Blennow, K; Brody, D L; Kochanek, P M; Levin, H; McKee, A; Ribbers, G M; Yaffe, K; Zetterberg, H
Traumatic brain injuries Journal Article
In: Nature Reviews Disease Primers, vol. 2, 2016.
Abstract | Links | BibTeX | Tags: amyloid beta protein, Article, axonal injury, biological marker, BIOPHYSICS, blood, brain, BRAIN damage, cerebrospinal fluid, Chronic traumatic encephalopathy, computer assisted tomography, disease severity, endocrine disease, heredity, human, molecular pathology, neuropathology, nonhuman, nuclear magnetic resonance imaging, Pathophysiology, positron emission tomography, postconcussion syndrome, priority journal, protein aggregation, quality of life, screening, tau protein, traumatic brain injury
@article{Blennow2016,
title = {Traumatic brain injuries},
author = {Blennow, K and Brody, D L and Kochanek, P M and Levin, H and McKee, A and Ribbers, G M and Yaffe, K and Zetterberg, H},
doi = {10.1038/nrdp.2016.84},
year = {2016},
date = {2016-01-01},
journal = {Nature Reviews Disease Primers},
volume = {2},
abstract = {Traumatic brain injuries (TBIs) are clinically grouped by severity: mild, moderate and severe. Mild TBI (the least severe form) is synonymous with concussion and is typically caused by blunt non-penetrating head trauma. The trauma causes stretching and tearing of axons, which leads to diffuse axonal injury-the best-studied pathogenetic mechanism of this disorder. However, mild TBI is defined on clinical grounds and no well-validated imaging or fluid biomarkers to determine the presence of neuronal damage in patients with mild TBI is available. Most patients with mild TBI will recover quickly, but others report persistent symptoms, called post-concussive syndrome, the underlying pathophysiology of which is largely unknown. Repeated concussive and subconcussive head injuries have been linked to the neurodegenerative condition chronic traumatic encephalopathy (CTE), which has been reported post-mortem in contact sports athletes and soldiers exposed to blasts. Insights from severe injuries and CTE plausibly shed light on the underlying cellular and molecular processes involved in mild TBI. MRI techniques and blood tests for axonal proteins to identify and grade axonal injury, in addition to PET for tau pathology, show promise as tools to explore CTE pathophysiology in longitudinal clinical studies, and might be developed into diagnostic tools for CTE. Given that CTE is attributed to repeated head trauma, prevention might be possible through rule changes by sports organizations and legislators. © 2016 Macmillan Publishers Limited, part of Springer Nature.},
keywords = {amyloid beta protein, Article, axonal injury, biological marker, BIOPHYSICS, blood, brain, BRAIN damage, cerebrospinal fluid, Chronic traumatic encephalopathy, computer assisted tomography, disease severity, endocrine disease, heredity, human, molecular pathology, neuropathology, nonhuman, nuclear magnetic resonance imaging, Pathophysiology, positron emission tomography, postconcussion syndrome, priority journal, protein aggregation, quality of life, screening, tau protein, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}
Ojo, J O; Mouzon, B C; Crawford, F
Repetitive head trauma, chronic traumatic encephalopathy and tau: Challenges in translating from mice to men Journal Article
In: Experimental Neurology, vol. 275, pp. 389–404, 2016.
Abstract | Links | BibTeX | Tags: amyloid beta protein, animal, Animal models, Animals, Astroglial tangles, Brain Injury, cell activation, Chronic, complication, Concussion, Craniocerebral Trauma, CTE, diffuse axonal injury, disease duration, disease model, Disease Models, genetic predisposition, gliosis, head injury, hippocampus, human, Humans, lifestyle modification, lithium, metabolism, Mice, microglia, minocycline, mouse, nervous system inflammation, Neurobehaviour, Neurofibrillary tangles, neuropathology, nonhuman, pathogenesis, pathology, priority journal, procedures, protein aggregation, protein analysis, protein blood level, protein cleavage, Repetitive TBI, Review, sex difference, stress activated protein kinase inhibitor, Systematic Review, Tau, tau protein, tau Proteins, Transgenic mice, Translational Medical Research, translational research, traumatic brain injury, trends
@article{Ojo2016,
title = {Repetitive head trauma, chronic traumatic encephalopathy and tau: Challenges in translating from mice to men},
author = {Ojo, J O and Mouzon, B C and Crawford, F},
doi = {10.1016/j.expneurol.2015.06.003},
year = {2016},
date = {2016-01-01},
journal = {Experimental Neurology},
volume = {275},
pages = {389--404},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurological and psychiatric condition marked by preferential perivascular foci of neurofibrillary and glial tangles (composed of hyperphosphorylated-tau proteins) in the depths of the sulci. Recent retrospective case series published over the last decade on athletes and military personnel have added considerably to our clinical and histopathological knowledge of CTE. This has marked a vital turning point in the traumatic brain injury (TBI) field, raising public awareness of the potential long-term effects of mild and moderate repetitive TBI, which has been recognized as one of the major risk factors associated with CTE. Although these human studies have been informative, their retrospective design carries certain inherent limitations that should be cautiously interpreted. In particular, the current overriding issue in the CTE literature remains confusing in regard to appropriate definitions of terminology, variability in individual pathologies and the potential case selection bias in autopsy based studies. There are currently no epidemiological or prospective studies on CTE. Controlled preclinical studies in animals therefore provide an alternative means for specifically interrogating aspects of CTE pathogenesis. In this article, we review the current literature and discuss difficulties and challenges of developing in-vivo TBI experimental paradigms to explore the link between repetitive head trauma and tau-dependent changes. We provide our current opinion list of recommended features to consider for successfully modeling CTE in animals to better understand the pathobiology and develop therapeutics and diagnostics, and critical factors, which might influence outcome. We finally discuss the possible directions of future experimental research in the repetitive TBI/CTE field. © 2015 Elsevier Inc..},
keywords = {amyloid beta protein, animal, Animal models, Animals, Astroglial tangles, Brain Injury, cell activation, Chronic, complication, Concussion, Craniocerebral Trauma, CTE, diffuse axonal injury, disease duration, disease model, Disease Models, genetic predisposition, gliosis, head injury, hippocampus, human, Humans, lifestyle modification, lithium, metabolism, Mice, microglia, minocycline, mouse, nervous system inflammation, Neurobehaviour, Neurofibrillary tangles, neuropathology, nonhuman, pathogenesis, pathology, priority journal, procedures, protein aggregation, protein analysis, protein blood level, protein cleavage, Repetitive TBI, Review, sex difference, stress activated protein kinase inhibitor, Systematic Review, Tau, tau protein, tau Proteins, Transgenic mice, Translational Medical Research, translational research, traumatic brain injury, trends},
pubstate = {published},
tppubtype = {article}
}
Lawrence, D W; Comper, P; Hutchison, M G; Sharma, B
The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review Journal Article
In: Brain Injury, vol. 29, no. 9, pp. 1018–1031, 2015.
Abstract | Links | BibTeX | Tags: 80 and over, aged, allele, Alleles, Alzheimer disease, amyloid beta protein, APOE, apolipoprotein E, apolipoprotein E4, Article, athlete, brain concussion, Brain Injuries, clinical evaluation, cognition, cognitive defect, disease severity, Female, follow up, genetic association, genetic risk, genetics, GENOTYPE, Glasgow Outcome Scale, heterozygote, histopathology, homozygote, human, Humans, Incidence, injury severity, Male, Memory, nerve cell necrosis, neuropathology, Neuroprotection, outcome assessment, pediatrics, Prevalence, Prognosis, prognostic assessment, protein function, psychologic test, psychology, Recovery, scoring system, Systematic Review, tau protein, traumatic brain injury, treatment outcome, very elderly, Wechsler Intelligence Scale
@article{Lawrence2015,
title = {The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review},
author = {Lawrence, D W and Comper, P and Hutchison, M G and Sharma, B},
doi = {10.3109/02699052.2015.1005131},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {9},
pages = {1018--1031},
abstract = {Background: The apolipoprotein E gene (APOE) has emerged as a candidate for prognosticating traumatic brain injury (TBI) recovery, with APOE$epsilon$4 identified as a susceptibility marker for poor outcome, despite large discrepancy in its reported influence post-TBI.Methods: A systematic review was conducted, including all primary articles investigating the role of APOE$epsilon$4 on TBI outcome. A total of 65 studies were included, including 24 predominantly investigating mild (mTBI), seven moderate (modTBI) and 33 severe (sTBI); severity was not reported in one study.Results: In mTBI studies, the association between APOE$epsilon$4 and post-TBI outcome was concluded as non-contributory in 14 studies (58.3%), hazardous in nine (37.5%) and protective in one (4.2%). In sTBI studies, the role of APOE$epsilon$4 was hazardous in 21 (63.6%), non-contributory in nine (27.3%) and protective in three (9.1%). Of the seven studies investigating dementia outcomes, four observed a hazardous association with APOE$epsilon$4, while three reported no association. Six studies examined Alzheimers dementia pathology, of which three reported a hazardous influence of APOE$epsilon$4.Conclusions: The influence of APOE$epsilon$4 on neuropsychological testing, functional outcome and in paediatric populations was incongruous. This review supports the majority of research indicating APOE$epsilon$4 adversely influences recovery following TBI, particularly with respect to dementia-related outcomes and outcomes following sTBI. © 2015 Taylor \& Francis Group, LLC.},
keywords = {80 and over, aged, allele, Alleles, Alzheimer disease, amyloid beta protein, APOE, apolipoprotein E, apolipoprotein E4, Article, athlete, brain concussion, Brain Injuries, clinical evaluation, cognition, cognitive defect, disease severity, Female, follow up, genetic association, genetic risk, genetics, GENOTYPE, Glasgow Outcome Scale, heterozygote, histopathology, homozygote, human, Humans, Incidence, injury severity, Male, Memory, nerve cell necrosis, neuropathology, Neuroprotection, outcome assessment, pediatrics, Prevalence, Prognosis, prognostic assessment, protein function, psychologic test, psychology, Recovery, scoring system, Systematic Review, tau protein, traumatic brain injury, treatment outcome, very elderly, Wechsler Intelligence Scale},
pubstate = {published},
tppubtype = {article}
}
Dessy, A M; Rasouli, J; Choudhri, T F
Second Impact Syndrome: A Rare, Devastating Consequence of Repetitive Head Injuries Journal Article
In: Neurosurgery Quarterly, vol. 25, no. 3, pp. 423–426, 2015.
Abstract | Links | BibTeX | Tags: Article, brain concussion, clinical feature, Concussion, Dizziness, fatigue, headache, human, hyperemia, intracranial hypertension, memory disorder, Neck pain, neuropathology, neurosurgeon, neurosurgery, Pathophysiology, postconcussion syndrome, priority journal, respiratory failure, Second impact syndrome, sport injury, traumatic brain injury
@article{Dessy2015,
title = {Second Impact Syndrome: A Rare, Devastating Consequence of Repetitive Head Injuries},
author = {Dessy, A M and Rasouli, J and Choudhri, T F},
doi = {10.1097/WNQ.0000000000000085},
year = {2015},
date = {2015-01-01},
journal = {Neurosurgery Quarterly},
volume = {25},
number = {3},
pages = {423--426},
abstract = {Sports-related concussion has been viewed as a developing public health crisis in recent years. Underrecognition of concussions can lead to premature clearance for athletic participation. Second impact syndrome (SIS) represents a rare, yet devastating, potential outcome of premature return to play. SIS is a condition in which rapid brain swelling occurs as a result of a repeat head injury sustained before symptoms of a previous head injury have resolved. Within minutes of the second impact, diffuse cerebral swelling, brain herniation, and death can occur. There are \<20 documented cases of SIS in the world literature to date, and the general understanding of the syndrome is based largely on interpretation of anecdotal cases. This article reviews current understanding of the epidemiology and pathology of SIS. Given neurosurgeons' role in management of head trauma, it is essential that neurosurgeons acquire and maintain thorough knowledge of concussion diagnosis, treatment, and management. © 2014 Wolters Kluwer Health, Inc. All rights reserved.},
keywords = {Article, brain concussion, clinical feature, Concussion, Dizziness, fatigue, headache, human, hyperemia, intracranial hypertension, memory disorder, Neck pain, neuropathology, neurosurgeon, neurosurgery, Pathophysiology, postconcussion syndrome, priority journal, respiratory failure, Second impact syndrome, sport injury, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}
Rapp, P E; Keyser, D O; Albano, A; Hernandez, R; Gibson, D B; Zambon, R A; David Hairston, W; Hughes, J D; Krystal, A; Nichols, A S
Traumatic brain injury detection using electrophysiological methods Journal Article
In: Frontiers in Human Neuroscience, vol. 9, no. FEB, 2015.
Abstract | Links | BibTeX | Tags: Article, brain electrophysiology, computer assisted tomography, Concussion, connectome, diagnostic accuracy, EEG, electroencephalogram, Electroencephalography, event related potential, Event-Related Potentials, evidence based medicine, executive function, human, intermethod comparison, latent period, neuroimaging, neuropathology, Non-linear dynamical analysis, nuclear magnetic resonance imaging, QEEG, Signal Processing, traumatic brain injury
@article{Rapp2015,
title = {Traumatic brain injury detection using electrophysiological methods},
author = {Rapp, P E and Keyser, D O and Albano, A and Hernandez, R and Gibson, D B and Zambon, R A and {David Hairston}, W and Hughes, J D and Krystal, A and Nichols, A S},
doi = {10.3389/fnhum.2015.00011},
year = {2015},
date = {2015-01-01},
journal = {Frontiers in Human Neuroscience},
volume = {9},
number = {FEB},
abstract = {Measuring neuronal activity with electrophysiological methods may be useful in detecting neurological dysfunctions, such as mild traumatic brain injury (mTBI).This approach may be particularly valuable for rapid detection in at-risk populations including military service members and athletes. Electrophysiological methods, such as quantitative electroencephalography (qEEG) and recording event-related potentials (ERPs) may be promising; however, the field is nascent and significant controversy exists on the efficacy and accuracy of the approaches as diagnostic tools. For example, the specific measures derived from an electroencephalogram (EEG) that are most suitable as markers of dysfunction have not been clearly established. A study was conducted to summarize and evaluate the statistical rigor of evidence on the overall utility of qEEG as an mTBI detection tool. The analysis evaluated qEEG measures/parameters that may be most suitable as fieldable diagnostic tools, identified other types of EEG measures and analysis methods of promise, recommended specific measures and analysis methods for further development as mTBI detection tools, identified research gaps in the field, and recommended future research and development thrust areas. The qEEG study group formed the following conclusions: (1) Individual qEEG measures provide limited diagnostic utility for mTBI. However, many measures can be important features of qEEG discriminant functions, which do show significant promise as mTBI detection tools. (2) ERPs offer utility in mTBI detection. In fact, evidence indicates that ERPs can identify abnormalities in cases where EEGs alone are non-disclosing. (3)The standard mathematical procedures used in the characterization of mTBI EEGs should be expanded to incorporate newer methods of analysis including non-linear dynamical analysis, complexity measures, analysis of causal interactions, graph theory, and information dynamics. (4) Reports of high specificity in qEEG evaluations of TBI must be interpreted with care. High specificities have been reported in carefully constructed clinical studies in which healthy controls were compared against a carefully selected TBI population. The published literature indicates, however, that similar abnormalities in qEEG measures are observed in other neuropsychiatric disorders. While it may be possible to distinguish a clinical patient from a healthy control participant with this technology, these measures are unlikely to discriminate between, for example, major depressive disorder, bipolar disorder, or TBI. The specificities observed in these clinical studies may well be lost in real world clinical practice. (5)The absence of specificity does not preclude clinical utility. The possibility of use as a longitudinal measure of treatment response remains. However, efficacy as a longitudinal clinical measure does require acceptable test-retest reliability. To date, very few test-retest reliability studies have been published with qEEG data obtained from TBI patients or from healthy controls. This is a particular concern because high variability is a known characteristic of the injured central nervous system. © 2015 Rapp, Keyser , Albano, Hernandez, Gibson, Zambon, Hairston, Hughes, Krystal and Nichols.},
keywords = {Article, brain electrophysiology, computer assisted tomography, Concussion, connectome, diagnostic accuracy, EEG, electroencephalogram, Electroencephalography, event related potential, Event-Related Potentials, evidence based medicine, executive function, human, intermethod comparison, latent period, neuroimaging, neuropathology, Non-linear dynamical analysis, nuclear magnetic resonance imaging, QEEG, Signal Processing, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}
Stein, T D; Alvarez, V E; McKee, A C
Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel Journal Article
In: Alzheimer's Research and Therapy, vol. 6, no. 1, 2014.
Abstract | Links | BibTeX | Tags: Aggression, Alzheimer disease, amnesia, army, astrocyte, athlete, behavior change, brain atrophy, brain stem, brain weight, central sulcus, chronic disease, Chronic Traumatic Encephalopathy TAR DNA binding p, cognitive defect, comorbidity, Dementia, depression, diencephalon, diffuse Lewy body disease, exposure, frontotemporal dementia, human, impulsiveness, irritability, Motor neuron disease, nerve fiber, neurite, neurofibrillary tangle, neuropathology, nonhuman, personality disorder, priority journal, Review, short term memory, soldier, staging, suicidal ideation, tau protein, tauopathy, temporal lobe, traumatic brain injury, veteran
@article{Stein2014,
title = {Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel},
author = {Stein, T D and Alvarez, V E and McKee, A C},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84892718392\&partnerID=40\&md5=c39a0e58ad33cee7a570b4681131d6ea},
doi = {10.1186/alzrt234},
year = {2014},
date = {2014-01-01},
journal = {Alzheimer's Research and Therapy},
volume = {6},
number = {1},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs in association with repetitive traumatic brain injury experienced in sport and military service. In most instances, the clinical symptoms of the disease begin after a long period of latency ranging from several years to several decades. The initial symptoms are typically insidious, consisting of irritability, impulsivity, aggression, depression, short-term memory loss and heightened suicidality. The symptoms progress slowly over decades to include cognitive deficits and dementia. The pathology of CTE is characterized by the accumulation of phosphorylated tau protein in neurons and astrocytes in a pattern that is unique from other tauopathies, including Alzheimer's disease. The hyperphosphorylated tau abnormalities begin focally, as perivascular neurofibrillary tangles and neurites at the depths of the cerebral sulci, and then spread to involve superficial layers of adjacent cortex before becoming a widespread degeneration affecting medial temporal lobe structures, diencephalon and brainstem. Most instances of CTE (\>85% of cases) show abnormal accumulations of phosphorylated 43 kDa TAR DNA binding protein that are partially colocalized with phosphorylated tau protein. As CTE is characterized pathologically by frontal and temporal lobe atrophy, by abnormal deposits of phosphorylated tau and by 43 kDa TAR DNA binding protein and is associated clinically with behavioral and personality changes, as well as cognitive impairments, CTE is increasingly categorized as an acquired frontotemporal lobar degeneration. Currently, some of the greatest challenges are that CTE cannot be diagnosed during life and the incidence and prevalence of the disorder remain uncertain. Furthermore, the contribution of age, gender, genetics, stress, alcohol and substance abuse to the development of CTE remains to be determined. © 2014 BioMed Central Ltd.},
keywords = {Aggression, Alzheimer disease, amnesia, army, astrocyte, athlete, behavior change, brain atrophy, brain stem, brain weight, central sulcus, chronic disease, Chronic Traumatic Encephalopathy TAR DNA binding p, cognitive defect, comorbidity, Dementia, depression, diencephalon, diffuse Lewy body disease, exposure, frontotemporal dementia, human, impulsiveness, irritability, Motor neuron disease, nerve fiber, neurite, neurofibrillary tangle, neuropathology, nonhuman, personality disorder, priority journal, Review, short term memory, soldier, staging, suicidal ideation, tau protein, tauopathy, temporal lobe, traumatic brain injury, veteran},
pubstate = {published},
tppubtype = {article}
}
Baugh, C M; Robbins, C A; Stern, R A; McKee, A C
Current understanding of chronic traumatic encephalopathy Journal Article
In: Current Treatment Options in Neurology, vol. 16, no. 9, 2014.
Links | BibTeX | Tags: Article, attention disturbance, axonal injury, biological marker, Biomarker, Brain trauma, Chronic traumatic encephalopathy, Chronic traumatic encephalopathy (CTE), Chronic Traumatic Encephalopathy APOE, clinical feature, concentration loss, Concussion, degenerative disease, football, genetic risk, headache, human, in vivo study, injury severity, lifestyle, neuropathology, risk factor, Tau, traumatic brain injury, Traumatic brain injury (TBI)
@article{Baugh2014,
title = {Current understanding of chronic traumatic encephalopathy},
author = {Baugh, C M and Robbins, C A and Stern, R A and McKee, A C},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84905669544\&partnerID=40\&md5=b7b1e2fe8132cad56800bf4102896b64},
doi = {10.1007/s11940-014-0306-5},
year = {2014},
date = {2014-01-01},
journal = {Current Treatment Options in Neurology},
volume = {16},
number = {9},
keywords = {Article, attention disturbance, axonal injury, biological marker, Biomarker, Brain trauma, Chronic traumatic encephalopathy, Chronic traumatic encephalopathy (CTE), Chronic Traumatic Encephalopathy APOE, clinical feature, concentration loss, Concussion, degenerative disease, football, genetic risk, headache, human, in vivo study, injury severity, lifestyle, neuropathology, risk factor, Tau, traumatic brain injury, Traumatic brain injury (TBI)},
pubstate = {published},
tppubtype = {article}
}
Gandy, S; Ikonomovic, M D; Mitsis, E; Elder, G; Ahlers, S T; Barth, J; Stone, J R; Dekosky, S T
Chronic traumatic encephalopathy: Clinical-biomarker correlations and current concepts in pathogenesis Journal Article
In: Molecular Neurodegeneration, vol. 9, no. 1, 2014.
Abstract | Links | BibTeX | Tags: animal model, army, Article, blast injury, body fluid, Boxing, chronic disease, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy biological marker, Dementia, dementia pugilistica, Diffusion Tensor Imaging, executive function, experimental animal, fluorine 18, football, functional magnetic resonance imaging, functional neuroimaging, human, molecular pathology, neuropathology, neuropsychology, nonhuman, nuclear magnetic resonance imaging, Occupational Exposure, positron emission tomography, punch drunk syndrome, systematic review (topic), traumatic brain injury, white matter, working memory
@article{Gandy2014a,
title = {Chronic traumatic encephalopathy: Clinical-biomarker correlations and current concepts in pathogenesis},
author = {Gandy, S and Ikonomovic, M D and Mitsis, E and Elder, G and Ahlers, S T and Barth, J and Stone, J R and Dekosky, S T},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84907464163\&partnerID=40\&md5=109c916e926417c11bab99fd7b44065c},
doi = {10.1186/1750-1326-9-37},
year = {2014},
date = {2014-01-01},
journal = {Molecular Neurodegeneration},
volume = {9},
number = {1},
abstract = {Background: Chronic traumatic encephalopathy (CTE) is a recently revived term used to describe a neurodegenerative process that occurs as a long term complication of repetitive mild traumatic brain injury (TBI). Corsellis provided one of the classic descriptions of CTE in boxers under the name "dementia pugilistica" (DP). Much recent attention has been drawn to the apparent association of CTE with contact sports (football, soccer, hockey) and with frequent battlefield exposure to blast waves generated by improvised explosive devices (IEDs). Recently, a promising serum biomarker has been identified by measurement of serum levels of the neuronal microtubule associated protein tau. New positron emission tomography (PET) ligands (e.g., [18F] T807) that identify brain tauopathy have been successfully deployed for the in vitro and in vivo detection of presumptive tauopathy in the brains of subjects with clinically probable CTE. Methods. Major academic and lay publications on DP/CTE were reviewed beginning with the 1928 paper describing the initial use of the term CTE by Martland. Results: The major current concepts in the neurological, psychiatric, neuropsychological, neuroimaging, and body fluid biomarker science of DP/CTE have been summarized. Newer achievements, such as serum tau and [18F] T807 tauopathy imaging, are also introduced and their significance has been explained. Conclusion: Recent advances in the science of DP/CTE hold promise for elucidating a long sought accurate determination of the true prevalence of CTE. This information holds potentially important public health implications for estimating the risk of contact sports in inflicting permanent and/or progressive brain damage on children, adolescents, and adults. © 2014Gandy et al.; licensee BioMed Central Ltd.},
keywords = {animal model, army, Article, blast injury, body fluid, Boxing, chronic disease, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy biological marker, Dementia, dementia pugilistica, Diffusion Tensor Imaging, executive function, experimental animal, fluorine 18, football, functional magnetic resonance imaging, functional neuroimaging, human, molecular pathology, neuropathology, neuropsychology, nonhuman, nuclear magnetic resonance imaging, Occupational Exposure, positron emission tomography, punch drunk syndrome, systematic review (topic), traumatic brain injury, white matter, working memory},
pubstate = {published},
tppubtype = {article}
}
Blennow, K; Brody, D L; Kochanek, P M; Levin, H; McKee, A; Ribbers, G M; Yaffe, K; Zetterberg, H
Traumatic brain injuries Journal Article
In: Nature Reviews Disease Primers, vol. 2, 2016.
@article{Blennow2016,
title = {Traumatic brain injuries},
author = {Blennow, K and Brody, D L and Kochanek, P M and Levin, H and McKee, A and Ribbers, G M and Yaffe, K and Zetterberg, H},
doi = {10.1038/nrdp.2016.84},
year = {2016},
date = {2016-01-01},
journal = {Nature Reviews Disease Primers},
volume = {2},
abstract = {Traumatic brain injuries (TBIs) are clinically grouped by severity: mild, moderate and severe. Mild TBI (the least severe form) is synonymous with concussion and is typically caused by blunt non-penetrating head trauma. The trauma causes stretching and tearing of axons, which leads to diffuse axonal injury-the best-studied pathogenetic mechanism of this disorder. However, mild TBI is defined on clinical grounds and no well-validated imaging or fluid biomarkers to determine the presence of neuronal damage in patients with mild TBI is available. Most patients with mild TBI will recover quickly, but others report persistent symptoms, called post-concussive syndrome, the underlying pathophysiology of which is largely unknown. Repeated concussive and subconcussive head injuries have been linked to the neurodegenerative condition chronic traumatic encephalopathy (CTE), which has been reported post-mortem in contact sports athletes and soldiers exposed to blasts. Insights from severe injuries and CTE plausibly shed light on the underlying cellular and molecular processes involved in mild TBI. MRI techniques and blood tests for axonal proteins to identify and grade axonal injury, in addition to PET for tau pathology, show promise as tools to explore CTE pathophysiology in longitudinal clinical studies, and might be developed into diagnostic tools for CTE. Given that CTE is attributed to repeated head trauma, prevention might be possible through rule changes by sports organizations and legislators. © 2016 Macmillan Publishers Limited, part of Springer Nature.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Ojo, J O; Mouzon, B C; Crawford, F
Repetitive head trauma, chronic traumatic encephalopathy and tau: Challenges in translating from mice to men Journal Article
In: Experimental Neurology, vol. 275, pp. 389–404, 2016.
@article{Ojo2016,
title = {Repetitive head trauma, chronic traumatic encephalopathy and tau: Challenges in translating from mice to men},
author = {Ojo, J O and Mouzon, B C and Crawford, F},
doi = {10.1016/j.expneurol.2015.06.003},
year = {2016},
date = {2016-01-01},
journal = {Experimental Neurology},
volume = {275},
pages = {389--404},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurological and psychiatric condition marked by preferential perivascular foci of neurofibrillary and glial tangles (composed of hyperphosphorylated-tau proteins) in the depths of the sulci. Recent retrospective case series published over the last decade on athletes and military personnel have added considerably to our clinical and histopathological knowledge of CTE. This has marked a vital turning point in the traumatic brain injury (TBI) field, raising public awareness of the potential long-term effects of mild and moderate repetitive TBI, which has been recognized as one of the major risk factors associated with CTE. Although these human studies have been informative, their retrospective design carries certain inherent limitations that should be cautiously interpreted. In particular, the current overriding issue in the CTE literature remains confusing in regard to appropriate definitions of terminology, variability in individual pathologies and the potential case selection bias in autopsy based studies. There are currently no epidemiological or prospective studies on CTE. Controlled preclinical studies in animals therefore provide an alternative means for specifically interrogating aspects of CTE pathogenesis. In this article, we review the current literature and discuss difficulties and challenges of developing in-vivo TBI experimental paradigms to explore the link between repetitive head trauma and tau-dependent changes. We provide our current opinion list of recommended features to consider for successfully modeling CTE in animals to better understand the pathobiology and develop therapeutics and diagnostics, and critical factors, which might influence outcome. We finally discuss the possible directions of future experimental research in the repetitive TBI/CTE field. © 2015 Elsevier Inc..},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Lawrence, D W; Comper, P; Hutchison, M G; Sharma, B
The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review Journal Article
In: Brain Injury, vol. 29, no. 9, pp. 1018–1031, 2015.
@article{Lawrence2015,
title = {The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review},
author = {Lawrence, D W and Comper, P and Hutchison, M G and Sharma, B},
doi = {10.3109/02699052.2015.1005131},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {9},
pages = {1018--1031},
abstract = {Background: The apolipoprotein E gene (APOE) has emerged as a candidate for prognosticating traumatic brain injury (TBI) recovery, with APOE$epsilon$4 identified as a susceptibility marker for poor outcome, despite large discrepancy in its reported influence post-TBI.Methods: A systematic review was conducted, including all primary articles investigating the role of APOE$epsilon$4 on TBI outcome. A total of 65 studies were included, including 24 predominantly investigating mild (mTBI), seven moderate (modTBI) and 33 severe (sTBI); severity was not reported in one study.Results: In mTBI studies, the association between APOE$epsilon$4 and post-TBI outcome was concluded as non-contributory in 14 studies (58.3%), hazardous in nine (37.5%) and protective in one (4.2%). In sTBI studies, the role of APOE$epsilon$4 was hazardous in 21 (63.6%), non-contributory in nine (27.3%) and protective in three (9.1%). Of the seven studies investigating dementia outcomes, four observed a hazardous association with APOE$epsilon$4, while three reported no association. Six studies examined Alzheimers dementia pathology, of which three reported a hazardous influence of APOE$epsilon$4.Conclusions: The influence of APOE$epsilon$4 on neuropsychological testing, functional outcome and in paediatric populations was incongruous. This review supports the majority of research indicating APOE$epsilon$4 adversely influences recovery following TBI, particularly with respect to dementia-related outcomes and outcomes following sTBI. © 2015 Taylor \& Francis Group, LLC.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Dessy, A M; Rasouli, J; Choudhri, T F
Second Impact Syndrome: A Rare, Devastating Consequence of Repetitive Head Injuries Journal Article
In: Neurosurgery Quarterly, vol. 25, no. 3, pp. 423–426, 2015.
@article{Dessy2015,
title = {Second Impact Syndrome: A Rare, Devastating Consequence of Repetitive Head Injuries},
author = {Dessy, A M and Rasouli, J and Choudhri, T F},
doi = {10.1097/WNQ.0000000000000085},
year = {2015},
date = {2015-01-01},
journal = {Neurosurgery Quarterly},
volume = {25},
number = {3},
pages = {423--426},
abstract = {Sports-related concussion has been viewed as a developing public health crisis in recent years. Underrecognition of concussions can lead to premature clearance for athletic participation. Second impact syndrome (SIS) represents a rare, yet devastating, potential outcome of premature return to play. SIS is a condition in which rapid brain swelling occurs as a result of a repeat head injury sustained before symptoms of a previous head injury have resolved. Within minutes of the second impact, diffuse cerebral swelling, brain herniation, and death can occur. There are \<20 documented cases of SIS in the world literature to date, and the general understanding of the syndrome is based largely on interpretation of anecdotal cases. This article reviews current understanding of the epidemiology and pathology of SIS. Given neurosurgeons' role in management of head trauma, it is essential that neurosurgeons acquire and maintain thorough knowledge of concussion diagnosis, treatment, and management. © 2014 Wolters Kluwer Health, Inc. All rights reserved.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Rapp, P E; Keyser, D O; Albano, A; Hernandez, R; Gibson, D B; Zambon, R A; David Hairston, W; Hughes, J D; Krystal, A; Nichols, A S
Traumatic brain injury detection using electrophysiological methods Journal Article
In: Frontiers in Human Neuroscience, vol. 9, no. FEB, 2015.
@article{Rapp2015,
title = {Traumatic brain injury detection using electrophysiological methods},
author = {Rapp, P E and Keyser, D O and Albano, A and Hernandez, R and Gibson, D B and Zambon, R A and {David Hairston}, W and Hughes, J D and Krystal, A and Nichols, A S},
doi = {10.3389/fnhum.2015.00011},
year = {2015},
date = {2015-01-01},
journal = {Frontiers in Human Neuroscience},
volume = {9},
number = {FEB},
abstract = {Measuring neuronal activity with electrophysiological methods may be useful in detecting neurological dysfunctions, such as mild traumatic brain injury (mTBI).This approach may be particularly valuable for rapid detection in at-risk populations including military service members and athletes. Electrophysiological methods, such as quantitative electroencephalography (qEEG) and recording event-related potentials (ERPs) may be promising; however, the field is nascent and significant controversy exists on the efficacy and accuracy of the approaches as diagnostic tools. For example, the specific measures derived from an electroencephalogram (EEG) that are most suitable as markers of dysfunction have not been clearly established. A study was conducted to summarize and evaluate the statistical rigor of evidence on the overall utility of qEEG as an mTBI detection tool. The analysis evaluated qEEG measures/parameters that may be most suitable as fieldable diagnostic tools, identified other types of EEG measures and analysis methods of promise, recommended specific measures and analysis methods for further development as mTBI detection tools, identified research gaps in the field, and recommended future research and development thrust areas. The qEEG study group formed the following conclusions: (1) Individual qEEG measures provide limited diagnostic utility for mTBI. However, many measures can be important features of qEEG discriminant functions, which do show significant promise as mTBI detection tools. (2) ERPs offer utility in mTBI detection. In fact, evidence indicates that ERPs can identify abnormalities in cases where EEGs alone are non-disclosing. (3)The standard mathematical procedures used in the characterization of mTBI EEGs should be expanded to incorporate newer methods of analysis including non-linear dynamical analysis, complexity measures, analysis of causal interactions, graph theory, and information dynamics. (4) Reports of high specificity in qEEG evaluations of TBI must be interpreted with care. High specificities have been reported in carefully constructed clinical studies in which healthy controls were compared against a carefully selected TBI population. The published literature indicates, however, that similar abnormalities in qEEG measures are observed in other neuropsychiatric disorders. While it may be possible to distinguish a clinical patient from a healthy control participant with this technology, these measures are unlikely to discriminate between, for example, major depressive disorder, bipolar disorder, or TBI. The specificities observed in these clinical studies may well be lost in real world clinical practice. (5)The absence of specificity does not preclude clinical utility. The possibility of use as a longitudinal measure of treatment response remains. However, efficacy as a longitudinal clinical measure does require acceptable test-retest reliability. To date, very few test-retest reliability studies have been published with qEEG data obtained from TBI patients or from healthy controls. This is a particular concern because high variability is a known characteristic of the injured central nervous system. © 2015 Rapp, Keyser , Albano, Hernandez, Gibson, Zambon, Hairston, Hughes, Krystal and Nichols.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Stein, T D; Alvarez, V E; McKee, A C
Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel Journal Article
In: Alzheimer's Research and Therapy, vol. 6, no. 1, 2014.
@article{Stein2014,
title = {Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel},
author = {Stein, T D and Alvarez, V E and McKee, A C},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84892718392\&partnerID=40\&md5=c39a0e58ad33cee7a570b4681131d6ea},
doi = {10.1186/alzrt234},
year = {2014},
date = {2014-01-01},
journal = {Alzheimer's Research and Therapy},
volume = {6},
number = {1},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs in association with repetitive traumatic brain injury experienced in sport and military service. In most instances, the clinical symptoms of the disease begin after a long period of latency ranging from several years to several decades. The initial symptoms are typically insidious, consisting of irritability, impulsivity, aggression, depression, short-term memory loss and heightened suicidality. The symptoms progress slowly over decades to include cognitive deficits and dementia. The pathology of CTE is characterized by the accumulation of phosphorylated tau protein in neurons and astrocytes in a pattern that is unique from other tauopathies, including Alzheimer's disease. The hyperphosphorylated tau abnormalities begin focally, as perivascular neurofibrillary tangles and neurites at the depths of the cerebral sulci, and then spread to involve superficial layers of adjacent cortex before becoming a widespread degeneration affecting medial temporal lobe structures, diencephalon and brainstem. Most instances of CTE (\>85% of cases) show abnormal accumulations of phosphorylated 43 kDa TAR DNA binding protein that are partially colocalized with phosphorylated tau protein. As CTE is characterized pathologically by frontal and temporal lobe atrophy, by abnormal deposits of phosphorylated tau and by 43 kDa TAR DNA binding protein and is associated clinically with behavioral and personality changes, as well as cognitive impairments, CTE is increasingly categorized as an acquired frontotemporal lobar degeneration. Currently, some of the greatest challenges are that CTE cannot be diagnosed during life and the incidence and prevalence of the disorder remain uncertain. Furthermore, the contribution of age, gender, genetics, stress, alcohol and substance abuse to the development of CTE remains to be determined. © 2014 BioMed Central Ltd.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Baugh, C M; Robbins, C A; Stern, R A; McKee, A C
Current understanding of chronic traumatic encephalopathy Journal Article
In: Current Treatment Options in Neurology, vol. 16, no. 9, 2014.
@article{Baugh2014,
title = {Current understanding of chronic traumatic encephalopathy},
author = {Baugh, C M and Robbins, C A and Stern, R A and McKee, A C},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84905669544\&partnerID=40\&md5=b7b1e2fe8132cad56800bf4102896b64},
doi = {10.1007/s11940-014-0306-5},
year = {2014},
date = {2014-01-01},
journal = {Current Treatment Options in Neurology},
volume = {16},
number = {9},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Gandy, S; Ikonomovic, M D; Mitsis, E; Elder, G; Ahlers, S T; Barth, J; Stone, J R; Dekosky, S T
Chronic traumatic encephalopathy: Clinical-biomarker correlations and current concepts in pathogenesis Journal Article
In: Molecular Neurodegeneration, vol. 9, no. 1, 2014.
@article{Gandy2014a,
title = {Chronic traumatic encephalopathy: Clinical-biomarker correlations and current concepts in pathogenesis},
author = {Gandy, S and Ikonomovic, M D and Mitsis, E and Elder, G and Ahlers, S T and Barth, J and Stone, J R and Dekosky, S T},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84907464163\&partnerID=40\&md5=109c916e926417c11bab99fd7b44065c},
doi = {10.1186/1750-1326-9-37},
year = {2014},
date = {2014-01-01},
journal = {Molecular Neurodegeneration},
volume = {9},
number = {1},
abstract = {Background: Chronic traumatic encephalopathy (CTE) is a recently revived term used to describe a neurodegenerative process that occurs as a long term complication of repetitive mild traumatic brain injury (TBI). Corsellis provided one of the classic descriptions of CTE in boxers under the name "dementia pugilistica" (DP). Much recent attention has been drawn to the apparent association of CTE with contact sports (football, soccer, hockey) and with frequent battlefield exposure to blast waves generated by improvised explosive devices (IEDs). Recently, a promising serum biomarker has been identified by measurement of serum levels of the neuronal microtubule associated protein tau. New positron emission tomography (PET) ligands (e.g., [18F] T807) that identify brain tauopathy have been successfully deployed for the in vitro and in vivo detection of presumptive tauopathy in the brains of subjects with clinically probable CTE. Methods. Major academic and lay publications on DP/CTE were reviewed beginning with the 1928 paper describing the initial use of the term CTE by Martland. Results: The major current concepts in the neurological, psychiatric, neuropsychological, neuroimaging, and body fluid biomarker science of DP/CTE have been summarized. Newer achievements, such as serum tau and [18F] T807 tauopathy imaging, are also introduced and their significance has been explained. Conclusion: Recent advances in the science of DP/CTE hold promise for elucidating a long sought accurate determination of the true prevalence of CTE. This information holds potentially important public health implications for estimating the risk of contact sports in inflicting permanent and/or progressive brain damage on children, adolescents, and adults. © 2014Gandy et al.; licensee BioMed Central Ltd.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Blennow, K; Brody, D L; Kochanek, P M; Levin, H; McKee, A; Ribbers, G M; Yaffe, K; Zetterberg, H
Traumatic brain injuries Journal Article
In: Nature Reviews Disease Primers, vol. 2, 2016.
Abstract | Links | BibTeX | Tags: amyloid beta protein, Article, axonal injury, biological marker, BIOPHYSICS, blood, brain, BRAIN damage, cerebrospinal fluid, Chronic traumatic encephalopathy, computer assisted tomography, disease severity, endocrine disease, heredity, human, molecular pathology, neuropathology, nonhuman, nuclear magnetic resonance imaging, Pathophysiology, positron emission tomography, postconcussion syndrome, priority journal, protein aggregation, quality of life, screening, tau protein, traumatic brain injury
@article{Blennow2016,
title = {Traumatic brain injuries},
author = {Blennow, K and Brody, D L and Kochanek, P M and Levin, H and McKee, A and Ribbers, G M and Yaffe, K and Zetterberg, H},
doi = {10.1038/nrdp.2016.84},
year = {2016},
date = {2016-01-01},
journal = {Nature Reviews Disease Primers},
volume = {2},
abstract = {Traumatic brain injuries (TBIs) are clinically grouped by severity: mild, moderate and severe. Mild TBI (the least severe form) is synonymous with concussion and is typically caused by blunt non-penetrating head trauma. The trauma causes stretching and tearing of axons, which leads to diffuse axonal injury-the best-studied pathogenetic mechanism of this disorder. However, mild TBI is defined on clinical grounds and no well-validated imaging or fluid biomarkers to determine the presence of neuronal damage in patients with mild TBI is available. Most patients with mild TBI will recover quickly, but others report persistent symptoms, called post-concussive syndrome, the underlying pathophysiology of which is largely unknown. Repeated concussive and subconcussive head injuries have been linked to the neurodegenerative condition chronic traumatic encephalopathy (CTE), which has been reported post-mortem in contact sports athletes and soldiers exposed to blasts. Insights from severe injuries and CTE plausibly shed light on the underlying cellular and molecular processes involved in mild TBI. MRI techniques and blood tests for axonal proteins to identify and grade axonal injury, in addition to PET for tau pathology, show promise as tools to explore CTE pathophysiology in longitudinal clinical studies, and might be developed into diagnostic tools for CTE. Given that CTE is attributed to repeated head trauma, prevention might be possible through rule changes by sports organizations and legislators. © 2016 Macmillan Publishers Limited, part of Springer Nature.},
keywords = {amyloid beta protein, Article, axonal injury, biological marker, BIOPHYSICS, blood, brain, BRAIN damage, cerebrospinal fluid, Chronic traumatic encephalopathy, computer assisted tomography, disease severity, endocrine disease, heredity, human, molecular pathology, neuropathology, nonhuman, nuclear magnetic resonance imaging, Pathophysiology, positron emission tomography, postconcussion syndrome, priority journal, protein aggregation, quality of life, screening, tau protein, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}
Ojo, J O; Mouzon, B C; Crawford, F
Repetitive head trauma, chronic traumatic encephalopathy and tau: Challenges in translating from mice to men Journal Article
In: Experimental Neurology, vol. 275, pp. 389–404, 2016.
Abstract | Links | BibTeX | Tags: amyloid beta protein, animal, Animal models, Animals, Astroglial tangles, Brain Injury, cell activation, Chronic, complication, Concussion, Craniocerebral Trauma, CTE, diffuse axonal injury, disease duration, disease model, Disease Models, genetic predisposition, gliosis, head injury, hippocampus, human, Humans, lifestyle modification, lithium, metabolism, Mice, microglia, minocycline, mouse, nervous system inflammation, Neurobehaviour, Neurofibrillary tangles, neuropathology, nonhuman, pathogenesis, pathology, priority journal, procedures, protein aggregation, protein analysis, protein blood level, protein cleavage, Repetitive TBI, Review, sex difference, stress activated protein kinase inhibitor, Systematic Review, Tau, tau protein, tau Proteins, Transgenic mice, Translational Medical Research, translational research, traumatic brain injury, trends
@article{Ojo2016,
title = {Repetitive head trauma, chronic traumatic encephalopathy and tau: Challenges in translating from mice to men},
author = {Ojo, J O and Mouzon, B C and Crawford, F},
doi = {10.1016/j.expneurol.2015.06.003},
year = {2016},
date = {2016-01-01},
journal = {Experimental Neurology},
volume = {275},
pages = {389--404},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurological and psychiatric condition marked by preferential perivascular foci of neurofibrillary and glial tangles (composed of hyperphosphorylated-tau proteins) in the depths of the sulci. Recent retrospective case series published over the last decade on athletes and military personnel have added considerably to our clinical and histopathological knowledge of CTE. This has marked a vital turning point in the traumatic brain injury (TBI) field, raising public awareness of the potential long-term effects of mild and moderate repetitive TBI, which has been recognized as one of the major risk factors associated with CTE. Although these human studies have been informative, their retrospective design carries certain inherent limitations that should be cautiously interpreted. In particular, the current overriding issue in the CTE literature remains confusing in regard to appropriate definitions of terminology, variability in individual pathologies and the potential case selection bias in autopsy based studies. There are currently no epidemiological or prospective studies on CTE. Controlled preclinical studies in animals therefore provide an alternative means for specifically interrogating aspects of CTE pathogenesis. In this article, we review the current literature and discuss difficulties and challenges of developing in-vivo TBI experimental paradigms to explore the link between repetitive head trauma and tau-dependent changes. We provide our current opinion list of recommended features to consider for successfully modeling CTE in animals to better understand the pathobiology and develop therapeutics and diagnostics, and critical factors, which might influence outcome. We finally discuss the possible directions of future experimental research in the repetitive TBI/CTE field. © 2015 Elsevier Inc..},
keywords = {amyloid beta protein, animal, Animal models, Animals, Astroglial tangles, Brain Injury, cell activation, Chronic, complication, Concussion, Craniocerebral Trauma, CTE, diffuse axonal injury, disease duration, disease model, Disease Models, genetic predisposition, gliosis, head injury, hippocampus, human, Humans, lifestyle modification, lithium, metabolism, Mice, microglia, minocycline, mouse, nervous system inflammation, Neurobehaviour, Neurofibrillary tangles, neuropathology, nonhuman, pathogenesis, pathology, priority journal, procedures, protein aggregation, protein analysis, protein blood level, protein cleavage, Repetitive TBI, Review, sex difference, stress activated protein kinase inhibitor, Systematic Review, Tau, tau protein, tau Proteins, Transgenic mice, Translational Medical Research, translational research, traumatic brain injury, trends},
pubstate = {published},
tppubtype = {article}
}
Lawrence, D W; Comper, P; Hutchison, M G; Sharma, B
The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review Journal Article
In: Brain Injury, vol. 29, no. 9, pp. 1018–1031, 2015.
Abstract | Links | BibTeX | Tags: 80 and over, aged, allele, Alleles, Alzheimer disease, amyloid beta protein, APOE, apolipoprotein E, apolipoprotein E4, Article, athlete, brain concussion, Brain Injuries, clinical evaluation, cognition, cognitive defect, disease severity, Female, follow up, genetic association, genetic risk, genetics, GENOTYPE, Glasgow Outcome Scale, heterozygote, histopathology, homozygote, human, Humans, Incidence, injury severity, Male, Memory, nerve cell necrosis, neuropathology, Neuroprotection, outcome assessment, pediatrics, Prevalence, Prognosis, prognostic assessment, protein function, psychologic test, psychology, Recovery, scoring system, Systematic Review, tau protein, traumatic brain injury, treatment outcome, very elderly, Wechsler Intelligence Scale
@article{Lawrence2015,
title = {The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review},
author = {Lawrence, D W and Comper, P and Hutchison, M G and Sharma, B},
doi = {10.3109/02699052.2015.1005131},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {9},
pages = {1018--1031},
abstract = {Background: The apolipoprotein E gene (APOE) has emerged as a candidate for prognosticating traumatic brain injury (TBI) recovery, with APOE$epsilon$4 identified as a susceptibility marker for poor outcome, despite large discrepancy in its reported influence post-TBI.Methods: A systematic review was conducted, including all primary articles investigating the role of APOE$epsilon$4 on TBI outcome. A total of 65 studies were included, including 24 predominantly investigating mild (mTBI), seven moderate (modTBI) and 33 severe (sTBI); severity was not reported in one study.Results: In mTBI studies, the association between APOE$epsilon$4 and post-TBI outcome was concluded as non-contributory in 14 studies (58.3%), hazardous in nine (37.5%) and protective in one (4.2%). In sTBI studies, the role of APOE$epsilon$4 was hazardous in 21 (63.6%), non-contributory in nine (27.3%) and protective in three (9.1%). Of the seven studies investigating dementia outcomes, four observed a hazardous association with APOE$epsilon$4, while three reported no association. Six studies examined Alzheimers dementia pathology, of which three reported a hazardous influence of APOE$epsilon$4.Conclusions: The influence of APOE$epsilon$4 on neuropsychological testing, functional outcome and in paediatric populations was incongruous. This review supports the majority of research indicating APOE$epsilon$4 adversely influences recovery following TBI, particularly with respect to dementia-related outcomes and outcomes following sTBI. © 2015 Taylor \& Francis Group, LLC.},
keywords = {80 and over, aged, allele, Alleles, Alzheimer disease, amyloid beta protein, APOE, apolipoprotein E, apolipoprotein E4, Article, athlete, brain concussion, Brain Injuries, clinical evaluation, cognition, cognitive defect, disease severity, Female, follow up, genetic association, genetic risk, genetics, GENOTYPE, Glasgow Outcome Scale, heterozygote, histopathology, homozygote, human, Humans, Incidence, injury severity, Male, Memory, nerve cell necrosis, neuropathology, Neuroprotection, outcome assessment, pediatrics, Prevalence, Prognosis, prognostic assessment, protein function, psychologic test, psychology, Recovery, scoring system, Systematic Review, tau protein, traumatic brain injury, treatment outcome, very elderly, Wechsler Intelligence Scale},
pubstate = {published},
tppubtype = {article}
}
Dessy, A M; Rasouli, J; Choudhri, T F
Second Impact Syndrome: A Rare, Devastating Consequence of Repetitive Head Injuries Journal Article
In: Neurosurgery Quarterly, vol. 25, no. 3, pp. 423–426, 2015.
Abstract | Links | BibTeX | Tags: Article, brain concussion, clinical feature, Concussion, Dizziness, fatigue, headache, human, hyperemia, intracranial hypertension, memory disorder, Neck pain, neuropathology, neurosurgeon, neurosurgery, Pathophysiology, postconcussion syndrome, priority journal, respiratory failure, Second impact syndrome, sport injury, traumatic brain injury
@article{Dessy2015,
title = {Second Impact Syndrome: A Rare, Devastating Consequence of Repetitive Head Injuries},
author = {Dessy, A M and Rasouli, J and Choudhri, T F},
doi = {10.1097/WNQ.0000000000000085},
year = {2015},
date = {2015-01-01},
journal = {Neurosurgery Quarterly},
volume = {25},
number = {3},
pages = {423--426},
abstract = {Sports-related concussion has been viewed as a developing public health crisis in recent years. Underrecognition of concussions can lead to premature clearance for athletic participation. Second impact syndrome (SIS) represents a rare, yet devastating, potential outcome of premature return to play. SIS is a condition in which rapid brain swelling occurs as a result of a repeat head injury sustained before symptoms of a previous head injury have resolved. Within minutes of the second impact, diffuse cerebral swelling, brain herniation, and death can occur. There are \<20 documented cases of SIS in the world literature to date, and the general understanding of the syndrome is based largely on interpretation of anecdotal cases. This article reviews current understanding of the epidemiology and pathology of SIS. Given neurosurgeons' role in management of head trauma, it is essential that neurosurgeons acquire and maintain thorough knowledge of concussion diagnosis, treatment, and management. © 2014 Wolters Kluwer Health, Inc. All rights reserved.},
keywords = {Article, brain concussion, clinical feature, Concussion, Dizziness, fatigue, headache, human, hyperemia, intracranial hypertension, memory disorder, Neck pain, neuropathology, neurosurgeon, neurosurgery, Pathophysiology, postconcussion syndrome, priority journal, respiratory failure, Second impact syndrome, sport injury, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}
Rapp, P E; Keyser, D O; Albano, A; Hernandez, R; Gibson, D B; Zambon, R A; David Hairston, W; Hughes, J D; Krystal, A; Nichols, A S
Traumatic brain injury detection using electrophysiological methods Journal Article
In: Frontiers in Human Neuroscience, vol. 9, no. FEB, 2015.
Abstract | Links | BibTeX | Tags: Article, brain electrophysiology, computer assisted tomography, Concussion, connectome, diagnostic accuracy, EEG, electroencephalogram, Electroencephalography, event related potential, Event-Related Potentials, evidence based medicine, executive function, human, intermethod comparison, latent period, neuroimaging, neuropathology, Non-linear dynamical analysis, nuclear magnetic resonance imaging, QEEG, Signal Processing, traumatic brain injury
@article{Rapp2015,
title = {Traumatic brain injury detection using electrophysiological methods},
author = {Rapp, P E and Keyser, D O and Albano, A and Hernandez, R and Gibson, D B and Zambon, R A and {David Hairston}, W and Hughes, J D and Krystal, A and Nichols, A S},
doi = {10.3389/fnhum.2015.00011},
year = {2015},
date = {2015-01-01},
journal = {Frontiers in Human Neuroscience},
volume = {9},
number = {FEB},
abstract = {Measuring neuronal activity with electrophysiological methods may be useful in detecting neurological dysfunctions, such as mild traumatic brain injury (mTBI).This approach may be particularly valuable for rapid detection in at-risk populations including military service members and athletes. Electrophysiological methods, such as quantitative electroencephalography (qEEG) and recording event-related potentials (ERPs) may be promising; however, the field is nascent and significant controversy exists on the efficacy and accuracy of the approaches as diagnostic tools. For example, the specific measures derived from an electroencephalogram (EEG) that are most suitable as markers of dysfunction have not been clearly established. A study was conducted to summarize and evaluate the statistical rigor of evidence on the overall utility of qEEG as an mTBI detection tool. The analysis evaluated qEEG measures/parameters that may be most suitable as fieldable diagnostic tools, identified other types of EEG measures and analysis methods of promise, recommended specific measures and analysis methods for further development as mTBI detection tools, identified research gaps in the field, and recommended future research and development thrust areas. The qEEG study group formed the following conclusions: (1) Individual qEEG measures provide limited diagnostic utility for mTBI. However, many measures can be important features of qEEG discriminant functions, which do show significant promise as mTBI detection tools. (2) ERPs offer utility in mTBI detection. In fact, evidence indicates that ERPs can identify abnormalities in cases where EEGs alone are non-disclosing. (3)The standard mathematical procedures used in the characterization of mTBI EEGs should be expanded to incorporate newer methods of analysis including non-linear dynamical analysis, complexity measures, analysis of causal interactions, graph theory, and information dynamics. (4) Reports of high specificity in qEEG evaluations of TBI must be interpreted with care. High specificities have been reported in carefully constructed clinical studies in which healthy controls were compared against a carefully selected TBI population. The published literature indicates, however, that similar abnormalities in qEEG measures are observed in other neuropsychiatric disorders. While it may be possible to distinguish a clinical patient from a healthy control participant with this technology, these measures are unlikely to discriminate between, for example, major depressive disorder, bipolar disorder, or TBI. The specificities observed in these clinical studies may well be lost in real world clinical practice. (5)The absence of specificity does not preclude clinical utility. The possibility of use as a longitudinal measure of treatment response remains. However, efficacy as a longitudinal clinical measure does require acceptable test-retest reliability. To date, very few test-retest reliability studies have been published with qEEG data obtained from TBI patients or from healthy controls. This is a particular concern because high variability is a known characteristic of the injured central nervous system. © 2015 Rapp, Keyser , Albano, Hernandez, Gibson, Zambon, Hairston, Hughes, Krystal and Nichols.},
keywords = {Article, brain electrophysiology, computer assisted tomography, Concussion, connectome, diagnostic accuracy, EEG, electroencephalogram, Electroencephalography, event related potential, Event-Related Potentials, evidence based medicine, executive function, human, intermethod comparison, latent period, neuroimaging, neuropathology, Non-linear dynamical analysis, nuclear magnetic resonance imaging, QEEG, Signal Processing, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}
Stein, T D; Alvarez, V E; McKee, A C
Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel Journal Article
In: Alzheimer's Research and Therapy, vol. 6, no. 1, 2014.
Abstract | Links | BibTeX | Tags: Aggression, Alzheimer disease, amnesia, army, astrocyte, athlete, behavior change, brain atrophy, brain stem, brain weight, central sulcus, chronic disease, Chronic Traumatic Encephalopathy TAR DNA binding p, cognitive defect, comorbidity, Dementia, depression, diencephalon, diffuse Lewy body disease, exposure, frontotemporal dementia, human, impulsiveness, irritability, Motor neuron disease, nerve fiber, neurite, neurofibrillary tangle, neuropathology, nonhuman, personality disorder, priority journal, Review, short term memory, soldier, staging, suicidal ideation, tau protein, tauopathy, temporal lobe, traumatic brain injury, veteran
@article{Stein2014,
title = {Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel},
author = {Stein, T D and Alvarez, V E and McKee, A C},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84892718392\&partnerID=40\&md5=c39a0e58ad33cee7a570b4681131d6ea},
doi = {10.1186/alzrt234},
year = {2014},
date = {2014-01-01},
journal = {Alzheimer's Research and Therapy},
volume = {6},
number = {1},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs in association with repetitive traumatic brain injury experienced in sport and military service. In most instances, the clinical symptoms of the disease begin after a long period of latency ranging from several years to several decades. The initial symptoms are typically insidious, consisting of irritability, impulsivity, aggression, depression, short-term memory loss and heightened suicidality. The symptoms progress slowly over decades to include cognitive deficits and dementia. The pathology of CTE is characterized by the accumulation of phosphorylated tau protein in neurons and astrocytes in a pattern that is unique from other tauopathies, including Alzheimer's disease. The hyperphosphorylated tau abnormalities begin focally, as perivascular neurofibrillary tangles and neurites at the depths of the cerebral sulci, and then spread to involve superficial layers of adjacent cortex before becoming a widespread degeneration affecting medial temporal lobe structures, diencephalon and brainstem. Most instances of CTE (\>85% of cases) show abnormal accumulations of phosphorylated 43 kDa TAR DNA binding protein that are partially colocalized with phosphorylated tau protein. As CTE is characterized pathologically by frontal and temporal lobe atrophy, by abnormal deposits of phosphorylated tau and by 43 kDa TAR DNA binding protein and is associated clinically with behavioral and personality changes, as well as cognitive impairments, CTE is increasingly categorized as an acquired frontotemporal lobar degeneration. Currently, some of the greatest challenges are that CTE cannot be diagnosed during life and the incidence and prevalence of the disorder remain uncertain. Furthermore, the contribution of age, gender, genetics, stress, alcohol and substance abuse to the development of CTE remains to be determined. © 2014 BioMed Central Ltd.},
keywords = {Aggression, Alzheimer disease, amnesia, army, astrocyte, athlete, behavior change, brain atrophy, brain stem, brain weight, central sulcus, chronic disease, Chronic Traumatic Encephalopathy TAR DNA binding p, cognitive defect, comorbidity, Dementia, depression, diencephalon, diffuse Lewy body disease, exposure, frontotemporal dementia, human, impulsiveness, irritability, Motor neuron disease, nerve fiber, neurite, neurofibrillary tangle, neuropathology, nonhuman, personality disorder, priority journal, Review, short term memory, soldier, staging, suicidal ideation, tau protein, tauopathy, temporal lobe, traumatic brain injury, veteran},
pubstate = {published},
tppubtype = {article}
}
Baugh, C M; Robbins, C A; Stern, R A; McKee, A C
Current understanding of chronic traumatic encephalopathy Journal Article
In: Current Treatment Options in Neurology, vol. 16, no. 9, 2014.
Links | BibTeX | Tags: Article, attention disturbance, axonal injury, biological marker, Biomarker, Brain trauma, Chronic traumatic encephalopathy, Chronic traumatic encephalopathy (CTE), Chronic Traumatic Encephalopathy APOE, clinical feature, concentration loss, Concussion, degenerative disease, football, genetic risk, headache, human, in vivo study, injury severity, lifestyle, neuropathology, risk factor, Tau, traumatic brain injury, Traumatic brain injury (TBI)
@article{Baugh2014,
title = {Current understanding of chronic traumatic encephalopathy},
author = {Baugh, C M and Robbins, C A and Stern, R A and McKee, A C},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84905669544\&partnerID=40\&md5=b7b1e2fe8132cad56800bf4102896b64},
doi = {10.1007/s11940-014-0306-5},
year = {2014},
date = {2014-01-01},
journal = {Current Treatment Options in Neurology},
volume = {16},
number = {9},
keywords = {Article, attention disturbance, axonal injury, biological marker, Biomarker, Brain trauma, Chronic traumatic encephalopathy, Chronic traumatic encephalopathy (CTE), Chronic Traumatic Encephalopathy APOE, clinical feature, concentration loss, Concussion, degenerative disease, football, genetic risk, headache, human, in vivo study, injury severity, lifestyle, neuropathology, risk factor, Tau, traumatic brain injury, Traumatic brain injury (TBI)},
pubstate = {published},
tppubtype = {article}
}
Gandy, S; Ikonomovic, M D; Mitsis, E; Elder, G; Ahlers, S T; Barth, J; Stone, J R; Dekosky, S T
Chronic traumatic encephalopathy: Clinical-biomarker correlations and current concepts in pathogenesis Journal Article
In: Molecular Neurodegeneration, vol. 9, no. 1, 2014.
Abstract | Links | BibTeX | Tags: animal model, army, Article, blast injury, body fluid, Boxing, chronic disease, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy biological marker, Dementia, dementia pugilistica, Diffusion Tensor Imaging, executive function, experimental animal, fluorine 18, football, functional magnetic resonance imaging, functional neuroimaging, human, molecular pathology, neuropathology, neuropsychology, nonhuman, nuclear magnetic resonance imaging, Occupational Exposure, positron emission tomography, punch drunk syndrome, systematic review (topic), traumatic brain injury, white matter, working memory
@article{Gandy2014a,
title = {Chronic traumatic encephalopathy: Clinical-biomarker correlations and current concepts in pathogenesis},
author = {Gandy, S and Ikonomovic, M D and Mitsis, E and Elder, G and Ahlers, S T and Barth, J and Stone, J R and Dekosky, S T},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84907464163\&partnerID=40\&md5=109c916e926417c11bab99fd7b44065c},
doi = {10.1186/1750-1326-9-37},
year = {2014},
date = {2014-01-01},
journal = {Molecular Neurodegeneration},
volume = {9},
number = {1},
abstract = {Background: Chronic traumatic encephalopathy (CTE) is a recently revived term used to describe a neurodegenerative process that occurs as a long term complication of repetitive mild traumatic brain injury (TBI). Corsellis provided one of the classic descriptions of CTE in boxers under the name "dementia pugilistica" (DP). Much recent attention has been drawn to the apparent association of CTE with contact sports (football, soccer, hockey) and with frequent battlefield exposure to blast waves generated by improvised explosive devices (IEDs). Recently, a promising serum biomarker has been identified by measurement of serum levels of the neuronal microtubule associated protein tau. New positron emission tomography (PET) ligands (e.g., [18F] T807) that identify brain tauopathy have been successfully deployed for the in vitro and in vivo detection of presumptive tauopathy in the brains of subjects with clinically probable CTE. Methods. Major academic and lay publications on DP/CTE were reviewed beginning with the 1928 paper describing the initial use of the term CTE by Martland. Results: The major current concepts in the neurological, psychiatric, neuropsychological, neuroimaging, and body fluid biomarker science of DP/CTE have been summarized. Newer achievements, such as serum tau and [18F] T807 tauopathy imaging, are also introduced and their significance has been explained. Conclusion: Recent advances in the science of DP/CTE hold promise for elucidating a long sought accurate determination of the true prevalence of CTE. This information holds potentially important public health implications for estimating the risk of contact sports in inflicting permanent and/or progressive brain damage on children, adolescents, and adults. © 2014Gandy et al.; licensee BioMed Central Ltd.},
keywords = {animal model, army, Article, blast injury, body fluid, Boxing, chronic disease, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy biological marker, Dementia, dementia pugilistica, Diffusion Tensor Imaging, executive function, experimental animal, fluorine 18, football, functional magnetic resonance imaging, functional neuroimaging, human, molecular pathology, neuropathology, neuropsychology, nonhuman, nuclear magnetic resonance imaging, Occupational Exposure, positron emission tomography, punch drunk syndrome, systematic review (topic), traumatic brain injury, white matter, working memory},
pubstate = {published},
tppubtype = {article}
}