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

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}

}

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

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

@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}

}

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

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 = {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}

}

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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2016

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