Biomarkers for traumatic brain injury: a short review

Gutierre, Marcela Usberti; Telles, João Paulo Mota; Welling, Leonardo C.; Rabelo, Ní­collas Nunes; Teixeira, Manoel Jacobsen; Figueiredo, Eberval Gadelha

doi:10.1007/s10143-020-01421-0

Cited by 11 publications

(20 citation statements)

References 39 publications

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“…In accordance with previous reports, TBI patients presented common abnormalities of brain morphology despite heterogeneity in injury severity and mechanisms, extent of focal insults, and time since injury [ 23 , 24 , 25 ]. Despite widespread atrophy across the cortical and subcortical regions, only a relatively small subset of this pattern of damage–mainly in the left inferior temporal gyrus and medial temporal lobe, supplementary motor area, thalamus, and ACC–were highly implicated in the post-traumatic cognitive impairment and psychiatric complaints.…”

Section: Discussionsupporting

confidence: 91%

Cortical and Subcortical Alterations and Clinical Correlates after Traumatic Brain Injury

Xue

Wang

Zhao

et al. 2022

JCM

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Background: Traumatic brain injury (TBI) often results in persistent cognitive impairment and psychiatric symptoms, while lesion location and severity are not consistent with its clinical complaints. Previous studies found cognitive deficits and psychiatric disorders following TBI are considered to be associated with prefrontal and medial temporal lobe lesions, however, the location and extent of contusions often cannot fully explain the patient′s impairments. Thus, we try to find the structural changes of gray matter (GM) and white matter (WM), clarify their correlation with psychiatric symptoms and memory following TBI, and determine the brain regions that primary correlate with clinical measurements. Methods: Overall, 32 TBI individuals and 23 healthy controls were recruited in the study. Cognitive impairment and psychiatric symptoms were examined by Mini-Mental State Examination (MMSE), Hospital Anxiety and Depression Scale (HADS), and Wechsler Memory Scale-Chinese Revision (WMS-CR). All MRI data were scanned using a Siemens Prisma 3.0 Tesla MRI system. T1 MRI data and diffusion tensor imaging (DTI) data were processed to analyze GM volume and WM microstructure separately. Results: In the present study, TBI patients underwent widespread decrease of GM volume in both cortical and subcortical regions. Among these regions, four brain areas including the left inferior temporal gyrus and medial temporal lobe, supplementary motor area, thalamus, and anterior cingulate cortex (ACC) were highly implicated in the post-traumatic cognitive impairment and psychiatric complaints. TBI patients also underwent changes of WM microstructure, involving decreased fractional anisotropy (FA) value in widespread WM tracts and increased mean diffusivity (MD) value in the forceps minor. The changes of WM microstructure were significantly correlated with the decrease of GM volume. Conclusions: TBI causes widespread cortical and subcortical alterations including a reduction in GM volume and change in WM microstructure related to clinical manifestation. Lesions in temporal lobe may lead to more serious cognitive and emotional dysfunction, which should attract our high clinical attention.

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Section: Discussionsupporting

confidence: 91%

Cortical and Subcortical Alterations and Clinical Correlates after Traumatic Brain Injury

Xue

Wang

Zhao

et al. 2022

JCM

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“…t-tau, NAA, αII-spectrin, GSH and NSE are all expressed in or associated with neurons and axons 83,173,212,249 , and their release after TBI therefore suggests neuronal and axonal damage 121,235 , such as retinal ganglion loss and RNFL thinning 119,123,[161][162][163] . NAA, NSE and GFAP are also associated with inflammation 185,206,233 , which is also an ocular response to TBI, particularly within the ON 111,123,166 . Disproving CSF compartmentalisation would suggest the possibility of biomarker detection in the CSF such as, the GFAP 40,173,203 , UCHL1 40,61 , S100B 61,196 , αII-spectrin 188 , and MicroRNAs 189 , in the retrolaminar CSF (behind the ON head) and potentially in the eye.…”

Section: 3mentioning

confidence: 99%

“…Studies have identified elevated levels in plasma after mild to moderate injuries (Figure 5a), as early as 1-hour post-injury, associated with axonal damage and DAI 170,172 . UCHL1 is sensitive to patients with positive CT scans and unfavourable outcomes 181,185,210 , but has low specificity, in the CSF, blood, peripheral nervous system, limiting its utility 66,211 . αII-spectrin is a cytoskeleton protein in axons and presynaptic terminals 212 .…”

Section: 1mentioning

confidence: 99%

“…Many TBI biomarkers are assayed in accessible biofluids [40] , [66] , [80] , [167] , [173] , [175] , [183] , [185] – [187] . Pineda et al , stated that ‘good’ biomarkers should be in easily accessible biofluids, with low background levels in healthy control groups, have high sensitivity and specificity to all injury severities and be released in a “time-locked sequence” after the injury [40] , [188] , [189] .…”

Section: Chemical Responses To Tbimentioning

confidence: 99%

“…Biomarkers associated with neuronal damage include NSE, a glycolytic enzyme and UCHL1, a protease expressed in red blood cells (RBCs) and CSF, respectively [40] , [61] , [173] . NSE is correlated to posttraumatic inflammation [185] , and raised NSE levels, within 4 hours of moderate-severe TBI may identify patients at higher risk of cognitive dysfunction [208] . The detectability of NSE in RBC makes it readily accessible but introduces a risk of cross-contamination in blood samples in the event of haemolysis (RBC rupture), rendering it less specific [209] .…”

Section: Chemical Responses To Tbimentioning

confidence: 99%

See 2 more Smart Citations

Review: Emerging Eye-Based Diagnostic Technologies for Traumatic Brain Injury

Harris

Rickard

Butt

et al. 2023

IEEE Rev. Biomed. Eng.

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The study of ocular manifestations of neurodegenerative disorders, Oculomics, is a growing field of investigation for early diagnostics, enabling structural and chemical biomarkers to be monitored overtime to predict prognosis. Traumatic brain injury (TBI) triggers a cascade of events harmful to the brain, which can lead to neurodegeneration. TBI, termed the "silent epidemic" is becoming a leading cause of death and disability worldwide. There is currently no effective diagnostic tool for TBI, and yet, earlyintervention is known to considerably shorten hospital stays, improve outcomes, fasten neurological recovery and lower mortality rates, highlighting the unmet need for techniques capable of rapid and accurate point-of-care diagnostics, implemented in the earliest stages. This review focuses on the latest advances in the main neuropathophysiological responses and the achievements and shortfalls of TBI diagnostic methods. Validated and emerging TBI-indicative biomarkers are outlined and linked to ocular neuro-disorders. Methods detecting structural and chemical ocular responses to TBI are categorised along with prospective chemical and physical sensing techniques. Particular attention is drawn to the potential of Raman spectroscopy as a non-invasive sensing of neurological molecular signatures in the ocular projections of the brain, laying the platform for the first tangible path towards alternative point-of-care diagnostic technologies for TBI.

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Head Injuries

Stahel

Buchanan²

2022

Textbook of Polytrauma Management

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Biomarkers for traumatic brain injury: a short review

Cited by 11 publications

References 39 publications

Cortical and Subcortical Alterations and Clinical Correlates after Traumatic Brain Injury

Cortical and Subcortical Alterations and Clinical Correlates after Traumatic Brain Injury

Review: Emerging Eye-Based Diagnostic Technologies for Traumatic Brain Injury

Head Injuries

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