Lyon, Louisa
High impact research: investigating the effects of repetitive head injury Journal Article
In: Brain: A Journal of Neurology, vol. 140, no. 1, pp. e6–e6, 2017, ISBN: 00068950.
Links | BibTeX | Tags: BRAIN -- Concussion, Chronic traumatic encephalopathy, DISEASE susceptibility, Head Injuries, NATIONAL Football League
@article{Lyon2017,
title = {High impact research: investigating the effects of repetitive head injury},
author = {Lyon, Louisa},
doi = {10.1093/brain/aww294},
isbn = {00068950},
year = {2017},
date = {2017-01-01},
journal = {Brain: A Journal of Neurology},
volume = {140},
number = {1},
pages = {e6--e6},
keywords = {BRAIN -- Concussion, Chronic traumatic encephalopathy, DISEASE susceptibility, Head Injuries, NATIONAL Football League},
pubstate = {published},
tppubtype = {article}
}
Webner, David; Iverson, Grant L
Suicide in professional American football players in the past 95 years Journal Article
In: Brain Injury, vol. 30, no. 13/14, pp. 1718–1721, 2016, ISBN: 02699052.
Abstract | Links | BibTeX | Tags: Athletes, BRAIN damage, CHRONIC diseases, CHRONIC pain, Chronic traumatic encephalopathy, depression, DESCRIPTIVE statistics, EPIDEMIOLOGY -- Research, football, Internet, Life change events, LONGITUDINAL method, MENTAL depression, MORTALITY, Professional athletes, Professional Sports, psychology, RESEARCH -- Methodology, Retirement, Retrospective Studies, Socioeconomic Factors, STRESS (Psychology), suicide, Suicide -- Risk factors, Suicide -- United States, UNITED States, WORK experience (Employment)
@article{Webner2016,
title = {Suicide in professional American football players in the past 95 years},
author = {Webner, David and Iverson, Grant L},
doi = {10.1080/02699052.2016.1202451},
isbn = {02699052},
year = {2016},
date = {2016-01-01},
journal = {Brain Injury},
volume = {30},
number = {13/14},
pages = {1718--1721},
abstract = {Objective: To examine publicly-available information on all identified cases of suicide in active or former American professional football players between 1920 and the spring of 2015. Design: Retrospective cohort study. Setting: Professional American Football in the US. Participants: A cohort of 26 702 athletes who had died, retired or were currently playing in the NFL from nfl.com since 1920 was identified. Main outcome measures: Internet queries identifying 26 professional football players who completed suicide. Obituaries and news reports were reviewed. The primary outcome measures included mortality, demographic characteristics and life circumstances in professional American football players completing suicide. Results: From 1920\textendash2015, the median age of the 26 men who completed suicide was 39.5 years (range = 23\textendash85). The median number of years after retirement was 6.5 (range = 0\textendash63). Most of the deaths since 1920 have occurred in the past 15 years (58.7%) and a large percentage have occurred since 2009 (42.3%). Most of the men suffered from multiple life stressors prior to their deaths, such as retirement from sport, loss of steady income, divorce, failed business ventures, estrangement from family members and medical, psychiatric and/or substance abuse problems. Conclusions: A disproportionate number of completed suicides in current and former professional football players have occurred since 2009 (42.3%). It is well established in the literature that the causes of depression and suicidality are diverse, often multifactorial and treatable. Providing at-risk retired athletes with mental health treatment will likely reduce their suffering and improve their quality-of-life. [ABSTRACT FROM AUTHOR]},
keywords = {Athletes, BRAIN damage, CHRONIC diseases, CHRONIC pain, Chronic traumatic encephalopathy, depression, DESCRIPTIVE statistics, EPIDEMIOLOGY -- Research, football, Internet, Life change events, LONGITUDINAL method, MENTAL depression, MORTALITY, Professional athletes, Professional Sports, psychology, RESEARCH -- Methodology, Retirement, Retrospective Studies, Socioeconomic Factors, STRESS (Psychology), suicide, Suicide -- Risk factors, Suicide -- United States, UNITED States, WORK experience (Employment)},
pubstate = {published},
tppubtype = {article}
}
Choe, M C
The Pathophysiology of Concussion Journal Article
In: Current Pain & Headache Reports, vol. 20, no. 6, 2016.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy, Concussion, diffuse axonal injury, Pathophysiology
@article{Choe2016b,
title = {The Pathophysiology of Concussion},
author = {Choe, M C},
doi = {10.1007/s11916-016-0573-9},
year = {2016},
date = {2016-01-01},
journal = {Current Pain \& Headache Reports},
volume = {20},
number = {6},
abstract = {Concussion is a significant issue in medicine and the media today. With growing interest on the long-term effects of sports participation, it is important to understand what occurs in the brain after an impact of any degree. While some of the basic pathophysiology has been elucidated, much is still unknown about what happens in the brain after traumatic brain injury, particularly with milder injuries where no damage can be seen at the structural level on standard neuroimaging. Understanding the chain of events from a cellular level using studies investigating more severe injuries can help to drive research efforts in understanding the symptomatology that is seen in the acute phase after concussion, as well as point to mechanisms that may underlie persistent post-concussive symptoms. This review discusses the basic neuropathology that occurs after traumatic brain injury at the cellular level. We also present the pathology of chronic traumatic encephalopathy and its similarities to other neurodegenerative diseases. We conclude with recent imaging and biomarker findings looking at changes that may occur after repeated subconcussive blows, which may help to guide efforts in understanding if cumulative subconcussive mechanical forces upon the brain are detrimental in the long term or if concussive symptoms mark the threshold for brain injury. © 2016, Springer Science+Business Media New York.},
keywords = {Chronic traumatic encephalopathy, Concussion, diffuse axonal injury, Pathophysiology},
pubstate = {published},
tppubtype = {article}
}
Chiroban, O; Perju-Dumbravă, L
Postmortem evaluation of chronic traumatic encephalopathy Journal Article
In: Romanian Journal of Legal Medicine, vol. 24, no. 4, pp. 266–272, 2016.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy, Forensic pathology, NEURODEGENERATION, Trauma
@article{Chiroban2016,
title = {Postmortem evaluation of chronic traumatic encephalopathy},
author = {Chiroban, O and Perju-Dumbrav\u{a}, L},
doi = {10.4323/rjlm.2016.266},
year = {2016},
date = {2016-01-01},
journal = {Romanian Journal of Legal Medicine},
volume = {24},
number = {4},
pages = {266--272},
abstract = {Chronic traumatic encephalopathy (CTE) is the modern concept naming the neurodegenerative processes occurring in patients with positive medical history of repeated brain trauma and progressive dementia. Morphologically, CTE is classified as being a distinct member of the tauopathies family, with different distribution of tau-positive neurofibrillary tangles (NFTs) and low to none beta-amyloid deposits, contrasting the most famous member of the family: Alzheimer’s disease (AD). As opposed to other of its kind, the neurofibrillary tangles (NFTs) are spread in the form of irregular, perivascular, patchy disseminations throughout frontal and temporal cortex, especially in the superficial cerebral layers, leaning for sulcal depths. The previously mentioned characteristics constitute the hallmark signature of CTE. Although the connection between repeated concussions and CTE has been recently proposed, the startup path is still a mysterious topic. It remains, up to a point, common to all tauopathies, yet overpasses all genders, sex and age. Initially, considered a professional disease in boxing, scientific overviews link CTE to military service, sports and even daily activities. It is a consensus that a moderate traumatic event sustained during life-spam was correlated with 2.3 fold increase in the risk of developing dementia, while severe concussion augments up 4 times the chances. By the same token, considering the broad population with potential exposure to repetitive insults, CTE represents an important public health issue. The main purpose of this scientific article is to highlight the neuropathological features encountered and discuss the limitations of proper diagnostic. © 2016 Romanian Society of Legal Medicine.},
keywords = {Chronic traumatic encephalopathy, Forensic pathology, NEURODEGENERATION, Trauma},
pubstate = {published},
tppubtype = {article}
}
Moon, K; Theodore, N
Football and Chronic Traumatic Encephalopathy: How Much Evidence Actually Exists? Journal Article
In: World Neurosurgery, vol. 89, pp. 720–721, 2016.
Links | BibTeX | Tags: Alzheimer disease, amyloid beta protein, amyloid plaque, anxiety disorder, apolipoprotein E, Article, behavior disorder, Boxing, brain atrophy, brain concussion, brain degeneration, chronic disease, Chronic traumatic encephalopathy, cognitive defect, degenerative disease, depression, environmental factor, football, frontotemporal dementia, genetic predisposition, genetic risk, genetic susceptibility, human, motor control, Neuroanatomy, opiate addiction, Parkinson disease, protein phosphorylation, scar formation, septum pellucidum, sport injury, substantia nigra, suicide, TAR DNA binding protein, tau protein, tauopathy, traumatic brain injury
@article{Moon2016,
title = {Football and Chronic Traumatic Encephalopathy: How Much Evidence Actually Exists?},
author = {Moon, K and Theodore, N},
doi = {10.1016/j.wneu.2016.03.073},
year = {2016},
date = {2016-01-01},
journal = {World Neurosurgery},
volume = {89},
pages = {720--721},
keywords = {Alzheimer disease, amyloid beta protein, amyloid plaque, anxiety disorder, apolipoprotein E, Article, behavior disorder, Boxing, brain atrophy, brain concussion, brain degeneration, chronic disease, Chronic traumatic encephalopathy, cognitive defect, degenerative disease, depression, environmental factor, football, frontotemporal dementia, genetic predisposition, genetic risk, genetic susceptibility, human, motor control, Neuroanatomy, opiate addiction, Parkinson disease, protein phosphorylation, scar formation, septum pellucidum, sport injury, substantia nigra, suicide, TAR DNA binding protein, tau protein, tauopathy, traumatic brain injury},
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}
}
Edlow, B L; Hinson, H E
Blowing the whistle on sports concussions Journal Article
In: Neurology, vol. 85, no. 17, pp. 1442–1443, 2015.
Abstract | Links | BibTeX | Tags: Alzheimer disease, Chronic traumatic encephalopathy, Concussion, contact sport, Diffusion Tensor Imaging, football, functional magnetic resonance imaging, histopathology, Hockey, human, memory disorder, mood disorder, pathogenesis, Pathophysiology, priority journal, Review, rugby, Soccer, sport injury, sports concussion, traumatic brain injury, wrestling
@article{Edlow2015,
title = {Blowing the whistle on sports concussions},
author = {Edlow, B L and Hinson, H E},
doi = {10.1212/WNL.0000000000001902},
year = {2015},
date = {2015-01-01},
journal = {Neurology},
volume = {85},
number = {17},
pages = {1442--1443},
abstract = {On March 13, 2015, Chris Borland, a star rookie linebacker on the San Francisco 49ers, announced his early retirement from professional football, citing concerns about chronic traumatic encephalopathy (CTE). Borland, who had a history of 2 diagnosed concussions, walked away from a multi-million-dollar contract and potential sports superstardom, explaining that "from what I've researched and what I've experienced, I don't think it's worth the risk." 1 Perhaps just as surprising as Borland's announcement was the support he received from teammates and other athletes-support that reflects a growing recognition in the athletic community that repetitive head trauma may be associated with CTE and other forms of dementia. 2 Indeed, in a recent legal settlement, the National Football League estimated that approximately 30% of its former players will develop dementia. At the high school and college levels, state legislatures and universities have enacted limits to the number of full-contact practices, citing similar concerns about concussions. These developments have prompted a societal conversation about the risks of contact sports. © 2015 American Academy of Neurology.},
keywords = {Alzheimer disease, Chronic traumatic encephalopathy, Concussion, contact sport, Diffusion Tensor Imaging, football, functional magnetic resonance imaging, histopathology, Hockey, human, memory disorder, mood disorder, pathogenesis, Pathophysiology, priority journal, Review, rugby, Soccer, sport injury, sports concussion, traumatic brain injury, wrestling},
pubstate = {published},
tppubtype = {article}
}
Montenigro, P H; Bernick, C; Cantu, R C
Clinical features of repetitive traumatic brain injury and chronic traumatic encephalopathy Journal Article
In: Brain Pathology, vol. 25, no. 3, pp. 304–317, 2015.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Montenigro2015,
title = {Clinical features of repetitive traumatic brain injury and chronic traumatic encephalopathy},
author = {Montenigro, P H and Bernick, C and Cantu, R C},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25904046},
year = {2015},
date = {2015-01-01},
journal = {Brain Pathology},
volume = {25},
number = {3},
pages = {304--317},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease characterized by a distinct pattern of hyperphosphorylated tau (p-tau). Thought to be caused by repetitive concussive and subconcussive injuries, CTE is considered largely preventable. The majority of neuropathologically confirmed cases have occurred in professional contact sport athletes (eg, boxing, football). A recent post-mortem case series has magnified concerns for the public's health following its identification in six high school level athletes. CTE is diagnosed with certainty only following a post-mortem autopsy. Efforts to define the etiology and clinical progression during life are ongoing. The goal of this article is to characterize the clinical concepts associated with short- and long-term effects of repetitive traumatic brain injury, with a special emphasis on new clinical diagnostic criteria for CTE. Utilizing these new diagnostic criteria, two cases of neuropathologically confirmed CTE, one in a professional football player and one in a professional boxer, are reported. Differences in cerebellar pathology in CTE confirmed cases in boxing and football are discussed. Copyright © 2015 International Society of Neuropathology.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Montenigro, P H; Corp, D T; Stein, T D; Cantu, R C; Stern, R A
Chronic traumatic encephalopathy: historical origins and current perspective Journal Article
In: Annual Review of Clinical Psychology, vol. 11, pp. 309–330, 2015.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Montenigro2015a,
title = {Chronic traumatic encephalopathy: historical origins and current perspective},
author = {Montenigro, P H and Corp, D T and Stein, T D and Cantu, R C and Stern, R A},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25581233},
year = {2015},
date = {2015-01-01},
journal = {Annual Review of Clinical Psychology},
volume = {11},
pages = {309--330},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that is most often identified in postmortem autopsies of individuals exposed to repetitive head impacts, such as boxers and football players. The neuropathology of CTE is characterized by the accumulation of hyperphosphorylated tau protein in a pattern that is unique from that of other neurodegenerative diseases, including Alzheimer's disease. The clinical features of CTE are often progressive, leading to dramatic changes in mood, behavior, and cognition, frequently resulting in debilitating dementia. In some cases, motor features, including parkinsonism, can also be present. In this review, the historical origins of CTE are revealed and an overview of the current state of knowledge of CTE is provided, including the neuropathology, clinical features, proposed clinical and pathological diagnostic criteria, potential in vivo biomarkers, known risk factors, and treatment options.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Daneshvar, Daniel H; Goldstein, Lee E; Kiernan, Patrick T; Stein, Thor D; McKee, Ann C
Post-traumatic neurodegeneration and chronic traumatic encephalopathy Journal Article
In: MCN: Molecular & Cellular Neuroscience, vol. 66, no. Part B, pp. 81–90, 2015, ISBN: 10447431.
Abstract | Links | BibTeX | Tags: A$beta$ beta-amyloid, AD Alzheimer's disease, APOE $epsilon$4 apolipoprotein $epsilon$4, axonal injury, Blast and impact neurotrauma, BRAIN -- Wounds & injuries, Brain trauma, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy NEURODEGENERATION, Concussion, CSF cerebrospinal fluid, CTE chronic traumatic encephalopathy, DIAGNOSIS, DISEASES -- Risk factors, DNA-binding proteins, MORTALITY, Motor neuron disease, mTBI mild traumatic brain injury, NERVOUS system -- Wounds & injuries, NFTs neurofibrillary tangles, p-tau hyperphosphorylated tau, PCS post-concussion syndrome, PET positron emission tomography, PHF-tau paired helical filament-tau, Posttraumatic neurodegeneration, tau protein, TBI traumatic brain injury, TDP-43 43 kDa TAR DNA-binding protein, traumatic brain injury
@article{Daneshvar2015,
title = {Post-traumatic neurodegeneration and chronic traumatic encephalopathy},
author = {Daneshvar, Daniel H and Goldstein, Lee E and Kiernan, Patrick T and Stein, Thor D and McKee, Ann C},
url = {http://search.ebscohost.com/login.aspx?direct=true\&db=aph\&AN=103136351\&site=ehost-live},
doi = {10.1016/j.mcn.2015.03.007},
isbn = {10447431},
year = {2015},
date = {2015-01-01},
journal = {MCN: Molecular \& Cellular Neuroscience},
volume = {66},
number = {Part B},
pages = {81--90},
abstract = {Traumatic brain injury (TBI) is a leading cause of mortality and morbidity around the world. Concussive and subconcussive forms of closed-head injury due to impact or blast neurotrauma represent the most common types of TBI in civilian and military settings. It is becoming increasingly evident that TBI can lead to persistent, long-term debilitating effects, and in some cases, progressive neurodegeneration and chronic traumatic encephalopathy (CTE). The epidemiological literature suggests that a single moderate-to-severe TBI may be associated with accelerated neurodegeneration and increased risk of Alzheimer's disease, Parkinson's disease, or motor neuron disease. However, the pathologic phenotype of these post-traumatic neurodegenerations is largely unknown and there may be pathobiological differences between post-traumatic disease and the corresponding sporadic disorder. By contrast, the pathology of CTE is increasingly well known and is characterized by a distinctive pattern of progressive brain atrophy and accumulation of hyperphosphorylated tau neurofibrillary and glial tangles, dystrophic neurites, 43 kDa TAR DNA-binding protein (TDP-43) neuronal and glial aggregates, microvasculopathy, myelinated axonopathy, neuroinflammation, and white matter degeneration. Clinically, CTE is associated with behavioral changes, executive dysfunction, memory deficits, and cognitive impairments that begin insidiously and most often progress slowly over decades. Although research on the long-term effects of TBI is advancing quickly, the incidence and prevalence of post-traumatic neurodegeneration and CTE are unknown. Critical knowledge gaps include elucidation of pathogenic mechanisms, identification of genetic risk factors, and clarification of relevant variables\textemdashincluding age at exposure to trauma, history of prior and subsequent head trauma, substance use, gender, stress, and comorbidities\textemdashall of which may contribute to risk profiles and the development of post-traumatic neurodegeneration and CTE. This article is part of a Special Issue entitled 'Traumatic Brain Injury'. [ABSTRACT FROM AUTHOR] Copyright of MCN: Molecular \& Cellular Neuroscience is the property of Academic Press Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)},
keywords = {A$beta$ beta-amyloid, AD Alzheimer's disease, APOE $epsilon$4 apolipoprotein $epsilon$4, axonal injury, Blast and impact neurotrauma, BRAIN -- Wounds \& injuries, Brain trauma, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy NEURODEGENERATION, Concussion, CSF cerebrospinal fluid, CTE chronic traumatic encephalopathy, DIAGNOSIS, DISEASES -- Risk factors, DNA-binding proteins, MORTALITY, Motor neuron disease, mTBI mild traumatic brain injury, NERVOUS system -- Wounds \& injuries, NFTs neurofibrillary tangles, p-tau hyperphosphorylated tau, PCS post-concussion syndrome, PET positron emission tomography, PHF-tau paired helical filament-tau, Posttraumatic neurodegeneration, tau protein, TBI traumatic brain injury, TDP-43 43 kDa TAR DNA-binding protein, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}
Ramalho, J; Castillo, M
Dementia resulting from traumatic brain injury Journal Article
In: Dementia e Neuropsychologia, vol. 9, no. 4, pp. 356–368, 2015.
Abstract | BibTeX | Tags: Chronic traumatic encephalopathy, Craniocerebral Trauma, Dementia, Magnetic resonance, Post-Concussion Syndrome
@article{Ramalho2015,
title = {Dementia resulting from traumatic brain injury},
author = {Ramalho, J and Castillo, M},
year = {2015},
date = {2015-01-01},
journal = {Dementia e Neuropsychologia},
volume = {9},
number = {4},
pages = {356--368},
abstract = {Traumatic brain injury (TBI) represents a significant public health problem in modern societies. It is primarily a consequence of traffic-related accidents and falls. Other recently recognized causes include sports injuries and indirect forces such as shock waves from battlefield explosions. TBI is an important cause of death and lifelong disability and represents the most well-established environmental risk factor for dementia. With the growing recognition that even mild head injury can lead to neurocognitive deficits, imaging of brain injury has assumed greater importance. However, there is no single imaging modality capable of characterizing TBI. Current advances, particularly in MR imaging, enable visualization and quantification of structural and functional brain changes not hitherto possible. In this review, we summarize data linking TBI with dementia, emphasizing the imaging techniques currently available in clinical practice along with some advances in medical knowledge. © 2015, Academia Brasileira de Neurologia. All rights reserved.},
keywords = {Chronic traumatic encephalopathy, Craniocerebral Trauma, Dementia, Magnetic resonance, Post-Concussion Syndrome},
pubstate = {published},
tppubtype = {article}
}
Lenihan, M W; Jordan, B D
The clinical presentation of chronic traumatic encephalopathy Journal Article
In: Current Neurology & Neuroscience Reports, vol. 15, no. 5, pp. 23, 2015.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Lenihan2015,
title = {The clinical presentation of chronic traumatic encephalopathy},
author = {Lenihan, M W and Jordan, B D},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25772999},
year = {2015},
date = {2015-01-01},
journal = {Current Neurology \& Neuroscience Reports},
volume = {15},
number = {5},
pages = {23},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder attributed to repetitive mild traumatic brain injury. The diagnosis in a living individual can be challenging and can be made definitively only at autopsy. The symptoms are often nonspecific and overlap with neurodegenerative disorders such as Alzheimer's disease (AD) and frontotemporal dementia (FTD). Higher exposure to repetitive head trauma increases the risk of CTE. Genetic risk factors such as presence of an apolipoprotein E epsilon4 allele may be important. Individuals have varying degrees of cognitive, behavioral, and motor decline. Limitations in the manner in which data have been obtained over the years have led to different clinical descriptions of CTE. At present, there are no biomarkers to assist in the diagnosis. Standard neuroimaging may show nonspecific atrophic changes; however, newer imaging modalities such as positron emission tomography (PET) and diffusion tensor imaging (DTI) show promise. Neuropsychological testing may be helpful in determining the pattern of cognitive or behavioral decline.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Riley, D O; Robbins, C A; Cantu, R C; Stern, R A
Chronic traumatic encephalopathy: contributions from the Boston University Center for the Study of Traumatic Encephalopathy Journal Article
In: Brain Injury, vol. 29, no. 2, pp. 154–163, 2015.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Riley2015,
title = {Chronic traumatic encephalopathy: contributions from the Boston University Center for the Study of Traumatic Encephalopathy},
author = {Riley, D O and Robbins, C A and Cantu, R C and Stern, R A},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25587744},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {2},
pages = {154--163},
abstract = {OBJECTIVE: Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disease associated with repetitive brain trauma (RBT). Initially described in boxers, CTE has now been found in other contact sport athletes with a history of RBT. In recent years, there has been tremendous media attention regarding CTE, primarily because of the deaths of high profile American football players who were found to have CTE upon neuropathological examination. However, the study of CTE remains in its infancy. This review focuses on research from the Centre for the Study of Traumatic Encephalopathy (CSTE) at Boston University. METHODS: This study reviews the formation of the CSTE, major CSTE publications and current ongoing research projects at the CSTE. RESULTS: The neuropathology of CTE has been well-described. Current research focuses on: methods of diagnosing the disease during life (including the development of biomarkers), examination of CTE risk factors (including genetic susceptibility and head impact exposure variables); description of the clinical presentation of CTE; development of research diagnostic criteria for Traumatic Encephalopathy Syndrome; and assessment of mechanism and pathogenesis. CONCLUSIONS: Current research at the BU CSTE is aimed at increasing understanding of the long-term consequences of repetitive head impacts and attempting to begin to answer several of the unanswered questions regarding CTE.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Solomon, G S; Zuckerman, S L
Chronic traumatic encephalopathy in professional sports: retrospective and prospective views Journal Article
In: Brain Injury, vol. 29, no. 2, pp. 164–170, 2015.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Solomon2015,
title = {Chronic traumatic encephalopathy in professional sports: retrospective and prospective views},
author = {Solomon, G S and Zuckerman, S L},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25314314},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {2},
pages = {164--170},
abstract = {PRIMARY OBJECTIVE: The purposes of this paper are to review: (1) the history of chronic traumatic encephalopathy (CTE) in sports, (2) the similarities and differences between historic and current definitions of CTE, (3) recent epidemiology and cohort studies of CTE and (4) controversies regarding the current CTE positions. RESEARCH DESIGN: Not applicable. METHODS AND PROCEDURES: Selective review of published articles relevant to CTE. MAIN OUTCOME AND RESULTS: The current definitions of CTE have evolved from its original definition and now rely heavily on the post-mortem detection of hyperphosphorylated tau for diagnosis. As of 2013, there is a blended cohort of 110 professional athletes diagnosed with CTE. It is being assumed that concussions and/or sub-concussive impacts in contact sports are the sole cause of CTE. CONCLUSIONS: There are multiple causes of abnormal tau protein deposition in the human brain and the pathogenesis of CTE may not be related solely to concussion and/or sub-concussive injury. In all likelihood, the causes of CTE are a multivariate, as opposed to a univariate, phenomenon.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Love, S; Solomon, G S
Talking with parents of high school football players about chronic traumatic encephalopathy: a concise summary Journal Article
In: American Journal of Sports Medicine, vol. 43, no. 5, pp. 1260–1264, 2015.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Love2015,
title = {Talking with parents of high school football players about chronic traumatic encephalopathy: a concise summary},
author = {Love, S and Solomon, G S},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=24907288},
year = {2015},
date = {2015-01-01},
journal = {American Journal of Sports Medicine},
volume = {43},
number = {5},
pages = {1260--1264},
abstract = {Over the past decade, athletic-related chronic traumatic encephalopathy (CTE) has garnered a great deal of attention in the popular press and, more recently, in the scientific press. With increasing frequency, sports medicine practitioners and providers are faced with questions from the parents of high school football players about CTE and the risk posed to children who participate in this or other contact or collision sports. The purpose of this review was to summarize the research on CTE in an attempt to provide some evidence-based answers to frequently asked questions in clinics from parents. Addressed are (1) the definitions of CTE and its symptoms, (2) the evidence for CTE in football, (3) abnormal tau protein, (4) the use of neuroimaging in CTE diagnosis, (5) risk for CTE, (6) CTE diagnosis in youth, (7) CTE and its relationship to suicide, and (8) contact and collision sports as a risk factor for permanent brain injury or death. Copyright © 2014 The Author(s).},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Castellani, R J
Chronic traumatic encephalopathy: A paradigm in search of evidence? Journal Article
In: Laboratory Investigation, vol. 95, no. 6, pp. 576–584, 2015.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Castellani2015,
title = {Chronic traumatic encephalopathy: A paradigm in search of evidence?},
author = {Castellani, R J},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25867769},
year = {2015},
date = {2015-01-01},
journal = {Laboratory Investigation},
volume = {95},
number = {6},
pages = {576--584},
abstract = {Chronic traumatic encephalopathy (CTE) has been in the medical literature since the 1920s. It is characterized clinically by diverse neuropsychiatric symptoms, and pathologically by variable degrees of phosphorylated tau accumulation in the brain. The evolving paradigm for the pathogenesis of CTE suggests that concussion or subconcussion from athletic participation initiates a cascade of pathologic events, encompassing neuroinflammation and protein templating with trans-synaptic neurotoxicity. The end result is neurologic and neurobehavioral deterioration, often with self-harm. Although these concepts warrant further investigation, the available evidence permits no conclusions as regards the pathogenesis of the reported findings. Investigations into the role of premorbid or co-morbid neurodegenerative diseases has been limited to date, and in-depth genetic analyses have not been performed. The role of concussion or subconcussion if any, whether and how the condition progresses over time, the extent of phosphorylated tau in clinically normal athletes, the role of phosphorylated tau as a toxic species versus an inert disease response, and whether protein templating has any in vivo relevance remain to be elucidated.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Antonius, D; Mathew, N; Picano, J; Hinds, A; Cogswell, A; Olympia, J; Brooks, T; Di Giacomo, M; Baker, J; Willer, B; Leddy, J
In: Journal of Neuropsychiatry and Clinical Neurosciences, vol. 26, no. 4, pp. 313–322, 2014.
Abstract | Links | BibTeX | Tags: Aggression, anxiety disorder, apathy, Article, behavior change, behavior disorder, brain concussion, buspirone, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy beta adrenergic r, cingulate gyrus, degenerative disease, depression, euphoria, head injury, human, hypersexuality, impulse control disorder, mental disease, mental instability, mood change, nerve degeneration, neurofibrillary tangle, olanzapine, parahippocampal gyrus, personality disorder, postconcussion syndrome, posttraumatic stress disorder, priority journal, serotonin uptake inhibitor, sexual behavior, suicidal behavior, traumatic brain injury
@article{Antonius2014,
title = {Behavioral health symptoms associated with chronic traumatic encephalopathy: A critical review of the literature and recommendations for treatment and research},
author = {Antonius, D and Mathew, N and Picano, J and Hinds, A and Cogswell, A and Olympia, J and Brooks, T and {Di Giacomo}, M and Baker, J and Willer, B and Leddy, J},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84920996232\&partnerID=40\&md5=cb8a1deab38101900f8d7a8ac0b7a80c},
year = {2014},
date = {2014-01-01},
journal = {Journal of Neuropsychiatry and Clinical Neurosciences},
volume = {26},
number = {4},
pages = {313--322},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative syndrome that has been linked to serious psychiatric symptoms, including depression, aggression, and suicidal behavior. This review critically examines the extant research on the behavioral manifestations of CTE and concludes that the paucity of longitudinal prospective studies on CTE, combined with a lack of research-accepted diagnostic criteria for identifying individuals who are considered at risk for CTE, makes it difficult to reliably establish a causal relationship between CTE and the onset of behavioral health problems. Selection and reporting bias and inconsistency in data collection methods are other concerns. To advance the field, there is a critical need for more empirical research on the behavioral manifestations of CTE. Recommendations and intervention models are also discussed. © 2014 American Psychiatric Association.},
keywords = {Aggression, anxiety disorder, apathy, Article, behavior change, behavior disorder, brain concussion, buspirone, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy beta adrenergic r, cingulate gyrus, degenerative disease, depression, euphoria, head injury, human, hypersexuality, impulse control disorder, mental disease, mental instability, mood change, nerve degeneration, neurofibrillary tangle, olanzapine, parahippocampal gyrus, personality disorder, postconcussion syndrome, posttraumatic stress disorder, priority journal, serotonin uptake inhibitor, sexual behavior, suicidal behavior, traumatic brain injury},
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}
}
Montenigro, P H; Baugh, C M; Daneshvar, D H; Mez, J; Budson, A E; Au, R; Katz, D I; Cantu, R C; Stern, R A
In: Alzheimer's Research and Therapy, vol. 6, no. 5-8, 2014.
Abstract | Links | BibTeX | Tags: Anxiety, apathy, ataxia, ataxic gait, attention, attention disturbance, behavior disorder, blunted affect, Boxing, chronic brain disease, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy aggression, clinical feature, clonus, cognitive defect, contact sport, delusion, Dementia, depression, depth perception, differential diagnosis, disease classification, dysarthria, dysgraphia, euphoria, executive function, fatigue, football, hopelessness, human, ice hockey, impulsiveness, insomnia, intelligence, irritability, language disability, mania, medical literature, memory disorder, mental concentration, mental instability, mood disorder, muscle weakness, neurologic gait disorder, paranoia, Parkinsonism, personality disorder, physical violence, preventive medicine, psychosis, Research Diagnostic Criteria, Review, risk factor, shuffling gait, social disability, social isolation, spastic gait, spasticity, speech disorder, sport injury, suicidal ideation, traumatic brain injury, traumatic encephalopathy syndrome, tremor, unsteady gait, violence, wrestling
@article{Montenigro2014,
title = {Clinical subtypes of chronic traumatic encephalopathy: Literature review and proposed research diagnostic criteria for traumatic encephalopathy syndrome},
author = {Montenigro, P H and Baugh, C M and Daneshvar, D H and Mez, J and Budson, A E and Au, R and Katz, D I and Cantu, R C and Stern, R A},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84908410645\&partnerID=40\&md5=bab59baeecd5adb22d0f84a4ce99bd5c},
doi = {10.1186/s13195-014-0068-z},
year = {2014},
date = {2014-01-01},
journal = {Alzheimer's Research and Therapy},
volume = {6},
number = {5-8},
abstract = {The long-term consequences of repetitive head impacts have been described since the early 20th century. Terms such as punch drunk and dementia pugilistica were first used to describe the clinical syndromes experienced by boxers. A more generic designation, chronic traumatic encephalopathy (CTE), has been employed since the mid-1900s and has been used in recent years to describe a neurodegenerative disease found not just in boxers but in American football players, other contact sport athletes, military veterans, and others with histories of repetitive brain trauma, including concussions and subconcussive trauma. This article reviews the literature of the clinical manifestations of CTE from 202 published cases. The clinical features include impairments in mood (for example, depression and hopelessness), behavior (for example, explosivity and violence), cognition (for example, impaired memory, executive functioning, attention, and dementia), and, less commonly, motor functioning (for example, parkinsonism, ataxia, and dysarthria). We present proposed research criteria for traumatic encephalopathy syndrome (TES) which consist of four variants or subtypes (TES behavioral/mood variant, TES cognitive variant, TES mixed variant, and TES dementia) as well as classifications of 'probable CTE' and 'possible CTE'. These proposed criteria are expected to be modified and updated as new research findings become available. They are not meant to be used for a clinical diagnosis. Rather, they should be viewed as research criteria that can be employed in studies of the underlying causes, risk factors, differential diagnosis, prevention, and treatment of CTE and related disorders. © 2014 Montenigro et al.; licensee BioMed Central Ltd.},
keywords = {Anxiety, apathy, ataxia, ataxic gait, attention, attention disturbance, behavior disorder, blunted affect, Boxing, chronic brain disease, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy aggression, clinical feature, clonus, cognitive defect, contact sport, delusion, Dementia, depression, depth perception, differential diagnosis, disease classification, dysarthria, dysgraphia, euphoria, executive function, fatigue, football, hopelessness, human, ice hockey, impulsiveness, insomnia, intelligence, irritability, language disability, mania, medical literature, memory disorder, mental concentration, mental instability, mood disorder, muscle weakness, neurologic gait disorder, paranoia, Parkinsonism, personality disorder, physical violence, preventive medicine, psychosis, Research Diagnostic Criteria, Review, risk factor, shuffling gait, social disability, social isolation, spastic gait, spasticity, speech disorder, sport injury, suicidal ideation, traumatic brain injury, traumatic encephalopathy syndrome, tremor, unsteady gait, violence, wrestling},
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}
}
Levin, B; Bhardwaj, A
Chronic traumatic encephalopathy: A critical appraisal Journal Article
In: Neurocritical Care, vol. 20, no. 2, pp. 334–344, 2014.
Abstract | Links | BibTeX | Tags: accident, alcohol consumption, amnesia, amyloid plaque, animal, Animals, Athletic Injuries, autopsy, behavior change, Brain Injury, Chronic, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy Dementia, complication, Diffusion Tensor Imaging, disease course, Encephalopathy, functional magnetic resonance imaging, histopathology, human, Humans, longitudinal study, Male, Neurodegenerative, Neurodegenerative Diseases, nonhuman, NUCLEAR magnetic resonance spectroscopy, Parkinsonism, pathogenesis, pathology, Pathophysiology, Prevalence, priority journal, Pugilistic, Review, risk factor, Risk Factors, sport injury, suicide, Systematic Review, traumatic brain injury, violence
@article{Levin2014,
title = {Chronic traumatic encephalopathy: A critical appraisal},
author = {Levin, B and Bhardwaj, A},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84896549537\&partnerID=40\&md5=138104db42f7ca99527a78bb9c821f59},
doi = {10.1007/s12028-013-9931-1},
year = {2014},
date = {2014-01-01},
journal = {Neurocritical Care},
volume = {20},
number = {2},
pages = {334--344},
abstract = {Chronic traumatic encephalopathy (CTE) formerly known as dementia pugilistica is a long-term neurodegenerative disorder associated with repeated subconcussive head injuries in high-contact sports. We reviewed the existing literature on CTE and examined epidemiological trends, risk factors, and its temporal progression, and proposed the underlying pathophysiological mechanisms that may provide unique insights to clinicians with an in-depth understanding of the disease to aid in the diagnosis and prevention, and provide future perspectives for research via search of Medline and Cochrane databases as well as manual review of bibliographies from selected articles and monographs. The prevalence of CTE in recent years is on the rise and almost exclusively affects men, with pathologic signs characterized by progressive memory loss, behavioral changes, and violent tendencies with some patients demonstrating Parkinsonian-like symptoms and signs. Many patients with CTE die following suicide, accident, or complications of drug or alcohol use. Postmortem pathologic analysis is characterized by neurofibrillary tangles and A$beta$ plaques in 50 % of cases. Currently, there are no ante-mortem diagnostic criteria, but modern imaging techniques such as functional magnetic resonance (MR) imaging, MR spectroscopy, and diffusion tension imaging hold promise for delineating the future diagnostic criteria. Further long-term longitudinal studies are warranted to investigate risk factors that will enhance understanding of the disease progression and its pathogenesis. © 2013 Springer Science+Business Media.},
keywords = {accident, alcohol consumption, amnesia, amyloid plaque, animal, Animals, Athletic Injuries, autopsy, behavior change, Brain Injury, Chronic, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy Dementia, complication, Diffusion Tensor Imaging, disease course, Encephalopathy, functional magnetic resonance imaging, histopathology, human, Humans, longitudinal study, Male, Neurodegenerative, Neurodegenerative Diseases, nonhuman, NUCLEAR magnetic resonance spectroscopy, Parkinsonism, pathogenesis, pathology, Pathophysiology, Prevalence, priority journal, Pugilistic, Review, risk factor, Risk Factors, sport injury, suicide, Systematic Review, traumatic brain injury, violence},
pubstate = {published},
tppubtype = {article}
}
Tator, C H
Chronic traumatic encephalopathy: how serious a sports problem is it? Journal Article
In: British Journal of Sports Medicine, vol. 48, pp. 81–83, 2014.
Abstract | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Tator2014,
title = {Chronic traumatic encephalopathy: how serious a sports problem is it?},
author = {Tator, C H},
year = {2014},
date = {2014-01-01},
journal = {British Journal of Sports Medicine},
volume = {48},
pages = {81--83},
address = {Division of Neurosurgery, Toronto Western Hospital, University of Toronto, , Toronto, Ontario, Canada.},
abstract = {It is now recognised that there is a spectrum of concussion disorders ranging from acute concussion at one end to various forms of brain degeneration at the other end. The spectrum includes acute concussion, second impact syndrome or acute cerebral swelling, postconcussion syndrome, depression or anxiety, chronic traumatic encephalopathy (CTE) and possibly other forms of central nervous system degeneration. It is essential to carefully evaluate the clinical and neuropathological correlations of CTE that have been published. This has been accomplished in an excellent paper on this subject by Gardner and colleagues in this issue. There have been significant advances in our knowledge of the clinical and neuropathological features of CTE in athletes in the past 10 years. However, we are just at the beginning of our appreciation of this entity due to the paucity of research and the inability to diagnose CTE during life. At present, it is not possible to assess the validity of the proposed methods of classification and grading of the severity of the disease. Additional studies of large numbers of at-risk athletes are essential, especially prospective longitudinal studies. Obviously, such studies would be even more effective if reliable in vivo biomarkers were discovered, especially non-invasive ones such as advanced MRI or MR spectroscopy or invasive ones such as blood or cerebrospinal fluid tests. The major questions that remain unanswered include the frequency of CTE in various collision sports, the causal or otherwise relationship between concussions and CTE, the number of concussions that need to be involved and their management.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Andrikopoulos, J
Creating a concussion crisis and chronic traumatic encephalopathy Journal Article
In: JAMA Neurology, vol. 71, pp. 654, 2014.
BibTeX | Tags: Chronic traumatic encephalopathy
@article{Andrikopoulos2014b,
title = {Creating a concussion crisis and chronic traumatic encephalopathy},
author = {Andrikopoulos, J},
year = {2014},
date = {2014-01-01},
journal = {JAMA Neurology},
volume = {71},
pages = {654},
address = {Mercy Hospital Medical Center, Ruan Neurology Clinic, Des Moines, Iowa.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Gardner, A; Iverson, G L; McCrory, P
Chronic traumatic encephalopathy in sport: a systematic review Journal Article
In: British Journal of Sports Medicine, vol. 48, pp. 84–90, 2014.
Abstract | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Gardner2014b,
title = {Chronic traumatic encephalopathy in sport: a systematic review},
author = {Gardner, A and Iverson, G L and McCrory, P},
year = {2014},
date = {2014-01-01},
journal = {British Journal of Sports Medicine},
volume = {48},
pages = {84--90},
address = {Centre for Translational Neuroscience and Mental Health, School of Medicine and Public Health, University of Newcastle, , Callaghan, New South Wales, Australia.},
abstract = {OBJECTIVE: To provide a critical review of chronic traumatic encephalopathy (CTE) by considering the range of clinical presentations, neuropathology and the strength of evidence for CTE as a distinct syndrome. DATA SOURCES: Seven electronic databases were searched using a combination of MeSH terms and key words to identify relevant articles. REVIEW METHODS: Specific inclusion and exclusion criteria were used to select studies for review. Data extracted where present included study population, exposure/outcome measures, clinical data, neurological examination findings, cognitive assessment, investigation results and neuropathology results. RESULTS: The data from 158 published case studies were reviewed. Critical differences between the older descriptions of CTE (the 'classic' syndrome) and the recent descriptions (the 'modern' syndrome) exist in the age of onset, natural history, clinical features, pathological findings and diagnostic criteria, which suggests that modern CTE is a different syndrome. The methodology of the current studies does not allow determination of aetiology or risk factors. CONCLUSIONS: The clinicopathological differences between the 'classic' CTE syndrome and the 'modern' syndrome suggest that the new syndrome needs a different nomenclature. Further research is required to clearly define the clinical phenotype of the modern CTE syndrome and establish the underlying aetiology. Future research needs to address these issues through large-scale, prospective clinicopathological studies.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Tartaglia, M C; Hazrati, L N; Davis, K D; Green, R E; Wennberg, R; Mikulis, D; Ezerins, L J; Keightley, M; Tator, C
Chronic traumatic encephalopathy and other neurodegenerative proteinopathies Journal Article
In: Frontiers in Human Neuroscience, vol. 8, pp. 30, 2014.
Abstract | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Tartaglia2014,
title = {Chronic traumatic encephalopathy and other neurodegenerative proteinopathies},
author = {Tartaglia, M C and Hazrati, L N and Davis, K D and Green, R E and Wennberg, R and Mikulis, D and Ezerins, L J and Keightley, M and Tator, C},
year = {2014},
date = {2014-01-01},
journal = {Frontiers in Human Neuroscience},
volume = {8},
pages = {30},
address = {Division of Neurology, Krembil Neuroscience Centre, University Health Network, University of Toronto Toronto, ON, Canada ; Tanz Centre for Research in Neurodegenerative Disease, University of Toronto Toronto, ON, Canada ; Canadian Sports Concussion Projec},
abstract = {"Chronic traumatic encephalopathy" (CTE) is described as a slowly progressive neurodegenerative disease believed to result from multiple concussions. Traditionally, concussions were considered benign events and although most people recover fully, about 10% develop a post-concussive syndrome with persisting neurological, cognitive and neuropsychiatric symptoms. CTE was once thought to be unique to boxers, but it has now been observed in many different athletes having suffered multiple concussions as well as in military personal after repeated blast injuries. Much remains unknown about the development of CTE but its pathological substrate is usually tau, similar to that seen in Alzheimer's disease (AD) and frontotemporal lobar degeneration (FTLD). The aim of this "perspective" is to compare and contrast clinical and pathological CTE with the other neurodegenerative proteinopathies and highlight that there is an urgent need for understanding the relationship between concussion and the development of CTE as it may provide a window into the development of a proteinopathy and thus new avenues for treatment.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Victoroff, J
Traumatic encephalopathy: Review and provisional research diagnostic criteria Journal Article
In: NeuroRehabilitation, vol. 32, pp. 211–224, 2013.
Abstract | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Victoroff2013,
title = {Traumatic encephalopathy: Review and provisional research diagnostic criteria},
author = {Victoroff, J},
year = {2013},
date = {2013-01-01},
journal = {NeuroRehabilitation},
volume = {32},
pages = {211--224},
abstract = {Objectives: To determine the frequency of neurobehavioral signs and symptoms reported in every published case of traumatic encephalopathy with a view toward the development of clinical diagnostic criteria with predictive validity. Introduction: Cases of persistent or progressive neurological or neurobehavioral change following exposure to one or more head injuries have been reported since 1928. This condition is often referred to as traumatic encephalopathy (TE). To date, however, no diagnostic criteria have been advanced or accepted for the clinical diagnosis of TE. Provisional research diagnostic criteria are required not only for meaningful diagnosis but also to facilitate research to determine the epidemiology, etiology, course, prognosis, imaging and biomarkers, neuropathological features and potentially effective treatments of TE. Methods: All 436 published cases of TE in all languages were reviewed. All symptoms and signs reported in these cases were classified and enumerated. Results: Ninety-seven cases met inclusion criteria based on sufficient documentation of the history and neurobehavioral examination. Provisional research diagnostic criteria for clinically probable and clinically possible TE were developed based on the most frequently reported clinical features. Conclusion: The provisional diagnostic criteria for TE presented here are the first published criteria for this condition based upon a systematic analysis of its clinical characteristics. This is the first a step toward scientifically derived consensus criteria, which are essential to accelerate progress in the investigation of this important condition. © 2013 - IOS Press and the authors. All rights reserved.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Andrews, Erin P
Avoiding the Technical Knockout: Tackling the Inadequacies of Youth Concussion Legislation Journal Article
In: New York Law School Law Review, vol. 58, no. 2, pp. 417–455, 2013, ISBN: 0145448X.
Abstract | BibTeX | Tags: ATHLETES -- Health, brain, BRAIN -- Degeneration, BRAIN -- Wounds & injuries, Chronic traumatic encephalopathy, Concussion, PATIENTS
@article{Andrews2013,
title = {Avoiding the Technical Knockout: Tackling the Inadequacies of Youth Concussion Legislation},
author = {Andrews, Erin P},
isbn = {0145448X},
year = {2013},
date = {2013-01-01},
journal = {New York Law School Law Review},
volume = {58},
number = {2},
pages = {417--455},
abstract = {The article discusses medical effects of football-related concussions on youths in the U.S. Topics discussed include shortcomings in the laws related to concussion epidemic among youth football players; a Uniform Concussion Management Code (UCMC) for concussion care; concussion symptoms and diagnosis; and the long-term effects of chronic traumatic encephalopathy (CTE).},
keywords = {ATHLETES -- Health, brain, BRAIN -- Degeneration, BRAIN -- Wounds \& injuries, Chronic traumatic encephalopathy, Concussion, PATIENTS},
pubstate = {published},
tppubtype = {article}
}
Gavett, Brandon E; Stern, Robert A; Cantu, Robert C; Nowinski, Christopher J; McKee, Ann C
Mild traumatic brain injury: a risk factor for neurodegeneration Journal Article
In: Alzheimer's Research & Therapy, vol. 2, pp. 18, 2010.
Abstract | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Gavett2010,
title = {Mild traumatic brain injury: a risk factor for neurodegeneration},
author = {Gavett, Brandon E and Stern, Robert A and Cantu, Robert C and Nowinski, Christopher J and McKee, Ann C},
year = {2010},
date = {2010-01-01},
journal = {Alzheimer's Research \& Therapy},
volume = {2},
pages = {18},
address = {Department of Neurology, Boston University School of Medicine, 72 East Concord St, B-7800, Boston, MA 02118, USA. begavett@bu.edu.},
abstract = {ABSTRACT : Recently, it has become clear that head trauma can lead to a progressive neurodegeneration known as chronic traumatic encephalopathy. Although the medical literature also implicates head trauma as a risk factor for Alzheimer's disease, these findings are predominantly based on clinical diagnostic criteria that lack specificity. The dementia that follows head injuries or repetitive mild trauma may be caused by chronic traumatic encephalopathy, alone or in conjunction with other neurodegenerations (for example, Alzheimer's disease). Prospective longitudinal studies of head-injured individuals, with neuropathological verification, will not only improve understanding of head trauma as a risk factor for dementia but will also enhance treatment and prevention of a variety of neurodegenerative diseases.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Watanabe, Thomas; Elovic, Elie; Zafonte, Ross
Chronic traumatic encephalopathy Journal Article
In: PM & R, vol. 2, pp. 671–675, 2010.
BibTeX | Tags: Chronic traumatic encephalopathy
@article{Watanabe2010,
title = {Chronic traumatic encephalopathy},
author = {Watanabe, Thomas and Elovic, Elie and Zafonte, Ross},
year = {2010},
date = {2010-01-01},
journal = {PM \& R},
volume = {2},
pages = {671--675},
address = {MossRehab, 60 Township Line Rd., Elkins Park, PA 19027, USA. watanabt@einstein.edu},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Gavett, B E; Stern, R A; Nowinski, C J; Cantu, R C; McKee, A C
Clinical and neuropathologic findings in chronic traumatic encephalopathy: A case series Journal Article
In: Archives of Clinical Neuropsychology, vol. 24, pp. 525, 2009, ISSN: 0887-6177.
BibTeX | Tags: Chronic traumatic encephalopathy
@article{Gavett2009,
title = {Clinical and neuropathologic findings in chronic traumatic encephalopathy: A case series},
author = {Gavett, B E and Stern, R A and Nowinski, C J and Cantu, R C and McKee, A C},
issn = {0887-6177},
year = {2009},
date = {2009-01-01},
journal = {Archives of Clinical Neuropsychology},
volume = {24},
pages = {525},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Forum, Alzheimer Research
Alzheimer Research Forum Live Discussion: Sports concussions, dementia, and ApoE genotyping: What can scientists tell the public? What's up for research? Journal Article
In: Journal of Alzheimer's Disease, vol. 16, no. 3, pp. 657–666, 2009.
BibTeX | Tags: Chronic traumatic encephalopathy, Education, genetics
@article{AlzheimerResearchForum2009,
title = {Alzheimer Research Forum Live Discussion: Sports concussions, dementia, and ApoE genotyping: What can scientists tell the public? What's up for research?},
author = {{Alzheimer Research Forum}},
year = {2009},
date = {2009-01-01},
journal = {Journal of Alzheimer's Disease},
volume = {16},
number = {3},
pages = {657--666},
keywords = {Chronic traumatic encephalopathy, Education, genetics},
pubstate = {published},
tppubtype = {article}
}
Lassonde, M; Theriault, M; de Beaumont, L
Electrophysiological anomalies 30 years post-concussion Journal Article
In: Clinical Neurophysiology, vol. 119, pp. e151–e151, 2008, ISSN: 1388-2457.
BibTeX | Tags: Chronic traumatic encephalopathy
@article{Lassonde2008,
title = {Electrophysiological anomalies 30 years post-concussion},
author = {Lassonde, M and Theriault, M and de Beaumont, L},
issn = {1388-2457},
year = {2008},
date = {2008-01-01},
journal = {Clinical Neurophysiology},
volume = {119},
pages = {e151--e151},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
for Disease Control, Centers; Prevention,
Nonfatal traumatic brain injuries from sports and recreation activities--United States, 2001-2005 Journal Article
In: MMWR - Morbidity & Mortality Weekly Report, vol. 56, no. 29, pp. 733–737, 2007.
Abstract | BibTeX | Tags: *Athletic Injuries/ep [Epidemiology], *Brain Injuries/ep [Epidemiology], Adolescent, adult, Child, Chronic traumatic encephalopathy, Female, Humans, Incidence/Epidemiology, Infant, Male, middle aged, Population Surveillance, Preschool, recreation, United States/ep [Epidemiology]
@article{CentersforDiseaseControlandPrevention2007,
title = {Nonfatal traumatic brain injuries from sports and recreation activities--United States, 2001-2005},
author = {{Centers for Disease Control and Prevention}},
year = {2007},
date = {2007-01-01},
journal = {MMWR - Morbidity \& Mortality Weekly Report},
volume = {56},
number = {29},
pages = {733--737},
abstract = {Each year in the United States, an estimated 38 million children and adolescents participate in organized sports, and approximately 170 million adults participate in some type of physical activity not related to work. The health benefits of these activities are tempered by the risk for injury, including traumatic brain injury (TBI). CDC estimates that 1.1 million persons with TBIs are treated and released from U.S. hospital emergency departments (EDs) each year, and an additional 235,000 are hospitalized for these injuries. TBIs can result in long-term, negative health effects (e.g., memory loss and behavioral changes). To characterize sports- and recreation-related (SR-related) TBIs among patients treated in U.S. hospital EDs, CDC analyzed data from the National Electronic Injury Surveillance System--All Injury Program (NEISS-AIP) for the period 2001-2005. This report summarizes the results of that analysis, which indicated that an estimated 207,830 patients with nonfatal SR-related TBIs were treated in EDs each year during this period. The highest rates of SR-related TBI ED visits for both males and females occurred among those aged 10-14 years. Increased awareness of TBI risks, prevention strategies, and the importance of timely identification and management is essential for reducing the incidence, severity, and long-term negative health effects of this type of injury.},
keywords = {*Athletic Injuries/ep [Epidemiology], *Brain Injuries/ep [Epidemiology], Adolescent, adult, Child, Chronic traumatic encephalopathy, Female, Humans, Incidence/Epidemiology, Infant, Male, middle aged, Population Surveillance, Preschool, recreation, United States/ep [Epidemiology]},
pubstate = {published},
tppubtype = {article}
}
Lyon, Louisa
High impact research: investigating the effects of repetitive head injury Journal Article
In: Brain: A Journal of Neurology, vol. 140, no. 1, pp. e6–e6, 2017, ISBN: 00068950.
@article{Lyon2017,
title = {High impact research: investigating the effects of repetitive head injury},
author = {Lyon, Louisa},
doi = {10.1093/brain/aww294},
isbn = {00068950},
year = {2017},
date = {2017-01-01},
journal = {Brain: A Journal of Neurology},
volume = {140},
number = {1},
pages = {e6--e6},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Webner, David; Iverson, Grant L
Suicide in professional American football players in the past 95 years Journal Article
In: Brain Injury, vol. 30, no. 13/14, pp. 1718–1721, 2016, ISBN: 02699052.
@article{Webner2016,
title = {Suicide in professional American football players in the past 95 years},
author = {Webner, David and Iverson, Grant L},
doi = {10.1080/02699052.2016.1202451},
isbn = {02699052},
year = {2016},
date = {2016-01-01},
journal = {Brain Injury},
volume = {30},
number = {13/14},
pages = {1718--1721},
abstract = {Objective: To examine publicly-available information on all identified cases of suicide in active or former American professional football players between 1920 and the spring of 2015. Design: Retrospective cohort study. Setting: Professional American Football in the US. Participants: A cohort of 26 702 athletes who had died, retired or were currently playing in the NFL from nfl.com since 1920 was identified. Main outcome measures: Internet queries identifying 26 professional football players who completed suicide. Obituaries and news reports were reviewed. The primary outcome measures included mortality, demographic characteristics and life circumstances in professional American football players completing suicide. Results: From 1920\textendash2015, the median age of the 26 men who completed suicide was 39.5 years (range = 23\textendash85). The median number of years after retirement was 6.5 (range = 0\textendash63). Most of the deaths since 1920 have occurred in the past 15 years (58.7%) and a large percentage have occurred since 2009 (42.3%). Most of the men suffered from multiple life stressors prior to their deaths, such as retirement from sport, loss of steady income, divorce, failed business ventures, estrangement from family members and medical, psychiatric and/or substance abuse problems. Conclusions: A disproportionate number of completed suicides in current and former professional football players have occurred since 2009 (42.3%). It is well established in the literature that the causes of depression and suicidality are diverse, often multifactorial and treatable. Providing at-risk retired athletes with mental health treatment will likely reduce their suffering and improve their quality-of-life. [ABSTRACT FROM AUTHOR]},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Choe, M C
The Pathophysiology of Concussion Journal Article
In: Current Pain & Headache Reports, vol. 20, no. 6, 2016.
@article{Choe2016b,
title = {The Pathophysiology of Concussion},
author = {Choe, M C},
doi = {10.1007/s11916-016-0573-9},
year = {2016},
date = {2016-01-01},
journal = {Current Pain \& Headache Reports},
volume = {20},
number = {6},
abstract = {Concussion is a significant issue in medicine and the media today. With growing interest on the long-term effects of sports participation, it is important to understand what occurs in the brain after an impact of any degree. While some of the basic pathophysiology has been elucidated, much is still unknown about what happens in the brain after traumatic brain injury, particularly with milder injuries where no damage can be seen at the structural level on standard neuroimaging. Understanding the chain of events from a cellular level using studies investigating more severe injuries can help to drive research efforts in understanding the symptomatology that is seen in the acute phase after concussion, as well as point to mechanisms that may underlie persistent post-concussive symptoms. This review discusses the basic neuropathology that occurs after traumatic brain injury at the cellular level. We also present the pathology of chronic traumatic encephalopathy and its similarities to other neurodegenerative diseases. We conclude with recent imaging and biomarker findings looking at changes that may occur after repeated subconcussive blows, which may help to guide efforts in understanding if cumulative subconcussive mechanical forces upon the brain are detrimental in the long term or if concussive symptoms mark the threshold for brain injury. © 2016, Springer Science+Business Media New York.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Chiroban, O; Perju-Dumbravă, L
Postmortem evaluation of chronic traumatic encephalopathy Journal Article
In: Romanian Journal of Legal Medicine, vol. 24, no. 4, pp. 266–272, 2016.
@article{Chiroban2016,
title = {Postmortem evaluation of chronic traumatic encephalopathy},
author = {Chiroban, O and Perju-Dumbrav\u{a}, L},
doi = {10.4323/rjlm.2016.266},
year = {2016},
date = {2016-01-01},
journal = {Romanian Journal of Legal Medicine},
volume = {24},
number = {4},
pages = {266--272},
abstract = {Chronic traumatic encephalopathy (CTE) is the modern concept naming the neurodegenerative processes occurring in patients with positive medical history of repeated brain trauma and progressive dementia. Morphologically, CTE is classified as being a distinct member of the tauopathies family, with different distribution of tau-positive neurofibrillary tangles (NFTs) and low to none beta-amyloid deposits, contrasting the most famous member of the family: Alzheimer’s disease (AD). As opposed to other of its kind, the neurofibrillary tangles (NFTs) are spread in the form of irregular, perivascular, patchy disseminations throughout frontal and temporal cortex, especially in the superficial cerebral layers, leaning for sulcal depths. The previously mentioned characteristics constitute the hallmark signature of CTE. Although the connection between repeated concussions and CTE has been recently proposed, the startup path is still a mysterious topic. It remains, up to a point, common to all tauopathies, yet overpasses all genders, sex and age. Initially, considered a professional disease in boxing, scientific overviews link CTE to military service, sports and even daily activities. It is a consensus that a moderate traumatic event sustained during life-spam was correlated with 2.3 fold increase in the risk of developing dementia, while severe concussion augments up 4 times the chances. By the same token, considering the broad population with potential exposure to repetitive insults, CTE represents an important public health issue. The main purpose of this scientific article is to highlight the neuropathological features encountered and discuss the limitations of proper diagnostic. © 2016 Romanian Society of Legal Medicine.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Moon, K; Theodore, N
Football and Chronic Traumatic Encephalopathy: How Much Evidence Actually Exists? Journal Article
In: World Neurosurgery, vol. 89, pp. 720–721, 2016.
@article{Moon2016,
title = {Football and Chronic Traumatic Encephalopathy: How Much Evidence Actually Exists?},
author = {Moon, K and Theodore, N},
doi = {10.1016/j.wneu.2016.03.073},
year = {2016},
date = {2016-01-01},
journal = {World Neurosurgery},
volume = {89},
pages = {720--721},
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.
@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}
}
Edlow, B L; Hinson, H E
Blowing the whistle on sports concussions Journal Article
In: Neurology, vol. 85, no. 17, pp. 1442–1443, 2015.
@article{Edlow2015,
title = {Blowing the whistle on sports concussions},
author = {Edlow, B L and Hinson, H E},
doi = {10.1212/WNL.0000000000001902},
year = {2015},
date = {2015-01-01},
journal = {Neurology},
volume = {85},
number = {17},
pages = {1442--1443},
abstract = {On March 13, 2015, Chris Borland, a star rookie linebacker on the San Francisco 49ers, announced his early retirement from professional football, citing concerns about chronic traumatic encephalopathy (CTE). Borland, who had a history of 2 diagnosed concussions, walked away from a multi-million-dollar contract and potential sports superstardom, explaining that "from what I've researched and what I've experienced, I don't think it's worth the risk." 1 Perhaps just as surprising as Borland's announcement was the support he received from teammates and other athletes-support that reflects a growing recognition in the athletic community that repetitive head trauma may be associated with CTE and other forms of dementia. 2 Indeed, in a recent legal settlement, the National Football League estimated that approximately 30% of its former players will develop dementia. At the high school and college levels, state legislatures and universities have enacted limits to the number of full-contact practices, citing similar concerns about concussions. These developments have prompted a societal conversation about the risks of contact sports. © 2015 American Academy of Neurology.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Montenigro, P H; Bernick, C; Cantu, R C
Clinical features of repetitive traumatic brain injury and chronic traumatic encephalopathy Journal Article
In: Brain Pathology, vol. 25, no. 3, pp. 304–317, 2015.
@article{Montenigro2015,
title = {Clinical features of repetitive traumatic brain injury and chronic traumatic encephalopathy},
author = {Montenigro, P H and Bernick, C and Cantu, R C},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25904046},
year = {2015},
date = {2015-01-01},
journal = {Brain Pathology},
volume = {25},
number = {3},
pages = {304--317},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease characterized by a distinct pattern of hyperphosphorylated tau (p-tau). Thought to be caused by repetitive concussive and subconcussive injuries, CTE is considered largely preventable. The majority of neuropathologically confirmed cases have occurred in professional contact sport athletes (eg, boxing, football). A recent post-mortem case series has magnified concerns for the public's health following its identification in six high school level athletes. CTE is diagnosed with certainty only following a post-mortem autopsy. Efforts to define the etiology and clinical progression during life are ongoing. The goal of this article is to characterize the clinical concepts associated with short- and long-term effects of repetitive traumatic brain injury, with a special emphasis on new clinical diagnostic criteria for CTE. Utilizing these new diagnostic criteria, two cases of neuropathologically confirmed CTE, one in a professional football player and one in a professional boxer, are reported. Differences in cerebellar pathology in CTE confirmed cases in boxing and football are discussed. Copyright © 2015 International Society of Neuropathology.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Montenigro, P H; Corp, D T; Stein, T D; Cantu, R C; Stern, R A
Chronic traumatic encephalopathy: historical origins and current perspective Journal Article
In: Annual Review of Clinical Psychology, vol. 11, pp. 309–330, 2015.
@article{Montenigro2015a,
title = {Chronic traumatic encephalopathy: historical origins and current perspective},
author = {Montenigro, P H and Corp, D T and Stein, T D and Cantu, R C and Stern, R A},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25581233},
year = {2015},
date = {2015-01-01},
journal = {Annual Review of Clinical Psychology},
volume = {11},
pages = {309--330},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that is most often identified in postmortem autopsies of individuals exposed to repetitive head impacts, such as boxers and football players. The neuropathology of CTE is characterized by the accumulation of hyperphosphorylated tau protein in a pattern that is unique from that of other neurodegenerative diseases, including Alzheimer's disease. The clinical features of CTE are often progressive, leading to dramatic changes in mood, behavior, and cognition, frequently resulting in debilitating dementia. In some cases, motor features, including parkinsonism, can also be present. In this review, the historical origins of CTE are revealed and an overview of the current state of knowledge of CTE is provided, including the neuropathology, clinical features, proposed clinical and pathological diagnostic criteria, potential in vivo biomarkers, known risk factors, and treatment options.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Daneshvar, Daniel H; Goldstein, Lee E; Kiernan, Patrick T; Stein, Thor D; McKee, Ann C
Post-traumatic neurodegeneration and chronic traumatic encephalopathy Journal Article
In: MCN: Molecular & Cellular Neuroscience, vol. 66, no. Part B, pp. 81–90, 2015, ISBN: 10447431.
@article{Daneshvar2015,
title = {Post-traumatic neurodegeneration and chronic traumatic encephalopathy},
author = {Daneshvar, Daniel H and Goldstein, Lee E and Kiernan, Patrick T and Stein, Thor D and McKee, Ann C},
url = {http://search.ebscohost.com/login.aspx?direct=true\&db=aph\&AN=103136351\&site=ehost-live},
doi = {10.1016/j.mcn.2015.03.007},
isbn = {10447431},
year = {2015},
date = {2015-01-01},
journal = {MCN: Molecular \& Cellular Neuroscience},
volume = {66},
number = {Part B},
pages = {81--90},
abstract = {Traumatic brain injury (TBI) is a leading cause of mortality and morbidity around the world. Concussive and subconcussive forms of closed-head injury due to impact or blast neurotrauma represent the most common types of TBI in civilian and military settings. It is becoming increasingly evident that TBI can lead to persistent, long-term debilitating effects, and in some cases, progressive neurodegeneration and chronic traumatic encephalopathy (CTE). The epidemiological literature suggests that a single moderate-to-severe TBI may be associated with accelerated neurodegeneration and increased risk of Alzheimer's disease, Parkinson's disease, or motor neuron disease. However, the pathologic phenotype of these post-traumatic neurodegenerations is largely unknown and there may be pathobiological differences between post-traumatic disease and the corresponding sporadic disorder. By contrast, the pathology of CTE is increasingly well known and is characterized by a distinctive pattern of progressive brain atrophy and accumulation of hyperphosphorylated tau neurofibrillary and glial tangles, dystrophic neurites, 43 kDa TAR DNA-binding protein (TDP-43) neuronal and glial aggregates, microvasculopathy, myelinated axonopathy, neuroinflammation, and white matter degeneration. Clinically, CTE is associated with behavioral changes, executive dysfunction, memory deficits, and cognitive impairments that begin insidiously and most often progress slowly over decades. Although research on the long-term effects of TBI is advancing quickly, the incidence and prevalence of post-traumatic neurodegeneration and CTE are unknown. Critical knowledge gaps include elucidation of pathogenic mechanisms, identification of genetic risk factors, and clarification of relevant variables\textemdashincluding age at exposure to trauma, history of prior and subsequent head trauma, substance use, gender, stress, and comorbidities\textemdashall of which may contribute to risk profiles and the development of post-traumatic neurodegeneration and CTE. This article is part of a Special Issue entitled 'Traumatic Brain Injury'. [ABSTRACT FROM AUTHOR] Copyright of MCN: Molecular \& Cellular Neuroscience is the property of Academic Press Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Ramalho, J; Castillo, M
Dementia resulting from traumatic brain injury Journal Article
In: Dementia e Neuropsychologia, vol. 9, no. 4, pp. 356–368, 2015.
@article{Ramalho2015,
title = {Dementia resulting from traumatic brain injury},
author = {Ramalho, J and Castillo, M},
year = {2015},
date = {2015-01-01},
journal = {Dementia e Neuropsychologia},
volume = {9},
number = {4},
pages = {356--368},
abstract = {Traumatic brain injury (TBI) represents a significant public health problem in modern societies. It is primarily a consequence of traffic-related accidents and falls. Other recently recognized causes include sports injuries and indirect forces such as shock waves from battlefield explosions. TBI is an important cause of death and lifelong disability and represents the most well-established environmental risk factor for dementia. With the growing recognition that even mild head injury can lead to neurocognitive deficits, imaging of brain injury has assumed greater importance. However, there is no single imaging modality capable of characterizing TBI. Current advances, particularly in MR imaging, enable visualization and quantification of structural and functional brain changes not hitherto possible. In this review, we summarize data linking TBI with dementia, emphasizing the imaging techniques currently available in clinical practice along with some advances in medical knowledge. © 2015, Academia Brasileira de Neurologia. All rights reserved.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Lenihan, M W; Jordan, B D
The clinical presentation of chronic traumatic encephalopathy Journal Article
In: Current Neurology & Neuroscience Reports, vol. 15, no. 5, pp. 23, 2015.
@article{Lenihan2015,
title = {The clinical presentation of chronic traumatic encephalopathy},
author = {Lenihan, M W and Jordan, B D},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25772999},
year = {2015},
date = {2015-01-01},
journal = {Current Neurology \& Neuroscience Reports},
volume = {15},
number = {5},
pages = {23},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder attributed to repetitive mild traumatic brain injury. The diagnosis in a living individual can be challenging and can be made definitively only at autopsy. The symptoms are often nonspecific and overlap with neurodegenerative disorders such as Alzheimer's disease (AD) and frontotemporal dementia (FTD). Higher exposure to repetitive head trauma increases the risk of CTE. Genetic risk factors such as presence of an apolipoprotein E epsilon4 allele may be important. Individuals have varying degrees of cognitive, behavioral, and motor decline. Limitations in the manner in which data have been obtained over the years have led to different clinical descriptions of CTE. At present, there are no biomarkers to assist in the diagnosis. Standard neuroimaging may show nonspecific atrophic changes; however, newer imaging modalities such as positron emission tomography (PET) and diffusion tensor imaging (DTI) show promise. Neuropsychological testing may be helpful in determining the pattern of cognitive or behavioral decline.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Riley, D O; Robbins, C A; Cantu, R C; Stern, R A
Chronic traumatic encephalopathy: contributions from the Boston University Center for the Study of Traumatic Encephalopathy Journal Article
In: Brain Injury, vol. 29, no. 2, pp. 154–163, 2015.
@article{Riley2015,
title = {Chronic traumatic encephalopathy: contributions from the Boston University Center for the Study of Traumatic Encephalopathy},
author = {Riley, D O and Robbins, C A and Cantu, R C and Stern, R A},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25587744},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {2},
pages = {154--163},
abstract = {OBJECTIVE: Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disease associated with repetitive brain trauma (RBT). Initially described in boxers, CTE has now been found in other contact sport athletes with a history of RBT. In recent years, there has been tremendous media attention regarding CTE, primarily because of the deaths of high profile American football players who were found to have CTE upon neuropathological examination. However, the study of CTE remains in its infancy. This review focuses on research from the Centre for the Study of Traumatic Encephalopathy (CSTE) at Boston University. METHODS: This study reviews the formation of the CSTE, major CSTE publications and current ongoing research projects at the CSTE. RESULTS: The neuropathology of CTE has been well-described. Current research focuses on: methods of diagnosing the disease during life (including the development of biomarkers), examination of CTE risk factors (including genetic susceptibility and head impact exposure variables); description of the clinical presentation of CTE; development of research diagnostic criteria for Traumatic Encephalopathy Syndrome; and assessment of mechanism and pathogenesis. CONCLUSIONS: Current research at the BU CSTE is aimed at increasing understanding of the long-term consequences of repetitive head impacts and attempting to begin to answer several of the unanswered questions regarding CTE.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Solomon, G S; Zuckerman, S L
Chronic traumatic encephalopathy in professional sports: retrospective and prospective views Journal Article
In: Brain Injury, vol. 29, no. 2, pp. 164–170, 2015.
@article{Solomon2015,
title = {Chronic traumatic encephalopathy in professional sports: retrospective and prospective views},
author = {Solomon, G S and Zuckerman, S L},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25314314},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {2},
pages = {164--170},
abstract = {PRIMARY OBJECTIVE: The purposes of this paper are to review: (1) the history of chronic traumatic encephalopathy (CTE) in sports, (2) the similarities and differences between historic and current definitions of CTE, (3) recent epidemiology and cohort studies of CTE and (4) controversies regarding the current CTE positions. RESEARCH DESIGN: Not applicable. METHODS AND PROCEDURES: Selective review of published articles relevant to CTE. MAIN OUTCOME AND RESULTS: The current definitions of CTE have evolved from its original definition and now rely heavily on the post-mortem detection of hyperphosphorylated tau for diagnosis. As of 2013, there is a blended cohort of 110 professional athletes diagnosed with CTE. It is being assumed that concussions and/or sub-concussive impacts in contact sports are the sole cause of CTE. CONCLUSIONS: There are multiple causes of abnormal tau protein deposition in the human brain and the pathogenesis of CTE may not be related solely to concussion and/or sub-concussive injury. In all likelihood, the causes of CTE are a multivariate, as opposed to a univariate, phenomenon.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Love, S; Solomon, G S
Talking with parents of high school football players about chronic traumatic encephalopathy: a concise summary Journal Article
In: American Journal of Sports Medicine, vol. 43, no. 5, pp. 1260–1264, 2015.
@article{Love2015,
title = {Talking with parents of high school football players about chronic traumatic encephalopathy: a concise summary},
author = {Love, S and Solomon, G S},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=24907288},
year = {2015},
date = {2015-01-01},
journal = {American Journal of Sports Medicine},
volume = {43},
number = {5},
pages = {1260--1264},
abstract = {Over the past decade, athletic-related chronic traumatic encephalopathy (CTE) has garnered a great deal of attention in the popular press and, more recently, in the scientific press. With increasing frequency, sports medicine practitioners and providers are faced with questions from the parents of high school football players about CTE and the risk posed to children who participate in this or other contact or collision sports. The purpose of this review was to summarize the research on CTE in an attempt to provide some evidence-based answers to frequently asked questions in clinics from parents. Addressed are (1) the definitions of CTE and its symptoms, (2) the evidence for CTE in football, (3) abnormal tau protein, (4) the use of neuroimaging in CTE diagnosis, (5) risk for CTE, (6) CTE diagnosis in youth, (7) CTE and its relationship to suicide, and (8) contact and collision sports as a risk factor for permanent brain injury or death. Copyright © 2014 The Author(s).},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Castellani, R J
Chronic traumatic encephalopathy: A paradigm in search of evidence? Journal Article
In: Laboratory Investigation, vol. 95, no. 6, pp. 576–584, 2015.
@article{Castellani2015,
title = {Chronic traumatic encephalopathy: A paradigm in search of evidence?},
author = {Castellani, R J},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25867769},
year = {2015},
date = {2015-01-01},
journal = {Laboratory Investigation},
volume = {95},
number = {6},
pages = {576--584},
abstract = {Chronic traumatic encephalopathy (CTE) has been in the medical literature since the 1920s. It is characterized clinically by diverse neuropsychiatric symptoms, and pathologically by variable degrees of phosphorylated tau accumulation in the brain. The evolving paradigm for the pathogenesis of CTE suggests that concussion or subconcussion from athletic participation initiates a cascade of pathologic events, encompassing neuroinflammation and protein templating with trans-synaptic neurotoxicity. The end result is neurologic and neurobehavioral deterioration, often with self-harm. Although these concepts warrant further investigation, the available evidence permits no conclusions as regards the pathogenesis of the reported findings. Investigations into the role of premorbid or co-morbid neurodegenerative diseases has been limited to date, and in-depth genetic analyses have not been performed. The role of concussion or subconcussion if any, whether and how the condition progresses over time, the extent of phosphorylated tau in clinically normal athletes, the role of phosphorylated tau as a toxic species versus an inert disease response, and whether protein templating has any in vivo relevance remain to be elucidated.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Antonius, D; Mathew, N; Picano, J; Hinds, A; Cogswell, A; Olympia, J; Brooks, T; Di Giacomo, M; Baker, J; Willer, B; Leddy, J
In: Journal of Neuropsychiatry and Clinical Neurosciences, vol. 26, no. 4, pp. 313–322, 2014.
@article{Antonius2014,
title = {Behavioral health symptoms associated with chronic traumatic encephalopathy: A critical review of the literature and recommendations for treatment and research},
author = {Antonius, D and Mathew, N and Picano, J and Hinds, A and Cogswell, A and Olympia, J and Brooks, T and {Di Giacomo}, M and Baker, J and Willer, B and Leddy, J},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84920996232\&partnerID=40\&md5=cb8a1deab38101900f8d7a8ac0b7a80c},
year = {2014},
date = {2014-01-01},
journal = {Journal of Neuropsychiatry and Clinical Neurosciences},
volume = {26},
number = {4},
pages = {313--322},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative syndrome that has been linked to serious psychiatric symptoms, including depression, aggression, and suicidal behavior. This review critically examines the extant research on the behavioral manifestations of CTE and concludes that the paucity of longitudinal prospective studies on CTE, combined with a lack of research-accepted diagnostic criteria for identifying individuals who are considered at risk for CTE, makes it difficult to reliably establish a causal relationship between CTE and the onset of behavioral health problems. Selection and reporting bias and inconsistency in data collection methods are other concerns. To advance the field, there is a critical need for more empirical research on the behavioral manifestations of CTE. Recommendations and intervention models are also discussed. © 2014 American Psychiatric Association.},
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}
}
Montenigro, P H; Baugh, C M; Daneshvar, D H; Mez, J; Budson, A E; Au, R; Katz, D I; Cantu, R C; Stern, R A
In: Alzheimer's Research and Therapy, vol. 6, no. 5-8, 2014.
@article{Montenigro2014,
title = {Clinical subtypes of chronic traumatic encephalopathy: Literature review and proposed research diagnostic criteria for traumatic encephalopathy syndrome},
author = {Montenigro, P H and Baugh, C M and Daneshvar, D H and Mez, J and Budson, A E and Au, R and Katz, D I and Cantu, R C and Stern, R A},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84908410645\&partnerID=40\&md5=bab59baeecd5adb22d0f84a4ce99bd5c},
doi = {10.1186/s13195-014-0068-z},
year = {2014},
date = {2014-01-01},
journal = {Alzheimer's Research and Therapy},
volume = {6},
number = {5-8},
abstract = {The long-term consequences of repetitive head impacts have been described since the early 20th century. Terms such as punch drunk and dementia pugilistica were first used to describe the clinical syndromes experienced by boxers. A more generic designation, chronic traumatic encephalopathy (CTE), has been employed since the mid-1900s and has been used in recent years to describe a neurodegenerative disease found not just in boxers but in American football players, other contact sport athletes, military veterans, and others with histories of repetitive brain trauma, including concussions and subconcussive trauma. This article reviews the literature of the clinical manifestations of CTE from 202 published cases. The clinical features include impairments in mood (for example, depression and hopelessness), behavior (for example, explosivity and violence), cognition (for example, impaired memory, executive functioning, attention, and dementia), and, less commonly, motor functioning (for example, parkinsonism, ataxia, and dysarthria). We present proposed research criteria for traumatic encephalopathy syndrome (TES) which consist of four variants or subtypes (TES behavioral/mood variant, TES cognitive variant, TES mixed variant, and TES dementia) as well as classifications of 'probable CTE' and 'possible CTE'. These proposed criteria are expected to be modified and updated as new research findings become available. They are not meant to be used for a clinical diagnosis. Rather, they should be viewed as research criteria that can be employed in studies of the underlying causes, risk factors, differential diagnosis, prevention, and treatment of CTE and related disorders. © 2014 Montenigro et al.; licensee BioMed Central Ltd.},
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}
}
Lyon, Louisa
High impact research: investigating the effects of repetitive head injury Journal Article
In: Brain: A Journal of Neurology, vol. 140, no. 1, pp. e6–e6, 2017, ISBN: 00068950.
Links | BibTeX | Tags: BRAIN -- Concussion, Chronic traumatic encephalopathy, DISEASE susceptibility, Head Injuries, NATIONAL Football League
@article{Lyon2017,
title = {High impact research: investigating the effects of repetitive head injury},
author = {Lyon, Louisa},
doi = {10.1093/brain/aww294},
isbn = {00068950},
year = {2017},
date = {2017-01-01},
journal = {Brain: A Journal of Neurology},
volume = {140},
number = {1},
pages = {e6--e6},
keywords = {BRAIN -- Concussion, Chronic traumatic encephalopathy, DISEASE susceptibility, Head Injuries, NATIONAL Football League},
pubstate = {published},
tppubtype = {article}
}
Webner, David; Iverson, Grant L
Suicide in professional American football players in the past 95 years Journal Article
In: Brain Injury, vol. 30, no. 13/14, pp. 1718–1721, 2016, ISBN: 02699052.
Abstract | Links | BibTeX | Tags: Athletes, BRAIN damage, CHRONIC diseases, CHRONIC pain, Chronic traumatic encephalopathy, depression, DESCRIPTIVE statistics, EPIDEMIOLOGY -- Research, football, Internet, Life change events, LONGITUDINAL method, MENTAL depression, MORTALITY, Professional athletes, Professional Sports, psychology, RESEARCH -- Methodology, Retirement, Retrospective Studies, Socioeconomic Factors, STRESS (Psychology), suicide, Suicide -- Risk factors, Suicide -- United States, UNITED States, WORK experience (Employment)
@article{Webner2016,
title = {Suicide in professional American football players in the past 95 years},
author = {Webner, David and Iverson, Grant L},
doi = {10.1080/02699052.2016.1202451},
isbn = {02699052},
year = {2016},
date = {2016-01-01},
journal = {Brain Injury},
volume = {30},
number = {13/14},
pages = {1718--1721},
abstract = {Objective: To examine publicly-available information on all identified cases of suicide in active or former American professional football players between 1920 and the spring of 2015. Design: Retrospective cohort study. Setting: Professional American Football in the US. Participants: A cohort of 26 702 athletes who had died, retired or were currently playing in the NFL from nfl.com since 1920 was identified. Main outcome measures: Internet queries identifying 26 professional football players who completed suicide. Obituaries and news reports were reviewed. The primary outcome measures included mortality, demographic characteristics and life circumstances in professional American football players completing suicide. Results: From 1920\textendash2015, the median age of the 26 men who completed suicide was 39.5 years (range = 23\textendash85). The median number of years after retirement was 6.5 (range = 0\textendash63). Most of the deaths since 1920 have occurred in the past 15 years (58.7%) and a large percentage have occurred since 2009 (42.3%). Most of the men suffered from multiple life stressors prior to their deaths, such as retirement from sport, loss of steady income, divorce, failed business ventures, estrangement from family members and medical, psychiatric and/or substance abuse problems. Conclusions: A disproportionate number of completed suicides in current and former professional football players have occurred since 2009 (42.3%). It is well established in the literature that the causes of depression and suicidality are diverse, often multifactorial and treatable. Providing at-risk retired athletes with mental health treatment will likely reduce their suffering and improve their quality-of-life. [ABSTRACT FROM AUTHOR]},
keywords = {Athletes, BRAIN damage, CHRONIC diseases, CHRONIC pain, Chronic traumatic encephalopathy, depression, DESCRIPTIVE statistics, EPIDEMIOLOGY -- Research, football, Internet, Life change events, LONGITUDINAL method, MENTAL depression, MORTALITY, Professional athletes, Professional Sports, psychology, RESEARCH -- Methodology, Retirement, Retrospective Studies, Socioeconomic Factors, STRESS (Psychology), suicide, Suicide -- Risk factors, Suicide -- United States, UNITED States, WORK experience (Employment)},
pubstate = {published},
tppubtype = {article}
}
Choe, M C
The Pathophysiology of Concussion Journal Article
In: Current Pain & Headache Reports, vol. 20, no. 6, 2016.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy, Concussion, diffuse axonal injury, Pathophysiology
@article{Choe2016b,
title = {The Pathophysiology of Concussion},
author = {Choe, M C},
doi = {10.1007/s11916-016-0573-9},
year = {2016},
date = {2016-01-01},
journal = {Current Pain \& Headache Reports},
volume = {20},
number = {6},
abstract = {Concussion is a significant issue in medicine and the media today. With growing interest on the long-term effects of sports participation, it is important to understand what occurs in the brain after an impact of any degree. While some of the basic pathophysiology has been elucidated, much is still unknown about what happens in the brain after traumatic brain injury, particularly with milder injuries where no damage can be seen at the structural level on standard neuroimaging. Understanding the chain of events from a cellular level using studies investigating more severe injuries can help to drive research efforts in understanding the symptomatology that is seen in the acute phase after concussion, as well as point to mechanisms that may underlie persistent post-concussive symptoms. This review discusses the basic neuropathology that occurs after traumatic brain injury at the cellular level. We also present the pathology of chronic traumatic encephalopathy and its similarities to other neurodegenerative diseases. We conclude with recent imaging and biomarker findings looking at changes that may occur after repeated subconcussive blows, which may help to guide efforts in understanding if cumulative subconcussive mechanical forces upon the brain are detrimental in the long term or if concussive symptoms mark the threshold for brain injury. © 2016, Springer Science+Business Media New York.},
keywords = {Chronic traumatic encephalopathy, Concussion, diffuse axonal injury, Pathophysiology},
pubstate = {published},
tppubtype = {article}
}
Chiroban, O; Perju-Dumbravă, L
Postmortem evaluation of chronic traumatic encephalopathy Journal Article
In: Romanian Journal of Legal Medicine, vol. 24, no. 4, pp. 266–272, 2016.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy, Forensic pathology, NEURODEGENERATION, Trauma
@article{Chiroban2016,
title = {Postmortem evaluation of chronic traumatic encephalopathy},
author = {Chiroban, O and Perju-Dumbrav\u{a}, L},
doi = {10.4323/rjlm.2016.266},
year = {2016},
date = {2016-01-01},
journal = {Romanian Journal of Legal Medicine},
volume = {24},
number = {4},
pages = {266--272},
abstract = {Chronic traumatic encephalopathy (CTE) is the modern concept naming the neurodegenerative processes occurring in patients with positive medical history of repeated brain trauma and progressive dementia. Morphologically, CTE is classified as being a distinct member of the tauopathies family, with different distribution of tau-positive neurofibrillary tangles (NFTs) and low to none beta-amyloid deposits, contrasting the most famous member of the family: Alzheimer’s disease (AD). As opposed to other of its kind, the neurofibrillary tangles (NFTs) are spread in the form of irregular, perivascular, patchy disseminations throughout frontal and temporal cortex, especially in the superficial cerebral layers, leaning for sulcal depths. The previously mentioned characteristics constitute the hallmark signature of CTE. Although the connection between repeated concussions and CTE has been recently proposed, the startup path is still a mysterious topic. It remains, up to a point, common to all tauopathies, yet overpasses all genders, sex and age. Initially, considered a professional disease in boxing, scientific overviews link CTE to military service, sports and even daily activities. It is a consensus that a moderate traumatic event sustained during life-spam was correlated with 2.3 fold increase in the risk of developing dementia, while severe concussion augments up 4 times the chances. By the same token, considering the broad population with potential exposure to repetitive insults, CTE represents an important public health issue. The main purpose of this scientific article is to highlight the neuropathological features encountered and discuss the limitations of proper diagnostic. © 2016 Romanian Society of Legal Medicine.},
keywords = {Chronic traumatic encephalopathy, Forensic pathology, NEURODEGENERATION, Trauma},
pubstate = {published},
tppubtype = {article}
}
Moon, K; Theodore, N
Football and Chronic Traumatic Encephalopathy: How Much Evidence Actually Exists? Journal Article
In: World Neurosurgery, vol. 89, pp. 720–721, 2016.
Links | BibTeX | Tags: Alzheimer disease, amyloid beta protein, amyloid plaque, anxiety disorder, apolipoprotein E, Article, behavior disorder, Boxing, brain atrophy, brain concussion, brain degeneration, chronic disease, Chronic traumatic encephalopathy, cognitive defect, degenerative disease, depression, environmental factor, football, frontotemporal dementia, genetic predisposition, genetic risk, genetic susceptibility, human, motor control, Neuroanatomy, opiate addiction, Parkinson disease, protein phosphorylation, scar formation, septum pellucidum, sport injury, substantia nigra, suicide, TAR DNA binding protein, tau protein, tauopathy, traumatic brain injury
@article{Moon2016,
title = {Football and Chronic Traumatic Encephalopathy: How Much Evidence Actually Exists?},
author = {Moon, K and Theodore, N},
doi = {10.1016/j.wneu.2016.03.073},
year = {2016},
date = {2016-01-01},
journal = {World Neurosurgery},
volume = {89},
pages = {720--721},
keywords = {Alzheimer disease, amyloid beta protein, amyloid plaque, anxiety disorder, apolipoprotein E, Article, behavior disorder, Boxing, brain atrophy, brain concussion, brain degeneration, chronic disease, Chronic traumatic encephalopathy, cognitive defect, degenerative disease, depression, environmental factor, football, frontotemporal dementia, genetic predisposition, genetic risk, genetic susceptibility, human, motor control, Neuroanatomy, opiate addiction, Parkinson disease, protein phosphorylation, scar formation, septum pellucidum, sport injury, substantia nigra, suicide, TAR DNA binding protein, tau protein, tauopathy, traumatic brain injury},
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}
}
Edlow, B L; Hinson, H E
Blowing the whistle on sports concussions Journal Article
In: Neurology, vol. 85, no. 17, pp. 1442–1443, 2015.
Abstract | Links | BibTeX | Tags: Alzheimer disease, Chronic traumatic encephalopathy, Concussion, contact sport, Diffusion Tensor Imaging, football, functional magnetic resonance imaging, histopathology, Hockey, human, memory disorder, mood disorder, pathogenesis, Pathophysiology, priority journal, Review, rugby, Soccer, sport injury, sports concussion, traumatic brain injury, wrestling
@article{Edlow2015,
title = {Blowing the whistle on sports concussions},
author = {Edlow, B L and Hinson, H E},
doi = {10.1212/WNL.0000000000001902},
year = {2015},
date = {2015-01-01},
journal = {Neurology},
volume = {85},
number = {17},
pages = {1442--1443},
abstract = {On March 13, 2015, Chris Borland, a star rookie linebacker on the San Francisco 49ers, announced his early retirement from professional football, citing concerns about chronic traumatic encephalopathy (CTE). Borland, who had a history of 2 diagnosed concussions, walked away from a multi-million-dollar contract and potential sports superstardom, explaining that "from what I've researched and what I've experienced, I don't think it's worth the risk." 1 Perhaps just as surprising as Borland's announcement was the support he received from teammates and other athletes-support that reflects a growing recognition in the athletic community that repetitive head trauma may be associated with CTE and other forms of dementia. 2 Indeed, in a recent legal settlement, the National Football League estimated that approximately 30% of its former players will develop dementia. At the high school and college levels, state legislatures and universities have enacted limits to the number of full-contact practices, citing similar concerns about concussions. These developments have prompted a societal conversation about the risks of contact sports. © 2015 American Academy of Neurology.},
keywords = {Alzheimer disease, Chronic traumatic encephalopathy, Concussion, contact sport, Diffusion Tensor Imaging, football, functional magnetic resonance imaging, histopathology, Hockey, human, memory disorder, mood disorder, pathogenesis, Pathophysiology, priority journal, Review, rugby, Soccer, sport injury, sports concussion, traumatic brain injury, wrestling},
pubstate = {published},
tppubtype = {article}
}
Montenigro, P H; Bernick, C; Cantu, R C
Clinical features of repetitive traumatic brain injury and chronic traumatic encephalopathy Journal Article
In: Brain Pathology, vol. 25, no. 3, pp. 304–317, 2015.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Montenigro2015,
title = {Clinical features of repetitive traumatic brain injury and chronic traumatic encephalopathy},
author = {Montenigro, P H and Bernick, C and Cantu, R C},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25904046},
year = {2015},
date = {2015-01-01},
journal = {Brain Pathology},
volume = {25},
number = {3},
pages = {304--317},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease characterized by a distinct pattern of hyperphosphorylated tau (p-tau). Thought to be caused by repetitive concussive and subconcussive injuries, CTE is considered largely preventable. The majority of neuropathologically confirmed cases have occurred in professional contact sport athletes (eg, boxing, football). A recent post-mortem case series has magnified concerns for the public's health following its identification in six high school level athletes. CTE is diagnosed with certainty only following a post-mortem autopsy. Efforts to define the etiology and clinical progression during life are ongoing. The goal of this article is to characterize the clinical concepts associated with short- and long-term effects of repetitive traumatic brain injury, with a special emphasis on new clinical diagnostic criteria for CTE. Utilizing these new diagnostic criteria, two cases of neuropathologically confirmed CTE, one in a professional football player and one in a professional boxer, are reported. Differences in cerebellar pathology in CTE confirmed cases in boxing and football are discussed. Copyright © 2015 International Society of Neuropathology.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Montenigro, P H; Corp, D T; Stein, T D; Cantu, R C; Stern, R A
Chronic traumatic encephalopathy: historical origins and current perspective Journal Article
In: Annual Review of Clinical Psychology, vol. 11, pp. 309–330, 2015.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Montenigro2015a,
title = {Chronic traumatic encephalopathy: historical origins and current perspective},
author = {Montenigro, P H and Corp, D T and Stein, T D and Cantu, R C and Stern, R A},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25581233},
year = {2015},
date = {2015-01-01},
journal = {Annual Review of Clinical Psychology},
volume = {11},
pages = {309--330},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that is most often identified in postmortem autopsies of individuals exposed to repetitive head impacts, such as boxers and football players. The neuropathology of CTE is characterized by the accumulation of hyperphosphorylated tau protein in a pattern that is unique from that of other neurodegenerative diseases, including Alzheimer's disease. The clinical features of CTE are often progressive, leading to dramatic changes in mood, behavior, and cognition, frequently resulting in debilitating dementia. In some cases, motor features, including parkinsonism, can also be present. In this review, the historical origins of CTE are revealed and an overview of the current state of knowledge of CTE is provided, including the neuropathology, clinical features, proposed clinical and pathological diagnostic criteria, potential in vivo biomarkers, known risk factors, and treatment options.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Daneshvar, Daniel H; Goldstein, Lee E; Kiernan, Patrick T; Stein, Thor D; McKee, Ann C
Post-traumatic neurodegeneration and chronic traumatic encephalopathy Journal Article
In: MCN: Molecular & Cellular Neuroscience, vol. 66, no. Part B, pp. 81–90, 2015, ISBN: 10447431.
Abstract | Links | BibTeX | Tags: A$beta$ beta-amyloid, AD Alzheimer's disease, APOE $epsilon$4 apolipoprotein $epsilon$4, axonal injury, Blast and impact neurotrauma, BRAIN -- Wounds & injuries, Brain trauma, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy NEURODEGENERATION, Concussion, CSF cerebrospinal fluid, CTE chronic traumatic encephalopathy, DIAGNOSIS, DISEASES -- Risk factors, DNA-binding proteins, MORTALITY, Motor neuron disease, mTBI mild traumatic brain injury, NERVOUS system -- Wounds & injuries, NFTs neurofibrillary tangles, p-tau hyperphosphorylated tau, PCS post-concussion syndrome, PET positron emission tomography, PHF-tau paired helical filament-tau, Posttraumatic neurodegeneration, tau protein, TBI traumatic brain injury, TDP-43 43 kDa TAR DNA-binding protein, traumatic brain injury
@article{Daneshvar2015,
title = {Post-traumatic neurodegeneration and chronic traumatic encephalopathy},
author = {Daneshvar, Daniel H and Goldstein, Lee E and Kiernan, Patrick T and Stein, Thor D and McKee, Ann C},
url = {http://search.ebscohost.com/login.aspx?direct=true\&db=aph\&AN=103136351\&site=ehost-live},
doi = {10.1016/j.mcn.2015.03.007},
isbn = {10447431},
year = {2015},
date = {2015-01-01},
journal = {MCN: Molecular \& Cellular Neuroscience},
volume = {66},
number = {Part B},
pages = {81--90},
abstract = {Traumatic brain injury (TBI) is a leading cause of mortality and morbidity around the world. Concussive and subconcussive forms of closed-head injury due to impact or blast neurotrauma represent the most common types of TBI in civilian and military settings. It is becoming increasingly evident that TBI can lead to persistent, long-term debilitating effects, and in some cases, progressive neurodegeneration and chronic traumatic encephalopathy (CTE). The epidemiological literature suggests that a single moderate-to-severe TBI may be associated with accelerated neurodegeneration and increased risk of Alzheimer's disease, Parkinson's disease, or motor neuron disease. However, the pathologic phenotype of these post-traumatic neurodegenerations is largely unknown and there may be pathobiological differences between post-traumatic disease and the corresponding sporadic disorder. By contrast, the pathology of CTE is increasingly well known and is characterized by a distinctive pattern of progressive brain atrophy and accumulation of hyperphosphorylated tau neurofibrillary and glial tangles, dystrophic neurites, 43 kDa TAR DNA-binding protein (TDP-43) neuronal and glial aggregates, microvasculopathy, myelinated axonopathy, neuroinflammation, and white matter degeneration. Clinically, CTE is associated with behavioral changes, executive dysfunction, memory deficits, and cognitive impairments that begin insidiously and most often progress slowly over decades. Although research on the long-term effects of TBI is advancing quickly, the incidence and prevalence of post-traumatic neurodegeneration and CTE are unknown. Critical knowledge gaps include elucidation of pathogenic mechanisms, identification of genetic risk factors, and clarification of relevant variables\textemdashincluding age at exposure to trauma, history of prior and subsequent head trauma, substance use, gender, stress, and comorbidities\textemdashall of which may contribute to risk profiles and the development of post-traumatic neurodegeneration and CTE. This article is part of a Special Issue entitled 'Traumatic Brain Injury'. [ABSTRACT FROM AUTHOR] Copyright of MCN: Molecular \& Cellular Neuroscience is the property of Academic Press Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)},
keywords = {A$beta$ beta-amyloid, AD Alzheimer's disease, APOE $epsilon$4 apolipoprotein $epsilon$4, axonal injury, Blast and impact neurotrauma, BRAIN -- Wounds \& injuries, Brain trauma, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy NEURODEGENERATION, Concussion, CSF cerebrospinal fluid, CTE chronic traumatic encephalopathy, DIAGNOSIS, DISEASES -- Risk factors, DNA-binding proteins, MORTALITY, Motor neuron disease, mTBI mild traumatic brain injury, NERVOUS system -- Wounds \& injuries, NFTs neurofibrillary tangles, p-tau hyperphosphorylated tau, PCS post-concussion syndrome, PET positron emission tomography, PHF-tau paired helical filament-tau, Posttraumatic neurodegeneration, tau protein, TBI traumatic brain injury, TDP-43 43 kDa TAR DNA-binding protein, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}
Ramalho, J; Castillo, M
Dementia resulting from traumatic brain injury Journal Article
In: Dementia e Neuropsychologia, vol. 9, no. 4, pp. 356–368, 2015.
Abstract | BibTeX | Tags: Chronic traumatic encephalopathy, Craniocerebral Trauma, Dementia, Magnetic resonance, Post-Concussion Syndrome
@article{Ramalho2015,
title = {Dementia resulting from traumatic brain injury},
author = {Ramalho, J and Castillo, M},
year = {2015},
date = {2015-01-01},
journal = {Dementia e Neuropsychologia},
volume = {9},
number = {4},
pages = {356--368},
abstract = {Traumatic brain injury (TBI) represents a significant public health problem in modern societies. It is primarily a consequence of traffic-related accidents and falls. Other recently recognized causes include sports injuries and indirect forces such as shock waves from battlefield explosions. TBI is an important cause of death and lifelong disability and represents the most well-established environmental risk factor for dementia. With the growing recognition that even mild head injury can lead to neurocognitive deficits, imaging of brain injury has assumed greater importance. However, there is no single imaging modality capable of characterizing TBI. Current advances, particularly in MR imaging, enable visualization and quantification of structural and functional brain changes not hitherto possible. In this review, we summarize data linking TBI with dementia, emphasizing the imaging techniques currently available in clinical practice along with some advances in medical knowledge. © 2015, Academia Brasileira de Neurologia. All rights reserved.},
keywords = {Chronic traumatic encephalopathy, Craniocerebral Trauma, Dementia, Magnetic resonance, Post-Concussion Syndrome},
pubstate = {published},
tppubtype = {article}
}
Lenihan, M W; Jordan, B D
The clinical presentation of chronic traumatic encephalopathy Journal Article
In: Current Neurology & Neuroscience Reports, vol. 15, no. 5, pp. 23, 2015.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Lenihan2015,
title = {The clinical presentation of chronic traumatic encephalopathy},
author = {Lenihan, M W and Jordan, B D},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25772999},
year = {2015},
date = {2015-01-01},
journal = {Current Neurology \& Neuroscience Reports},
volume = {15},
number = {5},
pages = {23},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder attributed to repetitive mild traumatic brain injury. The diagnosis in a living individual can be challenging and can be made definitively only at autopsy. The symptoms are often nonspecific and overlap with neurodegenerative disorders such as Alzheimer's disease (AD) and frontotemporal dementia (FTD). Higher exposure to repetitive head trauma increases the risk of CTE. Genetic risk factors such as presence of an apolipoprotein E epsilon4 allele may be important. Individuals have varying degrees of cognitive, behavioral, and motor decline. Limitations in the manner in which data have been obtained over the years have led to different clinical descriptions of CTE. At present, there are no biomarkers to assist in the diagnosis. Standard neuroimaging may show nonspecific atrophic changes; however, newer imaging modalities such as positron emission tomography (PET) and diffusion tensor imaging (DTI) show promise. Neuropsychological testing may be helpful in determining the pattern of cognitive or behavioral decline.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Riley, D O; Robbins, C A; Cantu, R C; Stern, R A
Chronic traumatic encephalopathy: contributions from the Boston University Center for the Study of Traumatic Encephalopathy Journal Article
In: Brain Injury, vol. 29, no. 2, pp. 154–163, 2015.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Riley2015,
title = {Chronic traumatic encephalopathy: contributions from the Boston University Center for the Study of Traumatic Encephalopathy},
author = {Riley, D O and Robbins, C A and Cantu, R C and Stern, R A},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25587744},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {2},
pages = {154--163},
abstract = {OBJECTIVE: Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disease associated with repetitive brain trauma (RBT). Initially described in boxers, CTE has now been found in other contact sport athletes with a history of RBT. In recent years, there has been tremendous media attention regarding CTE, primarily because of the deaths of high profile American football players who were found to have CTE upon neuropathological examination. However, the study of CTE remains in its infancy. This review focuses on research from the Centre for the Study of Traumatic Encephalopathy (CSTE) at Boston University. METHODS: This study reviews the formation of the CSTE, major CSTE publications and current ongoing research projects at the CSTE. RESULTS: The neuropathology of CTE has been well-described. Current research focuses on: methods of diagnosing the disease during life (including the development of biomarkers), examination of CTE risk factors (including genetic susceptibility and head impact exposure variables); description of the clinical presentation of CTE; development of research diagnostic criteria for Traumatic Encephalopathy Syndrome; and assessment of mechanism and pathogenesis. CONCLUSIONS: Current research at the BU CSTE is aimed at increasing understanding of the long-term consequences of repetitive head impacts and attempting to begin to answer several of the unanswered questions regarding CTE.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Solomon, G S; Zuckerman, S L
Chronic traumatic encephalopathy in professional sports: retrospective and prospective views Journal Article
In: Brain Injury, vol. 29, no. 2, pp. 164–170, 2015.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Solomon2015,
title = {Chronic traumatic encephalopathy in professional sports: retrospective and prospective views},
author = {Solomon, G S and Zuckerman, S L},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25314314},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {2},
pages = {164--170},
abstract = {PRIMARY OBJECTIVE: The purposes of this paper are to review: (1) the history of chronic traumatic encephalopathy (CTE) in sports, (2) the similarities and differences between historic and current definitions of CTE, (3) recent epidemiology and cohort studies of CTE and (4) controversies regarding the current CTE positions. RESEARCH DESIGN: Not applicable. METHODS AND PROCEDURES: Selective review of published articles relevant to CTE. MAIN OUTCOME AND RESULTS: The current definitions of CTE have evolved from its original definition and now rely heavily on the post-mortem detection of hyperphosphorylated tau for diagnosis. As of 2013, there is a blended cohort of 110 professional athletes diagnosed with CTE. It is being assumed that concussions and/or sub-concussive impacts in contact sports are the sole cause of CTE. CONCLUSIONS: There are multiple causes of abnormal tau protein deposition in the human brain and the pathogenesis of CTE may not be related solely to concussion and/or sub-concussive injury. In all likelihood, the causes of CTE are a multivariate, as opposed to a univariate, phenomenon.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Love, S; Solomon, G S
Talking with parents of high school football players about chronic traumatic encephalopathy: a concise summary Journal Article
In: American Journal of Sports Medicine, vol. 43, no. 5, pp. 1260–1264, 2015.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Love2015,
title = {Talking with parents of high school football players about chronic traumatic encephalopathy: a concise summary},
author = {Love, S and Solomon, G S},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=24907288},
year = {2015},
date = {2015-01-01},
journal = {American Journal of Sports Medicine},
volume = {43},
number = {5},
pages = {1260--1264},
abstract = {Over the past decade, athletic-related chronic traumatic encephalopathy (CTE) has garnered a great deal of attention in the popular press and, more recently, in the scientific press. With increasing frequency, sports medicine practitioners and providers are faced with questions from the parents of high school football players about CTE and the risk posed to children who participate in this or other contact or collision sports. The purpose of this review was to summarize the research on CTE in an attempt to provide some evidence-based answers to frequently asked questions in clinics from parents. Addressed are (1) the definitions of CTE and its symptoms, (2) the evidence for CTE in football, (3) abnormal tau protein, (4) the use of neuroimaging in CTE diagnosis, (5) risk for CTE, (6) CTE diagnosis in youth, (7) CTE and its relationship to suicide, and (8) contact and collision sports as a risk factor for permanent brain injury or death. Copyright © 2014 The Author(s).},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Castellani, R J
Chronic traumatic encephalopathy: A paradigm in search of evidence? Journal Article
In: Laboratory Investigation, vol. 95, no. 6, pp. 576–584, 2015.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Castellani2015,
title = {Chronic traumatic encephalopathy: A paradigm in search of evidence?},
author = {Castellani, R J},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=prem\&AN=25867769},
year = {2015},
date = {2015-01-01},
journal = {Laboratory Investigation},
volume = {95},
number = {6},
pages = {576--584},
abstract = {Chronic traumatic encephalopathy (CTE) has been in the medical literature since the 1920s. It is characterized clinically by diverse neuropsychiatric symptoms, and pathologically by variable degrees of phosphorylated tau accumulation in the brain. The evolving paradigm for the pathogenesis of CTE suggests that concussion or subconcussion from athletic participation initiates a cascade of pathologic events, encompassing neuroinflammation and protein templating with trans-synaptic neurotoxicity. The end result is neurologic and neurobehavioral deterioration, often with self-harm. Although these concepts warrant further investigation, the available evidence permits no conclusions as regards the pathogenesis of the reported findings. Investigations into the role of premorbid or co-morbid neurodegenerative diseases has been limited to date, and in-depth genetic analyses have not been performed. The role of concussion or subconcussion if any, whether and how the condition progresses over time, the extent of phosphorylated tau in clinically normal athletes, the role of phosphorylated tau as a toxic species versus an inert disease response, and whether protein templating has any in vivo relevance remain to be elucidated.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Antonius, D; Mathew, N; Picano, J; Hinds, A; Cogswell, A; Olympia, J; Brooks, T; Di Giacomo, M; Baker, J; Willer, B; Leddy, J
In: Journal of Neuropsychiatry and Clinical Neurosciences, vol. 26, no. 4, pp. 313–322, 2014.
Abstract | Links | BibTeX | Tags: Aggression, anxiety disorder, apathy, Article, behavior change, behavior disorder, brain concussion, buspirone, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy beta adrenergic r, cingulate gyrus, degenerative disease, depression, euphoria, head injury, human, hypersexuality, impulse control disorder, mental disease, mental instability, mood change, nerve degeneration, neurofibrillary tangle, olanzapine, parahippocampal gyrus, personality disorder, postconcussion syndrome, posttraumatic stress disorder, priority journal, serotonin uptake inhibitor, sexual behavior, suicidal behavior, traumatic brain injury
@article{Antonius2014,
title = {Behavioral health symptoms associated with chronic traumatic encephalopathy: A critical review of the literature and recommendations for treatment and research},
author = {Antonius, D and Mathew, N and Picano, J and Hinds, A and Cogswell, A and Olympia, J and Brooks, T and {Di Giacomo}, M and Baker, J and Willer, B and Leddy, J},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84920996232\&partnerID=40\&md5=cb8a1deab38101900f8d7a8ac0b7a80c},
year = {2014},
date = {2014-01-01},
journal = {Journal of Neuropsychiatry and Clinical Neurosciences},
volume = {26},
number = {4},
pages = {313--322},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative syndrome that has been linked to serious psychiatric symptoms, including depression, aggression, and suicidal behavior. This review critically examines the extant research on the behavioral manifestations of CTE and concludes that the paucity of longitudinal prospective studies on CTE, combined with a lack of research-accepted diagnostic criteria for identifying individuals who are considered at risk for CTE, makes it difficult to reliably establish a causal relationship between CTE and the onset of behavioral health problems. Selection and reporting bias and inconsistency in data collection methods are other concerns. To advance the field, there is a critical need for more empirical research on the behavioral manifestations of CTE. Recommendations and intervention models are also discussed. © 2014 American Psychiatric Association.},
keywords = {Aggression, anxiety disorder, apathy, Article, behavior change, behavior disorder, brain concussion, buspirone, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy beta adrenergic r, cingulate gyrus, degenerative disease, depression, euphoria, head injury, human, hypersexuality, impulse control disorder, mental disease, mental instability, mood change, nerve degeneration, neurofibrillary tangle, olanzapine, parahippocampal gyrus, personality disorder, postconcussion syndrome, posttraumatic stress disorder, priority journal, serotonin uptake inhibitor, sexual behavior, suicidal behavior, traumatic brain injury},
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}
}
Montenigro, P H; Baugh, C M; Daneshvar, D H; Mez, J; Budson, A E; Au, R; Katz, D I; Cantu, R C; Stern, R A
In: Alzheimer's Research and Therapy, vol. 6, no. 5-8, 2014.
Abstract | Links | BibTeX | Tags: Anxiety, apathy, ataxia, ataxic gait, attention, attention disturbance, behavior disorder, blunted affect, Boxing, chronic brain disease, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy aggression, clinical feature, clonus, cognitive defect, contact sport, delusion, Dementia, depression, depth perception, differential diagnosis, disease classification, dysarthria, dysgraphia, euphoria, executive function, fatigue, football, hopelessness, human, ice hockey, impulsiveness, insomnia, intelligence, irritability, language disability, mania, medical literature, memory disorder, mental concentration, mental instability, mood disorder, muscle weakness, neurologic gait disorder, paranoia, Parkinsonism, personality disorder, physical violence, preventive medicine, psychosis, Research Diagnostic Criteria, Review, risk factor, shuffling gait, social disability, social isolation, spastic gait, spasticity, speech disorder, sport injury, suicidal ideation, traumatic brain injury, traumatic encephalopathy syndrome, tremor, unsteady gait, violence, wrestling
@article{Montenigro2014,
title = {Clinical subtypes of chronic traumatic encephalopathy: Literature review and proposed research diagnostic criteria for traumatic encephalopathy syndrome},
author = {Montenigro, P H and Baugh, C M and Daneshvar, D H and Mez, J and Budson, A E and Au, R and Katz, D I and Cantu, R C and Stern, R A},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84908410645\&partnerID=40\&md5=bab59baeecd5adb22d0f84a4ce99bd5c},
doi = {10.1186/s13195-014-0068-z},
year = {2014},
date = {2014-01-01},
journal = {Alzheimer's Research and Therapy},
volume = {6},
number = {5-8},
abstract = {The long-term consequences of repetitive head impacts have been described since the early 20th century. Terms such as punch drunk and dementia pugilistica were first used to describe the clinical syndromes experienced by boxers. A more generic designation, chronic traumatic encephalopathy (CTE), has been employed since the mid-1900s and has been used in recent years to describe a neurodegenerative disease found not just in boxers but in American football players, other contact sport athletes, military veterans, and others with histories of repetitive brain trauma, including concussions and subconcussive trauma. This article reviews the literature of the clinical manifestations of CTE from 202 published cases. The clinical features include impairments in mood (for example, depression and hopelessness), behavior (for example, explosivity and violence), cognition (for example, impaired memory, executive functioning, attention, and dementia), and, less commonly, motor functioning (for example, parkinsonism, ataxia, and dysarthria). We present proposed research criteria for traumatic encephalopathy syndrome (TES) which consist of four variants or subtypes (TES behavioral/mood variant, TES cognitive variant, TES mixed variant, and TES dementia) as well as classifications of 'probable CTE' and 'possible CTE'. These proposed criteria are expected to be modified and updated as new research findings become available. They are not meant to be used for a clinical diagnosis. Rather, they should be viewed as research criteria that can be employed in studies of the underlying causes, risk factors, differential diagnosis, prevention, and treatment of CTE and related disorders. © 2014 Montenigro et al.; licensee BioMed Central Ltd.},
keywords = {Anxiety, apathy, ataxia, ataxic gait, attention, attention disturbance, behavior disorder, blunted affect, Boxing, chronic brain disease, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy aggression, clinical feature, clonus, cognitive defect, contact sport, delusion, Dementia, depression, depth perception, differential diagnosis, disease classification, dysarthria, dysgraphia, euphoria, executive function, fatigue, football, hopelessness, human, ice hockey, impulsiveness, insomnia, intelligence, irritability, language disability, mania, medical literature, memory disorder, mental concentration, mental instability, mood disorder, muscle weakness, neurologic gait disorder, paranoia, Parkinsonism, personality disorder, physical violence, preventive medicine, psychosis, Research Diagnostic Criteria, Review, risk factor, shuffling gait, social disability, social isolation, spastic gait, spasticity, speech disorder, sport injury, suicidal ideation, traumatic brain injury, traumatic encephalopathy syndrome, tremor, unsteady gait, violence, wrestling},
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}
}
Levin, B; Bhardwaj, A
Chronic traumatic encephalopathy: A critical appraisal Journal Article
In: Neurocritical Care, vol. 20, no. 2, pp. 334–344, 2014.
Abstract | Links | BibTeX | Tags: accident, alcohol consumption, amnesia, amyloid plaque, animal, Animals, Athletic Injuries, autopsy, behavior change, Brain Injury, Chronic, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy Dementia, complication, Diffusion Tensor Imaging, disease course, Encephalopathy, functional magnetic resonance imaging, histopathology, human, Humans, longitudinal study, Male, Neurodegenerative, Neurodegenerative Diseases, nonhuman, NUCLEAR magnetic resonance spectroscopy, Parkinsonism, pathogenesis, pathology, Pathophysiology, Prevalence, priority journal, Pugilistic, Review, risk factor, Risk Factors, sport injury, suicide, Systematic Review, traumatic brain injury, violence
@article{Levin2014,
title = {Chronic traumatic encephalopathy: A critical appraisal},
author = {Levin, B and Bhardwaj, A},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84896549537\&partnerID=40\&md5=138104db42f7ca99527a78bb9c821f59},
doi = {10.1007/s12028-013-9931-1},
year = {2014},
date = {2014-01-01},
journal = {Neurocritical Care},
volume = {20},
number = {2},
pages = {334--344},
abstract = {Chronic traumatic encephalopathy (CTE) formerly known as dementia pugilistica is a long-term neurodegenerative disorder associated with repeated subconcussive head injuries in high-contact sports. We reviewed the existing literature on CTE and examined epidemiological trends, risk factors, and its temporal progression, and proposed the underlying pathophysiological mechanisms that may provide unique insights to clinicians with an in-depth understanding of the disease to aid in the diagnosis and prevention, and provide future perspectives for research via search of Medline and Cochrane databases as well as manual review of bibliographies from selected articles and monographs. The prevalence of CTE in recent years is on the rise and almost exclusively affects men, with pathologic signs characterized by progressive memory loss, behavioral changes, and violent tendencies with some patients demonstrating Parkinsonian-like symptoms and signs. Many patients with CTE die following suicide, accident, or complications of drug or alcohol use. Postmortem pathologic analysis is characterized by neurofibrillary tangles and A$beta$ plaques in 50 % of cases. Currently, there are no ante-mortem diagnostic criteria, but modern imaging techniques such as functional magnetic resonance (MR) imaging, MR spectroscopy, and diffusion tension imaging hold promise for delineating the future diagnostic criteria. Further long-term longitudinal studies are warranted to investigate risk factors that will enhance understanding of the disease progression and its pathogenesis. © 2013 Springer Science+Business Media.},
keywords = {accident, alcohol consumption, amnesia, amyloid plaque, animal, Animals, Athletic Injuries, autopsy, behavior change, Brain Injury, Chronic, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy Dementia, complication, Diffusion Tensor Imaging, disease course, Encephalopathy, functional magnetic resonance imaging, histopathology, human, Humans, longitudinal study, Male, Neurodegenerative, Neurodegenerative Diseases, nonhuman, NUCLEAR magnetic resonance spectroscopy, Parkinsonism, pathogenesis, pathology, Pathophysiology, Prevalence, priority journal, Pugilistic, Review, risk factor, Risk Factors, sport injury, suicide, Systematic Review, traumatic brain injury, violence},
pubstate = {published},
tppubtype = {article}
}
Tator, C H
Chronic traumatic encephalopathy: how serious a sports problem is it? Journal Article
In: British Journal of Sports Medicine, vol. 48, pp. 81–83, 2014.
Abstract | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Tator2014,
title = {Chronic traumatic encephalopathy: how serious a sports problem is it?},
author = {Tator, C H},
year = {2014},
date = {2014-01-01},
journal = {British Journal of Sports Medicine},
volume = {48},
pages = {81--83},
address = {Division of Neurosurgery, Toronto Western Hospital, University of Toronto, , Toronto, Ontario, Canada.},
abstract = {It is now recognised that there is a spectrum of concussion disorders ranging from acute concussion at one end to various forms of brain degeneration at the other end. The spectrum includes acute concussion, second impact syndrome or acute cerebral swelling, postconcussion syndrome, depression or anxiety, chronic traumatic encephalopathy (CTE) and possibly other forms of central nervous system degeneration. It is essential to carefully evaluate the clinical and neuropathological correlations of CTE that have been published. This has been accomplished in an excellent paper on this subject by Gardner and colleagues in this issue. There have been significant advances in our knowledge of the clinical and neuropathological features of CTE in athletes in the past 10 years. However, we are just at the beginning of our appreciation of this entity due to the paucity of research and the inability to diagnose CTE during life. At present, it is not possible to assess the validity of the proposed methods of classification and grading of the severity of the disease. Additional studies of large numbers of at-risk athletes are essential, especially prospective longitudinal studies. Obviously, such studies would be even more effective if reliable in vivo biomarkers were discovered, especially non-invasive ones such as advanced MRI or MR spectroscopy or invasive ones such as blood or cerebrospinal fluid tests. The major questions that remain unanswered include the frequency of CTE in various collision sports, the causal or otherwise relationship between concussions and CTE, the number of concussions that need to be involved and their management.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Andrikopoulos, J
Creating a concussion crisis and chronic traumatic encephalopathy Journal Article
In: JAMA Neurology, vol. 71, pp. 654, 2014.
BibTeX | Tags: Chronic traumatic encephalopathy
@article{Andrikopoulos2014b,
title = {Creating a concussion crisis and chronic traumatic encephalopathy},
author = {Andrikopoulos, J},
year = {2014},
date = {2014-01-01},
journal = {JAMA Neurology},
volume = {71},
pages = {654},
address = {Mercy Hospital Medical Center, Ruan Neurology Clinic, Des Moines, Iowa.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Gardner, A; Iverson, G L; McCrory, P
Chronic traumatic encephalopathy in sport: a systematic review Journal Article
In: British Journal of Sports Medicine, vol. 48, pp. 84–90, 2014.
Abstract | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Gardner2014b,
title = {Chronic traumatic encephalopathy in sport: a systematic review},
author = {Gardner, A and Iverson, G L and McCrory, P},
year = {2014},
date = {2014-01-01},
journal = {British Journal of Sports Medicine},
volume = {48},
pages = {84--90},
address = {Centre for Translational Neuroscience and Mental Health, School of Medicine and Public Health, University of Newcastle, , Callaghan, New South Wales, Australia.},
abstract = {OBJECTIVE: To provide a critical review of chronic traumatic encephalopathy (CTE) by considering the range of clinical presentations, neuropathology and the strength of evidence for CTE as a distinct syndrome. DATA SOURCES: Seven electronic databases were searched using a combination of MeSH terms and key words to identify relevant articles. REVIEW METHODS: Specific inclusion and exclusion criteria were used to select studies for review. Data extracted where present included study population, exposure/outcome measures, clinical data, neurological examination findings, cognitive assessment, investigation results and neuropathology results. RESULTS: The data from 158 published case studies were reviewed. Critical differences between the older descriptions of CTE (the 'classic' syndrome) and the recent descriptions (the 'modern' syndrome) exist in the age of onset, natural history, clinical features, pathological findings and diagnostic criteria, which suggests that modern CTE is a different syndrome. The methodology of the current studies does not allow determination of aetiology or risk factors. CONCLUSIONS: The clinicopathological differences between the 'classic' CTE syndrome and the 'modern' syndrome suggest that the new syndrome needs a different nomenclature. Further research is required to clearly define the clinical phenotype of the modern CTE syndrome and establish the underlying aetiology. Future research needs to address these issues through large-scale, prospective clinicopathological studies.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Tartaglia, M C; Hazrati, L N; Davis, K D; Green, R E; Wennberg, R; Mikulis, D; Ezerins, L J; Keightley, M; Tator, C
Chronic traumatic encephalopathy and other neurodegenerative proteinopathies Journal Article
In: Frontiers in Human Neuroscience, vol. 8, pp. 30, 2014.
Abstract | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Tartaglia2014,
title = {Chronic traumatic encephalopathy and other neurodegenerative proteinopathies},
author = {Tartaglia, M C and Hazrati, L N and Davis, K D and Green, R E and Wennberg, R and Mikulis, D and Ezerins, L J and Keightley, M and Tator, C},
year = {2014},
date = {2014-01-01},
journal = {Frontiers in Human Neuroscience},
volume = {8},
pages = {30},
address = {Division of Neurology, Krembil Neuroscience Centre, University Health Network, University of Toronto Toronto, ON, Canada ; Tanz Centre for Research in Neurodegenerative Disease, University of Toronto Toronto, ON, Canada ; Canadian Sports Concussion Projec},
abstract = {"Chronic traumatic encephalopathy" (CTE) is described as a slowly progressive neurodegenerative disease believed to result from multiple concussions. Traditionally, concussions were considered benign events and although most people recover fully, about 10% develop a post-concussive syndrome with persisting neurological, cognitive and neuropsychiatric symptoms. CTE was once thought to be unique to boxers, but it has now been observed in many different athletes having suffered multiple concussions as well as in military personal after repeated blast injuries. Much remains unknown about the development of CTE but its pathological substrate is usually tau, similar to that seen in Alzheimer's disease (AD) and frontotemporal lobar degeneration (FTLD). The aim of this "perspective" is to compare and contrast clinical and pathological CTE with the other neurodegenerative proteinopathies and highlight that there is an urgent need for understanding the relationship between concussion and the development of CTE as it may provide a window into the development of a proteinopathy and thus new avenues for treatment.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Victoroff, J
Traumatic encephalopathy: Review and provisional research diagnostic criteria Journal Article
In: NeuroRehabilitation, vol. 32, pp. 211–224, 2013.
Abstract | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Victoroff2013,
title = {Traumatic encephalopathy: Review and provisional research diagnostic criteria},
author = {Victoroff, J},
year = {2013},
date = {2013-01-01},
journal = {NeuroRehabilitation},
volume = {32},
pages = {211--224},
abstract = {Objectives: To determine the frequency of neurobehavioral signs and symptoms reported in every published case of traumatic encephalopathy with a view toward the development of clinical diagnostic criteria with predictive validity. Introduction: Cases of persistent or progressive neurological or neurobehavioral change following exposure to one or more head injuries have been reported since 1928. This condition is often referred to as traumatic encephalopathy (TE). To date, however, no diagnostic criteria have been advanced or accepted for the clinical diagnosis of TE. Provisional research diagnostic criteria are required not only for meaningful diagnosis but also to facilitate research to determine the epidemiology, etiology, course, prognosis, imaging and biomarkers, neuropathological features and potentially effective treatments of TE. Methods: All 436 published cases of TE in all languages were reviewed. All symptoms and signs reported in these cases were classified and enumerated. Results: Ninety-seven cases met inclusion criteria based on sufficient documentation of the history and neurobehavioral examination. Provisional research diagnostic criteria for clinically probable and clinically possible TE were developed based on the most frequently reported clinical features. Conclusion: The provisional diagnostic criteria for TE presented here are the first published criteria for this condition based upon a systematic analysis of its clinical characteristics. This is the first a step toward scientifically derived consensus criteria, which are essential to accelerate progress in the investigation of this important condition. © 2013 - IOS Press and the authors. All rights reserved.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Andrews, Erin P
Avoiding the Technical Knockout: Tackling the Inadequacies of Youth Concussion Legislation Journal Article
In: New York Law School Law Review, vol. 58, no. 2, pp. 417–455, 2013, ISBN: 0145448X.
Abstract | BibTeX | Tags: ATHLETES -- Health, brain, BRAIN -- Degeneration, BRAIN -- Wounds & injuries, Chronic traumatic encephalopathy, Concussion, PATIENTS
@article{Andrews2013,
title = {Avoiding the Technical Knockout: Tackling the Inadequacies of Youth Concussion Legislation},
author = {Andrews, Erin P},
isbn = {0145448X},
year = {2013},
date = {2013-01-01},
journal = {New York Law School Law Review},
volume = {58},
number = {2},
pages = {417--455},
abstract = {The article discusses medical effects of football-related concussions on youths in the U.S. Topics discussed include shortcomings in the laws related to concussion epidemic among youth football players; a Uniform Concussion Management Code (UCMC) for concussion care; concussion symptoms and diagnosis; and the long-term effects of chronic traumatic encephalopathy (CTE).},
keywords = {ATHLETES -- Health, brain, BRAIN -- Degeneration, BRAIN -- Wounds \& injuries, Chronic traumatic encephalopathy, Concussion, PATIENTS},
pubstate = {published},
tppubtype = {article}
}
Gavett, Brandon E; Stern, Robert A; Cantu, Robert C; Nowinski, Christopher J; McKee, Ann C
Mild traumatic brain injury: a risk factor for neurodegeneration Journal Article
In: Alzheimer's Research & Therapy, vol. 2, pp. 18, 2010.
Abstract | BibTeX | Tags: Chronic traumatic encephalopathy
@article{Gavett2010,
title = {Mild traumatic brain injury: a risk factor for neurodegeneration},
author = {Gavett, Brandon E and Stern, Robert A and Cantu, Robert C and Nowinski, Christopher J and McKee, Ann C},
year = {2010},
date = {2010-01-01},
journal = {Alzheimer's Research \& Therapy},
volume = {2},
pages = {18},
address = {Department of Neurology, Boston University School of Medicine, 72 East Concord St, B-7800, Boston, MA 02118, USA. begavett@bu.edu.},
abstract = {ABSTRACT : Recently, it has become clear that head trauma can lead to a progressive neurodegeneration known as chronic traumatic encephalopathy. Although the medical literature also implicates head trauma as a risk factor for Alzheimer's disease, these findings are predominantly based on clinical diagnostic criteria that lack specificity. The dementia that follows head injuries or repetitive mild trauma may be caused by chronic traumatic encephalopathy, alone or in conjunction with other neurodegenerations (for example, Alzheimer's disease). Prospective longitudinal studies of head-injured individuals, with neuropathological verification, will not only improve understanding of head trauma as a risk factor for dementia but will also enhance treatment and prevention of a variety of neurodegenerative diseases.},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Watanabe, Thomas; Elovic, Elie; Zafonte, Ross
Chronic traumatic encephalopathy Journal Article
In: PM & R, vol. 2, pp. 671–675, 2010.
BibTeX | Tags: Chronic traumatic encephalopathy
@article{Watanabe2010,
title = {Chronic traumatic encephalopathy},
author = {Watanabe, Thomas and Elovic, Elie and Zafonte, Ross},
year = {2010},
date = {2010-01-01},
journal = {PM \& R},
volume = {2},
pages = {671--675},
address = {MossRehab, 60 Township Line Rd., Elkins Park, PA 19027, USA. watanabt@einstein.edu},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Gavett, B E; Stern, R A; Nowinski, C J; Cantu, R C; McKee, A C
Clinical and neuropathologic findings in chronic traumatic encephalopathy: A case series Journal Article
In: Archives of Clinical Neuropsychology, vol. 24, pp. 525, 2009, ISSN: 0887-6177.
BibTeX | Tags: Chronic traumatic encephalopathy
@article{Gavett2009,
title = {Clinical and neuropathologic findings in chronic traumatic encephalopathy: A case series},
author = {Gavett, B E and Stern, R A and Nowinski, C J and Cantu, R C and McKee, A C},
issn = {0887-6177},
year = {2009},
date = {2009-01-01},
journal = {Archives of Clinical Neuropsychology},
volume = {24},
pages = {525},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
Forum, Alzheimer Research
Alzheimer Research Forum Live Discussion: Sports concussions, dementia, and ApoE genotyping: What can scientists tell the public? What's up for research? Journal Article
In: Journal of Alzheimer's Disease, vol. 16, no. 3, pp. 657–666, 2009.
BibTeX | Tags: Chronic traumatic encephalopathy, Education, genetics
@article{AlzheimerResearchForum2009,
title = {Alzheimer Research Forum Live Discussion: Sports concussions, dementia, and ApoE genotyping: What can scientists tell the public? What's up for research?},
author = {{Alzheimer Research Forum}},
year = {2009},
date = {2009-01-01},
journal = {Journal of Alzheimer's Disease},
volume = {16},
number = {3},
pages = {657--666},
keywords = {Chronic traumatic encephalopathy, Education, genetics},
pubstate = {published},
tppubtype = {article}
}
Lassonde, M; Theriault, M; de Beaumont, L
Electrophysiological anomalies 30 years post-concussion Journal Article
In: Clinical Neurophysiology, vol. 119, pp. e151–e151, 2008, ISSN: 1388-2457.
BibTeX | Tags: Chronic traumatic encephalopathy
@article{Lassonde2008,
title = {Electrophysiological anomalies 30 years post-concussion},
author = {Lassonde, M and Theriault, M and de Beaumont, L},
issn = {1388-2457},
year = {2008},
date = {2008-01-01},
journal = {Clinical Neurophysiology},
volume = {119},
pages = {e151--e151},
keywords = {Chronic traumatic encephalopathy},
pubstate = {published},
tppubtype = {article}
}
for Disease Control, Centers; Prevention,
Nonfatal traumatic brain injuries from sports and recreation activities--United States, 2001-2005 Journal Article
In: MMWR - Morbidity & Mortality Weekly Report, vol. 56, no. 29, pp. 733–737, 2007.
Abstract | BibTeX | Tags: *Athletic Injuries/ep [Epidemiology], *Brain Injuries/ep [Epidemiology], Adolescent, adult, Child, Chronic traumatic encephalopathy, Female, Humans, Incidence/Epidemiology, Infant, Male, middle aged, Population Surveillance, Preschool, recreation, United States/ep [Epidemiology]
@article{CentersforDiseaseControlandPrevention2007,
title = {Nonfatal traumatic brain injuries from sports and recreation activities--United States, 2001-2005},
author = {{Centers for Disease Control and Prevention}},
year = {2007},
date = {2007-01-01},
journal = {MMWR - Morbidity \& Mortality Weekly Report},
volume = {56},
number = {29},
pages = {733--737},
abstract = {Each year in the United States, an estimated 38 million children and adolescents participate in organized sports, and approximately 170 million adults participate in some type of physical activity not related to work. The health benefits of these activities are tempered by the risk for injury, including traumatic brain injury (TBI). CDC estimates that 1.1 million persons with TBIs are treated and released from U.S. hospital emergency departments (EDs) each year, and an additional 235,000 are hospitalized for these injuries. TBIs can result in long-term, negative health effects (e.g., memory loss and behavioral changes). To characterize sports- and recreation-related (SR-related) TBIs among patients treated in U.S. hospital EDs, CDC analyzed data from the National Electronic Injury Surveillance System--All Injury Program (NEISS-AIP) for the period 2001-2005. This report summarizes the results of that analysis, which indicated that an estimated 207,830 patients with nonfatal SR-related TBIs were treated in EDs each year during this period. The highest rates of SR-related TBI ED visits for both males and females occurred among those aged 10-14 years. Increased awareness of TBI risks, prevention strategies, and the importance of timely identification and management is essential for reducing the incidence, severity, and long-term negative health effects of this type of injury.},
keywords = {*Athletic Injuries/ep [Epidemiology], *Brain Injuries/ep [Epidemiology], Adolescent, adult, Child, Chronic traumatic encephalopathy, Female, Humans, Incidence/Epidemiology, Infant, Male, middle aged, Population Surveillance, Preschool, recreation, United States/ep [Epidemiology]},
pubstate = {published},
tppubtype = {article}
}