Abstract
BackgroundMild traumatic brain injury (mTBI) is a significant healthcare burden and its diagnosis remains a challenge in the emergency department. Serum biomarkers and advanced magnetic resonance imaging (MRI) techniques have already demonstrated their potential to improve the detection of brain injury even in patients with negative computed tomography (CT) findings. The objective of this study was to determine the clinical value of a combinational use of both blood biomarkers and MRI in mTBI detection and their characterization in the acute setting (within 24 hours after injury).MethodsNine patients with mTBI were prospectively recruited from the emergency department. Serum samples were collected at the time of hospital admission and every 6 hours up to 24 hours post injury. Neuronal (Ubiquitin C-terminal Hydrolase-L1 [UCH-L1]) and glial (glial fibrillary acidic protein [GFAP]) biomarker levels were analyzed. Advanced MRI data were acquired at 9±6.91 hours after injury. Patients’ neurocognitive status was assessed by using the Standard Assessment of Concussion (SAC) instrument.ResultsThe median serum levels of UCH-L1 and GFAP on admission were increased 4.9 folds and 10.6 folds, respectively, compared to reference values. Three patients were found to have intracranial hemorrhages on SWI, all of whom had very high GFAP levels. Total volume of brain white matter (WM) with abnormal fractional anisotropy (FA) measures of diffusion tensor imaging (DTI) were negatively correlated with patients’ SAC scores, including delayed recall. Both increased and decreased DTI-FA values were observed in the same subjects. Serum biomarker level was not correlated with patients’ DTI data nor SAC score.ConclusionsBlood biomarkers and advanced MRI may correlate or complement each other in different aspects of mTBI detection and characterization. GFAP might have potential to serve as a clinical screening tool for intracranial bleeding. UCH-L1 complements MRI in injury detection. Impairment at WM tracts may account for the patients’ neurocognitive symptoms.
Highlights
Traumatic brain injury (TBI) is a significant public healthcare burden in the United States, accounting for 1.7 million incidents in the United States each year [1,2]
A total of 9 patients who sustained Mild traumatic brain injury (mTBI) were prospectively recruited from the emergency department (ED) of Detroit Receiving Hospital (DRH), a Level-1 trauma center, which is an affiliated hospital of Detroit Medical Center (DMC)
We found that a) the biomarker levels were significantly higher in mTBI patients after injury; b) the levels of Glial Fibrillary Acidic Protein (GFAP) were highest in all subjects with intracranial bleeding on susceptibility weighted imaging (SWI), which is new finding in mTBI research; c) the total volume of white matter (WM) voxels with abnormal diffusion tensor imaging (DTI) fractional anisotropy (FA) measures is correlated with patient’s neurocognitive status, including memory; and d) DTI FA values could both increase and decrease in the acute setting, which is a new finding in mTBI research
Summary
Traumatic brain injury (TBI) is a significant public healthcare burden in the United States, accounting for 1.7 million incidents in the United States each year [1,2]. Up to 50% of mTBI patients develop neurocognitive problems within the first month [7,8], and 5-15% of them continue to manifest neurocognitive sequelae at one year [7,9] Often, their neurocognitive outcomes inconsistently correlate with clinical measures such as the Glasgow Coma Scale (GCS) score and post-traumatic amnesia. Serum biomarkers and advanced magnetic resonance imaging (MRI) techniques have already demonstrated their potential to improve the detection of brain injury even in patients with negative computed tomography (CT) findings. Total volume of brain white matter (WM) with abnormal fractional anisotropy (FA) measures of diffusion tensor imaging (DTI) were negatively correlated with patients’ SAC scores, including delayed recall. Both increased and decreased DTI-FA values were observed in the same subjects. Impairment at WM tracts may account for the patients’ neurocognitive symptoms
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