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Mapping the Injured Brain
Published in Yu Chen, Babak Kateb, Neurophotonics and Brain Mapping, 2017
Chandler Sours, Jiachen Zhuo, Rao P. Gullapalli
Despite variable long-term outcomes across the range of severities based on the GCS classification, the majority of TBI cases, approximately 75%, are diagnosed as mild TBI (mTBI) (Centers for Disease Control and Prevention, 2003). Furthermore, these mild injuries can be further divided based on mechanism of injury into civilian or military blast injuries, each of which has unique features (Magnuson et al., 2012). The leading causes of civilian injuries, in order of prevalence include falls, unintentional blunt trauma, motor vehicle accidents, and assaults (CDC webpage). While civilian mTBI generally results from a direct impact to the brain, military blast mTBI can occur with or without a direct insult to the head, but is caused by overpressurization shock waves originating from high-energy explosives. It is the propagation of this shock wave that travels through the body into the head that is proposed to result in a portion of military mTBI in the absence of a direct impact (Chapman and Diaz-Arrastia, 2014). Further complicating matters, the latest research points to a cumulative effect of multiple concussive or subconcussive events. Referred to as chronic traumatic encephalopathy (CTE), this form of neurodegeneration results from repetitive subconcussive events and results in progressive memory loss and ultimately dementia similar to Alzheimer’s disease (Lakhan and Kirchgessner, 2012).
A mesoscale finite element modeling approach for understanding brain morphology and material heterogeneity effects in chronic traumatic encephalopathy
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2021
A. Bakhtiarydavijani, G. Khalid, M. A. Murphy, K. L. Johnson, L. E. Peterson, M. Jones, M. F. Horstemeyer, A. C. Dobbins, R. K. Prabhu
Chronic Traumatic Encephalopathy (CTE) is a progressive neurodegenerative disease common to a range of contact sports (Bailes et al. 2013). Parker (1934) first documented CTE, also known as punch drunk syndrome or dementia pugilistica, in boxers. This neurodegeneration has since been identified in multiple sports, including boxing (Saing et al. 2012), wrestling (Cajigal 2007), soccer (Geddes et al. 1999), and American professional football (Omalu et al. 2005). More recently, a postmortem study of National Football League (NFL) players found 110 out of 111 of the brains examined suffered from CTE (Mez et al. 2017). Considering the progressive nature of this disease and the lack of sufficient protection through protective gear and guidelines, further study of this disease and its underlying causes can help identify preventive measures and thus benefit the quality of life of these individuals.
Brain tissue analysis of impacts to American football helmets
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2018
Andrew Post, Marshall Kendall, Janie Cournoyer, Clara Karton, R. Anna Oeur, Lauren Dawson, T. Blaine Hoshizaki
In American football helmets were initially created to prevent severe head trauma including skull fractures and brain hematomas and as a result such injuries are rare (Hoshizaki and Brien 2004). Unfortunately, while traumatic brain injury (TBI) has become a rare event, the incidence of concussion has not been effectively managed by helmet technologies (Casson et al. 2010). Concussions in the National Football League (NFL) have been reported as 0.38 injuries per game (Casson et al. 2010) with the suggestion that this injury is greatly underreported (Delaney et al. 2002; McCrea et al. 2004). Youth in particular are at high risk, with over 55,000 reported concussions occurring as a result of participating in American football in 2005–2006 alone (CDC 2006). Head trauma including concussion has become a bigger concern with recent research linking it to chronic traumatic encephalopathy (CTE) in American football (McKee et al. 2009; Gavett et al. 2011; Tartaglia et al. 2014). There has been research examining concussion in American football, but little research has examined the relationship between head impact location and strains throughout the brain that are associated with concussion.
A quantitative risk assessment for chronic traumatic encephalopathy (CTE) in football: How public health science evaluates evidence
Published in Human and Ecological Risk Assessment: An International Journal, 2019
Adam M. Finkel, Kevin F. Bieniek
According to the 2017 Berlin Consensus Statement on Concussion in Sports by 36 neuroscientists, “chronic traumatic encephalopathy (CTE)… appears to represent a distinct tauopathy with an unknown incidence in athletic populations” (McCrory et al.2017). The term “tauopathy” refers to one of several neurodegenerative diseases, including frontotemporal lobar degeneration (FTLD) and progressive supranuclear palsy (PSP), in which the protein tau (found in normal human brain) becomes abnormally aggregated and forms inclusion bodies within nerve and glial cells in the brain. The abnormal tau becomes burdened by an excess of phosphate groups (hyperphosphorylation). A frequent inclusion body containing abnormal and insoluble tau is the “neurofibrillary tangle,” a lesion most often seen in the Alzheimer's disease (AD) brain.14AD also involves aggregation of hyperphosphorylated tau, but because its primary hallmark is the accumulation of fibrils of amyloid protein within plaques, it is considered a “secondary tauopathy.” CTE per se (when not co-existing with AD) does not display amyloid accumulation. In CTE, these tangles accumulate in a characteristic pattern that is different from AD and other tauopathies. A consensus conference of neuropathologists, sponsored by the National Institutes of Health, defined the pathognomonic lesion of CTE as hyperphosphorylated tau aggregates in neurons, astrocytes, and cell processes around small vessels in an irregular pattern at the depths of the cortical sulci (McKee et al.2016). There appear to be two different clinical presentations of CTE (Stern et al.2013); some cases begin relatively early in life (ages 30–50) and involve behavioral and mood disturbances with minimal cognitive impairment, while others begin later in life and display marked cognitive impairment and often motor disturbances as well.