Papa, L; Ramia, M M; Edwards, D; Johnson, B D; Slobounov, S M
Systematic review of clinical studies examining biomarkers of brain injury in athletes after sports-related concussion Journal Article
In: Journal of Neurotrauma, vol. 32, pp. 661–673, 2015.
Abstract | BibTeX | Tags: Physiopathology
@article{Papa2015,
title = {Systematic review of clinical studies examining biomarkers of brain injury in athletes after sports-related concussion},
author = {Papa, L and Ramia, M M and Edwards, D and Johnson, B D and Slobounov, S M},
year = {2015},
date = {2015-01-01},
journal = {Journal of Neurotrauma},
volume = {32},
pages = {661--673},
address = {Papa,Linda. 1 Department of Emergency Medicine, Orlando Regional Medical Center , Orlando, Florida.},
abstract = {The aim of this study was to systematically review clinical studies examining biofluid biomarkers of brain injury for concussion in athletes. Data sources included PubMed, MEDLINE, and the Cochrane Database from 1966 to October 2013. Studies were included if they recruited athletes participating in organized sports who experienced concussion or head injury during a sports-related activity and had brain injury biomarkers measured. Acceptable research designs included experimental, observational, and case-control studies. Review articles, opinion papers, and editorials were excluded. After title and abstract screening of potential articles, full texts were independently reviewed to identify articles that met inclusion criteria. A composite evidentiary table was then constructed and documented the study title, design, population, methods, sample size, outcome measures, and results. The search identified 52 publications, of which 13 were selected and critically reviewed. All of the included studies were prospective and were published either in or after the year 2000. Sports included boxing (six studies), soccer (five studies), running/jogging (two studies), hockey (one study), basketball (one study), cycling (one study), and swimming (one study). The majority of studies (92%) had fewer than 100 patients. Three studies (23%) evaluated biomarkers in cerebrospinal fluid (CSF), one in both serum and CSF, and 10 (77%) in serum exclusively. There were 11 different biomarkers assessed, including S100beta, glial fibrillary acidic protein, neuron-specific enolase, tau, neurofilament light protein, amyloid beta, brain-derived neurotrophic factor, creatine kinase and heart-type fatty acid binding protein, prolactin, cortisol, and albumin. A handful of biomarkers showed a correlation with number of hits to the head (soccer), acceleration/deceleration forces (jumps, collisions, and falls), postconcussive symptoms, trauma to the body versus the head, and dynamics of different sports. Although there are no validated biomarkers for concussion as yet, there is potential for biomarkers to provide diagnostic, prognostic, and monitoring information postinjury. They could also be combined with neuroimaging to assess injury evolution and recovery.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
McKee, A C; Daneshvar, D H
The neuropathology of traumatic brain injury Journal Article
In: Handbook of Clinical Neurology, vol. 127, pp. 45–66, 2015.
Abstract | BibTeX | Tags: Physiopathology
@article{McKee2015,
title = {The neuropathology of traumatic brain injury},
author = {McKee, A C and Daneshvar, D H},
year = {2015},
date = {2015-01-01},
journal = {Handbook of Clinical Neurology},
volume = {127},
pages = {45--66},
address = {Mckee,Ann C. VA Boston HealthCare System; Center for the Study of Traumatic Encephalopathy, Alzheimer's Disease Center, and Departments of Neurology and Pathology, Boston University School of Medicine, Boston, MA, USA. Electronic address: amckee@bu.edu. D},
abstract = {Traumatic brain injury, a leading cause of mortality and morbidity, is divided into three grades of severity: mild, moderate, and severe, based on the Glasgow Coma Scale, the loss of consciousness, and the development of post-traumatic amnesia. Although mild traumatic brain injury, including concussion and subconcussion, is by far the most common, it is also the most difficult to diagnose and the least well understood. Proper recognition, management, and treatment of acute concussion and mild traumatic brain injury are the fundamentals of an emerging clinical discipline. It is also becoming increasingly clear that some mild traumatic brain injuries have persistent, and sometimes progressive, long-term debilitating effects. Evidence indicates that a single traumatic brain injury can precipitate or accelerate multiple age-related neurodegenerations, increase the risk of developing Alzheimer's disease, Parkinson's disease, and motor neuron disease, and that repetitive mild traumatic brain injuries can provoke the development of a tauopathy, chronic traumatic encephalopathy. Clinically, chronic traumatic encephalopathy is associated with behavioral changes, executive dysfunction, memory loss, and cognitive impairments that begin insidiously and progress slowly over decades. Pathologically, chronic traumatic encephalopathy produces atrophy of the frontal and temporal lobes, thalamus, and hypothalamus, septal abnormalities, and abnormal deposits of hyperphosphorylated tau (tau) as neurofibrillary tangles and disordered neurites throughout the brain. The incidence and prevalence of chronic traumatic encephalopathy and the genetic risk factors critical to its development are currently unknown. Chronic traumatic encephalopathy frequently occurs as a sole diagnosis, but may be associated with other neurodegenerative disorders, including Alzheimer's disease, Lewy body disease, and motor neuron disease. Currently, chronic traumatic encephalopathy can be diagnosed only at autopsy; however, promising efforts to develop imaging, spinal fluid, and peripheral blood biomarkers are underway to diagnose and monitor the course of disease in living subjects.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Pham, N; Akonasu, H; Shishkin, R; Taghibiglou, C
Plasma soluble prion protein, a potential biomarker for sport-related concussions: a pilot study Journal Article
In: PLoS ONE, vol. 10, pp. e0117286, 2015.
Abstract | BibTeX | Tags: Physiopathology
@article{Pham2015b,
title = {Plasma soluble prion protein, a potential biomarker for sport-related concussions: a pilot study},
author = {Pham, N and Akonasu, H and Shishkin, R and Taghibiglou, C},
year = {2015},
date = {2015-01-01},
journal = {PLoS ONE},
volume = {10},
pages = {e0117286},
address = {Pham,Nam. Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Canada. Akonasu,Hungbo. Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Canada. Shishkin,Rhonda. College of Kinesiolo},
abstract = {Sport-related mild traumatic brain injury (mTBI) or concussion is a significant health concern to athletes with potential long-term consequences. The diagnosis of sport concussion and return to sport decision making is one of the greatest challenges facing health care clinicians working in sports. Blood biomarkers have recently demonstrated their potential in assisting the detection of brain injury particularly, in those cases with no obvious physical injury. We have recently discovered plasma soluble cellular prion protein (PrP(C)) as a potential reliable biomarker for blast induced TBI (bTBI) in a rodent animal model. In order to explore the application of this novel TBI biomarker to sport-related concussion, we conducted a pilot study at the University of Saskatchewan (U of S) by recruiting athlete and non-athlete 18 to 30 year-old students. Using a modified quantitative ELISA method, we first established normal values for the plasma soluble PrP(C) in male and female students. The measured plasma soluble PrP(C) in confirmed concussion cases demonstrated a significant elevation of this analyte in post-concussion samples. Data collected from our pilot study indicates that the plasma soluble PrP(C) is a potential biomarker for sport-related concussion, which may be further developed into a clinical diagnostic tool to assist clinicians in the assessment of sport concussion and return-to-play decision making.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Zetterberg, H; Blennow, K
Fluid markers of traumatic brain injury Journal Article
In: Molecular & Cellular Neurosciences, vol. 66, pp. 99–102, 2015.
Abstract | Links | BibTeX | Tags: Physiopathology
@article{Zetterberg2015,
title = {Fluid markers of traumatic brain injury},
author = {Zetterberg, H and Blennow, K},
doi = {10.1016/j.mcn.2015.02.003},
year = {2015},
date = {2015-01-01},
journal = {Molecular \& Cellular Neurosciences},
volume = {66},
pages = {99--102},
abstract = {Traumatic brain injury (TBI) occurs when an external force traumatically injures the brain. Whereas severe TBI can be diagnosed using a combination of clinical signs and standard neuroimaging techniques, mild TBI (also called concussion) is more difficult to detect. This is where fluid markers of injury to different cell types and subcellular compartments in the central nervous system come into play. These markers are often proteins, peptides or other molecules with selective or high expression in the brain, which can be measured in the cerebrospinal fluid or blood as they leak out or get secreted in response to the injury. Here, we review the literature on fluid markers of neuronal, axonal and astroglial injury to diagnose mild TBI and to predict clinical outcome in patients with head trauma. We also discuss chronic traumatic encephalopathy, a progressive neurodegenerative disease in individuals with a history of multiple mild TBIs in a biomarker context. This article is part of a Special Issue entitled 'Traumatic Brain Injury'. © 2015 Elsevier Inc.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Fakhran, S; Alhilali, L
Neurodegenerative changes after mild traumatic brain injury Miscellaneous
2014.
Abstract | Links | BibTeX | Tags: Physiopathology
@misc{Fakhran2014a,
title = {Neurodegenerative changes after mild traumatic brain injury},
author = {Fakhran, S and Alhilali, L},
doi = {10.1159/000358787},
year = {2014},
date = {2014-01-01},
booktitle = {Progress in Neurological Surgery},
volume = {28},
pages = {234--242},
abstract = {A link between mild traumatic brain injury (mTBI) and neurodegenerative diseases, specifically Alzheimer's disease and chronic traumatic encephalopathy (CTE), has long been suspected. Shared clinical symptomology - most notably the prominent role of central auditory dysfunction and sleepwake disturbances in both disease states - and similar findings on postmortem pathological examination has further reinforced suspected commonality between these seemingly disparate entities. However, conventional imaging techniques, including computed tomography and anatomic magnetic resonance, are unable to detect the symptomatic injuries in mTBI patients and therefore detection of neurodegenerative changes in vivo has previously not been reported. Recent research using diffusion tensor imaging, a novel imaging technique, and focused on patient-reported symptoms has for the first time demonstrated imaging findings in mTBI patients in vivo that are strikingly similar to Alzheimer's dementia and CTE. Moving forward, research will focus on identifying what renders certain patients with mTBI susceptible to developing full-fledged Alzheimer's disease and CTE later in life. © 2014 S. Karger AG, Basel.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {misc}
}
Slobounov, S
Metabolic integrity of primary motor cortex may be compromised in clinically asymptomatic concussed athletes Journal Article
In: Clinical Neurophysiology, vol. 125, pp. 1291–1292, 2014.
BibTeX | Tags: Physiopathology
@article{Slobounov2014,
title = {Metabolic integrity of primary motor cortex may be compromised in clinically asymptomatic concussed athletes},
author = {Slobounov, S},
year = {2014},
date = {2014-01-01},
journal = {Clinical Neurophysiology},
volume = {125},
pages = {1291--1292},
address = {The Pennsylvania State University, University Park, PA 16802, USA. Electronic address: sms18@psu.edu.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Morley, W A; Seneff, S
Diminished brain resilience syndrome: A modern day neurological pathology of increased susceptibility to mild brain trauma, concussion, and downstream neurodegeneration Journal Article
In: Surgical Neurology International, vol. 5, pp. 97, 2014.
Abstract | BibTeX | Tags: Physiopathology
@article{Morley2014,
title = {Diminished brain resilience syndrome: A modern day neurological pathology of increased susceptibility to mild brain trauma, concussion, and downstream neurodegeneration},
author = {Morley, W A and Seneff, S},
year = {2014},
date = {2014-01-01},
journal = {Surgical Neurology International},
volume = {5},
pages = {97},
address = {Morley,Wendy A. Thionetic Nutrition, Richmond Hill, ON L4C 7T3, Canada. Seneff,Stephanie. Spoken Language Systems Group, Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge MA 02139, USA.},
abstract = {The number of sports-related concussions has been steadily rising in recent years. Diminished brain resilience syndrome is a term coined by the lead author to describe a particular physiological state of nutrient functional deficiency and disrupted homeostatic mechanisms leading to increased susceptibility to previously considered innocuous concussion. We discuss how modern day environmental toxicant exposure, along with major changes in our food supply and lifestyle practices, profoundly reduce the bioavailability of neuro-critical nutrients such that the normal processes of homeostatic balance and resilience are no longer functional. Their diminished capacity triggers physiological and biochemical 'work around' processes that result in undesirable downstream consequences. Exposure to certain environmental chemicals, particularly glyphosate, the active ingredient in the herbicide, Roundup(), may disrupt the body's innate switching mechanism, which normally turns off the immune response to brain injury once danger has been removed. Deficiencies in serotonin, due to disruption of the shikimate pathway, may lead to impaired melatonin supply, which reduces the resiliency of the brain through reduced antioxidant capacity and alterations in the cerebrospinal fluid, reducing critical protective buffering mechanisms in impact trauma. Depletion of certain rare minerals, overuse of sunscreen and/or overprotection from sun exposure, as well as overindulgence in heavily processed, nutrient deficient foods, further compromise the brain's resilience. Modifications to lifestyle practices, if widely implemented, could significantly reduce this trend of neurological damage.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Schulte, S; Podlog, L W; Hamson-Utley, J J; Strathmann, F G; Struder, H K
A systematic review of the biomarker S100B: implications for sport-related concussion management Journal Article
In: Journal of Athletic Training, vol. 49, pp. 830–850, 2014.
Abstract | BibTeX | Tags: Physiopathology
@article{Schulte2014,
title = {A systematic review of the biomarker S100B: implications for sport-related concussion management},
author = {Schulte, S and Podlog, L W and Hamson-Utley, J J and Strathmann, F G and Struder, H K},
year = {2014},
date = {2014-01-01},
journal = {Journal of Athletic Training},
volume = {49},
pages = {830--850},
address = {Schulte,Stefanie. Department of Exercise and Sport Science, University of Utah, Salt Lake City;},
abstract = {OBJECTIVE: Elevated levels of the astroglial protein S100B have been shown to predict sport-related concussion. However, S100B levels within an athlete can vary depending on the type of physical activity (PA) engaged in and the methodologic approach used to measure them. Thus, appropriate reference values in the diagnosis of concussed athletes remain undefined. The purpose of our systematic literature review was to provide an overview of the current literature examining S100B measurement in the context of PA. The overall goal is to improve the use of the biomarker S100B in the context of sport-related concussion management. DATA SOURCES: PubMed, SciVerse Scopus, SPORTDiscus, CINAHL, and Cochrane. STUDY SELECTION: We selected articles that contained (1) research studies focusing exclusively on humans in which (2) either PA was used as an intervention or the test participants or athletes were involved in PA and (3) S100B was measured as a dependent variable. DATA EXTRACTION: We identified 24 articles. Study variations included the mode of PA used as an intervention, sample types, sample-processing procedures, and analytic techniques. DATA SYNTHESIS: Given the nonuniformity of the analytical methods used and the data samples collected, as well as differences in the types of PA investigated, we were not able to determine a single consistent reference value of S100B in the context of PA. Thus, a clear distinction between a concussed athlete and a healthy athlete based solely on the existing S100B cutoff value of 0.1 mug/L remains unclear. However, because of its high sensitivity and excellent negative predictive value, S100B measurement seems to have the potential to be a diagnostic adjunct for concussion in sports settings. We recommend that the interpretation of S100B values be based on congruent study designs to ensure measurement reliability and validity.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Di Battista, A P; Rhind, S G; Baker, A J
Application of blood-based biomarkers in human mild traumatic brain injury Journal Article
In: Frontiers in Neurology, vol. 4, pp. 44, 2013.
Abstract | BibTeX | Tags: Physiopathology
@article{DiBattista2013,
title = {Application of blood-based biomarkers in human mild traumatic brain injury},
author = {{Di Battista}, A P and Rhind, S G and Baker, A J},
year = {2013},
date = {2013-01-01},
journal = {Frontiers in Neurology},
volume = {4},
pages = {44},
address = {Faculty of Medicine, Institute of Medical Science, University of Toronto Toronto, ON, Canada.},
abstract = {Traumatic Brain Injury (TBI) is a global health concern. The majority of TBI's are mild, yet our ability to diagnose and treat mild traumatic brain injury (mTBI) is lacking. This deficiency results from a variety of issues including the difficulty in interpreting ambiguous clinically presented symptoms, and ineffective imaging techniques. Thus, researchers have begun to explore cellular and molecular based approaches to improve both diagnosis and prognosis. This has been met with a variety of challenges, including difficulty in relating biological markers to current clinical symptoms, and overcoming our lack of fundamental understanding of the pathophysiology of mTBI. However, recent adoption of high throughput technologies and a change in focus from the identification of single to multiple markers has given just optimism to mTBI research. The purpose of this review is to highlight a number of current experimental peripheral blood biomarkers of mTBI, as well as comment on the issues surrounding their clinical application and utility.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Keefer, Raina
In the game Journal Article
In: ACR Bulletin, vol. 67, no. 10, pp. 10–12, 2012, ISBN: 0098-6070.
BibTeX | Tags: Athletes, Brain -- Pathology, Brain Concussion -- Classification, Brain Concussion -- Complications, Brain Concussion -- Epidemiology -- United States, Brain Concussion -- Pathology, Brain Injuries -- Diagnosis, DIAGNOSTIC imaging, football, FOOTBALL injuries, Imaging & EEG, Physiopathology, Radiologists, Severity of Injury
@article{Keefer2012,
title = {In the game},
author = {Keefer, Raina},
isbn = {0098-6070},
year = {2012},
date = {2012-01-01},
journal = {ACR Bulletin},
volume = {67},
number = {10},
pages = {10--12},
keywords = {Athletes, Brain -- Pathology, Brain Concussion -- Classification, Brain Concussion -- Complications, Brain Concussion -- Epidemiology -- United States, Brain Concussion -- Pathology, Brain Injuries -- Diagnosis, DIAGNOSTIC imaging, football, FOOTBALL injuries, Imaging \& EEG, Physiopathology, Radiologists, Severity of Injury},
pubstate = {published},
tppubtype = {article}
}
Vaughan, C; VanMeter, J; McGuire, E; Gioia, G; Newman, J; Gerst, E; Fricke, S
Neurometabolic change over the course of recovery from concussion Journal Article
In: Archives of Clinical Neuropsychology, vol. 26, pp. 523, 2011, ISSN: 0887-6177.
BibTeX | Tags: Physiopathology
@article{Vaughan2011b,
title = {Neurometabolic change over the course of recovery from concussion},
author = {Vaughan, C and VanMeter, J and McGuire, E and Gioia, G and Newman, J and Gerst, E and Fricke, S},
issn = {0887-6177},
year = {2011},
date = {2011-01-01},
journal = {Archives of Clinical Neuropsychology},
volume = {26},
pages = {523},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Signoretti, S; Vagnozzi, R; Tavazzi, B; Lazzarino, G
Biochemical and neurochemical sequelae following mild traumatic brain injury: summary of experimental data and clinical implications Journal Article
In: Neurosurgical Focus, vol. 29, 2010, ISSN: 1092-0684.
Abstract | Links | BibTeX | Tags: Physiopathology
@article{Signoretti2010,
title = {Biochemical and neurochemical sequelae following mild traumatic brain injury: summary of experimental data and clinical implications},
author = {Signoretti, S and Vagnozzi, R and Tavazzi, B and Lazzarino, G},
doi = {E1 10.3171/2010.9.focus10183},
issn = {1092-0684},
year = {2010},
date = {2010-01-01},
journal = {Neurosurgical Focus},
volume = {29},
abstract = {Although numerous studies have been carried out to investigate the pathophysiology of mild traumatic brain injury (mTBI), there are still no standard criteria for the diagnosis and treatment of this peculiar condition. The dominant theory that diffuse axonal injury is the main neuropathological process behind mTBI is being revealed as weak at best or inconclusive, given the current literature and the fact that neuronal injury inherent to mTBI improves, with few lasting clinical sequelae in the vast majority of patients. Clinical and experimental evidence suggests that such a course, rather than being due to cell death, is based on temporal neuronal dysfunction, the inevitable consequence of complex biochemical and neurochemical cascade mechanisms directly and immediately triggered by the traumatic insult. This report is an attempt to summarize data from a long series of experiments conducted in the authors' laboratories and published during the past 12 years, together with an extensive analysis of the available literature, focused on understanding the biochemical damage produced by an mTBI. The overall clinical implications, as well as the metabolic nature of the post-mTBI brain vulnerability, are discussed. Finally, the application of proton MR spectroscopy as a possible tool to monitor the full recovery of brain metabolic functions is emphasized. (DOI: 10.3171/2010.9.FOCUS10183)},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Rees, Peter
Re: Whiplash and concussion: similar acute changes in middle-latency SEP's. Can J Neurol Sci. 2006; 33: 379-86 Journal Article
In: Canadian Journal of Neurological Sciences, vol. 34, pp. 260, 2007.
BibTeX | Tags: Physiopathology
@article{Rees2007,
title = {Re: Whiplash and concussion: similar acute changes in middle-latency SEP's. Can J Neurol Sci. 2006; 33: 379-86},
author = {Rees, Peter},
year = {2007},
date = {2007-01-01},
journal = {Canadian Journal of Neurological Sciences},
volume = {34},
pages = {260},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Bazarian, Jeffrey J; Zemlan, Frank P; Mookerjee, Sohug; Stigbrand, Torgney
Serum S-100B and cleaved-tau are poor predictors of long-term outcome after mild traumatic brain injury Journal Article
In: Brain Injury, vol. 20, pp. 759–765, 2006.
Abstract | BibTeX | Tags: Physiopathology
@article{Bazarian2006c,
title = {Serum S-100B and cleaved-tau are poor predictors of long-term outcome after mild traumatic brain injury},
author = {Bazarian, Jeffrey J and Zemlan, Frank P and Mookerjee, Sohug and Stigbrand, Torgney},
year = {2006},
date = {2006-01-01},
journal = {Brain Injury},
volume = {20},
pages = {759--765},
address = {Department of Emergency Medicine, University of Rochester School of Medicine, Rochester, New York 14472, USA. jeff_barzarian@urmc.rochester.edu},
abstract = {PRIMARY OBJECTIVE: To determine the relationship of serum S-100B and C-tau levels to long-term outcome after mild traumatic brain injury (mild TBI). RESEARCH DESIGN: A prospective study of 35 mild TBI subjects presenting to the emergency department. METHODS AND PROCEDURES: Six hour serum S-100B and C-tau levels compared to 3-month Rivermead Post Concussion Questionnaire (RPCQ) scores and post-concussive syndrome (PCS). MAIN OUTCOMES AND RESULTS: The linear correlation between marker levels and RPCQ scores was weak (S-100B: r = 0.071, C-tau: r = -0.21). There was no statistically significant correlation between marker levels and 3-month PCS (S-100B: AUC = 0.589, 95%CI. 038, 0.80; C-tau: AUC = 0.634, 95%CI 0.43, 0.84). The sensitivity of these markers ranged from 43.8-56.3% and the specificity from 35.7-71.4%. CONCLUSIONS: Initial serum S-100B and C-tau levels appear to be poor predictors of 3-month outcome after mild TBI.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Bazarian, Jeffrey J; Beck, Christopher; Blyth, Brian; von Ahsen, Nicolas; Hasselblatt, Martin
Impact of creatine kinase correction on the predictive value of S-100B after mild traumatic brain injury Journal Article
In: Restorative Neurology & Neuroscience, vol. 24, pp. 163–172, 2006.
Abstract | BibTeX | Tags: Physiopathology
@article{Bazarian2006b,
title = {Impact of creatine kinase correction on the predictive value of S-100B after mild traumatic brain injury},
author = {Bazarian, Jeffrey J and Beck, Christopher and Blyth, Brian and von Ahsen, Nicolas and Hasselblatt, Martin},
year = {2006},
date = {2006-01-01},
journal = {Restorative Neurology \& Neuroscience},
volume = {24},
pages = {163--172},
address = {Department of Emergency Medicine, University of Rochester School of Medicine, Rochester, NY, USA. jeff_bazarian@urmc.rochester.edu},
abstract = {PURPOSE: To validate a correction factor for the extracranial release of the astroglial protein, S-100B, based on concomitant creatine kinase (CK) levels. METHODS: The CK- S-100B relationship in non-head injured marathon runners was used to derive a correction factor for the extracranial release of S-100B. This factor was then applied to a separate cohort of 96 mild traumatic brain injury (TBI) patients in whom both CK and S-100B levels were measured. Corrected S-100B was compared to uncorrected S-100B for the prediction of initial head CT, three-month headache and three-month post concussive syndrome (PCS). RESULTS: Corrected S-100B resulted in a statistically significant improvement in the prediction of 3-month headache (area under curve [AUC] 0.46 vs 0.52},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Arciniegas, David B
The cholinergic hypothesis of cognitive impairment caused by traumatic brain injury Journal Article
In: Current Psychiatry Reports, vol. 5, pp. 391–399, 2003.
Abstract | BibTeX | Tags: Physiopathology
@article{Arciniegas2003,
title = {The cholinergic hypothesis of cognitive impairment caused by traumatic brain injury},
author = {Arciniegas, David B},
year = {2003},
date = {2003-01-01},
journal = {Current Psychiatry Reports},
volume = {5},
pages = {391--399},
address = {Brain Injury Rehabilitation Unit, Spalding Rehabilitation Hospital, Aurora, CO 80011, USA. david.arciniegas@UCHSC.edu},
abstract = {Cognitive impairments are among the most common neuropsychiatric sequelae of traumatic brain injury at all levels of severity. Cerebral cholinergic neurons and their ascending projections are particularly vulnerable to acute and chronic traumatically mediated dysfunction. In light of the important role of acetylcholine in arousal, attention, memory, and other aspects of cognition, cerebral cholinergic systems contribute to and may also be a target for pharmacologic remediation among individuals with post-traumatic cognitive impairments. This article will review the evidence in support of this hypothesis. Evidence of relatively selective damage to cholinergic injury, the development of persistent anticholinergic sensitivity, and the effects of cholinergic augmentation on memory performance are presented first. Thereafter, neuropathologic, electrophysiologic, and pharmacologic evidence of cholinergic dysfunction after traumatic brain injury in humans is reviewed. Finally, future directions for investigation of the cholinergic hypothesis and possible clinical applications of this information are discussed. [References: 80]},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Alessandri, B; Doppenberg, E; Zauner, A; Woodward, J; Young, H F; Bullock, R
Cortical extracellular sodium transients after human head injury: an indicator of secondary brain damage? Journal Article
In: Acta Neurochirurgica - Supplement, vol. 71, pp. 237–240, 1998.
Abstract | BibTeX | Tags: Physiopathology
@article{Alessandri1998,
title = {Cortical extracellular sodium transients after human head injury: an indicator of secondary brain damage?},
author = {Alessandri, B and Doppenberg, E and Zauner, A and Woodward, J and Young, H F and Bullock, R},
year = {1998},
date = {1998-01-01},
journal = {Acta Neurochirurgica - Supplement},
volume = {71},
pages = {237--240},
address = {Virginia Commonwealth University, Medical College of Virginia, USA.},
abstract = {Animal studies indicate that elevated extracellular sodium can increase glutamate-induced excitotoxicity. Therefore, we investigated the relationship between sodium and glutamate and the effect of changes in sodium concentrations on the outcome of head-injured patients. Thirty-four (34) patients were selected for this study and divided into a group of patients having episodes (\> or = 30-min) of high sodium in dialysates (\> or = 200 mM; HIGH},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Pogacnik, T
Characteristics of regional cerebral blood flow in patients with concussion Journal Article
In: Psychiatry Research, vol. 29, pp. 313–316, 1989.
BibTeX | Tags: Physiopathology
@article{Pogacnik1989,
title = {Characteristics of regional cerebral blood flow in patients with concussion},
author = {Pogacnik, T},
year = {1989},
date = {1989-01-01},
journal = {Psychiatry Research},
volume = {29},
pages = {313--316},
address = {University Department of Neurology, University Medical Centre, Ljubljana, Yugoslavia.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Papa, L; Ramia, M M; Edwards, D; Johnson, B D; Slobounov, S M
Systematic review of clinical studies examining biomarkers of brain injury in athletes after sports-related concussion Journal Article
In: Journal of Neurotrauma, vol. 32, pp. 661–673, 2015.
@article{Papa2015,
title = {Systematic review of clinical studies examining biomarkers of brain injury in athletes after sports-related concussion},
author = {Papa, L and Ramia, M M and Edwards, D and Johnson, B D and Slobounov, S M},
year = {2015},
date = {2015-01-01},
journal = {Journal of Neurotrauma},
volume = {32},
pages = {661--673},
address = {Papa,Linda. 1 Department of Emergency Medicine, Orlando Regional Medical Center , Orlando, Florida.},
abstract = {The aim of this study was to systematically review clinical studies examining biofluid biomarkers of brain injury for concussion in athletes. Data sources included PubMed, MEDLINE, and the Cochrane Database from 1966 to October 2013. Studies were included if they recruited athletes participating in organized sports who experienced concussion or head injury during a sports-related activity and had brain injury biomarkers measured. Acceptable research designs included experimental, observational, and case-control studies. Review articles, opinion papers, and editorials were excluded. After title and abstract screening of potential articles, full texts were independently reviewed to identify articles that met inclusion criteria. A composite evidentiary table was then constructed and documented the study title, design, population, methods, sample size, outcome measures, and results. The search identified 52 publications, of which 13 were selected and critically reviewed. All of the included studies were prospective and were published either in or after the year 2000. Sports included boxing (six studies), soccer (five studies), running/jogging (two studies), hockey (one study), basketball (one study), cycling (one study), and swimming (one study). The majority of studies (92%) had fewer than 100 patients. Three studies (23%) evaluated biomarkers in cerebrospinal fluid (CSF), one in both serum and CSF, and 10 (77%) in serum exclusively. There were 11 different biomarkers assessed, including S100beta, glial fibrillary acidic protein, neuron-specific enolase, tau, neurofilament light protein, amyloid beta, brain-derived neurotrophic factor, creatine kinase and heart-type fatty acid binding protein, prolactin, cortisol, and albumin. A handful of biomarkers showed a correlation with number of hits to the head (soccer), acceleration/deceleration forces (jumps, collisions, and falls), postconcussive symptoms, trauma to the body versus the head, and dynamics of different sports. Although there are no validated biomarkers for concussion as yet, there is potential for biomarkers to provide diagnostic, prognostic, and monitoring information postinjury. They could also be combined with neuroimaging to assess injury evolution and recovery.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
McKee, A C; Daneshvar, D H
The neuropathology of traumatic brain injury Journal Article
In: Handbook of Clinical Neurology, vol. 127, pp. 45–66, 2015.
@article{McKee2015,
title = {The neuropathology of traumatic brain injury},
author = {McKee, A C and Daneshvar, D H},
year = {2015},
date = {2015-01-01},
journal = {Handbook of Clinical Neurology},
volume = {127},
pages = {45--66},
address = {Mckee,Ann C. VA Boston HealthCare System; Center for the Study of Traumatic Encephalopathy, Alzheimer's Disease Center, and Departments of Neurology and Pathology, Boston University School of Medicine, Boston, MA, USA. Electronic address: amckee@bu.edu. D},
abstract = {Traumatic brain injury, a leading cause of mortality and morbidity, is divided into three grades of severity: mild, moderate, and severe, based on the Glasgow Coma Scale, the loss of consciousness, and the development of post-traumatic amnesia. Although mild traumatic brain injury, including concussion and subconcussion, is by far the most common, it is also the most difficult to diagnose and the least well understood. Proper recognition, management, and treatment of acute concussion and mild traumatic brain injury are the fundamentals of an emerging clinical discipline. It is also becoming increasingly clear that some mild traumatic brain injuries have persistent, and sometimes progressive, long-term debilitating effects. Evidence indicates that a single traumatic brain injury can precipitate or accelerate multiple age-related neurodegenerations, increase the risk of developing Alzheimer's disease, Parkinson's disease, and motor neuron disease, and that repetitive mild traumatic brain injuries can provoke the development of a tauopathy, chronic traumatic encephalopathy. Clinically, chronic traumatic encephalopathy is associated with behavioral changes, executive dysfunction, memory loss, and cognitive impairments that begin insidiously and progress slowly over decades. Pathologically, chronic traumatic encephalopathy produces atrophy of the frontal and temporal lobes, thalamus, and hypothalamus, septal abnormalities, and abnormal deposits of hyperphosphorylated tau (tau) as neurofibrillary tangles and disordered neurites throughout the brain. The incidence and prevalence of chronic traumatic encephalopathy and the genetic risk factors critical to its development are currently unknown. Chronic traumatic encephalopathy frequently occurs as a sole diagnosis, but may be associated with other neurodegenerative disorders, including Alzheimer's disease, Lewy body disease, and motor neuron disease. Currently, chronic traumatic encephalopathy can be diagnosed only at autopsy; however, promising efforts to develop imaging, spinal fluid, and peripheral blood biomarkers are underway to diagnose and monitor the course of disease in living subjects.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Pham, N; Akonasu, H; Shishkin, R; Taghibiglou, C
Plasma soluble prion protein, a potential biomarker for sport-related concussions: a pilot study Journal Article
In: PLoS ONE, vol. 10, pp. e0117286, 2015.
@article{Pham2015b,
title = {Plasma soluble prion protein, a potential biomarker for sport-related concussions: a pilot study},
author = {Pham, N and Akonasu, H and Shishkin, R and Taghibiglou, C},
year = {2015},
date = {2015-01-01},
journal = {PLoS ONE},
volume = {10},
pages = {e0117286},
address = {Pham,Nam. Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Canada. Akonasu,Hungbo. Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Canada. Shishkin,Rhonda. College of Kinesiolo},
abstract = {Sport-related mild traumatic brain injury (mTBI) or concussion is a significant health concern to athletes with potential long-term consequences. The diagnosis of sport concussion and return to sport decision making is one of the greatest challenges facing health care clinicians working in sports. Blood biomarkers have recently demonstrated their potential in assisting the detection of brain injury particularly, in those cases with no obvious physical injury. We have recently discovered plasma soluble cellular prion protein (PrP(C)) as a potential reliable biomarker for blast induced TBI (bTBI) in a rodent animal model. In order to explore the application of this novel TBI biomarker to sport-related concussion, we conducted a pilot study at the University of Saskatchewan (U of S) by recruiting athlete and non-athlete 18 to 30 year-old students. Using a modified quantitative ELISA method, we first established normal values for the plasma soluble PrP(C) in male and female students. The measured plasma soluble PrP(C) in confirmed concussion cases demonstrated a significant elevation of this analyte in post-concussion samples. Data collected from our pilot study indicates that the plasma soluble PrP(C) is a potential biomarker for sport-related concussion, which may be further developed into a clinical diagnostic tool to assist clinicians in the assessment of sport concussion and return-to-play decision making.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Zetterberg, H; Blennow, K
Fluid markers of traumatic brain injury Journal Article
In: Molecular & Cellular Neurosciences, vol. 66, pp. 99–102, 2015.
@article{Zetterberg2015,
title = {Fluid markers of traumatic brain injury},
author = {Zetterberg, H and Blennow, K},
doi = {10.1016/j.mcn.2015.02.003},
year = {2015},
date = {2015-01-01},
journal = {Molecular \& Cellular Neurosciences},
volume = {66},
pages = {99--102},
abstract = {Traumatic brain injury (TBI) occurs when an external force traumatically injures the brain. Whereas severe TBI can be diagnosed using a combination of clinical signs and standard neuroimaging techniques, mild TBI (also called concussion) is more difficult to detect. This is where fluid markers of injury to different cell types and subcellular compartments in the central nervous system come into play. These markers are often proteins, peptides or other molecules with selective or high expression in the brain, which can be measured in the cerebrospinal fluid or blood as they leak out or get secreted in response to the injury. Here, we review the literature on fluid markers of neuronal, axonal and astroglial injury to diagnose mild TBI and to predict clinical outcome in patients with head trauma. We also discuss chronic traumatic encephalopathy, a progressive neurodegenerative disease in individuals with a history of multiple mild TBIs in a biomarker context. This article is part of a Special Issue entitled 'Traumatic Brain Injury'. © 2015 Elsevier Inc.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Fakhran, S; Alhilali, L
Neurodegenerative changes after mild traumatic brain injury Miscellaneous
2014.
@misc{Fakhran2014a,
title = {Neurodegenerative changes after mild traumatic brain injury},
author = {Fakhran, S and Alhilali, L},
doi = {10.1159/000358787},
year = {2014},
date = {2014-01-01},
booktitle = {Progress in Neurological Surgery},
volume = {28},
pages = {234--242},
abstract = {A link between mild traumatic brain injury (mTBI) and neurodegenerative diseases, specifically Alzheimer's disease and chronic traumatic encephalopathy (CTE), has long been suspected. Shared clinical symptomology - most notably the prominent role of central auditory dysfunction and sleepwake disturbances in both disease states - and similar findings on postmortem pathological examination has further reinforced suspected commonality between these seemingly disparate entities. However, conventional imaging techniques, including computed tomography and anatomic magnetic resonance, are unable to detect the symptomatic injuries in mTBI patients and therefore detection of neurodegenerative changes in vivo has previously not been reported. Recent research using diffusion tensor imaging, a novel imaging technique, and focused on patient-reported symptoms has for the first time demonstrated imaging findings in mTBI patients in vivo that are strikingly similar to Alzheimer's dementia and CTE. Moving forward, research will focus on identifying what renders certain patients with mTBI susceptible to developing full-fledged Alzheimer's disease and CTE later in life. © 2014 S. Karger AG, Basel.},
keywords = {},
pubstate = {published},
tppubtype = {misc}
}
Slobounov, S
Metabolic integrity of primary motor cortex may be compromised in clinically asymptomatic concussed athletes Journal Article
In: Clinical Neurophysiology, vol. 125, pp. 1291–1292, 2014.
@article{Slobounov2014,
title = {Metabolic integrity of primary motor cortex may be compromised in clinically asymptomatic concussed athletes},
author = {Slobounov, S},
year = {2014},
date = {2014-01-01},
journal = {Clinical Neurophysiology},
volume = {125},
pages = {1291--1292},
address = {The Pennsylvania State University, University Park, PA 16802, USA. Electronic address: sms18@psu.edu.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Morley, W A; Seneff, S
Diminished brain resilience syndrome: A modern day neurological pathology of increased susceptibility to mild brain trauma, concussion, and downstream neurodegeneration Journal Article
In: Surgical Neurology International, vol. 5, pp. 97, 2014.
@article{Morley2014,
title = {Diminished brain resilience syndrome: A modern day neurological pathology of increased susceptibility to mild brain trauma, concussion, and downstream neurodegeneration},
author = {Morley, W A and Seneff, S},
year = {2014},
date = {2014-01-01},
journal = {Surgical Neurology International},
volume = {5},
pages = {97},
address = {Morley,Wendy A. Thionetic Nutrition, Richmond Hill, ON L4C 7T3, Canada. Seneff,Stephanie. Spoken Language Systems Group, Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge MA 02139, USA.},
abstract = {The number of sports-related concussions has been steadily rising in recent years. Diminished brain resilience syndrome is a term coined by the lead author to describe a particular physiological state of nutrient functional deficiency and disrupted homeostatic mechanisms leading to increased susceptibility to previously considered innocuous concussion. We discuss how modern day environmental toxicant exposure, along with major changes in our food supply and lifestyle practices, profoundly reduce the bioavailability of neuro-critical nutrients such that the normal processes of homeostatic balance and resilience are no longer functional. Their diminished capacity triggers physiological and biochemical 'work around' processes that result in undesirable downstream consequences. Exposure to certain environmental chemicals, particularly glyphosate, the active ingredient in the herbicide, Roundup(), may disrupt the body's innate switching mechanism, which normally turns off the immune response to brain injury once danger has been removed. Deficiencies in serotonin, due to disruption of the shikimate pathway, may lead to impaired melatonin supply, which reduces the resiliency of the brain through reduced antioxidant capacity and alterations in the cerebrospinal fluid, reducing critical protective buffering mechanisms in impact trauma. Depletion of certain rare minerals, overuse of sunscreen and/or overprotection from sun exposure, as well as overindulgence in heavily processed, nutrient deficient foods, further compromise the brain's resilience. Modifications to lifestyle practices, if widely implemented, could significantly reduce this trend of neurological damage.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Schulte, S; Podlog, L W; Hamson-Utley, J J; Strathmann, F G; Struder, H K
A systematic review of the biomarker S100B: implications for sport-related concussion management Journal Article
In: Journal of Athletic Training, vol. 49, pp. 830–850, 2014.
@article{Schulte2014,
title = {A systematic review of the biomarker S100B: implications for sport-related concussion management},
author = {Schulte, S and Podlog, L W and Hamson-Utley, J J and Strathmann, F G and Struder, H K},
year = {2014},
date = {2014-01-01},
journal = {Journal of Athletic Training},
volume = {49},
pages = {830--850},
address = {Schulte,Stefanie. Department of Exercise and Sport Science, University of Utah, Salt Lake City;},
abstract = {OBJECTIVE: Elevated levels of the astroglial protein S100B have been shown to predict sport-related concussion. However, S100B levels within an athlete can vary depending on the type of physical activity (PA) engaged in and the methodologic approach used to measure them. Thus, appropriate reference values in the diagnosis of concussed athletes remain undefined. The purpose of our systematic literature review was to provide an overview of the current literature examining S100B measurement in the context of PA. The overall goal is to improve the use of the biomarker S100B in the context of sport-related concussion management. DATA SOURCES: PubMed, SciVerse Scopus, SPORTDiscus, CINAHL, and Cochrane. STUDY SELECTION: We selected articles that contained (1) research studies focusing exclusively on humans in which (2) either PA was used as an intervention or the test participants or athletes were involved in PA and (3) S100B was measured as a dependent variable. DATA EXTRACTION: We identified 24 articles. Study variations included the mode of PA used as an intervention, sample types, sample-processing procedures, and analytic techniques. DATA SYNTHESIS: Given the nonuniformity of the analytical methods used and the data samples collected, as well as differences in the types of PA investigated, we were not able to determine a single consistent reference value of S100B in the context of PA. Thus, a clear distinction between a concussed athlete and a healthy athlete based solely on the existing S100B cutoff value of 0.1 mug/L remains unclear. However, because of its high sensitivity and excellent negative predictive value, S100B measurement seems to have the potential to be a diagnostic adjunct for concussion in sports settings. We recommend that the interpretation of S100B values be based on congruent study designs to ensure measurement reliability and validity.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Di Battista, A P; Rhind, S G; Baker, A J
Application of blood-based biomarkers in human mild traumatic brain injury Journal Article
In: Frontiers in Neurology, vol. 4, pp. 44, 2013.
@article{DiBattista2013,
title = {Application of blood-based biomarkers in human mild traumatic brain injury},
author = {{Di Battista}, A P and Rhind, S G and Baker, A J},
year = {2013},
date = {2013-01-01},
journal = {Frontiers in Neurology},
volume = {4},
pages = {44},
address = {Faculty of Medicine, Institute of Medical Science, University of Toronto Toronto, ON, Canada.},
abstract = {Traumatic Brain Injury (TBI) is a global health concern. The majority of TBI's are mild, yet our ability to diagnose and treat mild traumatic brain injury (mTBI) is lacking. This deficiency results from a variety of issues including the difficulty in interpreting ambiguous clinically presented symptoms, and ineffective imaging techniques. Thus, researchers have begun to explore cellular and molecular based approaches to improve both diagnosis and prognosis. This has been met with a variety of challenges, including difficulty in relating biological markers to current clinical symptoms, and overcoming our lack of fundamental understanding of the pathophysiology of mTBI. However, recent adoption of high throughput technologies and a change in focus from the identification of single to multiple markers has given just optimism to mTBI research. The purpose of this review is to highlight a number of current experimental peripheral blood biomarkers of mTBI, as well as comment on the issues surrounding their clinical application and utility.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Keefer, Raina
In the game Journal Article
In: ACR Bulletin, vol. 67, no. 10, pp. 10–12, 2012, ISBN: 0098-6070.
@article{Keefer2012,
title = {In the game},
author = {Keefer, Raina},
isbn = {0098-6070},
year = {2012},
date = {2012-01-01},
journal = {ACR Bulletin},
volume = {67},
number = {10},
pages = {10--12},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Vaughan, C; VanMeter, J; McGuire, E; Gioia, G; Newman, J; Gerst, E; Fricke, S
Neurometabolic change over the course of recovery from concussion Journal Article
In: Archives of Clinical Neuropsychology, vol. 26, pp. 523, 2011, ISSN: 0887-6177.
@article{Vaughan2011b,
title = {Neurometabolic change over the course of recovery from concussion},
author = {Vaughan, C and VanMeter, J and McGuire, E and Gioia, G and Newman, J and Gerst, E and Fricke, S},
issn = {0887-6177},
year = {2011},
date = {2011-01-01},
journal = {Archives of Clinical Neuropsychology},
volume = {26},
pages = {523},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Signoretti, S; Vagnozzi, R; Tavazzi, B; Lazzarino, G
Biochemical and neurochemical sequelae following mild traumatic brain injury: summary of experimental data and clinical implications Journal Article
In: Neurosurgical Focus, vol. 29, 2010, ISSN: 1092-0684.
@article{Signoretti2010,
title = {Biochemical and neurochemical sequelae following mild traumatic brain injury: summary of experimental data and clinical implications},
author = {Signoretti, S and Vagnozzi, R and Tavazzi, B and Lazzarino, G},
doi = {E1 10.3171/2010.9.focus10183},
issn = {1092-0684},
year = {2010},
date = {2010-01-01},
journal = {Neurosurgical Focus},
volume = {29},
abstract = {Although numerous studies have been carried out to investigate the pathophysiology of mild traumatic brain injury (mTBI), there are still no standard criteria for the diagnosis and treatment of this peculiar condition. The dominant theory that diffuse axonal injury is the main neuropathological process behind mTBI is being revealed as weak at best or inconclusive, given the current literature and the fact that neuronal injury inherent to mTBI improves, with few lasting clinical sequelae in the vast majority of patients. Clinical and experimental evidence suggests that such a course, rather than being due to cell death, is based on temporal neuronal dysfunction, the inevitable consequence of complex biochemical and neurochemical cascade mechanisms directly and immediately triggered by the traumatic insult. This report is an attempt to summarize data from a long series of experiments conducted in the authors' laboratories and published during the past 12 years, together with an extensive analysis of the available literature, focused on understanding the biochemical damage produced by an mTBI. The overall clinical implications, as well as the metabolic nature of the post-mTBI brain vulnerability, are discussed. Finally, the application of proton MR spectroscopy as a possible tool to monitor the full recovery of brain metabolic functions is emphasized. (DOI: 10.3171/2010.9.FOCUS10183)},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Rees, Peter
Re: Whiplash and concussion: similar acute changes in middle-latency SEP's. Can J Neurol Sci. 2006; 33: 379-86 Journal Article
In: Canadian Journal of Neurological Sciences, vol. 34, pp. 260, 2007.
@article{Rees2007,
title = {Re: Whiplash and concussion: similar acute changes in middle-latency SEP's. Can J Neurol Sci. 2006; 33: 379-86},
author = {Rees, Peter},
year = {2007},
date = {2007-01-01},
journal = {Canadian Journal of Neurological Sciences},
volume = {34},
pages = {260},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Bazarian, Jeffrey J; Zemlan, Frank P; Mookerjee, Sohug; Stigbrand, Torgney
Serum S-100B and cleaved-tau are poor predictors of long-term outcome after mild traumatic brain injury Journal Article
In: Brain Injury, vol. 20, pp. 759–765, 2006.
@article{Bazarian2006c,
title = {Serum S-100B and cleaved-tau are poor predictors of long-term outcome after mild traumatic brain injury},
author = {Bazarian, Jeffrey J and Zemlan, Frank P and Mookerjee, Sohug and Stigbrand, Torgney},
year = {2006},
date = {2006-01-01},
journal = {Brain Injury},
volume = {20},
pages = {759--765},
address = {Department of Emergency Medicine, University of Rochester School of Medicine, Rochester, New York 14472, USA. jeff_barzarian@urmc.rochester.edu},
abstract = {PRIMARY OBJECTIVE: To determine the relationship of serum S-100B and C-tau levels to long-term outcome after mild traumatic brain injury (mild TBI). RESEARCH DESIGN: A prospective study of 35 mild TBI subjects presenting to the emergency department. METHODS AND PROCEDURES: Six hour serum S-100B and C-tau levels compared to 3-month Rivermead Post Concussion Questionnaire (RPCQ) scores and post-concussive syndrome (PCS). MAIN OUTCOMES AND RESULTS: The linear correlation between marker levels and RPCQ scores was weak (S-100B: r = 0.071, C-tau: r = -0.21). There was no statistically significant correlation between marker levels and 3-month PCS (S-100B: AUC = 0.589, 95%CI. 038, 0.80; C-tau: AUC = 0.634, 95%CI 0.43, 0.84). The sensitivity of these markers ranged from 43.8-56.3% and the specificity from 35.7-71.4%. CONCLUSIONS: Initial serum S-100B and C-tau levels appear to be poor predictors of 3-month outcome after mild TBI.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Bazarian, Jeffrey J; Beck, Christopher; Blyth, Brian; von Ahsen, Nicolas; Hasselblatt, Martin
Impact of creatine kinase correction on the predictive value of S-100B after mild traumatic brain injury Journal Article
In: Restorative Neurology & Neuroscience, vol. 24, pp. 163–172, 2006.
@article{Bazarian2006b,
title = {Impact of creatine kinase correction on the predictive value of S-100B after mild traumatic brain injury},
author = {Bazarian, Jeffrey J and Beck, Christopher and Blyth, Brian and von Ahsen, Nicolas and Hasselblatt, Martin},
year = {2006},
date = {2006-01-01},
journal = {Restorative Neurology \& Neuroscience},
volume = {24},
pages = {163--172},
address = {Department of Emergency Medicine, University of Rochester School of Medicine, Rochester, NY, USA. jeff_bazarian@urmc.rochester.edu},
abstract = {PURPOSE: To validate a correction factor for the extracranial release of the astroglial protein, S-100B, based on concomitant creatine kinase (CK) levels. METHODS: The CK- S-100B relationship in non-head injured marathon runners was used to derive a correction factor for the extracranial release of S-100B. This factor was then applied to a separate cohort of 96 mild traumatic brain injury (TBI) patients in whom both CK and S-100B levels were measured. Corrected S-100B was compared to uncorrected S-100B for the prediction of initial head CT, three-month headache and three-month post concussive syndrome (PCS). RESULTS: Corrected S-100B resulted in a statistically significant improvement in the prediction of 3-month headache (area under curve [AUC] 0.46 vs 0.52},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Arciniegas, David B
The cholinergic hypothesis of cognitive impairment caused by traumatic brain injury Journal Article
In: Current Psychiatry Reports, vol. 5, pp. 391–399, 2003.
@article{Arciniegas2003,
title = {The cholinergic hypothesis of cognitive impairment caused by traumatic brain injury},
author = {Arciniegas, David B},
year = {2003},
date = {2003-01-01},
journal = {Current Psychiatry Reports},
volume = {5},
pages = {391--399},
address = {Brain Injury Rehabilitation Unit, Spalding Rehabilitation Hospital, Aurora, CO 80011, USA. david.arciniegas@UCHSC.edu},
abstract = {Cognitive impairments are among the most common neuropsychiatric sequelae of traumatic brain injury at all levels of severity. Cerebral cholinergic neurons and their ascending projections are particularly vulnerable to acute and chronic traumatically mediated dysfunction. In light of the important role of acetylcholine in arousal, attention, memory, and other aspects of cognition, cerebral cholinergic systems contribute to and may also be a target for pharmacologic remediation among individuals with post-traumatic cognitive impairments. This article will review the evidence in support of this hypothesis. Evidence of relatively selective damage to cholinergic injury, the development of persistent anticholinergic sensitivity, and the effects of cholinergic augmentation on memory performance are presented first. Thereafter, neuropathologic, electrophysiologic, and pharmacologic evidence of cholinergic dysfunction after traumatic brain injury in humans is reviewed. Finally, future directions for investigation of the cholinergic hypothesis and possible clinical applications of this information are discussed. [References: 80]},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Alessandri, B; Doppenberg, E; Zauner, A; Woodward, J; Young, H F; Bullock, R
Cortical extracellular sodium transients after human head injury: an indicator of secondary brain damage? Journal Article
In: Acta Neurochirurgica - Supplement, vol. 71, pp. 237–240, 1998.
@article{Alessandri1998,
title = {Cortical extracellular sodium transients after human head injury: an indicator of secondary brain damage?},
author = {Alessandri, B and Doppenberg, E and Zauner, A and Woodward, J and Young, H F and Bullock, R},
year = {1998},
date = {1998-01-01},
journal = {Acta Neurochirurgica - Supplement},
volume = {71},
pages = {237--240},
address = {Virginia Commonwealth University, Medical College of Virginia, USA.},
abstract = {Animal studies indicate that elevated extracellular sodium can increase glutamate-induced excitotoxicity. Therefore, we investigated the relationship between sodium and glutamate and the effect of changes in sodium concentrations on the outcome of head-injured patients. Thirty-four (34) patients were selected for this study and divided into a group of patients having episodes (\> or = 30-min) of high sodium in dialysates (\> or = 200 mM; HIGH},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Pogacnik, T
Characteristics of regional cerebral blood flow in patients with concussion Journal Article
In: Psychiatry Research, vol. 29, pp. 313–316, 1989.
@article{Pogacnik1989,
title = {Characteristics of regional cerebral blood flow in patients with concussion},
author = {Pogacnik, T},
year = {1989},
date = {1989-01-01},
journal = {Psychiatry Research},
volume = {29},
pages = {313--316},
address = {University Department of Neurology, University Medical Centre, Ljubljana, Yugoslavia.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Papa, L; Ramia, M M; Edwards, D; Johnson, B D; Slobounov, S M
Systematic review of clinical studies examining biomarkers of brain injury in athletes after sports-related concussion Journal Article
In: Journal of Neurotrauma, vol. 32, pp. 661–673, 2015.
Abstract | BibTeX | Tags: Physiopathology
@article{Papa2015,
title = {Systematic review of clinical studies examining biomarkers of brain injury in athletes after sports-related concussion},
author = {Papa, L and Ramia, M M and Edwards, D and Johnson, B D and Slobounov, S M},
year = {2015},
date = {2015-01-01},
journal = {Journal of Neurotrauma},
volume = {32},
pages = {661--673},
address = {Papa,Linda. 1 Department of Emergency Medicine, Orlando Regional Medical Center , Orlando, Florida.},
abstract = {The aim of this study was to systematically review clinical studies examining biofluid biomarkers of brain injury for concussion in athletes. Data sources included PubMed, MEDLINE, and the Cochrane Database from 1966 to October 2013. Studies were included if they recruited athletes participating in organized sports who experienced concussion or head injury during a sports-related activity and had brain injury biomarkers measured. Acceptable research designs included experimental, observational, and case-control studies. Review articles, opinion papers, and editorials were excluded. After title and abstract screening of potential articles, full texts were independently reviewed to identify articles that met inclusion criteria. A composite evidentiary table was then constructed and documented the study title, design, population, methods, sample size, outcome measures, and results. The search identified 52 publications, of which 13 were selected and critically reviewed. All of the included studies were prospective and were published either in or after the year 2000. Sports included boxing (six studies), soccer (five studies), running/jogging (two studies), hockey (one study), basketball (one study), cycling (one study), and swimming (one study). The majority of studies (92%) had fewer than 100 patients. Three studies (23%) evaluated biomarkers in cerebrospinal fluid (CSF), one in both serum and CSF, and 10 (77%) in serum exclusively. There were 11 different biomarkers assessed, including S100beta, glial fibrillary acidic protein, neuron-specific enolase, tau, neurofilament light protein, amyloid beta, brain-derived neurotrophic factor, creatine kinase and heart-type fatty acid binding protein, prolactin, cortisol, and albumin. A handful of biomarkers showed a correlation with number of hits to the head (soccer), acceleration/deceleration forces (jumps, collisions, and falls), postconcussive symptoms, trauma to the body versus the head, and dynamics of different sports. Although there are no validated biomarkers for concussion as yet, there is potential for biomarkers to provide diagnostic, prognostic, and monitoring information postinjury. They could also be combined with neuroimaging to assess injury evolution and recovery.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
McKee, A C; Daneshvar, D H
The neuropathology of traumatic brain injury Journal Article
In: Handbook of Clinical Neurology, vol. 127, pp. 45–66, 2015.
Abstract | BibTeX | Tags: Physiopathology
@article{McKee2015,
title = {The neuropathology of traumatic brain injury},
author = {McKee, A C and Daneshvar, D H},
year = {2015},
date = {2015-01-01},
journal = {Handbook of Clinical Neurology},
volume = {127},
pages = {45--66},
address = {Mckee,Ann C. VA Boston HealthCare System; Center for the Study of Traumatic Encephalopathy, Alzheimer's Disease Center, and Departments of Neurology and Pathology, Boston University School of Medicine, Boston, MA, USA. Electronic address: amckee@bu.edu. D},
abstract = {Traumatic brain injury, a leading cause of mortality and morbidity, is divided into three grades of severity: mild, moderate, and severe, based on the Glasgow Coma Scale, the loss of consciousness, and the development of post-traumatic amnesia. Although mild traumatic brain injury, including concussion and subconcussion, is by far the most common, it is also the most difficult to diagnose and the least well understood. Proper recognition, management, and treatment of acute concussion and mild traumatic brain injury are the fundamentals of an emerging clinical discipline. It is also becoming increasingly clear that some mild traumatic brain injuries have persistent, and sometimes progressive, long-term debilitating effects. Evidence indicates that a single traumatic brain injury can precipitate or accelerate multiple age-related neurodegenerations, increase the risk of developing Alzheimer's disease, Parkinson's disease, and motor neuron disease, and that repetitive mild traumatic brain injuries can provoke the development of a tauopathy, chronic traumatic encephalopathy. Clinically, chronic traumatic encephalopathy is associated with behavioral changes, executive dysfunction, memory loss, and cognitive impairments that begin insidiously and progress slowly over decades. Pathologically, chronic traumatic encephalopathy produces atrophy of the frontal and temporal lobes, thalamus, and hypothalamus, septal abnormalities, and abnormal deposits of hyperphosphorylated tau (tau) as neurofibrillary tangles and disordered neurites throughout the brain. The incidence and prevalence of chronic traumatic encephalopathy and the genetic risk factors critical to its development are currently unknown. Chronic traumatic encephalopathy frequently occurs as a sole diagnosis, but may be associated with other neurodegenerative disorders, including Alzheimer's disease, Lewy body disease, and motor neuron disease. Currently, chronic traumatic encephalopathy can be diagnosed only at autopsy; however, promising efforts to develop imaging, spinal fluid, and peripheral blood biomarkers are underway to diagnose and monitor the course of disease in living subjects.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Pham, N; Akonasu, H; Shishkin, R; Taghibiglou, C
Plasma soluble prion protein, a potential biomarker for sport-related concussions: a pilot study Journal Article
In: PLoS ONE, vol. 10, pp. e0117286, 2015.
Abstract | BibTeX | Tags: Physiopathology
@article{Pham2015b,
title = {Plasma soluble prion protein, a potential biomarker for sport-related concussions: a pilot study},
author = {Pham, N and Akonasu, H and Shishkin, R and Taghibiglou, C},
year = {2015},
date = {2015-01-01},
journal = {PLoS ONE},
volume = {10},
pages = {e0117286},
address = {Pham,Nam. Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Canada. Akonasu,Hungbo. Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Canada. Shishkin,Rhonda. College of Kinesiolo},
abstract = {Sport-related mild traumatic brain injury (mTBI) or concussion is a significant health concern to athletes with potential long-term consequences. The diagnosis of sport concussion and return to sport decision making is one of the greatest challenges facing health care clinicians working in sports. Blood biomarkers have recently demonstrated their potential in assisting the detection of brain injury particularly, in those cases with no obvious physical injury. We have recently discovered plasma soluble cellular prion protein (PrP(C)) as a potential reliable biomarker for blast induced TBI (bTBI) in a rodent animal model. In order to explore the application of this novel TBI biomarker to sport-related concussion, we conducted a pilot study at the University of Saskatchewan (U of S) by recruiting athlete and non-athlete 18 to 30 year-old students. Using a modified quantitative ELISA method, we first established normal values for the plasma soluble PrP(C) in male and female students. The measured plasma soluble PrP(C) in confirmed concussion cases demonstrated a significant elevation of this analyte in post-concussion samples. Data collected from our pilot study indicates that the plasma soluble PrP(C) is a potential biomarker for sport-related concussion, which may be further developed into a clinical diagnostic tool to assist clinicians in the assessment of sport concussion and return-to-play decision making.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Zetterberg, H; Blennow, K
Fluid markers of traumatic brain injury Journal Article
In: Molecular & Cellular Neurosciences, vol. 66, pp. 99–102, 2015.
Abstract | Links | BibTeX | Tags: Physiopathology
@article{Zetterberg2015,
title = {Fluid markers of traumatic brain injury},
author = {Zetterberg, H and Blennow, K},
doi = {10.1016/j.mcn.2015.02.003},
year = {2015},
date = {2015-01-01},
journal = {Molecular \& Cellular Neurosciences},
volume = {66},
pages = {99--102},
abstract = {Traumatic brain injury (TBI) occurs when an external force traumatically injures the brain. Whereas severe TBI can be diagnosed using a combination of clinical signs and standard neuroimaging techniques, mild TBI (also called concussion) is more difficult to detect. This is where fluid markers of injury to different cell types and subcellular compartments in the central nervous system come into play. These markers are often proteins, peptides or other molecules with selective or high expression in the brain, which can be measured in the cerebrospinal fluid or blood as they leak out or get secreted in response to the injury. Here, we review the literature on fluid markers of neuronal, axonal and astroglial injury to diagnose mild TBI and to predict clinical outcome in patients with head trauma. We also discuss chronic traumatic encephalopathy, a progressive neurodegenerative disease in individuals with a history of multiple mild TBIs in a biomarker context. This article is part of a Special Issue entitled 'Traumatic Brain Injury'. © 2015 Elsevier Inc.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Fakhran, S; Alhilali, L
Neurodegenerative changes after mild traumatic brain injury Miscellaneous
2014.
Abstract | Links | BibTeX | Tags: Physiopathology
@misc{Fakhran2014a,
title = {Neurodegenerative changes after mild traumatic brain injury},
author = {Fakhran, S and Alhilali, L},
doi = {10.1159/000358787},
year = {2014},
date = {2014-01-01},
booktitle = {Progress in Neurological Surgery},
volume = {28},
pages = {234--242},
abstract = {A link between mild traumatic brain injury (mTBI) and neurodegenerative diseases, specifically Alzheimer's disease and chronic traumatic encephalopathy (CTE), has long been suspected. Shared clinical symptomology - most notably the prominent role of central auditory dysfunction and sleepwake disturbances in both disease states - and similar findings on postmortem pathological examination has further reinforced suspected commonality between these seemingly disparate entities. However, conventional imaging techniques, including computed tomography and anatomic magnetic resonance, are unable to detect the symptomatic injuries in mTBI patients and therefore detection of neurodegenerative changes in vivo has previously not been reported. Recent research using diffusion tensor imaging, a novel imaging technique, and focused on patient-reported symptoms has for the first time demonstrated imaging findings in mTBI patients in vivo that are strikingly similar to Alzheimer's dementia and CTE. Moving forward, research will focus on identifying what renders certain patients with mTBI susceptible to developing full-fledged Alzheimer's disease and CTE later in life. © 2014 S. Karger AG, Basel.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {misc}
}
Slobounov, S
Metabolic integrity of primary motor cortex may be compromised in clinically asymptomatic concussed athletes Journal Article
In: Clinical Neurophysiology, vol. 125, pp. 1291–1292, 2014.
BibTeX | Tags: Physiopathology
@article{Slobounov2014,
title = {Metabolic integrity of primary motor cortex may be compromised in clinically asymptomatic concussed athletes},
author = {Slobounov, S},
year = {2014},
date = {2014-01-01},
journal = {Clinical Neurophysiology},
volume = {125},
pages = {1291--1292},
address = {The Pennsylvania State University, University Park, PA 16802, USA. Electronic address: sms18@psu.edu.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Morley, W A; Seneff, S
Diminished brain resilience syndrome: A modern day neurological pathology of increased susceptibility to mild brain trauma, concussion, and downstream neurodegeneration Journal Article
In: Surgical Neurology International, vol. 5, pp. 97, 2014.
Abstract | BibTeX | Tags: Physiopathology
@article{Morley2014,
title = {Diminished brain resilience syndrome: A modern day neurological pathology of increased susceptibility to mild brain trauma, concussion, and downstream neurodegeneration},
author = {Morley, W A and Seneff, S},
year = {2014},
date = {2014-01-01},
journal = {Surgical Neurology International},
volume = {5},
pages = {97},
address = {Morley,Wendy A. Thionetic Nutrition, Richmond Hill, ON L4C 7T3, Canada. Seneff,Stephanie. Spoken Language Systems Group, Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge MA 02139, USA.},
abstract = {The number of sports-related concussions has been steadily rising in recent years. Diminished brain resilience syndrome is a term coined by the lead author to describe a particular physiological state of nutrient functional deficiency and disrupted homeostatic mechanisms leading to increased susceptibility to previously considered innocuous concussion. We discuss how modern day environmental toxicant exposure, along with major changes in our food supply and lifestyle practices, profoundly reduce the bioavailability of neuro-critical nutrients such that the normal processes of homeostatic balance and resilience are no longer functional. Their diminished capacity triggers physiological and biochemical 'work around' processes that result in undesirable downstream consequences. Exposure to certain environmental chemicals, particularly glyphosate, the active ingredient in the herbicide, Roundup(), may disrupt the body's innate switching mechanism, which normally turns off the immune response to brain injury once danger has been removed. Deficiencies in serotonin, due to disruption of the shikimate pathway, may lead to impaired melatonin supply, which reduces the resiliency of the brain through reduced antioxidant capacity and alterations in the cerebrospinal fluid, reducing critical protective buffering mechanisms in impact trauma. Depletion of certain rare minerals, overuse of sunscreen and/or overprotection from sun exposure, as well as overindulgence in heavily processed, nutrient deficient foods, further compromise the brain's resilience. Modifications to lifestyle practices, if widely implemented, could significantly reduce this trend of neurological damage.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Schulte, S; Podlog, L W; Hamson-Utley, J J; Strathmann, F G; Struder, H K
A systematic review of the biomarker S100B: implications for sport-related concussion management Journal Article
In: Journal of Athletic Training, vol. 49, pp. 830–850, 2014.
Abstract | BibTeX | Tags: Physiopathology
@article{Schulte2014,
title = {A systematic review of the biomarker S100B: implications for sport-related concussion management},
author = {Schulte, S and Podlog, L W and Hamson-Utley, J J and Strathmann, F G and Struder, H K},
year = {2014},
date = {2014-01-01},
journal = {Journal of Athletic Training},
volume = {49},
pages = {830--850},
address = {Schulte,Stefanie. Department of Exercise and Sport Science, University of Utah, Salt Lake City;},
abstract = {OBJECTIVE: Elevated levels of the astroglial protein S100B have been shown to predict sport-related concussion. However, S100B levels within an athlete can vary depending on the type of physical activity (PA) engaged in and the methodologic approach used to measure them. Thus, appropriate reference values in the diagnosis of concussed athletes remain undefined. The purpose of our systematic literature review was to provide an overview of the current literature examining S100B measurement in the context of PA. The overall goal is to improve the use of the biomarker S100B in the context of sport-related concussion management. DATA SOURCES: PubMed, SciVerse Scopus, SPORTDiscus, CINAHL, and Cochrane. STUDY SELECTION: We selected articles that contained (1) research studies focusing exclusively on humans in which (2) either PA was used as an intervention or the test participants or athletes were involved in PA and (3) S100B was measured as a dependent variable. DATA EXTRACTION: We identified 24 articles. Study variations included the mode of PA used as an intervention, sample types, sample-processing procedures, and analytic techniques. DATA SYNTHESIS: Given the nonuniformity of the analytical methods used and the data samples collected, as well as differences in the types of PA investigated, we were not able to determine a single consistent reference value of S100B in the context of PA. Thus, a clear distinction between a concussed athlete and a healthy athlete based solely on the existing S100B cutoff value of 0.1 mug/L remains unclear. However, because of its high sensitivity and excellent negative predictive value, S100B measurement seems to have the potential to be a diagnostic adjunct for concussion in sports settings. We recommend that the interpretation of S100B values be based on congruent study designs to ensure measurement reliability and validity.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Di Battista, A P; Rhind, S G; Baker, A J
Application of blood-based biomarkers in human mild traumatic brain injury Journal Article
In: Frontiers in Neurology, vol. 4, pp. 44, 2013.
Abstract | BibTeX | Tags: Physiopathology
@article{DiBattista2013,
title = {Application of blood-based biomarkers in human mild traumatic brain injury},
author = {{Di Battista}, A P and Rhind, S G and Baker, A J},
year = {2013},
date = {2013-01-01},
journal = {Frontiers in Neurology},
volume = {4},
pages = {44},
address = {Faculty of Medicine, Institute of Medical Science, University of Toronto Toronto, ON, Canada.},
abstract = {Traumatic Brain Injury (TBI) is a global health concern. The majority of TBI's are mild, yet our ability to diagnose and treat mild traumatic brain injury (mTBI) is lacking. This deficiency results from a variety of issues including the difficulty in interpreting ambiguous clinically presented symptoms, and ineffective imaging techniques. Thus, researchers have begun to explore cellular and molecular based approaches to improve both diagnosis and prognosis. This has been met with a variety of challenges, including difficulty in relating biological markers to current clinical symptoms, and overcoming our lack of fundamental understanding of the pathophysiology of mTBI. However, recent adoption of high throughput technologies and a change in focus from the identification of single to multiple markers has given just optimism to mTBI research. The purpose of this review is to highlight a number of current experimental peripheral blood biomarkers of mTBI, as well as comment on the issues surrounding their clinical application and utility.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Keefer, Raina
In the game Journal Article
In: ACR Bulletin, vol. 67, no. 10, pp. 10–12, 2012, ISBN: 0098-6070.
BibTeX | Tags: Athletes, Brain -- Pathology, Brain Concussion -- Classification, Brain Concussion -- Complications, Brain Concussion -- Epidemiology -- United States, Brain Concussion -- Pathology, Brain Injuries -- Diagnosis, DIAGNOSTIC imaging, football, FOOTBALL injuries, Imaging & EEG, Physiopathology, Radiologists, Severity of Injury
@article{Keefer2012,
title = {In the game},
author = {Keefer, Raina},
isbn = {0098-6070},
year = {2012},
date = {2012-01-01},
journal = {ACR Bulletin},
volume = {67},
number = {10},
pages = {10--12},
keywords = {Athletes, Brain -- Pathology, Brain Concussion -- Classification, Brain Concussion -- Complications, Brain Concussion -- Epidemiology -- United States, Brain Concussion -- Pathology, Brain Injuries -- Diagnosis, DIAGNOSTIC imaging, football, FOOTBALL injuries, Imaging \& EEG, Physiopathology, Radiologists, Severity of Injury},
pubstate = {published},
tppubtype = {article}
}
Vaughan, C; VanMeter, J; McGuire, E; Gioia, G; Newman, J; Gerst, E; Fricke, S
Neurometabolic change over the course of recovery from concussion Journal Article
In: Archives of Clinical Neuropsychology, vol. 26, pp. 523, 2011, ISSN: 0887-6177.
BibTeX | Tags: Physiopathology
@article{Vaughan2011b,
title = {Neurometabolic change over the course of recovery from concussion},
author = {Vaughan, C and VanMeter, J and McGuire, E and Gioia, G and Newman, J and Gerst, E and Fricke, S},
issn = {0887-6177},
year = {2011},
date = {2011-01-01},
journal = {Archives of Clinical Neuropsychology},
volume = {26},
pages = {523},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Signoretti, S; Vagnozzi, R; Tavazzi, B; Lazzarino, G
Biochemical and neurochemical sequelae following mild traumatic brain injury: summary of experimental data and clinical implications Journal Article
In: Neurosurgical Focus, vol. 29, 2010, ISSN: 1092-0684.
Abstract | Links | BibTeX | Tags: Physiopathology
@article{Signoretti2010,
title = {Biochemical and neurochemical sequelae following mild traumatic brain injury: summary of experimental data and clinical implications},
author = {Signoretti, S and Vagnozzi, R and Tavazzi, B and Lazzarino, G},
doi = {E1 10.3171/2010.9.focus10183},
issn = {1092-0684},
year = {2010},
date = {2010-01-01},
journal = {Neurosurgical Focus},
volume = {29},
abstract = {Although numerous studies have been carried out to investigate the pathophysiology of mild traumatic brain injury (mTBI), there are still no standard criteria for the diagnosis and treatment of this peculiar condition. The dominant theory that diffuse axonal injury is the main neuropathological process behind mTBI is being revealed as weak at best or inconclusive, given the current literature and the fact that neuronal injury inherent to mTBI improves, with few lasting clinical sequelae in the vast majority of patients. Clinical and experimental evidence suggests that such a course, rather than being due to cell death, is based on temporal neuronal dysfunction, the inevitable consequence of complex biochemical and neurochemical cascade mechanisms directly and immediately triggered by the traumatic insult. This report is an attempt to summarize data from a long series of experiments conducted in the authors' laboratories and published during the past 12 years, together with an extensive analysis of the available literature, focused on understanding the biochemical damage produced by an mTBI. The overall clinical implications, as well as the metabolic nature of the post-mTBI brain vulnerability, are discussed. Finally, the application of proton MR spectroscopy as a possible tool to monitor the full recovery of brain metabolic functions is emphasized. (DOI: 10.3171/2010.9.FOCUS10183)},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Rees, Peter
Re: Whiplash and concussion: similar acute changes in middle-latency SEP's. Can J Neurol Sci. 2006; 33: 379-86 Journal Article
In: Canadian Journal of Neurological Sciences, vol. 34, pp. 260, 2007.
BibTeX | Tags: Physiopathology
@article{Rees2007,
title = {Re: Whiplash and concussion: similar acute changes in middle-latency SEP's. Can J Neurol Sci. 2006; 33: 379-86},
author = {Rees, Peter},
year = {2007},
date = {2007-01-01},
journal = {Canadian Journal of Neurological Sciences},
volume = {34},
pages = {260},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Bazarian, Jeffrey J; Zemlan, Frank P; Mookerjee, Sohug; Stigbrand, Torgney
Serum S-100B and cleaved-tau are poor predictors of long-term outcome after mild traumatic brain injury Journal Article
In: Brain Injury, vol. 20, pp. 759–765, 2006.
Abstract | BibTeX | Tags: Physiopathology
@article{Bazarian2006c,
title = {Serum S-100B and cleaved-tau are poor predictors of long-term outcome after mild traumatic brain injury},
author = {Bazarian, Jeffrey J and Zemlan, Frank P and Mookerjee, Sohug and Stigbrand, Torgney},
year = {2006},
date = {2006-01-01},
journal = {Brain Injury},
volume = {20},
pages = {759--765},
address = {Department of Emergency Medicine, University of Rochester School of Medicine, Rochester, New York 14472, USA. jeff_barzarian@urmc.rochester.edu},
abstract = {PRIMARY OBJECTIVE: To determine the relationship of serum S-100B and C-tau levels to long-term outcome after mild traumatic brain injury (mild TBI). RESEARCH DESIGN: A prospective study of 35 mild TBI subjects presenting to the emergency department. METHODS AND PROCEDURES: Six hour serum S-100B and C-tau levels compared to 3-month Rivermead Post Concussion Questionnaire (RPCQ) scores and post-concussive syndrome (PCS). MAIN OUTCOMES AND RESULTS: The linear correlation between marker levels and RPCQ scores was weak (S-100B: r = 0.071, C-tau: r = -0.21). There was no statistically significant correlation between marker levels and 3-month PCS (S-100B: AUC = 0.589, 95%CI. 038, 0.80; C-tau: AUC = 0.634, 95%CI 0.43, 0.84). The sensitivity of these markers ranged from 43.8-56.3% and the specificity from 35.7-71.4%. CONCLUSIONS: Initial serum S-100B and C-tau levels appear to be poor predictors of 3-month outcome after mild TBI.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Bazarian, Jeffrey J; Beck, Christopher; Blyth, Brian; von Ahsen, Nicolas; Hasselblatt, Martin
Impact of creatine kinase correction on the predictive value of S-100B after mild traumatic brain injury Journal Article
In: Restorative Neurology & Neuroscience, vol. 24, pp. 163–172, 2006.
Abstract | BibTeX | Tags: Physiopathology
@article{Bazarian2006b,
title = {Impact of creatine kinase correction on the predictive value of S-100B after mild traumatic brain injury},
author = {Bazarian, Jeffrey J and Beck, Christopher and Blyth, Brian and von Ahsen, Nicolas and Hasselblatt, Martin},
year = {2006},
date = {2006-01-01},
journal = {Restorative Neurology \& Neuroscience},
volume = {24},
pages = {163--172},
address = {Department of Emergency Medicine, University of Rochester School of Medicine, Rochester, NY, USA. jeff_bazarian@urmc.rochester.edu},
abstract = {PURPOSE: To validate a correction factor for the extracranial release of the astroglial protein, S-100B, based on concomitant creatine kinase (CK) levels. METHODS: The CK- S-100B relationship in non-head injured marathon runners was used to derive a correction factor for the extracranial release of S-100B. This factor was then applied to a separate cohort of 96 mild traumatic brain injury (TBI) patients in whom both CK and S-100B levels were measured. Corrected S-100B was compared to uncorrected S-100B for the prediction of initial head CT, three-month headache and three-month post concussive syndrome (PCS). RESULTS: Corrected S-100B resulted in a statistically significant improvement in the prediction of 3-month headache (area under curve [AUC] 0.46 vs 0.52},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Arciniegas, David B
The cholinergic hypothesis of cognitive impairment caused by traumatic brain injury Journal Article
In: Current Psychiatry Reports, vol. 5, pp. 391–399, 2003.
Abstract | BibTeX | Tags: Physiopathology
@article{Arciniegas2003,
title = {The cholinergic hypothesis of cognitive impairment caused by traumatic brain injury},
author = {Arciniegas, David B},
year = {2003},
date = {2003-01-01},
journal = {Current Psychiatry Reports},
volume = {5},
pages = {391--399},
address = {Brain Injury Rehabilitation Unit, Spalding Rehabilitation Hospital, Aurora, CO 80011, USA. david.arciniegas@UCHSC.edu},
abstract = {Cognitive impairments are among the most common neuropsychiatric sequelae of traumatic brain injury at all levels of severity. Cerebral cholinergic neurons and their ascending projections are particularly vulnerable to acute and chronic traumatically mediated dysfunction. In light of the important role of acetylcholine in arousal, attention, memory, and other aspects of cognition, cerebral cholinergic systems contribute to and may also be a target for pharmacologic remediation among individuals with post-traumatic cognitive impairments. This article will review the evidence in support of this hypothesis. Evidence of relatively selective damage to cholinergic injury, the development of persistent anticholinergic sensitivity, and the effects of cholinergic augmentation on memory performance are presented first. Thereafter, neuropathologic, electrophysiologic, and pharmacologic evidence of cholinergic dysfunction after traumatic brain injury in humans is reviewed. Finally, future directions for investigation of the cholinergic hypothesis and possible clinical applications of this information are discussed. [References: 80]},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Alessandri, B; Doppenberg, E; Zauner, A; Woodward, J; Young, H F; Bullock, R
Cortical extracellular sodium transients after human head injury: an indicator of secondary brain damage? Journal Article
In: Acta Neurochirurgica - Supplement, vol. 71, pp. 237–240, 1998.
Abstract | BibTeX | Tags: Physiopathology
@article{Alessandri1998,
title = {Cortical extracellular sodium transients after human head injury: an indicator of secondary brain damage?},
author = {Alessandri, B and Doppenberg, E and Zauner, A and Woodward, J and Young, H F and Bullock, R},
year = {1998},
date = {1998-01-01},
journal = {Acta Neurochirurgica - Supplement},
volume = {71},
pages = {237--240},
address = {Virginia Commonwealth University, Medical College of Virginia, USA.},
abstract = {Animal studies indicate that elevated extracellular sodium can increase glutamate-induced excitotoxicity. Therefore, we investigated the relationship between sodium and glutamate and the effect of changes in sodium concentrations on the outcome of head-injured patients. Thirty-four (34) patients were selected for this study and divided into a group of patients having episodes (\> or = 30-min) of high sodium in dialysates (\> or = 200 mM; HIGH},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}
Pogacnik, T
Characteristics of regional cerebral blood flow in patients with concussion Journal Article
In: Psychiatry Research, vol. 29, pp. 313–316, 1989.
BibTeX | Tags: Physiopathology
@article{Pogacnik1989,
title = {Characteristics of regional cerebral blood flow in patients with concussion},
author = {Pogacnik, T},
year = {1989},
date = {1989-01-01},
journal = {Psychiatry Research},
volume = {29},
pages = {313--316},
address = {University Department of Neurology, University Medical Centre, Ljubljana, Yugoslavia.},
keywords = {Physiopathology},
pubstate = {published},
tppubtype = {article}
}