scholarly journals Consider the woodpecker: The contested more-than-human ethics of biomimetic technology and traumatic brain injury

2021 ◽  
pp. 030631272110525
Author(s):  
Gregory Hollin

Chronic Traumatic Encephalopathy, or CTE, is a neurodegenerative disease caused by traumatic brain injury and most frequently associated with contact sports such as American Football. Perhaps surprisingly, the woodpecker – an animal apparently immune to the effects of head impacts – has increasingly figured into debates surrounding CTE. On the one hand, the woodpecker is described as being contra-human and used to underscore the radical inappropriateness of humans playing football. On the other, there have been attempts to mitigate against the risk of CTE through the creation of biomimetic technologies inspired by woodpeckers. In this article I examine the highly politicized encounters between humans and woodpeckers and discuss how the politics of re-/dis-/en-tanglement during these interspecies relations is rendered meaningful. I show here, first, that those who seek to keep the human and the woodpecker apart envisage social overhaul while biomimetic technologies are put to work for the status quo. Second, I stress that different forms of entanglement have diverse sociopolitical consequences. I conclude by suggesting that the case of the woodpecker troubles a strand of contemporary scholarship in Science and Technology Studies that argues that biotechnologies are inherently transformatory and that foregrounding entanglement and interspecies relations is ethically generative. Instead, a discursive separation of nature and culture may be innovative.

2018 ◽  
Vol 120 (1) ◽  
pp. 1-3
Author(s):  
Megan E. Huibregtse

Chronic traumatic encephalopathy (CTE) is thought to be caused by repetitive head impacts. Consequently, there is a need to develop rodent models to better understand the behavioral and pathophysiological changes of repetitive mild traumatic brain injury (rmTBI) and to determine the link between rmTBI and CTE. This Neuro Forum article reviews recent rodent rmTBI models, comparing the impact methods and outcome measures in terms of translational potential.


Author(s):  
Nicole L. Ackermans ◽  
Merina Varghese ◽  
Bridget Wicinski ◽  
Joshua Torres ◽  
Rita De Gasperi ◽  
...  

Biomarkers ◽  
2020 ◽  
Vol 25 (3) ◽  
pp. 213-227 ◽  
Author(s):  
Matthew I. Hiskens ◽  
Anthony G. Schneiders ◽  
Mariana Angoa-Pérez ◽  
Rebecca K. Vella ◽  
Andrew S. Fenning

2014 ◽  
Vol 8 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Jéssica Natuline Ianof ◽  
Fabio Rios Freire ◽  
Vanessa Tomé Gonçalves Calado ◽  
Juliana Rhein Lacerda ◽  
Fernanda Coelho ◽  
...  

ABSTRACT Traumatic brain injury (TBI) is a major cause of lifelong disability and death worldwide. Sport-related traumatic brain injury is an important public health concern. The purpose of this review was to highlight the importance of sport-related concussions. Concussion refers to a transient alteration in consciousness induced by external biomechanical forces transmitted directly or indirectly to the brain. It is a common, although most likely underreported, condition. Contact sports such as American football, rugby, soccer, boxing, basketball and hockey are associated with a relatively high prevalence of concussion. Various factors may be associated with a greater risk of sport-related concussion, such as age, sex, sport played, level of sport played and equipment used. Physical complaints (headache, fatigue, dizziness), behavioral changes (depression, anxiety, irritability) and cognitive impairment are very common after a concussion. The risk of premature return to activities includes the prolongation of post-concussive symptoms and increased risk of concussion recurrence.


Author(s):  
Thomas Blaine Hoshizaki ◽  
Clara Karton ◽  
R. Anna Oeur ◽  
Marshall Kendall ◽  
Lauren Dawson ◽  
...  

Brain injuries are prevalent in the sport of American football. Helmets have been used which effectively have reduced the incidence of traumatic brain injury, but have had a limited effect on concussion rates. In an effort to improve the protective capacity of American football helmets, a standard has been proposed by National Operating Committee on Standards for Athletic Equipment that may better represent helmet-to-helmet impacts common to football concussions. The purpose of this research was to examine the National Operating Committee on Standards for Athletic Equipment standard and a new impact method similar to the proposed National Operating Committee on Standards for Athletic Equipment standard to examine the information these methods provide on helmet performance. Five National Operating Committee on Standards for Athletic Equipment–certified American football helmets were impacted according to the National Operating Committee on Standards for Athletic Equipment standard test and a new method based on the proposed standard test. The results demonstrated that the National Operating Committee on Standards for Athletic Equipment test produced larger linear accelerations than the new method, which were a reflection of the stiffer compliance of the standard meant to replicate traumatic brain injury mechanisms of injury. When the helmets were impacted using a new helmet-to-helmet method, the results reflected significant risk of concussive injury but showed differences in rotational acceleration responses between different helmet models. This suggests that the new system is sensitive enough to detect the effect of different design changes on rotational acceleration, a metric more closely associated with risk of concussion. As only one helmet produced magnitudes of response lower than the National Operating Committee on Standards for Athletic Equipment pass/fail using the new system, and all helmets passed the National Operating Committee on Standards for Athletic Equipment standard, these results suggest that further development of helmet technologies must be undertaken to reduce this risk in the future. Finally, these results show that it would be prudent to use both standards together to address risk of injury from traumatic brain injury and concussion.


2018 ◽  
Vol 89 (10) ◽  
pp. A42.1-A42
Author(s):  
Graham Neil SN ◽  
Jolly Amy E ◽  
Bourke Niall J ◽  
Scott Gregory ◽  
Cole James H ◽  
...  

BackgroundDementia rates are elevated after traumatic brain injury (TBI) and a subgroup develops chronic traumatic encephalopathy. Post-traumatic neurodegeneration can be measured by brain atrophy rates derived from neuroimaging, but it is unclear how atrophy relates to the initial pattern of injury.ObjectivesTo investigate the relationship between baseline TBI patterns and subsequent neurodegeneration measured by progressive brain atrophy.Methods55 patients after moderate-severe TBI (mean 3 years post-injury) and 20 controls underwent longitudinal MRI. Brain atrophy was quantified using the Jacobian determinant defined from volumetric T1 scans approximately one year apart. Diffuse axonal injury was measured using diffusion tensor imaging and focal injuries defined from T1 and FLAIR. Neuropsychological assessment was performed.ResultsAbnormal progressive brain atrophy was seen after TBI (~1.8%/year in white matter). This was accompanied by widespread reductions in fractional anisotropy, in keeping with the presence of diffuse axonal injury. There was a strong negative correlation between FA and brain atrophy, whereby areas of greater white matter damage showed greater atrophy over time.ConclusionsThe results show a strong relationship between the location of diffuse axonal injury and subsequent neurodegeneration. This suggests that TBI triggers progressive neurodegeneration through the long-lasting effects of diffuse axonal injury.


2019 ◽  
Vol 13 ◽  
pp. 117906951984993 ◽  
Author(s):  
Melissa Demock ◽  
Steven Kornguth

A mechanism that describes the progression of traumatic brain injury (TBI) to end-stage chronic traumatic encephalopathy (CTE) is offered in this article. This mechanism is based upon the observed increase in the concentration of both tau protein and of human leukocyte antigen (HLA) class I proteins; the HLA increase is expressed on the cell membrane of neural cells. These events follow the inflammatory responses caused by the repetitive TBI. Associated inflammatory changes include macrophage entry into the brain parenchyma from increased permeability of the blood-brain barrier (BBB) and microglial activation at the base of the sulci. The release of interferon gamma from the microglia and macrophages induces the marked increased expression of HLA class I proteins by the neural cells and subsequent redistribution of the tau proteins to the glial and neuronal surface. In those individuals with highly expressed HLA class I C, the high level of HLA binds tau protein electrostatically. The ionic region of HLA class I C (amino acid positions 50-90) binds to the oppositely charged ionic region of tau (amino acid positions 93-133). These interactions thereby shift the cellular localization of the tau and orient the tau spatially so that the cross-linking sites of tau (275-280 and 306-311) are aligned. This alignment facilitates the cross-linking of tau to form the intracellular and extracellular microfibrils of tau, the primary physiological characteristic of tauopathy. Following endocytosis of the membrane HLA/tau complex, these microfibrils accumulate and produce a tau-storage-like disease. Therefore, tauopathy is the secondary collateral process of brain injury, resulting from the substantial increase in tau and HLA expression on neural cells. This proposed mechanism suggests several potential targets for mitigating the clinical progression of TBI to CTE.


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