CTE, or chronic traumatic encephalopathy, is caused by repetitive head trauma and detected by a distinctive stain for a protein called ‘tau’ in autopsied brain tissue. While the number of diagnosed patients is only in the hundreds, the cultural footprint of the disease in North America is huge, both because those diagnosed are often celebrity-athletes and because millions of children, adolescents and young men and women play collision sports like football and hockey. We argue that the widespread attention to CTE provides a useful wedge to crack open another, heretofore neglected public health concern: repetitive acts of violence in and around hypermasculine sports create subjects whose brains—and characters—are materially shaped by that violence. Brains change materially when delivering blows as well as receiving them, when participating in degrading hazing rituals as victim or assailant, when belittled or assaulted by a coach, when approaching an upcoming game riddled with fear. We adopt a biosocial model of the brain’s becoming to intervene in a linear discourse around CTE that medicalizes and oversimplifies violence, a story that prematurely dissects one slice of the problem from a noxious whole.

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The article Concussion killjoys: CTE, violence and the brain’s becoming, written by Aryn Martin and Alasdair McMillan, was originally published electronically on the publisher’s internet portal on 30 October 2020 without open access. With the author(s)’ decision to opt for Open Choice the copyright of the article changed on 9 February 2021 to © The Author(s) 2021 and the article is forthwith distributed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licen ses/by/4.0/.

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Schizophrenia. antipsychotics and neuroimaging 421s outside of 2 standard deviations were considered abnormal. In contrastto a group of 61 age-matched normal controls. Vmean in MCA and ACA was significantly increased in the schizophrenic group on admission (p < 0.05). PI was not significantly changed in any of the ultrasounded vessels.Vmeanshoweda significant positivecorrelation to the degreeof positivesymptomatology in PANSS(p < 0.05). After psychopathological improvement, a significant decrease of Vmean was found(p < 0.05). First results indicate a correlation between the increased blood flowvelocity found inTCD and brain SPECTresults. Thus. increased Vmean in frontal brain circulation may be seen as an indication of increased perfusion (SPECT), which correlates positively with the degree of productive schizophrenic symptomatology. Further study will show ifTCD may be used routinelyto add to. or even substitute. SPECTor PET examinations, thus constitutingan alternative method to radionuclides.