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
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Herrmann, M
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机构:Otto Von Guericke Univ, Fac Med, Div Neuropsychol & Behav Neurol, D-39120 Magdeburg, Germany
Herrmann, M
Jost, S
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机构:Otto Von Guericke Univ, Fac Med, Div Neuropsychol & Behav Neurol, D-39120 Magdeburg, Germany
Jost, S
Kutz, S
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机构:Otto Von Guericke Univ, Fac Med, Div Neuropsychol & Behav Neurol, D-39120 Magdeburg, Germany
Kutz, S
Ebert, AD
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机构:Otto Von Guericke Univ, Fac Med, Div Neuropsychol & Behav Neurol, D-39120 Magdeburg, Germany
Ebert, AD
Kratz, T
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机构:Otto Von Guericke Univ, Fac Med, Div Neuropsychol & Behav Neurol, D-39120 Magdeburg, Germany
Kratz, T
Wunderlich, MT
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机构:Otto Von Guericke Univ, Fac Med, Div Neuropsychol & Behav Neurol, D-39120 Magdeburg, Germany
Wunderlich, MT
Synowitz, H
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机构:Otto Von Guericke Univ, Fac Med, Div Neuropsychol & Behav Neurol, D-39120 Magdeburg, Germany
Synowitz, H
机构:
[1] Otto Von Guericke Univ, Fac Med, Div Neuropsychol & Behav Neurol, D-39120 Magdeburg, Germany
[2] Otto Von Guericke Univ, Dept Neurol, D-39120 Magdeburg, Germany
[3] Otto Von Guericke Univ, Dept Neurosurg, D-39120 Magdeburg, Germany
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 less than or equal to 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.