What’s New in Traumatic Brain Injury: Update on Tracking, Monitoring and Treatment
Abstract
:1. Introduction
2. Gene Expression Profiles after TBI
2.1. Genetic Polymorphisms Influence Recovery
2.2. Local and Remote Gene Expression Profiles
2.3. miRNAs Expression Profiles
3. Biochemical Markers for TBI Diagnosis, Prognosis and Management
3.1. miRNAs as Diagnostic and Prognostic Biomarkers
3.2. Serum Autoantibodies as Long-Term Biomarkers
Serum Auto-Antibodies | Significance | Reference |
---|---|---|
Anti-GFAP and GFAP break down products (BDPs) | Strong diagnostic marker and prognostic factor | Zhang et al. 2014 [36] |
Anti-BMP (basic myelinprotein) | Weak diagnostic marker and prognostic factor | Ngankam et al. 2011 [37] |
Anti-PL (phospholipid) | Weak diagnostic marker and prognostic factor | Ngankam et al. 2011 [37] |
Anti-NMDA and Anti-AMPA | Moderate prognostic factor | Goryunova et al. 2007 [38] |
3.3. Early Generation Biomarkers
Candidate Marker | Marker Origins | Attributes | References |
---|---|---|---|
pNF-H (Phosphorylated Neurofilament H) | Neuron | Neuronal injury Blood levels of pNF-H levels showed significant correlations with the level of consciousness and CT findings | Ghonemi et al., 2013 [41] |
NSE (neuron-specific enolase) | Neuron | Neuronal injury Neuron-specific Elevated blood NSE levels have been linked to poor outcome in severe and mild TBI | Topolovec-Vranic et al., 2011 [42] |
SBDP150/SBDP145 (spectrin breakdown products) (Calpain-generated) αII-spectrin proteolysis | Axons and presynaptic terminals | Acute necrosis High level is associated with worse Glasgow Coma Scale (GCS), longer ICP elevation, and poor outcome following TBI | Mondello et al., 2010 [43] |
SBDP120 (caspase-3-generated) | Axons and presynaptic terminals | Delayed apoptosis Underlying cell death mechanisms | Brophy et al., 2009 [27] |
UCH-L1 (ubiquitin carboxyl-terminalhydrolase-L1) | Neuronal cell body | Neuronal cell body injury sensitive and specific biomarker elevated UCH-L1 levels are associated with lower Glasgow Coma Scale (GCS) and poor outcome after TBI | Papa et al., 2012 [44] |
MAP2 (microtubule-associated protein 2) | Dendrites | Dendritic injury | Kobeissy et al., 2006 [45] |
MBP (myelin basic protein) | Oligoden-drocytes/Schwann cells | Demyelination Excellent specificity, limited sensitivity | Berger et al., 2005 [46] |
S100B (Calcium-Binding Protein B) and its isoforms s100A1B and s100BB | Glia cells | Glial injury Elevated blood and urine levels of s100b, 100A1B and s100BB are associated with poor outcome in TBI | Rodriguez et al., 2012 [47] |
GFAP (glialfibrillary acidic protein) | Glia cells | Glial injury CNS-specificity Elevated blood GFAP levels to predict TBI outcome | Vos et al., 2010 [48] |
GFAP breakdown products (GFAP-BDP) | Glia cells | Specific marker of brain damage GFAPBDP >0.68 lg/L within 24 h of injury was associated with acute traumatic lesions on the CT and with unfavorable 6-month outcome | Okonkwo et al., 2013 [49] |
Angiopoietins-1/2(Ang-1/2) | Endothelia cells | Vascular injury and regeneration evaluation in plasma, serum and cerebrospinal fluid | Chittiboina et al., 2013 [50] |
3.4. Clinical Limitations and Outlook
4. Neuroimaging Advances for TBI Diagnosis and Prognosis
Neuroimaging Techniques | Attributes | Limitation |
---|---|---|
Susceptibility-weighted imaging (SWI) | Microbleeding in diffuse axonal injury | Long acquisition time and sensitivity to motion artifacts |
Diffusion-weighted imaging (DWI) | Non hemorrhagic diffuse axonal injury | Heterogeneity with large standard deviation of the ADC changes |
Diffusion tensor imaging (DTI) | White matter integrity | FA measurement is compromised by interstitial fluid content |
High definition fiber tractography (HDFT) | Structural brain connectivity | Restricted ability to determine crossing of fibers within a voxel |
Functional MRI (fMRI) | Neuronal activity with cerebral oxygen consumption | Physics based factors of signal and the field inhomogeneity generated by deoxyhemoglobin |
Magnetoencephalography (MEG) | Magnetic fields of postsynaptic ionic currents | Variety of incomparable approaches and absence of standard analyzing protocols |
Magnetic resonance spectroscopy (MRS) | Intracellular neuronal metabolic status | Limited spatiotemporal resolution and small brain fields are challenging to analyze |
Single-photon emission computed tomography (SPECT) | Regional cerebral blood flow | Regional cerebral blood flow changes after TBI do not always correspond to metabolism |
4.1. Susceptibility-Weighted Imaging (SWI)
4.2. Diffusion-Weighted Imaging (DWI)
4.3. Diffusion Tensor Imaging (DTI)
4.4. High Definition Fiber Tractography (HDFT)
4.5. Functional MRI (fMRI)
4.6. Magnetoencephalography (MEG)
4.7. Magnetic Resonance Spectroscopy (MRS)
4.8. Single-Photon Emission Computed Tomography (SPECT)
5. Neuromonitoring after TBI
5.1. Intracranial Pressure (ICP) Monitoring and Cerebral Autoregulation
Index | Reference | Title |
---|---|---|
PRx (pressure reactivity index) | Howells et al., 2014 [171] | An optimal frequency range for assessing the pressure reactivity index in patients with traumatic brain injury |
L-PRx (low-frequency pressure reactivity index) | Depreitere et al., 2014 [172] | Pressure autoregulation monitoring and cerebral perfusion pressure target recommendation in patients with severe traumatic brain injury based on minute-by-minute monitoring data |
Mx (mean index, TCD-derived) | Zweifel et al., 2008 [173] | Continuous monitoring of cerebrovascular pressure reactivity in patients with head injury |
Sx (systolic flow index, TCD-derived) | Budohoski et al., 2012 [174] | Monitoring cerebral autoregulation after head injury. Which component of transcranial Doppler flow velocity is optimal |
PAx (pressure-amplitude index, TCD-derived) | Radolovich et al., 2011 [175] | Pulsatile intracranial pressure and cerebral autoregulation after traumatic brain injury |
PI (pulsatility index, TCD-derived) | Melo et al., 2011 [176] | Transcranial Doppler can predict intracranial hypertension in children with severe traumatic brain injuries |
COx (cerebral oximetry index, NIRS-derived, Somanetics) | Brady et al., 2007 [177] | Continuous time-domain analysis of cerebrovascular autoregulation using NIRS |
TOx (tissue oxygenation index, NIRS-derived, Hämamatsu) | Steiner et al., 2009 [178] | NIRS can monitor dynamic cerebral autoregulation in adults |
HVx (haemoglobin volume index, NIRS-derived, Somanetics) | Lee et al., 2012 [179] | Noninvasive autoregulation monitoring in a swine model of pediatric cardiac arrest |
THx (total haemoglobin reactivity index, IRS-derived, Hämamatsu) | Zweifel et al., 2010 [180] | Noninvasive monitoring of cerebrovascular reactivity with NIRS in head-injured patients |
ORx (brain tissue oxygen reactivity index) | Lang et al., 2014 [181] | Changes in cerebral partial oxygen pressure and cerebrovascular reactivity during intracranial pressure plateau waves |
5.2. Brain Oxygen Monitoring
5.3. Electrophysiologic Monitoring
5.4. Microdialysis
Marker for | Biomarker | Clinical Significance |
---|---|---|
Energy metabolism | Glucose | ↓ in hypoxia/ischemia |
Lactate | ↑ in hypoxia/ischemia | |
Pyruvate | ↓ in hypoxia/ischemia | |
Lactate/Pyruvate Ratio | ↑ in hypoxia/ischemia = best marker for anaerobic metabolism | |
Cellular distress | Glycerol | ↑ with destruction of cell membrane structure and generation of free radicals |
Glutamate | ↑ in hypoxia/ischemia and excitotoxicity |
Biomarker | Significance | Reference |
---|---|---|
Serum albumin | BBB disruption | Blyth et al., 2009 [212] |
Hemoglobin subunit α and ß | Red blood cell degradation | Babu et al., 2012 [213] |
Serotransferrin | Free iron in the brain tissue | Park et al., 2011 [214] |
Creatine kinase B-type | Enhancing predictive sensitivity of S100B as a biomarker | Bazarian et al., 2006 [215] |
Cystatin C | Increased autophagy | Liu et al., 2013 [216] |
Apolipoprotein A-1 and E | Membrane remodeling due to cellular trauma | Mahley et al., 2012 [217] |
α-2-HS-glycoprotein (Fetuin-A) | Systemic response to cerebral injury | Wang and Sama et al., 2012 [218] |
Complement C3 | Activation of the innate immune response to injury | Ducruet et al., 2009 [219] |
5.5. Brain-on-Chip
6. Treatment Strategies and Modalities after TBI
6.1. Stem Cell Based Therapy
6.1.2. Stabilized BBB by Stem Cells
6.1.3. Reduction of Oxidative Stress by Stem Cells
6.1.4. Immunomodulation by Stem Cells
6.1.5. White Matter Protection and Microvascular Integrity by Stem Cells
6.2. Nanotechnology Based Therapy
6.2.1. Perfluorocarbons
6.2.2. Polyethylene Glycol-Functionalized Hydrophilic Carbon Clusters (PEG-HCCs)
6.3. Preconditioning in TBI Treatment
6.3.1. Hyperbaric Oxygen Treatment (HBOT)
6.3.2. Glutaminergic Precoditioning
6.4. Hormones in TBI Treatment
6.4.1. Erythropoietin
6.4.2. Progesterone
6.5. Antioxidants in TBI Treatment
6.5.1. U-83836E
6.5.2. Melatonin
6.5.3. Tempol
6.5.4. Resveratrol
6.6. Hypothermia
6.7. Inhibitor Interventions for TBI Treatment
6.7.1. CR8
6.7.2. Statins
6.7.3. Acetylcholinesterase Inhibitors
6.8. Lithium Used for TBI Treatment
7. Conclusions
Conflicts of Interest
References
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Reis, C.; Wang, Y.; Akyol, O.; Ho, W.M.; II, R.A.; Stier, G.; Martin, R.; Zhang, J.H. What’s New in Traumatic Brain Injury: Update on Tracking, Monitoring and Treatment. Int. J. Mol. Sci. 2015, 16, 11903-11965. https://doi.org/10.3390/ijms160611903
Reis C, Wang Y, Akyol O, Ho WM, II RA, Stier G, Martin R, Zhang JH. What’s New in Traumatic Brain Injury: Update on Tracking, Monitoring and Treatment. International Journal of Molecular Sciences. 2015; 16(6):11903-11965. https://doi.org/10.3390/ijms160611903
Chicago/Turabian StyleReis, Cesar, Yuechun Wang, Onat Akyol, Wing Mann Ho, Richard Applegate II, Gary Stier, Robert Martin, and John H. Zhang. 2015. "What’s New in Traumatic Brain Injury: Update on Tracking, Monitoring and Treatment" International Journal of Molecular Sciences 16, no. 6: 11903-11965. https://doi.org/10.3390/ijms160611903
APA StyleReis, C., Wang, Y., Akyol, O., Ho, W. M., II, R. A., Stier, G., Martin, R., & Zhang, J. H. (2015). What’s New in Traumatic Brain Injury: Update on Tracking, Monitoring and Treatment. International Journal of Molecular Sciences, 16(6), 11903-11965. https://doi.org/10.3390/ijms160611903