Holtkamp, M D; Grimes, J; Ling, G
Concussion in the Military: an Evidence-Base Review of mTBI in US Military Personnel Focused on Posttraumatic Headache Journal Article
In: Current Pain & Headache Reports, vol. 20, no. 6, 2016.
Abstract | Links | BibTeX | Tags: apolipoprotein E4, assessment, biological marker, botulinum toxin, brain concussion, calcitonin gene related peptide receptor antagonis, comorbidity, Concussion, depression, DIAGNOSTIC imaging, disease course, genetic polymorphism, genetic predisposition, glial fibrillary acidic protein, headache, Headache disorder, human, MANAGEMENT, migraine, Military personnel, mTBI, neuroimaging, Pathophysiology, postconcussion syndrome, posttraumatic headache, posttraumatic stress disorder, Prognosis, Review, serotonin 1 agonist, serotonin 1F agonist, soldier, traumatic brain injury, Treatment, tricyclic antidepressant agent, triptan derivative, unclassified drug, UNITED States
@article{Holtkamp2016,
title = {Concussion in the Military: an Evidence-Base Review of mTBI in US Military Personnel Focused on Posttraumatic Headache},
author = {Holtkamp, M D and Grimes, J and Ling, G},
doi = {10.1007/s11916-016-0572-x},
year = {2016},
date = {2016-01-01},
journal = {Current Pain \& Headache Reports},
volume = {20},
number = {6},
abstract = {Traumatic brain injury (TBI) is defined as an alteration in brain function caused by an external force. Mild TBI or concussion is now well recognized to be a risk of military service as well as participation in athletic sports such as football. Posttraumatic headache (PTH) is the most common symptom after mTBI in US service members. PTH most commonly presents with migraine-like headache features. The following is an overview of the epidemiology, pathophysiology, clinical course, prognosis, complications, and treatment of mTBI and associated comorbidities with a focus on PTH. There is a particular emphasis on emerging evidence-based clinical practice. One important medical consequence of the recognition that mTBI is a highly prevalent among military service members is that the Department of Defense (DoD) is dedicating significant financial and intellectual resources to better understanding and developing treatments for TBI. The identification of the importance of TBI among the US military population has had the added benefit of increasing awareness of this condition among civilian populations, particularly those engaged in both professional and youth sports. The NIH and NSF are also supporting important TBI research. President Obama’s Brain Initiative is also providing additional impetus for these efforts. Unfortunately, the understanding of the acute and chronic effects of mTBI on the brain remains limited. Gratefully, there is hope that through innovative research, there will be advances in elucidating the underlying pathophysiology, which will lead to clinical and prognostic indicators, ultimately resulting in new treatment options for this very complicated set of disorders. © 2016, Springer Science+Business Media New York (outside the USA).},
keywords = {apolipoprotein E4, assessment, biological marker, botulinum toxin, brain concussion, calcitonin gene related peptide receptor antagonis, comorbidity, Concussion, depression, DIAGNOSTIC imaging, disease course, genetic polymorphism, genetic predisposition, glial fibrillary acidic protein, headache, Headache disorder, human, MANAGEMENT, migraine, Military personnel, mTBI, neuroimaging, Pathophysiology, postconcussion syndrome, posttraumatic headache, posttraumatic stress disorder, Prognosis, Review, serotonin 1 agonist, serotonin 1F agonist, soldier, traumatic brain injury, Treatment, tricyclic antidepressant agent, triptan derivative, unclassified drug, UNITED States},
pubstate = {published},
tppubtype = {article}
}
Stein, T D; Montenigro, P H; Alvarez, V E; Xia, W; Crary, J F; Tripodis, Y; Daneshvar, D H; Mez, J; Solomon, T; Meng, G; Kubilus, C A; Cormier, K A; Meng, S; Babcock, K; Kiernan, P; Murphy, L; Nowinski, C J; Martin, B; Dixon, D; Stern, R A; Cantu, R C; Kowall, N W; McKee, A C
Beta-amyloid deposition in chronic traumatic encephalopathy Journal Article
In: Acta Neuropathologica, vol. 130, no. 1, pp. 21–34, 2015.
Abstract | BibTeX | Tags: *Amyloid beta-Peptides/me [Metabolism], *Brain Injury, *Brain/pa [Pathology], *Neurodegenerative Diseases/pa [Pathology], *tau Proteins/me [Metabolism], 0 (Amyloid beta-Peptides), 0 (Apolipoprotein E4), 0 (MAPT protein, 0 (tau Proteins), 80 and over, adult, Age Factors, aged, Amyloid/et [Etiology], Amyloid/me [Metabolism], Amyloid/pa [Pathology], Apolipoprotein E4/ge [Genetics], Athletes, Athletic Injuries/ep [Epidemiology], Athletic Injuries/ge [Genetics], Athletic Injuries/me [Metabolism], Athletic Injuries/pa [Pathology], Brain Injury, Brain/me [Metabolism], Chronic/ep [Epidemiology], Chronic/ge [Genetics], Chronic/me [Metabolism], Chronic/pa [Pathology], Cohort Studies, comorbidity, human), Humans, middle aged, Neurodegenerative Diseases/ep [Epidemiology], Neurodegenerative Diseases/ge [Genetics], Neurodegenerative Diseases/me [Metabolism], Plaque, SEVERITY of illness index, veterans, War-Related Injuries/ep [Epidemiology], War-Related Injuries/ge [Genetics], War-Related Injuries/me [Metabolism], War-Related Injuries/pa [Pathology]
@article{Stein2015b,
title = {Beta-amyloid deposition in chronic traumatic encephalopathy},
author = {Stein, T D and Montenigro, P H and Alvarez, V E and Xia, W and Crary, J F and Tripodis, Y and Daneshvar, D H and Mez, J and Solomon, T and Meng, G and Kubilus, C A and Cormier, K A and Meng, S and Babcock, K and Kiernan, P and Murphy, L and Nowinski, C J and Martin, B and Dixon, D and Stern, R A and Cantu, R C and Kowall, N W and McKee, A C},
year = {2015},
date = {2015-01-01},
journal = {Acta Neuropathologica},
volume = {130},
number = {1},
pages = {21--34},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer's disease (AD). Although trauma has been suggested to increase amyloid beta peptide (Abeta) levels, the extent of Abeta deposition in CTE has not been thoroughly characterized. We studied a heterogeneous cohort of deceased athletes and military veterans with neuropathologically diagnosed CTE (n = 114, mean age at death = 60) to test the hypothesis that Abeta deposition is altered in CTE and associated with more severe pathology and worse clinical outcomes. We found that Abeta deposition, either as diffuse or neuritic plaques, was present in 52 % of CTE subjects. Moreover, Abeta deposition in CTE occurred at an accelerated rate and with altered dynamics in CTE compared to a normal aging population (OR = 3.8, p \< 0.001). We also found a clear pathological and clinical dichotomy between those CTE cases with Abeta plaques and those without. Abeta deposition was significantly associated with the presence of the APOE epsilon4 allele (p = 0.035), older age at symptom onset (p \< 0.001), and older age at death (p \< 0.001). In addition, when controlling for age, neuritic plaques were significantly associated with increased CTE tauopathy stage (beta = 2.43},
keywords = {*Amyloid beta-Peptides/me [Metabolism], *Brain Injury, *Brain/pa [Pathology], *Neurodegenerative Diseases/pa [Pathology], *tau Proteins/me [Metabolism], 0 (Amyloid beta-Peptides), 0 (Apolipoprotein E4), 0 (MAPT protein, 0 (tau Proteins), 80 and over, adult, Age Factors, aged, Amyloid/et [Etiology], Amyloid/me [Metabolism], Amyloid/pa [Pathology], Apolipoprotein E4/ge [Genetics], Athletes, Athletic Injuries/ep [Epidemiology], Athletic Injuries/ge [Genetics], Athletic Injuries/me [Metabolism], Athletic Injuries/pa [Pathology], Brain Injury, Brain/me [Metabolism], Chronic/ep [Epidemiology], Chronic/ge [Genetics], Chronic/me [Metabolism], Chronic/pa [Pathology], Cohort Studies, comorbidity, human), Humans, middle aged, Neurodegenerative Diseases/ep [Epidemiology], Neurodegenerative Diseases/ge [Genetics], Neurodegenerative Diseases/me [Metabolism], Plaque, SEVERITY of illness index, veterans, War-Related Injuries/ep [Epidemiology], War-Related Injuries/ge [Genetics], War-Related Injuries/me [Metabolism], War-Related Injuries/pa [Pathology]},
pubstate = {published},
tppubtype = {article}
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Stein, T D; Alvarez, V E; McKee, A C
Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel Journal Article
In: Alzheimer's Research and Therapy, vol. 6, no. 1, 2014.
Abstract | Links | BibTeX | Tags: Aggression, Alzheimer disease, amnesia, army, astrocyte, athlete, behavior change, brain atrophy, brain stem, brain weight, central sulcus, chronic disease, Chronic Traumatic Encephalopathy TAR DNA binding p, cognitive defect, comorbidity, Dementia, depression, diencephalon, diffuse Lewy body disease, exposure, frontotemporal dementia, human, impulsiveness, irritability, Motor neuron disease, nerve fiber, neurite, neurofibrillary tangle, neuropathology, nonhuman, personality disorder, priority journal, Review, short term memory, soldier, staging, suicidal ideation, tau protein, tauopathy, temporal lobe, traumatic brain injury, veteran
@article{Stein2014,
title = {Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel},
author = {Stein, T D and Alvarez, V E and McKee, A C},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84892718392\&partnerID=40\&md5=c39a0e58ad33cee7a570b4681131d6ea},
doi = {10.1186/alzrt234},
year = {2014},
date = {2014-01-01},
journal = {Alzheimer's Research and Therapy},
volume = {6},
number = {1},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs in association with repetitive traumatic brain injury experienced in sport and military service. In most instances, the clinical symptoms of the disease begin after a long period of latency ranging from several years to several decades. The initial symptoms are typically insidious, consisting of irritability, impulsivity, aggression, depression, short-term memory loss and heightened suicidality. The symptoms progress slowly over decades to include cognitive deficits and dementia. The pathology of CTE is characterized by the accumulation of phosphorylated tau protein in neurons and astrocytes in a pattern that is unique from other tauopathies, including Alzheimer's disease. The hyperphosphorylated tau abnormalities begin focally, as perivascular neurofibrillary tangles and neurites at the depths of the cerebral sulci, and then spread to involve superficial layers of adjacent cortex before becoming a widespread degeneration affecting medial temporal lobe structures, diencephalon and brainstem. Most instances of CTE (\>85% of cases) show abnormal accumulations of phosphorylated 43 kDa TAR DNA binding protein that are partially colocalized with phosphorylated tau protein. As CTE is characterized pathologically by frontal and temporal lobe atrophy, by abnormal deposits of phosphorylated tau and by 43 kDa TAR DNA binding protein and is associated clinically with behavioral and personality changes, as well as cognitive impairments, CTE is increasingly categorized as an acquired frontotemporal lobar degeneration. Currently, some of the greatest challenges are that CTE cannot be diagnosed during life and the incidence and prevalence of the disorder remain uncertain. Furthermore, the contribution of age, gender, genetics, stress, alcohol and substance abuse to the development of CTE remains to be determined. © 2014 BioMed Central Ltd.},
keywords = {Aggression, Alzheimer disease, amnesia, army, astrocyte, athlete, behavior change, brain atrophy, brain stem, brain weight, central sulcus, chronic disease, Chronic Traumatic Encephalopathy TAR DNA binding p, cognitive defect, comorbidity, Dementia, depression, diencephalon, diffuse Lewy body disease, exposure, frontotemporal dementia, human, impulsiveness, irritability, Motor neuron disease, nerve fiber, neurite, neurofibrillary tangle, neuropathology, nonhuman, personality disorder, priority journal, Review, short term memory, soldier, staging, suicidal ideation, tau protein, tauopathy, temporal lobe, traumatic brain injury, veteran},
pubstate = {published},
tppubtype = {article}
}
Gandy, S; DeKosky, S T
[18F]-T807 tauopathy PET imaging in chronic traumatic encephalopathy Journal Article
In: F1000Research, vol. 3, 2014.
Abstract | Links | BibTeX | Tags: aging, Article, athlete, brain region, Chronic Traumatic Encephalopathy radiopharmaceutic, comorbidity, cumulative trauma disorder, diagnostic value, disease association, disease severity, human, image analysis, ligand binding, neurofibrillary tangle, positron emission tomography, progressive supranuclear palsy, t 807 f 18, tauopathy, temporal lobe, traumatic brain injury, unclassified drug, veteran
@article{Gandy2014,
title = {[18F]-T807 tauopathy PET imaging in chronic traumatic encephalopathy},
author = {Gandy, S and DeKosky, S T},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84923165667\&partnerID=40\&md5=90ae38a9d3536705acb61b5e1fbbc81a},
doi = {10.12688/f1000research.5372.1},
year = {2014},
date = {2014-01-01},
journal = {F1000Research},
volume = {3},
abstract = {A new molecular ligand for positron emission tomography (PET) of the human brain, [18F]-T807, is under investigation for the antemortem detection of pathological neurofibrillary aggregates, which are evidence of neurofibrillary tangle (NFT) diseases, also known as tauopathies. Repetitive mild traumatic brain injuries in athletes and battlefield veterans are associated with one such tauopathy, known as chronic traumatic encephalopathy (CTE). In a recent case report, a former NFL player with clinically probable CTE and a concurrent Progressive Supranuclear Palsy (PSP) -like syndrome was studied using [18F]-T807. The interpretation of this player's [18F]-T807 PET imaging was complicated by the overlap of tracer uptake in brain regions involved in CTE and PSP with regions associated with either nonspecific [18F]-T807 ligand binding or "aging-associated" binding of [18F]-T807 to authentic tauopathy known to be associated with aging and disease severity (i.e., NFT in the mesial temporal lobe). The implications of these data for the utility of [18F]-T807 in the pre-mortem detection of CTE are summarized. © 2014 Gandy S and DeKosky ST.},
keywords = {aging, Article, athlete, brain region, Chronic Traumatic Encephalopathy radiopharmaceutic, comorbidity, cumulative trauma disorder, diagnostic value, disease association, disease severity, human, image analysis, ligand binding, neurofibrillary tangle, positron emission tomography, progressive supranuclear palsy, t 807 f 18, tauopathy, temporal lobe, traumatic brain injury, unclassified drug, veteran},
pubstate = {published},
tppubtype = {article}
}
Holtkamp, M D; Grimes, J; Ling, G
Concussion in the Military: an Evidence-Base Review of mTBI in US Military Personnel Focused on Posttraumatic Headache Journal Article
In: Current Pain & Headache Reports, vol. 20, no. 6, 2016.
@article{Holtkamp2016,
title = {Concussion in the Military: an Evidence-Base Review of mTBI in US Military Personnel Focused on Posttraumatic Headache},
author = {Holtkamp, M D and Grimes, J and Ling, G},
doi = {10.1007/s11916-016-0572-x},
year = {2016},
date = {2016-01-01},
journal = {Current Pain \& Headache Reports},
volume = {20},
number = {6},
abstract = {Traumatic brain injury (TBI) is defined as an alteration in brain function caused by an external force. Mild TBI or concussion is now well recognized to be a risk of military service as well as participation in athletic sports such as football. Posttraumatic headache (PTH) is the most common symptom after mTBI in US service members. PTH most commonly presents with migraine-like headache features. The following is an overview of the epidemiology, pathophysiology, clinical course, prognosis, complications, and treatment of mTBI and associated comorbidities with a focus on PTH. There is a particular emphasis on emerging evidence-based clinical practice. One important medical consequence of the recognition that mTBI is a highly prevalent among military service members is that the Department of Defense (DoD) is dedicating significant financial and intellectual resources to better understanding and developing treatments for TBI. The identification of the importance of TBI among the US military population has had the added benefit of increasing awareness of this condition among civilian populations, particularly those engaged in both professional and youth sports. The NIH and NSF are also supporting important TBI research. President Obama’s Brain Initiative is also providing additional impetus for these efforts. Unfortunately, the understanding of the acute and chronic effects of mTBI on the brain remains limited. Gratefully, there is hope that through innovative research, there will be advances in elucidating the underlying pathophysiology, which will lead to clinical and prognostic indicators, ultimately resulting in new treatment options for this very complicated set of disorders. © 2016, Springer Science+Business Media New York (outside the USA).},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Stein, T D; Montenigro, P H; Alvarez, V E; Xia, W; Crary, J F; Tripodis, Y; Daneshvar, D H; Mez, J; Solomon, T; Meng, G; Kubilus, C A; Cormier, K A; Meng, S; Babcock, K; Kiernan, P; Murphy, L; Nowinski, C J; Martin, B; Dixon, D; Stern, R A; Cantu, R C; Kowall, N W; McKee, A C
Beta-amyloid deposition in chronic traumatic encephalopathy Journal Article
In: Acta Neuropathologica, vol. 130, no. 1, pp. 21–34, 2015.
@article{Stein2015b,
title = {Beta-amyloid deposition in chronic traumatic encephalopathy},
author = {Stein, T D and Montenigro, P H and Alvarez, V E and Xia, W and Crary, J F and Tripodis, Y and Daneshvar, D H and Mez, J and Solomon, T and Meng, G and Kubilus, C A and Cormier, K A and Meng, S and Babcock, K and Kiernan, P and Murphy, L and Nowinski, C J and Martin, B and Dixon, D and Stern, R A and Cantu, R C and Kowall, N W and McKee, A C},
year = {2015},
date = {2015-01-01},
journal = {Acta Neuropathologica},
volume = {130},
number = {1},
pages = {21--34},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer's disease (AD). Although trauma has been suggested to increase amyloid beta peptide (Abeta) levels, the extent of Abeta deposition in CTE has not been thoroughly characterized. We studied a heterogeneous cohort of deceased athletes and military veterans with neuropathologically diagnosed CTE (n = 114, mean age at death = 60) to test the hypothesis that Abeta deposition is altered in CTE and associated with more severe pathology and worse clinical outcomes. We found that Abeta deposition, either as diffuse or neuritic plaques, was present in 52 % of CTE subjects. Moreover, Abeta deposition in CTE occurred at an accelerated rate and with altered dynamics in CTE compared to a normal aging population (OR = 3.8, p \< 0.001). We also found a clear pathological and clinical dichotomy between those CTE cases with Abeta plaques and those without. Abeta deposition was significantly associated with the presence of the APOE epsilon4 allele (p = 0.035), older age at symptom onset (p \< 0.001), and older age at death (p \< 0.001). In addition, when controlling for age, neuritic plaques were significantly associated with increased CTE tauopathy stage (beta = 2.43},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Stein, T D; Alvarez, V E; McKee, A C
Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel Journal Article
In: Alzheimer's Research and Therapy, vol. 6, no. 1, 2014.
@article{Stein2014,
title = {Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel},
author = {Stein, T D and Alvarez, V E and McKee, A C},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84892718392\&partnerID=40\&md5=c39a0e58ad33cee7a570b4681131d6ea},
doi = {10.1186/alzrt234},
year = {2014},
date = {2014-01-01},
journal = {Alzheimer's Research and Therapy},
volume = {6},
number = {1},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs in association with repetitive traumatic brain injury experienced in sport and military service. In most instances, the clinical symptoms of the disease begin after a long period of latency ranging from several years to several decades. The initial symptoms are typically insidious, consisting of irritability, impulsivity, aggression, depression, short-term memory loss and heightened suicidality. The symptoms progress slowly over decades to include cognitive deficits and dementia. The pathology of CTE is characterized by the accumulation of phosphorylated tau protein in neurons and astrocytes in a pattern that is unique from other tauopathies, including Alzheimer's disease. The hyperphosphorylated tau abnormalities begin focally, as perivascular neurofibrillary tangles and neurites at the depths of the cerebral sulci, and then spread to involve superficial layers of adjacent cortex before becoming a widespread degeneration affecting medial temporal lobe structures, diencephalon and brainstem. Most instances of CTE (\>85% of cases) show abnormal accumulations of phosphorylated 43 kDa TAR DNA binding protein that are partially colocalized with phosphorylated tau protein. As CTE is characterized pathologically by frontal and temporal lobe atrophy, by abnormal deposits of phosphorylated tau and by 43 kDa TAR DNA binding protein and is associated clinically with behavioral and personality changes, as well as cognitive impairments, CTE is increasingly categorized as an acquired frontotemporal lobar degeneration. Currently, some of the greatest challenges are that CTE cannot be diagnosed during life and the incidence and prevalence of the disorder remain uncertain. Furthermore, the contribution of age, gender, genetics, stress, alcohol and substance abuse to the development of CTE remains to be determined. © 2014 BioMed Central Ltd.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Gandy, S; DeKosky, S T
[18F]-T807 tauopathy PET imaging in chronic traumatic encephalopathy Journal Article
In: F1000Research, vol. 3, 2014.
@article{Gandy2014,
title = {[18F]-T807 tauopathy PET imaging in chronic traumatic encephalopathy},
author = {Gandy, S and DeKosky, S T},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84923165667\&partnerID=40\&md5=90ae38a9d3536705acb61b5e1fbbc81a},
doi = {10.12688/f1000research.5372.1},
year = {2014},
date = {2014-01-01},
journal = {F1000Research},
volume = {3},
abstract = {A new molecular ligand for positron emission tomography (PET) of the human brain, [18F]-T807, is under investigation for the antemortem detection of pathological neurofibrillary aggregates, which are evidence of neurofibrillary tangle (NFT) diseases, also known as tauopathies. Repetitive mild traumatic brain injuries in athletes and battlefield veterans are associated with one such tauopathy, known as chronic traumatic encephalopathy (CTE). In a recent case report, a former NFL player with clinically probable CTE and a concurrent Progressive Supranuclear Palsy (PSP) -like syndrome was studied using [18F]-T807. The interpretation of this player's [18F]-T807 PET imaging was complicated by the overlap of tracer uptake in brain regions involved in CTE and PSP with regions associated with either nonspecific [18F]-T807 ligand binding or "aging-associated" binding of [18F]-T807 to authentic tauopathy known to be associated with aging and disease severity (i.e., NFT in the mesial temporal lobe). The implications of these data for the utility of [18F]-T807 in the pre-mortem detection of CTE are summarized. © 2014 Gandy S and DeKosky ST.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Holtkamp, M D; Grimes, J; Ling, G
Concussion in the Military: an Evidence-Base Review of mTBI in US Military Personnel Focused on Posttraumatic Headache Journal Article
In: Current Pain & Headache Reports, vol. 20, no. 6, 2016.
Abstract | Links | BibTeX | Tags: apolipoprotein E4, assessment, biological marker, botulinum toxin, brain concussion, calcitonin gene related peptide receptor antagonis, comorbidity, Concussion, depression, DIAGNOSTIC imaging, disease course, genetic polymorphism, genetic predisposition, glial fibrillary acidic protein, headache, Headache disorder, human, MANAGEMENT, migraine, Military personnel, mTBI, neuroimaging, Pathophysiology, postconcussion syndrome, posttraumatic headache, posttraumatic stress disorder, Prognosis, Review, serotonin 1 agonist, serotonin 1F agonist, soldier, traumatic brain injury, Treatment, tricyclic antidepressant agent, triptan derivative, unclassified drug, UNITED States
@article{Holtkamp2016,
title = {Concussion in the Military: an Evidence-Base Review of mTBI in US Military Personnel Focused on Posttraumatic Headache},
author = {Holtkamp, M D and Grimes, J and Ling, G},
doi = {10.1007/s11916-016-0572-x},
year = {2016},
date = {2016-01-01},
journal = {Current Pain \& Headache Reports},
volume = {20},
number = {6},
abstract = {Traumatic brain injury (TBI) is defined as an alteration in brain function caused by an external force. Mild TBI or concussion is now well recognized to be a risk of military service as well as participation in athletic sports such as football. Posttraumatic headache (PTH) is the most common symptom after mTBI in US service members. PTH most commonly presents with migraine-like headache features. The following is an overview of the epidemiology, pathophysiology, clinical course, prognosis, complications, and treatment of mTBI and associated comorbidities with a focus on PTH. There is a particular emphasis on emerging evidence-based clinical practice. One important medical consequence of the recognition that mTBI is a highly prevalent among military service members is that the Department of Defense (DoD) is dedicating significant financial and intellectual resources to better understanding and developing treatments for TBI. The identification of the importance of TBI among the US military population has had the added benefit of increasing awareness of this condition among civilian populations, particularly those engaged in both professional and youth sports. The NIH and NSF are also supporting important TBI research. President Obama’s Brain Initiative is also providing additional impetus for these efforts. Unfortunately, the understanding of the acute and chronic effects of mTBI on the brain remains limited. Gratefully, there is hope that through innovative research, there will be advances in elucidating the underlying pathophysiology, which will lead to clinical and prognostic indicators, ultimately resulting in new treatment options for this very complicated set of disorders. © 2016, Springer Science+Business Media New York (outside the USA).},
keywords = {apolipoprotein E4, assessment, biological marker, botulinum toxin, brain concussion, calcitonin gene related peptide receptor antagonis, comorbidity, Concussion, depression, DIAGNOSTIC imaging, disease course, genetic polymorphism, genetic predisposition, glial fibrillary acidic protein, headache, Headache disorder, human, MANAGEMENT, migraine, Military personnel, mTBI, neuroimaging, Pathophysiology, postconcussion syndrome, posttraumatic headache, posttraumatic stress disorder, Prognosis, Review, serotonin 1 agonist, serotonin 1F agonist, soldier, traumatic brain injury, Treatment, tricyclic antidepressant agent, triptan derivative, unclassified drug, UNITED States},
pubstate = {published},
tppubtype = {article}
}
Stein, T D; Montenigro, P H; Alvarez, V E; Xia, W; Crary, J F; Tripodis, Y; Daneshvar, D H; Mez, J; Solomon, T; Meng, G; Kubilus, C A; Cormier, K A; Meng, S; Babcock, K; Kiernan, P; Murphy, L; Nowinski, C J; Martin, B; Dixon, D; Stern, R A; Cantu, R C; Kowall, N W; McKee, A C
Beta-amyloid deposition in chronic traumatic encephalopathy Journal Article
In: Acta Neuropathologica, vol. 130, no. 1, pp. 21–34, 2015.
Abstract | BibTeX | Tags: *Amyloid beta-Peptides/me [Metabolism], *Brain Injury, *Brain/pa [Pathology], *Neurodegenerative Diseases/pa [Pathology], *tau Proteins/me [Metabolism], 0 (Amyloid beta-Peptides), 0 (Apolipoprotein E4), 0 (MAPT protein, 0 (tau Proteins), 80 and over, adult, Age Factors, aged, Amyloid/et [Etiology], Amyloid/me [Metabolism], Amyloid/pa [Pathology], Apolipoprotein E4/ge [Genetics], Athletes, Athletic Injuries/ep [Epidemiology], Athletic Injuries/ge [Genetics], Athletic Injuries/me [Metabolism], Athletic Injuries/pa [Pathology], Brain Injury, Brain/me [Metabolism], Chronic/ep [Epidemiology], Chronic/ge [Genetics], Chronic/me [Metabolism], Chronic/pa [Pathology], Cohort Studies, comorbidity, human), Humans, middle aged, Neurodegenerative Diseases/ep [Epidemiology], Neurodegenerative Diseases/ge [Genetics], Neurodegenerative Diseases/me [Metabolism], Plaque, SEVERITY of illness index, veterans, War-Related Injuries/ep [Epidemiology], War-Related Injuries/ge [Genetics], War-Related Injuries/me [Metabolism], War-Related Injuries/pa [Pathology]
@article{Stein2015b,
title = {Beta-amyloid deposition in chronic traumatic encephalopathy},
author = {Stein, T D and Montenigro, P H and Alvarez, V E and Xia, W and Crary, J F and Tripodis, Y and Daneshvar, D H and Mez, J and Solomon, T and Meng, G and Kubilus, C A and Cormier, K A and Meng, S and Babcock, K and Kiernan, P and Murphy, L and Nowinski, C J and Martin, B and Dixon, D and Stern, R A and Cantu, R C and Kowall, N W and McKee, A C},
year = {2015},
date = {2015-01-01},
journal = {Acta Neuropathologica},
volume = {130},
number = {1},
pages = {21--34},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer's disease (AD). Although trauma has been suggested to increase amyloid beta peptide (Abeta) levels, the extent of Abeta deposition in CTE has not been thoroughly characterized. We studied a heterogeneous cohort of deceased athletes and military veterans with neuropathologically diagnosed CTE (n = 114, mean age at death = 60) to test the hypothesis that Abeta deposition is altered in CTE and associated with more severe pathology and worse clinical outcomes. We found that Abeta deposition, either as diffuse or neuritic plaques, was present in 52 % of CTE subjects. Moreover, Abeta deposition in CTE occurred at an accelerated rate and with altered dynamics in CTE compared to a normal aging population (OR = 3.8, p \< 0.001). We also found a clear pathological and clinical dichotomy between those CTE cases with Abeta plaques and those without. Abeta deposition was significantly associated with the presence of the APOE epsilon4 allele (p = 0.035), older age at symptom onset (p \< 0.001), and older age at death (p \< 0.001). In addition, when controlling for age, neuritic plaques were significantly associated with increased CTE tauopathy stage (beta = 2.43},
keywords = {*Amyloid beta-Peptides/me [Metabolism], *Brain Injury, *Brain/pa [Pathology], *Neurodegenerative Diseases/pa [Pathology], *tau Proteins/me [Metabolism], 0 (Amyloid beta-Peptides), 0 (Apolipoprotein E4), 0 (MAPT protein, 0 (tau Proteins), 80 and over, adult, Age Factors, aged, Amyloid/et [Etiology], Amyloid/me [Metabolism], Amyloid/pa [Pathology], Apolipoprotein E4/ge [Genetics], Athletes, Athletic Injuries/ep [Epidemiology], Athletic Injuries/ge [Genetics], Athletic Injuries/me [Metabolism], Athletic Injuries/pa [Pathology], Brain Injury, Brain/me [Metabolism], Chronic/ep [Epidemiology], Chronic/ge [Genetics], Chronic/me [Metabolism], Chronic/pa [Pathology], Cohort Studies, comorbidity, human), Humans, middle aged, Neurodegenerative Diseases/ep [Epidemiology], Neurodegenerative Diseases/ge [Genetics], Neurodegenerative Diseases/me [Metabolism], Plaque, SEVERITY of illness index, veterans, War-Related Injuries/ep [Epidemiology], War-Related Injuries/ge [Genetics], War-Related Injuries/me [Metabolism], War-Related Injuries/pa [Pathology]},
pubstate = {published},
tppubtype = {article}
}
Stein, T D; Alvarez, V E; McKee, A C
Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel Journal Article
In: Alzheimer's Research and Therapy, vol. 6, no. 1, 2014.
Abstract | Links | BibTeX | Tags: Aggression, Alzheimer disease, amnesia, army, astrocyte, athlete, behavior change, brain atrophy, brain stem, brain weight, central sulcus, chronic disease, Chronic Traumatic Encephalopathy TAR DNA binding p, cognitive defect, comorbidity, Dementia, depression, diencephalon, diffuse Lewy body disease, exposure, frontotemporal dementia, human, impulsiveness, irritability, Motor neuron disease, nerve fiber, neurite, neurofibrillary tangle, neuropathology, nonhuman, personality disorder, priority journal, Review, short term memory, soldier, staging, suicidal ideation, tau protein, tauopathy, temporal lobe, traumatic brain injury, veteran
@article{Stein2014,
title = {Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel},
author = {Stein, T D and Alvarez, V E and McKee, A C},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84892718392\&partnerID=40\&md5=c39a0e58ad33cee7a570b4681131d6ea},
doi = {10.1186/alzrt234},
year = {2014},
date = {2014-01-01},
journal = {Alzheimer's Research and Therapy},
volume = {6},
number = {1},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs in association with repetitive traumatic brain injury experienced in sport and military service. In most instances, the clinical symptoms of the disease begin after a long period of latency ranging from several years to several decades. The initial symptoms are typically insidious, consisting of irritability, impulsivity, aggression, depression, short-term memory loss and heightened suicidality. The symptoms progress slowly over decades to include cognitive deficits and dementia. The pathology of CTE is characterized by the accumulation of phosphorylated tau protein in neurons and astrocytes in a pattern that is unique from other tauopathies, including Alzheimer's disease. The hyperphosphorylated tau abnormalities begin focally, as perivascular neurofibrillary tangles and neurites at the depths of the cerebral sulci, and then spread to involve superficial layers of adjacent cortex before becoming a widespread degeneration affecting medial temporal lobe structures, diencephalon and brainstem. Most instances of CTE (\>85% of cases) show abnormal accumulations of phosphorylated 43 kDa TAR DNA binding protein that are partially colocalized with phosphorylated tau protein. As CTE is characterized pathologically by frontal and temporal lobe atrophy, by abnormal deposits of phosphorylated tau and by 43 kDa TAR DNA binding protein and is associated clinically with behavioral and personality changes, as well as cognitive impairments, CTE is increasingly categorized as an acquired frontotemporal lobar degeneration. Currently, some of the greatest challenges are that CTE cannot be diagnosed during life and the incidence and prevalence of the disorder remain uncertain. Furthermore, the contribution of age, gender, genetics, stress, alcohol and substance abuse to the development of CTE remains to be determined. © 2014 BioMed Central Ltd.},
keywords = {Aggression, Alzheimer disease, amnesia, army, astrocyte, athlete, behavior change, brain atrophy, brain stem, brain weight, central sulcus, chronic disease, Chronic Traumatic Encephalopathy TAR DNA binding p, cognitive defect, comorbidity, Dementia, depression, diencephalon, diffuse Lewy body disease, exposure, frontotemporal dementia, human, impulsiveness, irritability, Motor neuron disease, nerve fiber, neurite, neurofibrillary tangle, neuropathology, nonhuman, personality disorder, priority journal, Review, short term memory, soldier, staging, suicidal ideation, tau protein, tauopathy, temporal lobe, traumatic brain injury, veteran},
pubstate = {published},
tppubtype = {article}
}
Gandy, S; DeKosky, S T
[18F]-T807 tauopathy PET imaging in chronic traumatic encephalopathy Journal Article
In: F1000Research, vol. 3, 2014.
Abstract | Links | BibTeX | Tags: aging, Article, athlete, brain region, Chronic Traumatic Encephalopathy radiopharmaceutic, comorbidity, cumulative trauma disorder, diagnostic value, disease association, disease severity, human, image analysis, ligand binding, neurofibrillary tangle, positron emission tomography, progressive supranuclear palsy, t 807 f 18, tauopathy, temporal lobe, traumatic brain injury, unclassified drug, veteran
@article{Gandy2014,
title = {[18F]-T807 tauopathy PET imaging in chronic traumatic encephalopathy},
author = {Gandy, S and DeKosky, S T},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84923165667\&partnerID=40\&md5=90ae38a9d3536705acb61b5e1fbbc81a},
doi = {10.12688/f1000research.5372.1},
year = {2014},
date = {2014-01-01},
journal = {F1000Research},
volume = {3},
abstract = {A new molecular ligand for positron emission tomography (PET) of the human brain, [18F]-T807, is under investigation for the antemortem detection of pathological neurofibrillary aggregates, which are evidence of neurofibrillary tangle (NFT) diseases, also known as tauopathies. Repetitive mild traumatic brain injuries in athletes and battlefield veterans are associated with one such tauopathy, known as chronic traumatic encephalopathy (CTE). In a recent case report, a former NFL player with clinically probable CTE and a concurrent Progressive Supranuclear Palsy (PSP) -like syndrome was studied using [18F]-T807. The interpretation of this player's [18F]-T807 PET imaging was complicated by the overlap of tracer uptake in brain regions involved in CTE and PSP with regions associated with either nonspecific [18F]-T807 ligand binding or "aging-associated" binding of [18F]-T807 to authentic tauopathy known to be associated with aging and disease severity (i.e., NFT in the mesial temporal lobe). The implications of these data for the utility of [18F]-T807 in the pre-mortem detection of CTE are summarized. © 2014 Gandy S and DeKosky ST.},
keywords = {aging, Article, athlete, brain region, Chronic Traumatic Encephalopathy radiopharmaceutic, comorbidity, cumulative trauma disorder, diagnostic value, disease association, disease severity, human, image analysis, ligand binding, neurofibrillary tangle, positron emission tomography, progressive supranuclear palsy, t 807 f 18, tauopathy, temporal lobe, traumatic brain injury, unclassified drug, veteran},
pubstate = {published},
tppubtype = {article}
}