References

2016

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

2014

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}

}

Mitsis, E M; Riggio, S; Kostakoglu, L; Dickstein, D L; Machac, J; Delman, B; Goldstein, M; Jennings, D; D'Antonio, E; Martin, J; Naidich, T P; Aloysi, A; Fernandez, C; Seibyl, J; DeKosky, S T; Elder, G A; Marek, K; Gordon, W; Hof, P R; Sano, M; Gandy, S

Tauopathy PET and amyloid PET in the diagnosis of chronic traumatic encephalopathies: Studies of a retired NFL player and of a man with FTD and a severe head injury Journal Article

In: Translational Psychiatry, vol. 4, no. 9, 2014.

Abstract | Links | BibTeX | Tags: adult, aged, amyloid plaque, arachnoid cyst, Article, case report, Chronic Traumatic Encephalopathy florbetapir f 18, Concussion, diagnostic accuracy, eye movement, football, frontotemporal dementia, head injury, human, injury severity, ligand binding, Male, memory disorder, middle aged, molecular imaging, motor dysfunction, muscle tone, personality disorder, positron emission tomography, short term memory, subdural hematoma, tauopathy, traumatic brain injury

@article{Mitsis2014,

title = {Tauopathy PET and amyloid PET in the diagnosis of chronic traumatic encephalopathies: Studies of a retired NFL player and of a man with FTD and a severe head injury},

author = {Mitsis, E M and Riggio, S and Kostakoglu, L and Dickstein, D L and Machac, J and Delman, B and Goldstein, M and Jennings, D and D'Antonio, E and Martin, J and Naidich, T P and Aloysi, A and Fernandez, C and Seibyl, J and DeKosky, S T and Elder, G A and Marek, K and Gordon, W and Hof, P R and Sano, M and Gandy, S},

url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84918535750\&partnerID=40\&md5=704b918a7429432cbd631e703c44eb63},

doi = {10.1038/tp.2014.91},

year  = {2014},

date = {2014-01-01},

journal = {Translational Psychiatry},

volume = {4},

number = {9},

abstract = {Single, severe traumatic brain injury (TBI) which elevates CNS amyloid, increases the risk of Alzheimer's disease (AD); while repetitive concussive and subconcussive events as observed in athletes and military personnel, may increase the risk of chronic traumatic encephalopathy (CTE). We describe two clinical cases, one with a history of multiple concussions during a career in the National Football League (NFL) and the second with frontotemporal dementia and a single, severe TBI. Both patients presented with cognitive decline and underwent [18F]-Florbetapir positron emission tomography (PET) imaging for amyloid plaques; the retired NFL player also underwent [18F]-T807 PET imaging, a new ligand binding to tau, the main constituent of neurofibrillary tangles (NFT). Case 1, the former NFL player, was 71 years old when he presented with memory impairment and a clinical profile highly similar to AD. [18F]-Florbetapir PET imaging was negative, essentially excluding AD as a diagnosis. CTE was suspected clinically, and [18F]-T807 PET imaging revealed striatal and nigral [18F]-T807 retention consistent with the presence of tauopathy. Case 2 was a 56- year-old man with personality changes and cognitive decline who had sustained a fall complicated by a subdural hematoma. At 1 year post injury, [18F]-Florbetapir PET imaging was negative for an AD pattern of amyloid accumulation in this subject. Focal [18F]- Florbetapir retention was noted at the site of impact. In case 1, amyloid imaging provided improved diagnostic accuracy where standard clinical and laboratory criteria were inadequate. In that same case, tau imaging with [18F]-T807 revealed a subcortical tauopathy that we interpret as a novel form of CTE with a distribution of tauopathy that mimics, to some extent, that of progressive supranuclear palsy (PSP), despite a clinical presentation of amnesia without any movement disorder complaints or signs. A key distinguishing feature is that our patient presented with hippocampal involvement, which is more frequently seen in CTE than in PSP. In case 2, focal [18F]-Florbetapir retention at the site of injury in an otherwise negative scan suggests focal amyloid aggregation. In each of these complex cases, a combination of [18F]-fluorodeoxyglucose, [18F]-Florbetapir and/or [18F]-T807 PET molecular imaging improved the accuracy of diagnosis and prevented inappropriate interventions. © 2014 Macmillan Publishers Limited.},

keywords = {adult, aged, amyloid plaque, arachnoid cyst, Article, case report, Chronic Traumatic Encephalopathy florbetapir f 18, Concussion, diagnostic accuracy, eye movement, football, frontotemporal dementia, head injury, human, injury severity, ligand binding, Male, memory disorder, middle aged, molecular imaging, motor dysfunction, muscle tone, personality disorder, positron emission tomography, short term memory, subdural hematoma, tauopathy, traumatic brain injury},

pubstate = {published},

tppubtype = {article}

}

Single, severe traumatic brain injury (TBI) which elevates CNS amyloid, increases the risk of Alzheimer's disease (AD); while repetitive concussive and subconcussive events as observed in athletes and military personnel, may increase the risk of chronic traumatic encephalopathy (CTE). We describe two clinical cases, one with a history of multiple concussions during a career in the National Football League (NFL) and the second with frontotemporal dementia and a single, severe TBI. Both patients presented with cognitive decline and underwent [18F]-Florbetapir positron emission tomography (PET) imaging for amyloid plaques; the retired NFL player also underwent [18F]-T807 PET imaging, a new ligand binding to tau, the main constituent of neurofibrillary tangles (NFT). Case 1, the former NFL player, was 71 years old when he presented with memory impairment and a clinical profile highly similar to AD. [18F]-Florbetapir PET imaging was negative, essentially excluding AD as a diagnosis. CTE was suspected clinically, and [18F]-T807 PET imaging revealed striatal and nigral [18F]-T807 retention consistent with the presence of tauopathy. Case 2 was a 56- year-old man with personality changes and cognitive decline who had sustained a fall complicated by a subdural hematoma. At 1 year post injury, [18F]-Florbetapir PET imaging was negative for an AD pattern of amyloid accumulation in this subject. Focal [18F]- Florbetapir retention was noted at the site of impact. In case 1, amyloid imaging provided improved diagnostic accuracy where standard clinical and laboratory criteria were inadequate. In that same case, tau imaging with [18F]-T807 revealed a subcortical tauopathy that we interpret as a novel form of CTE with a distribution of tauopathy that mimics, to some extent, that of progressive supranuclear palsy (PSP), despite a clinical presentation of amnesia without any movement disorder complaints or signs. A key distinguishing feature is that our patient presented with hippocampal involvement, which is more frequently seen in CTE than in PSP. In case 2, focal [18F]-Florbetapir retention at the site of injury in an otherwise negative scan suggests focal amyloid aggregation. In each of these complex cases, a combination of [18F]-fluorodeoxyglucose, [18F]-Florbetapir and/or [18F]-T807 PET molecular imaging improved the accuracy of diagnosis and prevented inappropriate interventions. © 2014 Macmillan Publishers Limited.

Reference Search

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

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

@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 = {},

pubstate = {published},

tppubtype = {article}

}

Tauopathy PET and amyloid PET in the diagnosis of chronic traumatic encephalopathies: Studies of a retired NFL player and of a man with FTD and a severe head injury Journal Article

In: Translational Psychiatry, vol. 4, no. 9, 2014.

Abstract | Links | BibTeX

@article{Mitsis2014,

title = {Tauopathy PET and amyloid PET in the diagnosis of chronic traumatic encephalopathies: Studies of a retired NFL player and of a man with FTD and a severe head injury},

author = {Mitsis, E M and Riggio, S and Kostakoglu, L and Dickstein, D L and Machac, J and Delman, B and Goldstein, M and Jennings, D and D'Antonio, E and Martin, J and Naidich, T P and Aloysi, A and Fernandez, C and Seibyl, J and DeKosky, S T and Elder, G A and Marek, K and Gordon, W and Hof, P R and Sano, M and Gandy, S},

url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84918535750\&partnerID=40\&md5=704b918a7429432cbd631e703c44eb63},

doi = {10.1038/tp.2014.91},

year  = {2014},

date = {2014-01-01},

journal = {Translational Psychiatry},

volume = {4},

number = {9},

abstract = {Single, severe traumatic brain injury (TBI) which elevates CNS amyloid, increases the risk of Alzheimer's disease (AD); while repetitive concussive and subconcussive events as observed in athletes and military personnel, may increase the risk of chronic traumatic encephalopathy (CTE). We describe two clinical cases, one with a history of multiple concussions during a career in the National Football League (NFL) and the second with frontotemporal dementia and a single, severe TBI. Both patients presented with cognitive decline and underwent [18F]-Florbetapir positron emission tomography (PET) imaging for amyloid plaques; the retired NFL player also underwent [18F]-T807 PET imaging, a new ligand binding to tau, the main constituent of neurofibrillary tangles (NFT). Case 1, the former NFL player, was 71 years old when he presented with memory impairment and a clinical profile highly similar to AD. [18F]-Florbetapir PET imaging was negative, essentially excluding AD as a diagnosis. CTE was suspected clinically, and [18F]-T807 PET imaging revealed striatal and nigral [18F]-T807 retention consistent with the presence of tauopathy. Case 2 was a 56- year-old man with personality changes and cognitive decline who had sustained a fall complicated by a subdural hematoma. At 1 year post injury, [18F]-Florbetapir PET imaging was negative for an AD pattern of amyloid accumulation in this subject. Focal [18F]- Florbetapir retention was noted at the site of impact. In case 1, amyloid imaging provided improved diagnostic accuracy where standard clinical and laboratory criteria were inadequate. In that same case, tau imaging with [18F]-T807 revealed a subcortical tauopathy that we interpret as a novel form of CTE with a distribution of tauopathy that mimics, to some extent, that of progressive supranuclear palsy (PSP), despite a clinical presentation of amnesia without any movement disorder complaints or signs. A key distinguishing feature is that our patient presented with hippocampal involvement, which is more frequently seen in CTE than in PSP. In case 2, focal [18F]-Florbetapir retention at the site of injury in an otherwise negative scan suggests focal amyloid aggregation. In each of these complex cases, a combination of [18F]-fluorodeoxyglucose, [18F]-Florbetapir and/or [18F]-T807 PET molecular imaging improved the accuracy of diagnosis and prevented inappropriate interventions. © 2014 Macmillan Publishers Limited.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

Most Referenced Keywords

Show all

2016

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.

2014

Levin, B; Bhardwaj, A

Chronic traumatic encephalopathy: A critical appraisal Journal Article

In: Neurocritical Care, vol. 20, no. 2, pp. 334–344, 2014.

@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}

}

Tauopathy PET and amyloid PET in the diagnosis of chronic traumatic encephalopathies: Studies of a retired NFL player and of a man with FTD and a severe head injury Journal Article

In: Translational Psychiatry, vol. 4, no. 9, 2014.

@article{Mitsis2014,

title = {Tauopathy PET and amyloid PET in the diagnosis of chronic traumatic encephalopathies: Studies of a retired NFL player and of a man with FTD and a severe head injury},

author = {Mitsis, E M and Riggio, S and Kostakoglu, L and Dickstein, D L and Machac, J and Delman, B and Goldstein, M and Jennings, D and D'Antonio, E and Martin, J and Naidich, T P and Aloysi, A and Fernandez, C and Seibyl, J and DeKosky, S T and Elder, G A and Marek, K and Gordon, W and Hof, P R and Sano, M and Gandy, S},

url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84918535750\&partnerID=40\&md5=704b918a7429432cbd631e703c44eb63},

doi = {10.1038/tp.2014.91},

year  = {2014},

date = {2014-01-01},

journal = {Translational Psychiatry},

volume = {4},

number = {9},

abstract = {Single, severe traumatic brain injury (TBI) which elevates CNS amyloid, increases the risk of Alzheimer's disease (AD); while repetitive concussive and subconcussive events as observed in athletes and military personnel, may increase the risk of chronic traumatic encephalopathy (CTE). We describe two clinical cases, one with a history of multiple concussions during a career in the National Football League (NFL) and the second with frontotemporal dementia and a single, severe TBI. Both patients presented with cognitive decline and underwent [18F]-Florbetapir positron emission tomography (PET) imaging for amyloid plaques; the retired NFL player also underwent [18F]-T807 PET imaging, a new ligand binding to tau, the main constituent of neurofibrillary tangles (NFT). Case 1, the former NFL player, was 71 years old when he presented with memory impairment and a clinical profile highly similar to AD. [18F]-Florbetapir PET imaging was negative, essentially excluding AD as a diagnosis. CTE was suspected clinically, and [18F]-T807 PET imaging revealed striatal and nigral [18F]-T807 retention consistent with the presence of tauopathy. Case 2 was a 56- year-old man with personality changes and cognitive decline who had sustained a fall complicated by a subdural hematoma. At 1 year post injury, [18F]-Florbetapir PET imaging was negative for an AD pattern of amyloid accumulation in this subject. Focal [18F]- Florbetapir retention was noted at the site of impact. In case 1, amyloid imaging provided improved diagnostic accuracy where standard clinical and laboratory criteria were inadequate. In that same case, tau imaging with [18F]-T807 revealed a subcortical tauopathy that we interpret as a novel form of CTE with a distribution of tauopathy that mimics, to some extent, that of progressive supranuclear palsy (PSP), despite a clinical presentation of amnesia without any movement disorder complaints or signs. A key distinguishing feature is that our patient presented with hippocampal involvement, which is more frequently seen in CTE than in PSP. In case 2, focal [18F]-Florbetapir retention at the site of injury in an otherwise negative scan suggests focal amyloid aggregation. In each of these complex cases, a combination of [18F]-fluorodeoxyglucose, [18F]-Florbetapir and/or [18F]-T807 PET molecular imaging improved the accuracy of diagnosis and prevented inappropriate interventions. © 2014 Macmillan Publishers Limited.},

keywords = {adult, aged, amyloid plaque, arachnoid cyst, Article, case report, Chronic Traumatic Encephalopathy florbetapir f 18, Concussion, diagnostic accuracy, eye movement, football, frontotemporal dementia, head injury, human, injury severity, ligand binding, Male, memory disorder, middle aged, molecular imaging, motor dysfunction, muscle tone, personality disorder, positron emission tomography, short term memory, subdural hematoma, tauopathy, traumatic brain injury},

pubstate = {published},

tppubtype = {article}

}

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