Tényi, D; Gyimesi, C; Horváth, R; Kovács, N; Ábrahám, H; Darnai, G; Fogarasi, A; Büki, A; Janszky, J
Concussive convulsions: A YouTube video analysis Journal Article
In: Epilepsia, vol. 57, no. 8, pp. 1310–1316, 2016.
Abstract | Links | BibTeX | Tags: Brain trauma, Concussive convulsion, Nonepileptic seizure, Seizure semiology
@article{Tenyi2016,
title = {Concussive convulsions: A YouTube video analysis},
author = {T\'{e}nyi, D and Gyimesi, C and Horv\'{a}th, R and Kov\'{a}cs, N and \'{A}brah\'{a}m, H and Darnai, G and Fogarasi, A and B\"{u}ki, A and Janszky, J},
doi = {10.1111/epi.13432},
year = {2016},
date = {2016-01-01},
journal = {Epilepsia},
volume = {57},
number = {8},
pages = {1310--1316},
abstract = {Objective: To analyze seizure-like motor phenomena immediately occurring after concussion (concussive convulsions). Methods: Twenty-five videos of concussive convulsions were obtained from YouTube as a result of numerous sports-related search terms. The videos were analyzed by four independent observers, documenting observations of the casualty, the head injury, motor symptoms of the concussive convulsions, the postictal period, and the outcome. Results: Immediate responses included the fencing response, bear hug position, and bilateral leg extension. Fencing response was the most common. The side of the hit (p = 0.039) and the head turning (p = 0.0002) was ipsilateral to the extended arm. There was a tendency that if the blow had only a vertical component, the bear hug position appeared more frequently (p = 0.12). The motor symptom that appeared with latency of 6 ± 3 s was clonus, sometimes superimposed with tonic motor phenomena. Clonus was focal, focally evolving bilateral or bilateral, with a duration of 27 ± 19 s (5\textendash72 s). Where lateralization of clonus could be determined, the side of clonus and the side of hit were contralateral (p = 0.039). Significance: Concussive convulsions consist of two phases. The short-latency first phase encompasses motor phenomena resembling neonatal reflexes and may be of brainstem origin. The long-latency second phase consists of clonus. We hypothesize that the motor symptoms of the long-latency phase are attributed to cortical structures; however, they are probably not epileptic in origin but rather a result of a transient cortical neuronal disturbance induced by mechanical forces. Wiley Periodicals, Inc. © 2016 International League Against Epilepsy},
keywords = {Brain trauma, Concussive convulsion, Nonepileptic seizure, Seizure semiology},
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},
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}
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},
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Tényi, D; Gyimesi, C; Horváth, R; Kovács, N; Ábrahám, H; Darnai, G; Fogarasi, A; Büki, A; Janszky, J
Concussive convulsions: A YouTube video analysis Journal Article
In: Epilepsia, vol. 57, no. 8, pp. 1310–1316, 2016.
@article{Tenyi2016,
title = {Concussive convulsions: A YouTube video analysis},
author = {T\'{e}nyi, D and Gyimesi, C and Horv\'{a}th, R and Kov\'{a}cs, N and \'{A}brah\'{a}m, H and Darnai, G and Fogarasi, A and B\"{u}ki, A and Janszky, J},
doi = {10.1111/epi.13432},
year = {2016},
date = {2016-01-01},
journal = {Epilepsia},
volume = {57},
number = {8},
pages = {1310--1316},
abstract = {Objective: To analyze seizure-like motor phenomena immediately occurring after concussion (concussive convulsions). Methods: Twenty-five videos of concussive convulsions were obtained from YouTube as a result of numerous sports-related search terms. The videos were analyzed by four independent observers, documenting observations of the casualty, the head injury, motor symptoms of the concussive convulsions, the postictal period, and the outcome. Results: Immediate responses included the fencing response, bear hug position, and bilateral leg extension. Fencing response was the most common. The side of the hit (p = 0.039) and the head turning (p = 0.0002) was ipsilateral to the extended arm. There was a tendency that if the blow had only a vertical component, the bear hug position appeared more frequently (p = 0.12). The motor symptom that appeared with latency of 6 ± 3 s was clonus, sometimes superimposed with tonic motor phenomena. Clonus was focal, focally evolving bilateral or bilateral, with a duration of 27 ± 19 s (5\textendash72 s). Where lateralization of clonus could be determined, the side of clonus and the side of hit were contralateral (p = 0.039). Significance: Concussive convulsions consist of two phases. The short-latency first phase encompasses motor phenomena resembling neonatal reflexes and may be of brainstem origin. The long-latency second phase consists of clonus. We hypothesize that the motor symptoms of the long-latency phase are attributed to cortical structures; however, they are probably not epileptic in origin but rather a result of a transient cortical neuronal disturbance induced by mechanical forces. Wiley Periodicals, Inc. © 2016 International League Against Epilepsy},
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}
}
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}
}
Tényi, D; Gyimesi, C; Horváth, R; Kovács, N; Ábrahám, H; Darnai, G; Fogarasi, A; Büki, A; Janszky, J
Concussive convulsions: A YouTube video analysis Journal Article
In: Epilepsia, vol. 57, no. 8, pp. 1310–1316, 2016.
Abstract | Links | BibTeX | Tags: Brain trauma, Concussive convulsion, Nonepileptic seizure, Seizure semiology
@article{Tenyi2016,
title = {Concussive convulsions: A YouTube video analysis},
author = {T\'{e}nyi, D and Gyimesi, C and Horv\'{a}th, R and Kov\'{a}cs, N and \'{A}brah\'{a}m, H and Darnai, G and Fogarasi, A and B\"{u}ki, A and Janszky, J},
doi = {10.1111/epi.13432},
year = {2016},
date = {2016-01-01},
journal = {Epilepsia},
volume = {57},
number = {8},
pages = {1310--1316},
abstract = {Objective: To analyze seizure-like motor phenomena immediately occurring after concussion (concussive convulsions). Methods: Twenty-five videos of concussive convulsions were obtained from YouTube as a result of numerous sports-related search terms. The videos were analyzed by four independent observers, documenting observations of the casualty, the head injury, motor symptoms of the concussive convulsions, the postictal period, and the outcome. Results: Immediate responses included the fencing response, bear hug position, and bilateral leg extension. Fencing response was the most common. The side of the hit (p = 0.039) and the head turning (p = 0.0002) was ipsilateral to the extended arm. There was a tendency that if the blow had only a vertical component, the bear hug position appeared more frequently (p = 0.12). The motor symptom that appeared with latency of 6 ± 3 s was clonus, sometimes superimposed with tonic motor phenomena. Clonus was focal, focally evolving bilateral or bilateral, with a duration of 27 ± 19 s (5\textendash72 s). Where lateralization of clonus could be determined, the side of clonus and the side of hit were contralateral (p = 0.039). Significance: Concussive convulsions consist of two phases. The short-latency first phase encompasses motor phenomena resembling neonatal reflexes and may be of brainstem origin. The long-latency second phase consists of clonus. We hypothesize that the motor symptoms of the long-latency phase are attributed to cortical structures; however, they are probably not epileptic in origin but rather a result of a transient cortical neuronal disturbance induced by mechanical forces. Wiley Periodicals, Inc. © 2016 International League Against Epilepsy},
keywords = {Brain trauma, Concussive convulsion, Nonepileptic seizure, Seizure semiology},
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}
}
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}
}