI [Glasgow Coma Scale (GCS) score at the site of accident < or =12] exhibited significantly higher NSE and S-100B concentrations and a significantly longer release compared to patients with minor head injury (GCS: 13-15). Both, patients with and without visible intracerebral pathology in CT scans exhibited elevated concentrations of NSE and S-100B after TBI and a significant decrease in the follow-up blood samples. Release patterns of S-100B and NSE differed in patients with primary cortical contusions, diffuse axonal injury (DAI), and signs of cerebral edema (ICP) without focal mass lesions. All serum concentrations of NSE and S-100B were significantly correlated with the volume of contusions. The data of the present study indicate that the early release patterns of NSE and S-100 may mirror different pathophysiological consequences of traumatic brain injury.
authors.affiliation: Division of Neuropsychology and Behavioral Neurology, Otto-von-Guericke-University, Magdeburg, Germany. herrmann@medizin.uni-magdeburg.de
authors.forename: M
authors.initials: M
authors.lastname: Herrmann
authors.forename: S
authors.initials: S
authors.lastname: Jost
authors.forename: S
authors.initials: S
authors.lastname: Kutz
authors.forename: A D
authors.initials: AD
authors.lastname: Ebert
authors.forename: T
authors.initials: T
authors.lastname: Kratz
authors.forename: M T
authors.initials: MT
authors.lastname: Wunderlich
authors.forename: H
authors.initials: H
authors.lastname: Synowitz
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000032:analysis; D001921:Brain / Q000000981:diagnostic imaging* / Q000473:pathology*; D001925:Brain Damage, Chronic / Q000000981:diagnostic imaging* / Q000473:pathology; D001930:Brain Injuries / Q000000981:diagnostic imaging* / Q000473:pathology*; D002135:Calcium-Binding Proteins / Q000032:analysis; D006259:Craniocerebral Trauma / Q000000981:diagnostic imaging / Q000473:pathology; D015600:Glasgow Coma Scale; D006801:Humans; D008875:Middle Aged; D009414:Nerve Growth Factors; D010751:Phosphopyruvate Hydratase / Q000032:analysis*; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000032:analysis*; D013997:Time Factors; D014057:Tomography, X-Ray Computed
chemical_list: D015415:Biomarkers; D002135:Calcium-Binding Proteins; D009414:Nerve Growth Factors; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; D010751:Phosphopyruvate Hydratase