Chiroban, O; Perju-Dumbravă, L
Postmortem evaluation of chronic traumatic encephalopathy Journal Article
In: Romanian Journal of Legal Medicine, vol. 24, no. 4, pp. 266–272, 2016.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy, Forensic pathology, NEURODEGENERATION, Trauma
@article{Chiroban2016,
title = {Postmortem evaluation of chronic traumatic encephalopathy},
author = {Chiroban, O and Perju-Dumbrav\u{a}, L},
doi = {10.4323/rjlm.2016.266},
year = {2016},
date = {2016-01-01},
journal = {Romanian Journal of Legal Medicine},
volume = {24},
number = {4},
pages = {266--272},
abstract = {Chronic traumatic encephalopathy (CTE) is the modern concept naming the neurodegenerative processes occurring in patients with positive medical history of repeated brain trauma and progressive dementia. Morphologically, CTE is classified as being a distinct member of the tauopathies family, with different distribution of tau-positive neurofibrillary tangles (NFTs) and low to none beta-amyloid deposits, contrasting the most famous member of the family: Alzheimer’s disease (AD). As opposed to other of its kind, the neurofibrillary tangles (NFTs) are spread in the form of irregular, perivascular, patchy disseminations throughout frontal and temporal cortex, especially in the superficial cerebral layers, leaning for sulcal depths. The previously mentioned characteristics constitute the hallmark signature of CTE. Although the connection between repeated concussions and CTE has been recently proposed, the startup path is still a mysterious topic. It remains, up to a point, common to all tauopathies, yet overpasses all genders, sex and age. Initially, considered a professional disease in boxing, scientific overviews link CTE to military service, sports and even daily activities. It is a consensus that a moderate traumatic event sustained during life-spam was correlated with 2.3 fold increase in the risk of developing dementia, while severe concussion augments up 4 times the chances. By the same token, considering the broad population with potential exposure to repetitive insults, CTE represents an important public health issue. The main purpose of this scientific article is to highlight the neuropathological features encountered and discuss the limitations of proper diagnostic. © 2016 Romanian Society of Legal Medicine.},
keywords = {Chronic traumatic encephalopathy, Forensic pathology, NEURODEGENERATION, Trauma},
pubstate = {published},
tppubtype = {article}
}
Caron, A M; Stephenson, R
Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat Journal Article
In: Nature and Science of Sleep, vol. 7, pp. 63–72, 2015.
Abstract | Links | BibTeX | Tags: Concussion, Dark neuron, NEURODEGENERATION, Rat cortex, sleep deprivation, traumatic brain injury
@article{Caron2015b,
title = {Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat},
author = {Caron, A M and Stephenson, R},
doi = {10.2147/NSS.S82888},
year = {2015},
date = {2015-01-01},
journal = {Nature and Science of Sleep},
volume = {7},
pages = {63--72},
abstract = {Mild and moderate traumatic brain injuries (TBIs) (and concussion) occur frequently as a result of falls, automobile accidents, and sporting activities, and are a major cause of acute and chronic disability. Fatigue and excessive sleepiness are associated with increased risk of accidents, but it is unknown whether prior sleep debt also affects the pathophysiological outcome of concussive injury. Using the "dark neuron" (DN) as a marker of reversible neuronal damage, we tested the hypothesis that acute (48 hours) total sleep deprivation (TSD) and chronic sleep restriction (CSR; 10 days, 6-hour sleep/day) affect DN formation following mild TBI in the rat. TSD and CSR were administered using a walking wheel apparatus. Mild TBI was administered under anesthesia using a weight-drop impact model, and the acute neuronal response was observed without recovery. DNs were detected using standard bright-field microscopy with toluidine blue stain following appropriate tissue fixation. DN density was low under home cage and sleep deprivation control conditions (respective median DN densities, 0.14% and 0.22% of neurons), and this was unaffected by TSD alone (0.1%). Mild TBI caused significantly higher DN densities (0.76%), and this was unchanged by preexisting acute or chronic sleep debt (TSD, 0.23%; CSR, 0.7%). Thus, although sleep debt may be predicted to increase the incidence of concussive injury, the present data suggest that sleep debt does not exacerbate the resulting neuronal damage. © 2015 Caron and Stephenson.},
keywords = {Concussion, Dark neuron, NEURODEGENERATION, Rat cortex, sleep deprivation, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}
Chiroban, O; Perju-Dumbravă, L
Postmortem evaluation of chronic traumatic encephalopathy Journal Article
In: Romanian Journal of Legal Medicine, vol. 24, no. 4, pp. 266–272, 2016.
@article{Chiroban2016,
title = {Postmortem evaluation of chronic traumatic encephalopathy},
author = {Chiroban, O and Perju-Dumbrav\u{a}, L},
doi = {10.4323/rjlm.2016.266},
year = {2016},
date = {2016-01-01},
journal = {Romanian Journal of Legal Medicine},
volume = {24},
number = {4},
pages = {266--272},
abstract = {Chronic traumatic encephalopathy (CTE) is the modern concept naming the neurodegenerative processes occurring in patients with positive medical history of repeated brain trauma and progressive dementia. Morphologically, CTE is classified as being a distinct member of the tauopathies family, with different distribution of tau-positive neurofibrillary tangles (NFTs) and low to none beta-amyloid deposits, contrasting the most famous member of the family: Alzheimer’s disease (AD). As opposed to other of its kind, the neurofibrillary tangles (NFTs) are spread in the form of irregular, perivascular, patchy disseminations throughout frontal and temporal cortex, especially in the superficial cerebral layers, leaning for sulcal depths. The previously mentioned characteristics constitute the hallmark signature of CTE. Although the connection between repeated concussions and CTE has been recently proposed, the startup path is still a mysterious topic. It remains, up to a point, common to all tauopathies, yet overpasses all genders, sex and age. Initially, considered a professional disease in boxing, scientific overviews link CTE to military service, sports and even daily activities. It is a consensus that a moderate traumatic event sustained during life-spam was correlated with 2.3 fold increase in the risk of developing dementia, while severe concussion augments up 4 times the chances. By the same token, considering the broad population with potential exposure to repetitive insults, CTE represents an important public health issue. The main purpose of this scientific article is to highlight the neuropathological features encountered and discuss the limitations of proper diagnostic. © 2016 Romanian Society of Legal Medicine.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Caron, A M; Stephenson, R
Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat Journal Article
In: Nature and Science of Sleep, vol. 7, pp. 63–72, 2015.
@article{Caron2015b,
title = {Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat},
author = {Caron, A M and Stephenson, R},
doi = {10.2147/NSS.S82888},
year = {2015},
date = {2015-01-01},
journal = {Nature and Science of Sleep},
volume = {7},
pages = {63--72},
abstract = {Mild and moderate traumatic brain injuries (TBIs) (and concussion) occur frequently as a result of falls, automobile accidents, and sporting activities, and are a major cause of acute and chronic disability. Fatigue and excessive sleepiness are associated with increased risk of accidents, but it is unknown whether prior sleep debt also affects the pathophysiological outcome of concussive injury. Using the "dark neuron" (DN) as a marker of reversible neuronal damage, we tested the hypothesis that acute (48 hours) total sleep deprivation (TSD) and chronic sleep restriction (CSR; 10 days, 6-hour sleep/day) affect DN formation following mild TBI in the rat. TSD and CSR were administered using a walking wheel apparatus. Mild TBI was administered under anesthesia using a weight-drop impact model, and the acute neuronal response was observed without recovery. DNs were detected using standard bright-field microscopy with toluidine blue stain following appropriate tissue fixation. DN density was low under home cage and sleep deprivation control conditions (respective median DN densities, 0.14% and 0.22% of neurons), and this was unaffected by TSD alone (0.1%). Mild TBI caused significantly higher DN densities (0.76%), and this was unchanged by preexisting acute or chronic sleep debt (TSD, 0.23%; CSR, 0.7%). Thus, although sleep debt may be predicted to increase the incidence of concussive injury, the present data suggest that sleep debt does not exacerbate the resulting neuronal damage. © 2015 Caron and Stephenson.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Chiroban, O; Perju-Dumbravă, L
Postmortem evaluation of chronic traumatic encephalopathy Journal Article
In: Romanian Journal of Legal Medicine, vol. 24, no. 4, pp. 266–272, 2016.
Abstract | Links | BibTeX | Tags: Chronic traumatic encephalopathy, Forensic pathology, NEURODEGENERATION, Trauma
@article{Chiroban2016,
title = {Postmortem evaluation of chronic traumatic encephalopathy},
author = {Chiroban, O and Perju-Dumbrav\u{a}, L},
doi = {10.4323/rjlm.2016.266},
year = {2016},
date = {2016-01-01},
journal = {Romanian Journal of Legal Medicine},
volume = {24},
number = {4},
pages = {266--272},
abstract = {Chronic traumatic encephalopathy (CTE) is the modern concept naming the neurodegenerative processes occurring in patients with positive medical history of repeated brain trauma and progressive dementia. Morphologically, CTE is classified as being a distinct member of the tauopathies family, with different distribution of tau-positive neurofibrillary tangles (NFTs) and low to none beta-amyloid deposits, contrasting the most famous member of the family: Alzheimer’s disease (AD). As opposed to other of its kind, the neurofibrillary tangles (NFTs) are spread in the form of irregular, perivascular, patchy disseminations throughout frontal and temporal cortex, especially in the superficial cerebral layers, leaning for sulcal depths. The previously mentioned characteristics constitute the hallmark signature of CTE. Although the connection between repeated concussions and CTE has been recently proposed, the startup path is still a mysterious topic. It remains, up to a point, common to all tauopathies, yet overpasses all genders, sex and age. Initially, considered a professional disease in boxing, scientific overviews link CTE to military service, sports and even daily activities. It is a consensus that a moderate traumatic event sustained during life-spam was correlated with 2.3 fold increase in the risk of developing dementia, while severe concussion augments up 4 times the chances. By the same token, considering the broad population with potential exposure to repetitive insults, CTE represents an important public health issue. The main purpose of this scientific article is to highlight the neuropathological features encountered and discuss the limitations of proper diagnostic. © 2016 Romanian Society of Legal Medicine.},
keywords = {Chronic traumatic encephalopathy, Forensic pathology, NEURODEGENERATION, Trauma},
pubstate = {published},
tppubtype = {article}
}
Caron, A M; Stephenson, R
Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat Journal Article
In: Nature and Science of Sleep, vol. 7, pp. 63–72, 2015.
Abstract | Links | BibTeX | Tags: Concussion, Dark neuron, NEURODEGENERATION, Rat cortex, sleep deprivation, traumatic brain injury
@article{Caron2015b,
title = {Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat},
author = {Caron, A M and Stephenson, R},
doi = {10.2147/NSS.S82888},
year = {2015},
date = {2015-01-01},
journal = {Nature and Science of Sleep},
volume = {7},
pages = {63--72},
abstract = {Mild and moderate traumatic brain injuries (TBIs) (and concussion) occur frequently as a result of falls, automobile accidents, and sporting activities, and are a major cause of acute and chronic disability. Fatigue and excessive sleepiness are associated with increased risk of accidents, but it is unknown whether prior sleep debt also affects the pathophysiological outcome of concussive injury. Using the "dark neuron" (DN) as a marker of reversible neuronal damage, we tested the hypothesis that acute (48 hours) total sleep deprivation (TSD) and chronic sleep restriction (CSR; 10 days, 6-hour sleep/day) affect DN formation following mild TBI in the rat. TSD and CSR were administered using a walking wheel apparatus. Mild TBI was administered under anesthesia using a weight-drop impact model, and the acute neuronal response was observed without recovery. DNs were detected using standard bright-field microscopy with toluidine blue stain following appropriate tissue fixation. DN density was low under home cage and sleep deprivation control conditions (respective median DN densities, 0.14% and 0.22% of neurons), and this was unaffected by TSD alone (0.1%). Mild TBI caused significantly higher DN densities (0.76%), and this was unchanged by preexisting acute or chronic sleep debt (TSD, 0.23%; CSR, 0.7%). Thus, although sleep debt may be predicted to increase the incidence of concussive injury, the present data suggest that sleep debt does not exacerbate the resulting neuronal damage. © 2015 Caron and Stephenson.},
keywords = {Concussion, Dark neuron, NEURODEGENERATION, Rat cortex, sleep deprivation, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}