Omalu, B
Chronic traumatic encephalopathy Journal Article
In: Progress in Neurological Surgery, vol. 28, pp. 38–49, 2014.
Abstract | Links | BibTeX | Tags: *Brain Injuries/pa [Pathology], *Brain Injury, Brain Concussion/pa [Pathology], Chronic Traumatic Encephalopathy Animals, Chronic/pa [Pathology], Humans, Tauopathies
@article{Omalu2014,
title = {Chronic traumatic encephalopathy},
author = {Omalu, B},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=medl\&AN=24923391},
year = {2014},
date = {2014-01-01},
journal = {Progress in Neurological Surgery},
volume = {28},
pages = {38--49},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative syndrome, which is caused by single, episodic, or repetitive blunt force impacts to the head and transfer of acceleration-deceleration forces to the brain. CTE presents clinically as a composite syndrome of mood disorders and behavioral and cognitive impairment, with or without sensorimotor impairment. Symptoms of CTE may begin with persistent symptoms of acute traumatic brain injury (TBI) following a documented episode of brain trauma or after a latent period that may range from days to weeks to months and years, up to 40 years following a documented episode of brain trauma or cessation of repetitive TBI. Posttraumatic encephalopathy is distinct from CTE, can be comorbid with CTE, and is a clinicopathologic syndrome induced by focal and/or diffuse, gross and/or microscopic destruction of brain tissue following brain trauma. The brain of a CTE sufferer may appear grossly unremarkable, but shows microscopic evidence of primary and secondary proteinopathies. The primary proteinopathy of CTE is tauopathy, while secondary proteinopathies may include, but are not limited to, amyloidopathy and TDP proteinopathy. Reported prevalence rates of CTE in cohorts exposed to TBI ranges from 3 to 80% across age groups.Copyright © 2014 S. Karger AG, Basel.},
keywords = {*Brain Injuries/pa [Pathology], *Brain Injury, Brain Concussion/pa [Pathology], Chronic Traumatic Encephalopathy Animals, Chronic/pa [Pathology], Humans, Tauopathies},
pubstate = {published},
tppubtype = {article}
}
Omalu, B
Chronic traumatic encephalopathy Journal Article
In: Progress in Neurological Surgery, vol. 28, pp. 38–49, 2014.
@article{Omalu2014,
title = {Chronic traumatic encephalopathy},
author = {Omalu, B},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=medl\&AN=24923391},
year = {2014},
date = {2014-01-01},
journal = {Progress in Neurological Surgery},
volume = {28},
pages = {38--49},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative syndrome, which is caused by single, episodic, or repetitive blunt force impacts to the head and transfer of acceleration-deceleration forces to the brain. CTE presents clinically as a composite syndrome of mood disorders and behavioral and cognitive impairment, with or without sensorimotor impairment. Symptoms of CTE may begin with persistent symptoms of acute traumatic brain injury (TBI) following a documented episode of brain trauma or after a latent period that may range from days to weeks to months and years, up to 40 years following a documented episode of brain trauma or cessation of repetitive TBI. Posttraumatic encephalopathy is distinct from CTE, can be comorbid with CTE, and is a clinicopathologic syndrome induced by focal and/or diffuse, gross and/or microscopic destruction of brain tissue following brain trauma. The brain of a CTE sufferer may appear grossly unremarkable, but shows microscopic evidence of primary and secondary proteinopathies. The primary proteinopathy of CTE is tauopathy, while secondary proteinopathies may include, but are not limited to, amyloidopathy and TDP proteinopathy. Reported prevalence rates of CTE in cohorts exposed to TBI ranges from 3 to 80% across age groups.Copyright © 2014 S. Karger AG, Basel.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Omalu, B
Chronic traumatic encephalopathy Journal Article
In: Progress in Neurological Surgery, vol. 28, pp. 38–49, 2014.
Abstract | Links | BibTeX | Tags: *Brain Injuries/pa [Pathology], *Brain Injury, Brain Concussion/pa [Pathology], Chronic Traumatic Encephalopathy Animals, Chronic/pa [Pathology], Humans, Tauopathies
@article{Omalu2014,
title = {Chronic traumatic encephalopathy},
author = {Omalu, B},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=medl\&AN=24923391},
year = {2014},
date = {2014-01-01},
journal = {Progress in Neurological Surgery},
volume = {28},
pages = {38--49},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative syndrome, which is caused by single, episodic, or repetitive blunt force impacts to the head and transfer of acceleration-deceleration forces to the brain. CTE presents clinically as a composite syndrome of mood disorders and behavioral and cognitive impairment, with or without sensorimotor impairment. Symptoms of CTE may begin with persistent symptoms of acute traumatic brain injury (TBI) following a documented episode of brain trauma or after a latent period that may range from days to weeks to months and years, up to 40 years following a documented episode of brain trauma or cessation of repetitive TBI. Posttraumatic encephalopathy is distinct from CTE, can be comorbid with CTE, and is a clinicopathologic syndrome induced by focal and/or diffuse, gross and/or microscopic destruction of brain tissue following brain trauma. The brain of a CTE sufferer may appear grossly unremarkable, but shows microscopic evidence of primary and secondary proteinopathies. The primary proteinopathy of CTE is tauopathy, while secondary proteinopathies may include, but are not limited to, amyloidopathy and TDP proteinopathy. Reported prevalence rates of CTE in cohorts exposed to TBI ranges from 3 to 80% across age groups.Copyright © 2014 S. Karger AG, Basel.},
keywords = {*Brain Injuries/pa [Pathology], *Brain Injury, Brain Concussion/pa [Pathology], Chronic Traumatic Encephalopathy Animals, Chronic/pa [Pathology], Humans, Tauopathies},
pubstate = {published},
tppubtype = {article}
}