Mollayeva, T; Mollayeva, S; Colantonio, A
The Risk of Sleep Disorder Among Persons with Mild Traumatic Brain Injury Journal Article
In: Current Neurology & Neuroscience Reports, vol. 16, no. 6, pp. 55, 2016.
Abstract | BibTeX | Tags: *Brain Concussion/co [Complications], *Sleep Wake Disorders/et [Etiology], Animals, Brain Concussion/pa [Pathology], Brain/pa [Pathology], Humans, Risk Factors, Sleep Wake Disorders/ge [Genetics], wakefulness
@article{Mollayeva2016,
title = {The Risk of Sleep Disorder Among Persons with Mild Traumatic Brain Injury},
author = {Mollayeva, T and Mollayeva, S and Colantonio, A},
year = {2016},
date = {2016-01-01},
journal = {Current Neurology \& Neuroscience Reports},
volume = {16},
number = {6},
pages = {55},
abstract = {Sleep disorders and mild traumatic brain injury (mTBI) are among the most commonly occurring neurological problems clinicians encounter simultaneously. Each can cause the other, and both share common predisposing factors. An important question that remains to be addressed is whether high-risk groups can be defined. We observed an accumulation of considerable knowledge on sleep dysfunction in mTBI in recently published works. The results highlight sleep disturbances in mTBI as the product of diverse internal and external influences, acting on a genetically determined substrate. This may partially explain the clinical heterogeneity of mTBI, pointing to the importance of establishing an accurate history on the onset and course of a specific sleep disorder in the early stages post-mTBI in the individual patient. Such an approach will aid not only diagnosis and treatment but may also lead to identification of disorders whose symptoms mimic those of TBI and thereby direct the most suitable treatment and management.},
keywords = {*Brain Concussion/co [Complications], *Sleep Wake Disorders/et [Etiology], Animals, Brain Concussion/pa [Pathology], Brain/pa [Pathology], Humans, Risk Factors, Sleep Wake Disorders/ge [Genetics], wakefulness},
pubstate = {published},
tppubtype = {article}
}
Puvenna, V; Engeler, M; Banjara, M; Brennan, C; Schreiber, P; Dadas, A; Bahrami, A; Solanki, J; Bandyopadhyay, A; Morris, J K; Bernick, C; Ghosh, C; Rapp, E; Bazarian, J J; Janigro, D
Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy Journal Article
In: Brain Research, vol. 1630, pp. 225–240, 2016.
Abstract | BibTeX | Tags: *Brain Injury, *Brain/me [Metabolism], *Epilepsy/me [Metabolism], *tau Proteins/me [Metabolism], 0 (MAPT protein, 0 (tau Proteins), 80 and over, Adolescent, adult, aged, Brain Injury, Brain/pa [Pathology], Brain/su [Surgery], Child, Chronic/me [Metabolism], Chronic/pa [Pathology], ENZYME-linked immunosorbent assay, Epilepsy/pa [Pathology], Epilepsy/su [Surgery], Female, human), Humans, immunohistochemistry, Infant, Male, middle aged, Phosphorylation, Preschool, Young Adult
@article{Puvenna2016,
title = {Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy},
author = {Puvenna, V and Engeler, M and Banjara, M and Brennan, C and Schreiber, P and Dadas, A and Bahrami, A and Solanki, J and Bandyopadhyay, A and Morris, J K and Bernick, C and Ghosh, C and Rapp, E and Bazarian, J J and Janigro, D},
year = {2016},
date = {2016-01-01},
journal = {Brain Research},
volume = {1630},
pages = {225--240},
abstract = {Repetitive traumatic brain injury (rTBI) is one of the major risk factors for the abnormal deposition of phosphorylated tau (PT) in the brain and chronic traumatic encephalopathy (CTE). CTE and temporal lobe epilepsy (TLE) affect the limbic system, but no comparative studies on PT distribution in TLE and CTE are available. It is also unclear whether PT pathology results from repeated head hits (rTBI). These gaps prevent a thorough understanding of the pathogenesis and clinical significance of PT, limiting our ability to develop preventative and therapeutic interventions. We quantified PT in TLE and CTE to unveil whether a history of rTBI is a prerequisite for PT accumulation in the brain. Six postmortem CTE (mean 73.3 years) and age matched control samples were compared to 19 surgically resected TLE brain specimens (4 months-58 years; mean 27.6 years). No history of TBI was present in TLE or control; all CTE patients had a history of rTBI. TLE and CTE brain displayed increased levels of PT as revealed by immunohistochemistry. No age-dependent changes were noted, as PT was present as early as 4 months after birth. In TLE and CTE, cortical neurons, perivascular regions around penetrating pial vessels and meninges were immunopositive for PT; white matter tracts also displayed robust expression of extracellular PT organized in bundles parallel to venules. Microscopically, there were extensive tau-immunoreactive neuronal, astrocytic and degenerating neurites throughout the brain. In CTE perivascular tangles were most prominent. Overall, significant differences in staining intensities were found between CTE and control (P\<0.01) but not between CTE and TLE (P=0.08). pS199 tau analysis showed that CTE had the most high molecular weight tangle-associated tau, whereas epileptic brain contained low molecular weight tau. Tau deposition may not be specific to rTBI since TLE recapitulated most of the pathological features of CTE. Copyright © 2015 Elsevier B.V. All rights reserved.},
keywords = {*Brain Injury, *Brain/me [Metabolism], *Epilepsy/me [Metabolism], *tau Proteins/me [Metabolism], 0 (MAPT protein, 0 (tau Proteins), 80 and over, Adolescent, adult, aged, Brain Injury, Brain/pa [Pathology], Brain/su [Surgery], Child, Chronic/me [Metabolism], Chronic/pa [Pathology], ENZYME-linked immunosorbent assay, Epilepsy/pa [Pathology], Epilepsy/su [Surgery], Female, human), Humans, immunohistochemistry, Infant, Male, middle aged, Phosphorylation, Preschool, Young Adult},
pubstate = {published},
tppubtype = {article}
}
Davis, A E
Mechanisms of traumatic brain injury: biomechanical, structural and cellular considerations Journal Article
In: Critical Care Nursing Quarterly, vol. 23, no. 3, pp. 1–13, 2000.
Abstract | BibTeX | Tags: *Brain Injuries/pa [Pathology], *Brain Injuries/pp [Physiopathology], Biomechanical Phenomena, Brain Injuries/cl [Classification], Brain Injuries/co [Complications], Brain/me [Metabolism], Brain/pa [Pathology], Humans, intracranial hemorrhage, Neurons/me [Metabolism], Neurons/pa [Pathology], Nonpenetrating/pa [Pathology], Nonpenetrating/pp [Physiopathology], Skull Fractures/pa [Pathology], Skull Fractures/pp [Physiopathology], Traumatic/pa [Pathology], Traumatic/pp [Physiopatho, Wounds
@article{Davis2000,
title = {Mechanisms of traumatic brain injury: biomechanical, structural and cellular considerations},
author = {Davis, A E},
year = {2000},
date = {2000-01-01},
journal = {Critical Care Nursing Quarterly},
volume = {23},
number = {3},
pages = {1--13},
abstract = {Traumatic brain injury (TBI) is a public health problem of great concern, because it affects more than 2 million individuals each year. TBI occurs as a result of motor vehicle crashes, falls, and sports-related events. Biomechanical mechanisms occurring at the time of the injury initiate primary and secondary injuries that evolve over several days. In this article the relationship between an blunt injury event and the subsequent damage produced is addressed. Mechanisms of brain injury from biomechanics to cellular pathobiology are presented. Primary and secondary injuries are differentiated, and specific focal and diffuse clinical syndromes are described. Cellular mechanisms responsible for injury are also addressed, because they provide the unifying concepts across the many clinical syndromes so often discussed separately in reviews of traumatic brain injury. [References: 26]},
keywords = {*Brain Injuries/pa [Pathology], *Brain Injuries/pp [Physiopathology], Biomechanical Phenomena, Brain Injuries/cl [Classification], Brain Injuries/co [Complications], Brain/me [Metabolism], Brain/pa [Pathology], Humans, intracranial hemorrhage, Neurons/me [Metabolism], Neurons/pa [Pathology], Nonpenetrating/pa [Pathology], Nonpenetrating/pp [Physiopathology], Skull Fractures/pa [Pathology], Skull Fractures/pp [Physiopathology], Traumatic/pa [Pathology], Traumatic/pp [Physiopatho, Wounds},
pubstate = {published},
tppubtype = {article}
}
Mollayeva, T; Mollayeva, S; Colantonio, A
The Risk of Sleep Disorder Among Persons with Mild Traumatic Brain Injury Journal Article
In: Current Neurology & Neuroscience Reports, vol. 16, no. 6, pp. 55, 2016.
@article{Mollayeva2016,
title = {The Risk of Sleep Disorder Among Persons with Mild Traumatic Brain Injury},
author = {Mollayeva, T and Mollayeva, S and Colantonio, A},
year = {2016},
date = {2016-01-01},
journal = {Current Neurology \& Neuroscience Reports},
volume = {16},
number = {6},
pages = {55},
abstract = {Sleep disorders and mild traumatic brain injury (mTBI) are among the most commonly occurring neurological problems clinicians encounter simultaneously. Each can cause the other, and both share common predisposing factors. An important question that remains to be addressed is whether high-risk groups can be defined. We observed an accumulation of considerable knowledge on sleep dysfunction in mTBI in recently published works. The results highlight sleep disturbances in mTBI as the product of diverse internal and external influences, acting on a genetically determined substrate. This may partially explain the clinical heterogeneity of mTBI, pointing to the importance of establishing an accurate history on the onset and course of a specific sleep disorder in the early stages post-mTBI in the individual patient. Such an approach will aid not only diagnosis and treatment but may also lead to identification of disorders whose symptoms mimic those of TBI and thereby direct the most suitable treatment and management.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Puvenna, V; Engeler, M; Banjara, M; Brennan, C; Schreiber, P; Dadas, A; Bahrami, A; Solanki, J; Bandyopadhyay, A; Morris, J K; Bernick, C; Ghosh, C; Rapp, E; Bazarian, J J; Janigro, D
Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy Journal Article
In: Brain Research, vol. 1630, pp. 225–240, 2016.
@article{Puvenna2016,
title = {Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy},
author = {Puvenna, V and Engeler, M and Banjara, M and Brennan, C and Schreiber, P and Dadas, A and Bahrami, A and Solanki, J and Bandyopadhyay, A and Morris, J K and Bernick, C and Ghosh, C and Rapp, E and Bazarian, J J and Janigro, D},
year = {2016},
date = {2016-01-01},
journal = {Brain Research},
volume = {1630},
pages = {225--240},
abstract = {Repetitive traumatic brain injury (rTBI) is one of the major risk factors for the abnormal deposition of phosphorylated tau (PT) in the brain and chronic traumatic encephalopathy (CTE). CTE and temporal lobe epilepsy (TLE) affect the limbic system, but no comparative studies on PT distribution in TLE and CTE are available. It is also unclear whether PT pathology results from repeated head hits (rTBI). These gaps prevent a thorough understanding of the pathogenesis and clinical significance of PT, limiting our ability to develop preventative and therapeutic interventions. We quantified PT in TLE and CTE to unveil whether a history of rTBI is a prerequisite for PT accumulation in the brain. Six postmortem CTE (mean 73.3 years) and age matched control samples were compared to 19 surgically resected TLE brain specimens (4 months-58 years; mean 27.6 years). No history of TBI was present in TLE or control; all CTE patients had a history of rTBI. TLE and CTE brain displayed increased levels of PT as revealed by immunohistochemistry. No age-dependent changes were noted, as PT was present as early as 4 months after birth. In TLE and CTE, cortical neurons, perivascular regions around penetrating pial vessels and meninges were immunopositive for PT; white matter tracts also displayed robust expression of extracellular PT organized in bundles parallel to venules. Microscopically, there were extensive tau-immunoreactive neuronal, astrocytic and degenerating neurites throughout the brain. In CTE perivascular tangles were most prominent. Overall, significant differences in staining intensities were found between CTE and control (P\<0.01) but not between CTE and TLE (P=0.08). pS199 tau analysis showed that CTE had the most high molecular weight tangle-associated tau, whereas epileptic brain contained low molecular weight tau. Tau deposition may not be specific to rTBI since TLE recapitulated most of the pathological features of CTE. Copyright © 2015 Elsevier B.V. All rights reserved.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Davis, A E
Mechanisms of traumatic brain injury: biomechanical, structural and cellular considerations Journal Article
In: Critical Care Nursing Quarterly, vol. 23, no. 3, pp. 1–13, 2000.
@article{Davis2000,
title = {Mechanisms of traumatic brain injury: biomechanical, structural and cellular considerations},
author = {Davis, A E},
year = {2000},
date = {2000-01-01},
journal = {Critical Care Nursing Quarterly},
volume = {23},
number = {3},
pages = {1--13},
abstract = {Traumatic brain injury (TBI) is a public health problem of great concern, because it affects more than 2 million individuals each year. TBI occurs as a result of motor vehicle crashes, falls, and sports-related events. Biomechanical mechanisms occurring at the time of the injury initiate primary and secondary injuries that evolve over several days. In this article the relationship between an blunt injury event and the subsequent damage produced is addressed. Mechanisms of brain injury from biomechanics to cellular pathobiology are presented. Primary and secondary injuries are differentiated, and specific focal and diffuse clinical syndromes are described. Cellular mechanisms responsible for injury are also addressed, because they provide the unifying concepts across the many clinical syndromes so often discussed separately in reviews of traumatic brain injury. [References: 26]},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Mollayeva, T; Mollayeva, S; Colantonio, A
The Risk of Sleep Disorder Among Persons with Mild Traumatic Brain Injury Journal Article
In: Current Neurology & Neuroscience Reports, vol. 16, no. 6, pp. 55, 2016.
Abstract | BibTeX | Tags: *Brain Concussion/co [Complications], *Sleep Wake Disorders/et [Etiology], Animals, Brain Concussion/pa [Pathology], Brain/pa [Pathology], Humans, Risk Factors, Sleep Wake Disorders/ge [Genetics], wakefulness
@article{Mollayeva2016,
title = {The Risk of Sleep Disorder Among Persons with Mild Traumatic Brain Injury},
author = {Mollayeva, T and Mollayeva, S and Colantonio, A},
year = {2016},
date = {2016-01-01},
journal = {Current Neurology \& Neuroscience Reports},
volume = {16},
number = {6},
pages = {55},
abstract = {Sleep disorders and mild traumatic brain injury (mTBI) are among the most commonly occurring neurological problems clinicians encounter simultaneously. Each can cause the other, and both share common predisposing factors. An important question that remains to be addressed is whether high-risk groups can be defined. We observed an accumulation of considerable knowledge on sleep dysfunction in mTBI in recently published works. The results highlight sleep disturbances in mTBI as the product of diverse internal and external influences, acting on a genetically determined substrate. This may partially explain the clinical heterogeneity of mTBI, pointing to the importance of establishing an accurate history on the onset and course of a specific sleep disorder in the early stages post-mTBI in the individual patient. Such an approach will aid not only diagnosis and treatment but may also lead to identification of disorders whose symptoms mimic those of TBI and thereby direct the most suitable treatment and management.},
keywords = {*Brain Concussion/co [Complications], *Sleep Wake Disorders/et [Etiology], Animals, Brain Concussion/pa [Pathology], Brain/pa [Pathology], Humans, Risk Factors, Sleep Wake Disorders/ge [Genetics], wakefulness},
pubstate = {published},
tppubtype = {article}
}
Puvenna, V; Engeler, M; Banjara, M; Brennan, C; Schreiber, P; Dadas, A; Bahrami, A; Solanki, J; Bandyopadhyay, A; Morris, J K; Bernick, C; Ghosh, C; Rapp, E; Bazarian, J J; Janigro, D
Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy Journal Article
In: Brain Research, vol. 1630, pp. 225–240, 2016.
Abstract | BibTeX | Tags: *Brain Injury, *Brain/me [Metabolism], *Epilepsy/me [Metabolism], *tau Proteins/me [Metabolism], 0 (MAPT protein, 0 (tau Proteins), 80 and over, Adolescent, adult, aged, Brain Injury, Brain/pa [Pathology], Brain/su [Surgery], Child, Chronic/me [Metabolism], Chronic/pa [Pathology], ENZYME-linked immunosorbent assay, Epilepsy/pa [Pathology], Epilepsy/su [Surgery], Female, human), Humans, immunohistochemistry, Infant, Male, middle aged, Phosphorylation, Preschool, Young Adult
@article{Puvenna2016,
title = {Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy},
author = {Puvenna, V and Engeler, M and Banjara, M and Brennan, C and Schreiber, P and Dadas, A and Bahrami, A and Solanki, J and Bandyopadhyay, A and Morris, J K and Bernick, C and Ghosh, C and Rapp, E and Bazarian, J J and Janigro, D},
year = {2016},
date = {2016-01-01},
journal = {Brain Research},
volume = {1630},
pages = {225--240},
abstract = {Repetitive traumatic brain injury (rTBI) is one of the major risk factors for the abnormal deposition of phosphorylated tau (PT) in the brain and chronic traumatic encephalopathy (CTE). CTE and temporal lobe epilepsy (TLE) affect the limbic system, but no comparative studies on PT distribution in TLE and CTE are available. It is also unclear whether PT pathology results from repeated head hits (rTBI). These gaps prevent a thorough understanding of the pathogenesis and clinical significance of PT, limiting our ability to develop preventative and therapeutic interventions. We quantified PT in TLE and CTE to unveil whether a history of rTBI is a prerequisite for PT accumulation in the brain. Six postmortem CTE (mean 73.3 years) and age matched control samples were compared to 19 surgically resected TLE brain specimens (4 months-58 years; mean 27.6 years). No history of TBI was present in TLE or control; all CTE patients had a history of rTBI. TLE and CTE brain displayed increased levels of PT as revealed by immunohistochemistry. No age-dependent changes were noted, as PT was present as early as 4 months after birth. In TLE and CTE, cortical neurons, perivascular regions around penetrating pial vessels and meninges were immunopositive for PT; white matter tracts also displayed robust expression of extracellular PT organized in bundles parallel to venules. Microscopically, there were extensive tau-immunoreactive neuronal, astrocytic and degenerating neurites throughout the brain. In CTE perivascular tangles were most prominent. Overall, significant differences in staining intensities were found between CTE and control (P\<0.01) but not between CTE and TLE (P=0.08). pS199 tau analysis showed that CTE had the most high molecular weight tangle-associated tau, whereas epileptic brain contained low molecular weight tau. Tau deposition may not be specific to rTBI since TLE recapitulated most of the pathological features of CTE. Copyright © 2015 Elsevier B.V. All rights reserved.},
keywords = {*Brain Injury, *Brain/me [Metabolism], *Epilepsy/me [Metabolism], *tau Proteins/me [Metabolism], 0 (MAPT protein, 0 (tau Proteins), 80 and over, Adolescent, adult, aged, Brain Injury, Brain/pa [Pathology], Brain/su [Surgery], Child, Chronic/me [Metabolism], Chronic/pa [Pathology], ENZYME-linked immunosorbent assay, Epilepsy/pa [Pathology], Epilepsy/su [Surgery], Female, human), Humans, immunohistochemistry, Infant, Male, middle aged, Phosphorylation, Preschool, Young Adult},
pubstate = {published},
tppubtype = {article}
}
Davis, A E
Mechanisms of traumatic brain injury: biomechanical, structural and cellular considerations Journal Article
In: Critical Care Nursing Quarterly, vol. 23, no. 3, pp. 1–13, 2000.
Abstract | BibTeX | Tags: *Brain Injuries/pa [Pathology], *Brain Injuries/pp [Physiopathology], Biomechanical Phenomena, Brain Injuries/cl [Classification], Brain Injuries/co [Complications], Brain/me [Metabolism], Brain/pa [Pathology], Humans, intracranial hemorrhage, Neurons/me [Metabolism], Neurons/pa [Pathology], Nonpenetrating/pa [Pathology], Nonpenetrating/pp [Physiopathology], Skull Fractures/pa [Pathology], Skull Fractures/pp [Physiopathology], Traumatic/pa [Pathology], Traumatic/pp [Physiopatho, Wounds
@article{Davis2000,
title = {Mechanisms of traumatic brain injury: biomechanical, structural and cellular considerations},
author = {Davis, A E},
year = {2000},
date = {2000-01-01},
journal = {Critical Care Nursing Quarterly},
volume = {23},
number = {3},
pages = {1--13},
abstract = {Traumatic brain injury (TBI) is a public health problem of great concern, because it affects more than 2 million individuals each year. TBI occurs as a result of motor vehicle crashes, falls, and sports-related events. Biomechanical mechanisms occurring at the time of the injury initiate primary and secondary injuries that evolve over several days. In this article the relationship between an blunt injury event and the subsequent damage produced is addressed. Mechanisms of brain injury from biomechanics to cellular pathobiology are presented. Primary and secondary injuries are differentiated, and specific focal and diffuse clinical syndromes are described. Cellular mechanisms responsible for injury are also addressed, because they provide the unifying concepts across the many clinical syndromes so often discussed separately in reviews of traumatic brain injury. [References: 26]},
keywords = {*Brain Injuries/pa [Pathology], *Brain Injuries/pp [Physiopathology], Biomechanical Phenomena, Brain Injuries/cl [Classification], Brain Injuries/co [Complications], Brain/me [Metabolism], Brain/pa [Pathology], Humans, intracranial hemorrhage, Neurons/me [Metabolism], Neurons/pa [Pathology], Nonpenetrating/pa [Pathology], Nonpenetrating/pp [Physiopathology], Skull Fractures/pa [Pathology], Skull Fractures/pp [Physiopathology], Traumatic/pa [Pathology], Traumatic/pp [Physiopatho, Wounds},
pubstate = {published},
tppubtype = {article}
}