Ellis, M J; Leiter, J; Hall, T; McDonald, P J; Sawyer, S; Silver, N; Bunge, M; Essig, M
Neuroimaging findings in pediatric sports-related concussion Journal Article
In: Journal of Neurosurgery. Pediatrics., vol. 16, no. 3, pp. 241–247, 2015.
Abstract | BibTeX | Tags: *Athletic Injuries/di [Diagnosis], *Brain Concussion/di [Diagnosis], *Brain Concussion/et [Etiology], *Neuroimaging, Adolescent, Arachnoid Cysts/di [Diagnosis], Athletic Injuries/co [Complications], Athletic Injuries/pa [Pathology], Brain Concussion/pa [Pathology], Brain Injuries/di [Diagnosis], Brain Injuries/et [Etiology], Child, Contusions/di [Diagnosis], Dizziness/et [Etiology], Female, Follow-Up Studies, Headache/et [Etiology], Humans, Intracranial Hemorrhages/di [Diagnosis], Magnetic Resonance Imaging, Male, Neuroimaging/mt [Methods], postural balance, Predictive Value of Tests, Retrospective Studies, Skull Fractures/di [Diagnosis], Tomography, Unconsciousness/et [Etiology], X-Ray Computed
@article{Ellis2015b,
title = {Neuroimaging findings in pediatric sports-related concussion},
author = {Ellis, M J and Leiter, J and Hall, T and McDonald, P J and Sawyer, S and Silver, N and Bunge, M and Essig, M},
year = {2015},
date = {2015-01-01},
journal = {Journal of Neurosurgery. Pediatrics.},
volume = {16},
number = {3},
pages = {241--247},
abstract = {OBJECT: The goal in this review was to summarize the results of clinical neuroimaging studies performed in patients with sports-related concussion (SRC) who were referred to a multidisciplinar ypediatric concussion program. METHODS: The authors conducted a retrospective review of medical records and neuroimaging findings for all patients referred to a multidisciplinary pediatric concussion program between September 2013 and July 2014. Inclusion criteria were as follows: 1) age \< 19 years; and 2) physician-diagnosed SRC. All patients underwent evaluation and follow-up by the same neurosurgeon. The 2 outcomes examined in this review were the frequency of neuroimaging studies performed in this population (including CT and MRI) and the findings of those studies. Clinical indications for neuroimaging and the impact of neuroimaging findings on clinical decision making were summarized where available. This investigation was approved by the local institutional ethics review board. RESULTS: A total of 151 patients (mean age 14 years, 59% female) were included this study. Overall, 36 patients (24%) underwent neuroimaging studies, the results of which were normal in 78% of cases. Sixteen percent of patients underwent CT imaging; results were normal in 79% of cases. Abnormal CT findings included the following: arachnoid cyst (1 patient), skull fracture (2 patients), suspected intracranial hemorrhage (1 patient), and suspected hemorrhage into an arachnoid cyst (1 patient). Eleven percent of patients underwent MRI; results were normal in 75% of cases. Abnormal MRI findings included the following: intraparenchymal hemorrhage and sylvian fissure arachnoid cyst (1 patient); nonhemorrhagic contusion (1 patient); demyelinating disease (1 patient); and posterior fossa arachnoid cyst, cerebellar volume loss, and nonspecific white matter changes (1 patient). CONCLUSIONS: Results of clinical neuroimaging studies are normal in the majority of pediatric patients with SRC. However, in selected cases neuroimaging can provide information that impacts decision making about return to play and retirement from the sport.},
keywords = {*Athletic Injuries/di [Diagnosis], *Brain Concussion/di [Diagnosis], *Brain Concussion/et [Etiology], *Neuroimaging, Adolescent, Arachnoid Cysts/di [Diagnosis], Athletic Injuries/co [Complications], Athletic Injuries/pa [Pathology], Brain Concussion/pa [Pathology], Brain Injuries/di [Diagnosis], Brain Injuries/et [Etiology], Child, Contusions/di [Diagnosis], Dizziness/et [Etiology], Female, Follow-Up Studies, Headache/et [Etiology], Humans, Intracranial Hemorrhages/di [Diagnosis], Magnetic Resonance Imaging, Male, Neuroimaging/mt [Methods], postural balance, Predictive Value of Tests, Retrospective Studies, Skull Fractures/di [Diagnosis], Tomography, Unconsciousness/et [Etiology], X-Ray Computed},
pubstate = {published},
tppubtype = {article}
}
Bieniek, K F; Ross, O A; Cormier, K A; Walton, R L; Soto-Ortolaza, A; Johnston, A E; DeSaro, P; Boylan, K B; Graff-Radford, N R; Wszolek, Z K; Rademakers, R; Boeve, B F; McKee, A C; Dickson, D W
Chronic traumatic encephalopathy pathology in a neurodegenerative disorders brain bank Journal Article
In: Acta Neuropathologica, vol. 130, no. 6, pp. 877–889, 2015.
Abstract | BibTeX | Tags: *Brain Injury, *Brain/pa [Pathology], *Neurodegenerative Diseases/et [Etiology], *Neurodegenerative Diseases/pa [Pathology], 0 (Apolipoproteins E), 0 (MAPT protein, 0 (Membrane Proteins), 0 (Nerve Tissue Proteins), 0 (tau Proteins), 0 (TMEM106B protein, aged, Apolipoproteins E/ge [Genetics], Athletic Injuries/co [Complications], Athletic Injuries/ge [Genetics], Athletic Injuries/me [Metabolism], Athletic Injuries/pa [Pathology], Brain Injury, Brain/me [Metabolism], Chronic/et [Etiology], Chronic/ge [Genetics], Chronic/me [Metabolism], Chronic/pa [Pathology], Female, human), Humans, immunohistochemistry, Male, Membrane Proteins/ge [Genetics], Nerve Tissue Proteins/ge [Genetics], Neurodegenerative Diseases/ge [Genetics], Neurodegenerative Diseases/me [Metabolism], Retrospective Studies, tau Proteins/ge [Genetics], tau Proteins/me [Metabolism], Tissue Banks
@article{Bieniek2015,
title = {Chronic traumatic encephalopathy pathology in a neurodegenerative disorders brain bank},
author = {Bieniek, K F and Ross, O A and Cormier, K A and Walton, R L and Soto-Ortolaza, A and Johnston, A E and DeSaro, P and Boylan, K B and Graff-Radford, N R and Wszolek, Z K and Rademakers, R and Boeve, B F and McKee, A C and Dickson, D W},
year = {2015},
date = {2015-01-01},
journal = {Acta Neuropathologica},
volume = {130},
number = {6},
pages = {877--889},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder linked to repetitive traumatic brain injury (TBI) and characterized by deposition of hyperphosphorylated tau at the depths of sulci. We sought to determine the presence of CTE pathology in a brain bank for neurodegenerative disorders for individuals with and without a history of contact sports participation. Available medical records of 1721 men were reviewed for evidence of past history of injury or participation in contact sports. Subsequently, cerebral cortical samples were processed for tau immunohistochemistry in cases with a documented history of sports exposure as well as age- and disease-matched men and women without such exposure. For cases with available frozen tissue, genetic analysis was performed for variants in APOE, MAPT, and TMEM106B. Immunohistochemistry revealed 21 of 66 former athletes had cortical tau pathology consistent with CTE. CTE pathology was not detected in 198 individuals without exposure to contact sports, including 33 individuals with documented single-incident TBI sustained from falls, motor vehicle accidents, domestic violence, or assaults. Among those exposed to contact sports, those with CTE pathology did not differ from those without CTE pathology with respect to noted clinicopathologic features. There were no significant differences in genetic variants for those with CTE pathology, but we observed a slight increase in MAPT H1 haplotype, and there tended to be fewer homozygous carriers of the protective TMEM106B rs3173615 minor allele in those with sports exposure and CTE pathology compared to those without CTE pathology. In conclusion, this study has identified a small, yet significant, subset of individuals with neurodegenerative disorders and concomitant CTE pathology. CTE pathology was only detected in individuals with documented participation in contact sports. Exposure to contact sports was the greatest risk factor for CTE pathology. Future studies addressing clinical correlates of CTE pathology are needed.},
keywords = {*Brain Injury, *Brain/pa [Pathology], *Neurodegenerative Diseases/et [Etiology], *Neurodegenerative Diseases/pa [Pathology], 0 (Apolipoproteins E), 0 (MAPT protein, 0 (Membrane Proteins), 0 (Nerve Tissue Proteins), 0 (tau Proteins), 0 (TMEM106B protein, aged, Apolipoproteins E/ge [Genetics], Athletic Injuries/co [Complications], Athletic Injuries/ge [Genetics], Athletic Injuries/me [Metabolism], Athletic Injuries/pa [Pathology], Brain Injury, Brain/me [Metabolism], Chronic/et [Etiology], Chronic/ge [Genetics], Chronic/me [Metabolism], Chronic/pa [Pathology], Female, human), Humans, immunohistochemistry, Male, Membrane Proteins/ge [Genetics], Nerve Tissue Proteins/ge [Genetics], Neurodegenerative Diseases/ge [Genetics], Neurodegenerative Diseases/me [Metabolism], Retrospective Studies, tau Proteins/ge [Genetics], tau Proteins/me [Metabolism], Tissue Banks},
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}
}
Jordan, B D
Neurologic aspects of boxing Journal Article
In: Archives of Neurology, vol. 44, no. 4, pp. 453–459, 1987.
Abstract | BibTeX | Tags: *Athletic Injuries, *Boxing, *Brain Injuries, Athletic Injuries/ep [Epidemiology], Athletic Injuries/pa [Pathology], Athletic Injuries/pc [Prevention & Control], Athletic Injuries/pp [Physiopathology], Brain Concussion/et [Etiology], Brain Injuries/ep [Epidemiology], Brain Injuries/pa [Pathology], Brain Injuries/pc [Prevention & Control], Brain Injuries/pp [Physiopathology], Humans, Magnetic Resonance Spectroscopy, Tomography, X-Ray Computed
@article{Jordan1987,
title = {Neurologic aspects of boxing},
author = {Jordan, B D},
year = {1987},
date = {1987-01-01},
journal = {Archives of Neurology},
volume = {44},
number = {4},
pages = {453--459},
abstract = {The assessment and prevention of potentially adverse neurologic consequences of boxing requires two important considerations. Acute neurologic injuries should be distinguished from chronic brain injuries and the level of competitive boxing (ie, amateur vs professional) must also be taken into account. Acute neurologic injuries such as concussion, post-concussion syndrome, intracranial hemorrhage, and brain contusion are more readily identified than chronic neurologic injuries because of their immediate devastation of the nervous system. In contrast, chronic neurologic injuries differ in their pathophysiologic mechanisms that are exemplified by an insidious onset and progression after the cessation of boxing. Accordingly, the chronic traumatic encephalopathy of boxing poses the most serious neurologic threat of boxing. Amateur boxing differs from professional boxing in the duration of fights, rules and regulatory policies, medical evaluation, and protective devices. These factors could produce a differential effect on the risk of injury to the brain. The prevention of neurologic injuries in boxing requires the integration of proper neurologic evaluation by qualified ring-side physicians, the design and utilization of effective protective devices, and the establishment of national regulatory agencies.},
keywords = {*Athletic Injuries, *Boxing, *Brain Injuries, Athletic Injuries/ep [Epidemiology], Athletic Injuries/pa [Pathology], Athletic Injuries/pc [Prevention \& Control], Athletic Injuries/pp [Physiopathology], Brain Concussion/et [Etiology], Brain Injuries/ep [Epidemiology], Brain Injuries/pa [Pathology], Brain Injuries/pc [Prevention \& Control], Brain Injuries/pp [Physiopathology], Humans, Magnetic Resonance Spectroscopy, Tomography, X-Ray Computed},
pubstate = {published},
tppubtype = {article}
}
Ellis, M J; Leiter, J; Hall, T; McDonald, P J; Sawyer, S; Silver, N; Bunge, M; Essig, M
Neuroimaging findings in pediatric sports-related concussion Journal Article
In: Journal of Neurosurgery. Pediatrics., vol. 16, no. 3, pp. 241–247, 2015.
@article{Ellis2015b,
title = {Neuroimaging findings in pediatric sports-related concussion},
author = {Ellis, M J and Leiter, J and Hall, T and McDonald, P J and Sawyer, S and Silver, N and Bunge, M and Essig, M},
year = {2015},
date = {2015-01-01},
journal = {Journal of Neurosurgery. Pediatrics.},
volume = {16},
number = {3},
pages = {241--247},
abstract = {OBJECT: The goal in this review was to summarize the results of clinical neuroimaging studies performed in patients with sports-related concussion (SRC) who were referred to a multidisciplinar ypediatric concussion program. METHODS: The authors conducted a retrospective review of medical records and neuroimaging findings for all patients referred to a multidisciplinary pediatric concussion program between September 2013 and July 2014. Inclusion criteria were as follows: 1) age \< 19 years; and 2) physician-diagnosed SRC. All patients underwent evaluation and follow-up by the same neurosurgeon. The 2 outcomes examined in this review were the frequency of neuroimaging studies performed in this population (including CT and MRI) and the findings of those studies. Clinical indications for neuroimaging and the impact of neuroimaging findings on clinical decision making were summarized where available. This investigation was approved by the local institutional ethics review board. RESULTS: A total of 151 patients (mean age 14 years, 59% female) were included this study. Overall, 36 patients (24%) underwent neuroimaging studies, the results of which were normal in 78% of cases. Sixteen percent of patients underwent CT imaging; results were normal in 79% of cases. Abnormal CT findings included the following: arachnoid cyst (1 patient), skull fracture (2 patients), suspected intracranial hemorrhage (1 patient), and suspected hemorrhage into an arachnoid cyst (1 patient). Eleven percent of patients underwent MRI; results were normal in 75% of cases. Abnormal MRI findings included the following: intraparenchymal hemorrhage and sylvian fissure arachnoid cyst (1 patient); nonhemorrhagic contusion (1 patient); demyelinating disease (1 patient); and posterior fossa arachnoid cyst, cerebellar volume loss, and nonspecific white matter changes (1 patient). CONCLUSIONS: Results of clinical neuroimaging studies are normal in the majority of pediatric patients with SRC. However, in selected cases neuroimaging can provide information that impacts decision making about return to play and retirement from the sport.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Bieniek, K F; Ross, O A; Cormier, K A; Walton, R L; Soto-Ortolaza, A; Johnston, A E; DeSaro, P; Boylan, K B; Graff-Radford, N R; Wszolek, Z K; Rademakers, R; Boeve, B F; McKee, A C; Dickson, D W
Chronic traumatic encephalopathy pathology in a neurodegenerative disorders brain bank Journal Article
In: Acta Neuropathologica, vol. 130, no. 6, pp. 877–889, 2015.
@article{Bieniek2015,
title = {Chronic traumatic encephalopathy pathology in a neurodegenerative disorders brain bank},
author = {Bieniek, K F and Ross, O A and Cormier, K A and Walton, R L and Soto-Ortolaza, A and Johnston, A E and DeSaro, P and Boylan, K B and Graff-Radford, N R and Wszolek, Z K and Rademakers, R and Boeve, B F and McKee, A C and Dickson, D W},
year = {2015},
date = {2015-01-01},
journal = {Acta Neuropathologica},
volume = {130},
number = {6},
pages = {877--889},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder linked to repetitive traumatic brain injury (TBI) and characterized by deposition of hyperphosphorylated tau at the depths of sulci. We sought to determine the presence of CTE pathology in a brain bank for neurodegenerative disorders for individuals with and without a history of contact sports participation. Available medical records of 1721 men were reviewed for evidence of past history of injury or participation in contact sports. Subsequently, cerebral cortical samples were processed for tau immunohistochemistry in cases with a documented history of sports exposure as well as age- and disease-matched men and women without such exposure. For cases with available frozen tissue, genetic analysis was performed for variants in APOE, MAPT, and TMEM106B. Immunohistochemistry revealed 21 of 66 former athletes had cortical tau pathology consistent with CTE. CTE pathology was not detected in 198 individuals without exposure to contact sports, including 33 individuals with documented single-incident TBI sustained from falls, motor vehicle accidents, domestic violence, or assaults. Among those exposed to contact sports, those with CTE pathology did not differ from those without CTE pathology with respect to noted clinicopathologic features. There were no significant differences in genetic variants for those with CTE pathology, but we observed a slight increase in MAPT H1 haplotype, and there tended to be fewer homozygous carriers of the protective TMEM106B rs3173615 minor allele in those with sports exposure and CTE pathology compared to those without CTE pathology. In conclusion, this study has identified a small, yet significant, subset of individuals with neurodegenerative disorders and concomitant CTE pathology. CTE pathology was only detected in individuals with documented participation in contact sports. Exposure to contact sports was the greatest risk factor for CTE pathology. Future studies addressing clinical correlates of CTE pathology are needed.},
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}
}
Jordan, B D
Neurologic aspects of boxing Journal Article
In: Archives of Neurology, vol. 44, no. 4, pp. 453–459, 1987.
@article{Jordan1987,
title = {Neurologic aspects of boxing},
author = {Jordan, B D},
year = {1987},
date = {1987-01-01},
journal = {Archives of Neurology},
volume = {44},
number = {4},
pages = {453--459},
abstract = {The assessment and prevention of potentially adverse neurologic consequences of boxing requires two important considerations. Acute neurologic injuries should be distinguished from chronic brain injuries and the level of competitive boxing (ie, amateur vs professional) must also be taken into account. Acute neurologic injuries such as concussion, post-concussion syndrome, intracranial hemorrhage, and brain contusion are more readily identified than chronic neurologic injuries because of their immediate devastation of the nervous system. In contrast, chronic neurologic injuries differ in their pathophysiologic mechanisms that are exemplified by an insidious onset and progression after the cessation of boxing. Accordingly, the chronic traumatic encephalopathy of boxing poses the most serious neurologic threat of boxing. Amateur boxing differs from professional boxing in the duration of fights, rules and regulatory policies, medical evaluation, and protective devices. These factors could produce a differential effect on the risk of injury to the brain. The prevention of neurologic injuries in boxing requires the integration of proper neurologic evaluation by qualified ring-side physicians, the design and utilization of effective protective devices, and the establishment of national regulatory agencies.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Ellis, M J; Leiter, J; Hall, T; McDonald, P J; Sawyer, S; Silver, N; Bunge, M; Essig, M
Neuroimaging findings in pediatric sports-related concussion Journal Article
In: Journal of Neurosurgery. Pediatrics., vol. 16, no. 3, pp. 241–247, 2015.
Abstract | BibTeX | Tags: *Athletic Injuries/di [Diagnosis], *Brain Concussion/di [Diagnosis], *Brain Concussion/et [Etiology], *Neuroimaging, Adolescent, Arachnoid Cysts/di [Diagnosis], Athletic Injuries/co [Complications], Athletic Injuries/pa [Pathology], Brain Concussion/pa [Pathology], Brain Injuries/di [Diagnosis], Brain Injuries/et [Etiology], Child, Contusions/di [Diagnosis], Dizziness/et [Etiology], Female, Follow-Up Studies, Headache/et [Etiology], Humans, Intracranial Hemorrhages/di [Diagnosis], Magnetic Resonance Imaging, Male, Neuroimaging/mt [Methods], postural balance, Predictive Value of Tests, Retrospective Studies, Skull Fractures/di [Diagnosis], Tomography, Unconsciousness/et [Etiology], X-Ray Computed
@article{Ellis2015b,
title = {Neuroimaging findings in pediatric sports-related concussion},
author = {Ellis, M J and Leiter, J and Hall, T and McDonald, P J and Sawyer, S and Silver, N and Bunge, M and Essig, M},
year = {2015},
date = {2015-01-01},
journal = {Journal of Neurosurgery. Pediatrics.},
volume = {16},
number = {3},
pages = {241--247},
abstract = {OBJECT: The goal in this review was to summarize the results of clinical neuroimaging studies performed in patients with sports-related concussion (SRC) who were referred to a multidisciplinar ypediatric concussion program. METHODS: The authors conducted a retrospective review of medical records and neuroimaging findings for all patients referred to a multidisciplinary pediatric concussion program between September 2013 and July 2014. Inclusion criteria were as follows: 1) age \< 19 years; and 2) physician-diagnosed SRC. All patients underwent evaluation and follow-up by the same neurosurgeon. The 2 outcomes examined in this review were the frequency of neuroimaging studies performed in this population (including CT and MRI) and the findings of those studies. Clinical indications for neuroimaging and the impact of neuroimaging findings on clinical decision making were summarized where available. This investigation was approved by the local institutional ethics review board. RESULTS: A total of 151 patients (mean age 14 years, 59% female) were included this study. Overall, 36 patients (24%) underwent neuroimaging studies, the results of which were normal in 78% of cases. Sixteen percent of patients underwent CT imaging; results were normal in 79% of cases. Abnormal CT findings included the following: arachnoid cyst (1 patient), skull fracture (2 patients), suspected intracranial hemorrhage (1 patient), and suspected hemorrhage into an arachnoid cyst (1 patient). Eleven percent of patients underwent MRI; results were normal in 75% of cases. Abnormal MRI findings included the following: intraparenchymal hemorrhage and sylvian fissure arachnoid cyst (1 patient); nonhemorrhagic contusion (1 patient); demyelinating disease (1 patient); and posterior fossa arachnoid cyst, cerebellar volume loss, and nonspecific white matter changes (1 patient). CONCLUSIONS: Results of clinical neuroimaging studies are normal in the majority of pediatric patients with SRC. However, in selected cases neuroimaging can provide information that impacts decision making about return to play and retirement from the sport.},
keywords = {*Athletic Injuries/di [Diagnosis], *Brain Concussion/di [Diagnosis], *Brain Concussion/et [Etiology], *Neuroimaging, Adolescent, Arachnoid Cysts/di [Diagnosis], Athletic Injuries/co [Complications], Athletic Injuries/pa [Pathology], Brain Concussion/pa [Pathology], Brain Injuries/di [Diagnosis], Brain Injuries/et [Etiology], Child, Contusions/di [Diagnosis], Dizziness/et [Etiology], Female, Follow-Up Studies, Headache/et [Etiology], Humans, Intracranial Hemorrhages/di [Diagnosis], Magnetic Resonance Imaging, Male, Neuroimaging/mt [Methods], postural balance, Predictive Value of Tests, Retrospective Studies, Skull Fractures/di [Diagnosis], Tomography, Unconsciousness/et [Etiology], X-Ray Computed},
pubstate = {published},
tppubtype = {article}
}
Bieniek, K F; Ross, O A; Cormier, K A; Walton, R L; Soto-Ortolaza, A; Johnston, A E; DeSaro, P; Boylan, K B; Graff-Radford, N R; Wszolek, Z K; Rademakers, R; Boeve, B F; McKee, A C; Dickson, D W
Chronic traumatic encephalopathy pathology in a neurodegenerative disorders brain bank Journal Article
In: Acta Neuropathologica, vol. 130, no. 6, pp. 877–889, 2015.
Abstract | BibTeX | Tags: *Brain Injury, *Brain/pa [Pathology], *Neurodegenerative Diseases/et [Etiology], *Neurodegenerative Diseases/pa [Pathology], 0 (Apolipoproteins E), 0 (MAPT protein, 0 (Membrane Proteins), 0 (Nerve Tissue Proteins), 0 (tau Proteins), 0 (TMEM106B protein, aged, Apolipoproteins E/ge [Genetics], Athletic Injuries/co [Complications], Athletic Injuries/ge [Genetics], Athletic Injuries/me [Metabolism], Athletic Injuries/pa [Pathology], Brain Injury, Brain/me [Metabolism], Chronic/et [Etiology], Chronic/ge [Genetics], Chronic/me [Metabolism], Chronic/pa [Pathology], Female, human), Humans, immunohistochemistry, Male, Membrane Proteins/ge [Genetics], Nerve Tissue Proteins/ge [Genetics], Neurodegenerative Diseases/ge [Genetics], Neurodegenerative Diseases/me [Metabolism], Retrospective Studies, tau Proteins/ge [Genetics], tau Proteins/me [Metabolism], Tissue Banks
@article{Bieniek2015,
title = {Chronic traumatic encephalopathy pathology in a neurodegenerative disorders brain bank},
author = {Bieniek, K F and Ross, O A and Cormier, K A and Walton, R L and Soto-Ortolaza, A and Johnston, A E and DeSaro, P and Boylan, K B and Graff-Radford, N R and Wszolek, Z K and Rademakers, R and Boeve, B F and McKee, A C and Dickson, D W},
year = {2015},
date = {2015-01-01},
journal = {Acta Neuropathologica},
volume = {130},
number = {6},
pages = {877--889},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder linked to repetitive traumatic brain injury (TBI) and characterized by deposition of hyperphosphorylated tau at the depths of sulci. We sought to determine the presence of CTE pathology in a brain bank for neurodegenerative disorders for individuals with and without a history of contact sports participation. Available medical records of 1721 men were reviewed for evidence of past history of injury or participation in contact sports. Subsequently, cerebral cortical samples were processed for tau immunohistochemistry in cases with a documented history of sports exposure as well as age- and disease-matched men and women without such exposure. For cases with available frozen tissue, genetic analysis was performed for variants in APOE, MAPT, and TMEM106B. Immunohistochemistry revealed 21 of 66 former athletes had cortical tau pathology consistent with CTE. CTE pathology was not detected in 198 individuals without exposure to contact sports, including 33 individuals with documented single-incident TBI sustained from falls, motor vehicle accidents, domestic violence, or assaults. Among those exposed to contact sports, those with CTE pathology did not differ from those without CTE pathology with respect to noted clinicopathologic features. There were no significant differences in genetic variants for those with CTE pathology, but we observed a slight increase in MAPT H1 haplotype, and there tended to be fewer homozygous carriers of the protective TMEM106B rs3173615 minor allele in those with sports exposure and CTE pathology compared to those without CTE pathology. In conclusion, this study has identified a small, yet significant, subset of individuals with neurodegenerative disorders and concomitant CTE pathology. CTE pathology was only detected in individuals with documented participation in contact sports. Exposure to contact sports was the greatest risk factor for CTE pathology. Future studies addressing clinical correlates of CTE pathology are needed.},
keywords = {*Brain Injury, *Brain/pa [Pathology], *Neurodegenerative Diseases/et [Etiology], *Neurodegenerative Diseases/pa [Pathology], 0 (Apolipoproteins E), 0 (MAPT protein, 0 (Membrane Proteins), 0 (Nerve Tissue Proteins), 0 (tau Proteins), 0 (TMEM106B protein, aged, Apolipoproteins E/ge [Genetics], Athletic Injuries/co [Complications], Athletic Injuries/ge [Genetics], Athletic Injuries/me [Metabolism], Athletic Injuries/pa [Pathology], Brain Injury, Brain/me [Metabolism], Chronic/et [Etiology], Chronic/ge [Genetics], Chronic/me [Metabolism], Chronic/pa [Pathology], Female, human), Humans, immunohistochemistry, Male, Membrane Proteins/ge [Genetics], Nerve Tissue Proteins/ge [Genetics], Neurodegenerative Diseases/ge [Genetics], Neurodegenerative Diseases/me [Metabolism], Retrospective Studies, tau Proteins/ge [Genetics], tau Proteins/me [Metabolism], Tissue Banks},
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}
}
Jordan, B D
Neurologic aspects of boxing Journal Article
In: Archives of Neurology, vol. 44, no. 4, pp. 453–459, 1987.
Abstract | BibTeX | Tags: *Athletic Injuries, *Boxing, *Brain Injuries, Athletic Injuries/ep [Epidemiology], Athletic Injuries/pa [Pathology], Athletic Injuries/pc [Prevention & Control], Athletic Injuries/pp [Physiopathology], Brain Concussion/et [Etiology], Brain Injuries/ep [Epidemiology], Brain Injuries/pa [Pathology], Brain Injuries/pc [Prevention & Control], Brain Injuries/pp [Physiopathology], Humans, Magnetic Resonance Spectroscopy, Tomography, X-Ray Computed
@article{Jordan1987,
title = {Neurologic aspects of boxing},
author = {Jordan, B D},
year = {1987},
date = {1987-01-01},
journal = {Archives of Neurology},
volume = {44},
number = {4},
pages = {453--459},
abstract = {The assessment and prevention of potentially adverse neurologic consequences of boxing requires two important considerations. Acute neurologic injuries should be distinguished from chronic brain injuries and the level of competitive boxing (ie, amateur vs professional) must also be taken into account. Acute neurologic injuries such as concussion, post-concussion syndrome, intracranial hemorrhage, and brain contusion are more readily identified than chronic neurologic injuries because of their immediate devastation of the nervous system. In contrast, chronic neurologic injuries differ in their pathophysiologic mechanisms that are exemplified by an insidious onset and progression after the cessation of boxing. Accordingly, the chronic traumatic encephalopathy of boxing poses the most serious neurologic threat of boxing. Amateur boxing differs from professional boxing in the duration of fights, rules and regulatory policies, medical evaluation, and protective devices. These factors could produce a differential effect on the risk of injury to the brain. The prevention of neurologic injuries in boxing requires the integration of proper neurologic evaluation by qualified ring-side physicians, the design and utilization of effective protective devices, and the establishment of national regulatory agencies.},
keywords = {*Athletic Injuries, *Boxing, *Brain Injuries, Athletic Injuries/ep [Epidemiology], Athletic Injuries/pa [Pathology], Athletic Injuries/pc [Prevention \& Control], Athletic Injuries/pp [Physiopathology], Brain Concussion/et [Etiology], Brain Injuries/ep [Epidemiology], Brain Injuries/pa [Pathology], Brain Injuries/pc [Prevention \& Control], Brain Injuries/pp [Physiopathology], Humans, Magnetic Resonance Spectroscopy, Tomography, X-Ray Computed},
pubstate = {published},
tppubtype = {article}
}