AbstractRepetitive subconcussive head impacts occur regularly in sports. However, the exact relationship between their biomechanical properties and their consequences on brain structure and function has not been clarified yet. We therefore reviewed prospective cohort studies that objectively reported the biomechanical characteristics of repetitive subconcussive head impacts and their impact on brain anatomy and function. Only studies with a pre- to post-measurement design were included. Twenty-four studies met the inclusion criteria. Structural white matter alterations, such as reduced fractional anisotropy and an increase in mean diffusivity values, seem to be evident in athletes exposed to repetitive subconcussive head impacts exceeding 10 g. Such changes are observable after only one season of play. Furthermore, a dose-response relationship exists between white matter abnormalities and the total number of subconcussive head impacts. However, functional changes after repetitive subconcussive head impacts remain inconclusive. We therefore conclude that repetitive subconcussive head impacts induce structural changes, but thus far without overt functional changes.

Contact events in rugby codes such as tackling, running into contact, scrums, rucks, and contact with the playing surface may expose athletes to muscle damage known as impact-induced muscle damage. These repetitive impacts to muscle tissue have the potential to diminish muscle force production and delay recovery following contact-focused training and match-play. Repetitive exposure to contacts may also affect the surrounding vascular and neuronal tissues, an area that has received little attention in the collision sports. Depending on the severity and duration of tissue damage, repetitive contact exposure without sufficient recovery or noticeable adaptation may predispose collision sport athletes to impaired performance and long-term health complications. The aim of this narrative review is to provide a conceptual framework for understanding the physiological implications of contact exposure in collision sports. We examine the current understanding of impact-induced muscle damage (IIMD), how it differs from exercise-induced muscle damage (EIMD), and its relationship with contact exposure in collision sports. Drawing on both experimental animal models of contusion injury and limited human observational research, we explore the effects of repeated contact exposure on the microvasculature and its implications for both athletic performance and player welfare. To account for all tissues that may be affected by impacts, including muscle, nerve, vascular, connective tissue, skin, other organs and bones, we recommend impact-induced tissue damage (IITD) as the preferred descriptor rather than IIMD. Finally, we discuss the concept of contact adaptation and provide recommendations for future research on IITD in collision sports.

Traumatic brain injury (TBI) remains a significant public health concern, particularly among military personnel and contact sport athletes who are frequently exposed to repeated blast overpressure waves and mild concussive impacts, respectively. While moderate and severe TBIs have been extensively studied, the long-term neuroendocrine consequences of mild, repetitive brain trauma are poorly understood. In this study, we investigated the temporal dynamics of hypothalamic-pituitary-adrenal (HPA) axis dysregulation following repeated mild concussive head impacts and blast exposures using two clinically relevant rodent models. Male Sprague-Dawley rats were subjected to repeated mild concussive impacts using a modified weight drop model or repeated blast exposures using an advanced blast simulator. Plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone were measured on days 1 and 30 post-injuries. Our findings revealed that repeated blast exposures induced elevation of plasma ACTH and corticosterone on days 1 and 30 post-blasts. After the repeated mild concussive impacts, increased plasma levels of corticosterone were observed on days 1 and 30, but ACTH levels were increased only on day 30. This study is among the first to directly compare neuroendocrine outcomes of repeated mild concussive impacts and blast exposures within a unified experimental framework. Our findings demonstrate distinct temporal trajectories of HPA axis dysregulation depending on injury type and highlight plasma levels of ACTH and corticosterone as potential biomarkers of subclinical brain trauma. These insights may inform early diagnostic approaches and therapeutic strategies aimed at mitigating long-term stress-related complications following mild traumatic brain injuries.

Abstract Blood-based biomarkers of brain injury may be useful for monitoring brain health in athletes at risk for concussions. Two putative biomarkers of sport-related concussion, neurofilament light (NfL), an axonal structural protein, and S100 calcium-binding protein beta (S100B), an astrocyte-derived protein, were measured in saliva, a biofluid which can be sampled in an athletic setting without the risks and burdens associated with blood sampled by venipuncture. Samples were collected from men’s and women’s collegiate water polo players (n = 65) before and after a competitive tournament. Head impacts were measured using sensors previously evaluated for use in water polo, and video recordings were independently reviewed for the purpose of validating impacts recorded by the sensors. Athletes sustained a total of 107 head impacts, all of which were asymptomatic (i.e., no athlete was diagnosed with a concussion or more serious). Post-tournament salivary NfL was directly associated with head impact frequency (RR = 1.151, p = 0.025) and cumulative head impact magnitude (RR = 1.008, p = 0.014), while controlling for baseline salivary NfL. Change in S100B was not associated with head impact exposure (RR 0.483). These patterns suggest that repeated head impacts may cause axonal injury, even in asymptomatic athletes.

In vitro studies of multiple impact injury to mammalian CNS neurons: prevention of perikaryal damage and death by ketamine. We have developed an in vitro model of rapid acceleration injury (RAI) to study the effects of multiple impact (220 g/impact, 3-5 s intervals) trauma on cultures of mammalian CNS cells. Our initial investigations have shown that: (1) multiple impacts delivered tangential to the plane of growth caused neuronal death while normal impacts did not; (2) glia were not affected by tangential or normal RAI; (3) most neuronal death occurred within 15 min; (4) the threshold for neuronal death was above 440 g (cumulative); (5) neuronal death reached a maximum of 50% at cumulative accelerations greater than or equal to 1100 g; (6) somal swelling and increased nuclear prominence were often observed after tangential RAI, and the frequency of these changes increased with the cumulative acceleration; and (7) ketamine prevented neuronal death and morphological changes during tangential RAI. We hypothesize that neuronal sensitivity to multiple impact RAI depends on the density of N-methyl-D-aspartate (NMDA) complexes in the dendrosomatic membranes.

About Repeated Head Impacts | Traumatic Brain Injury & Concussion | CDC Skip directly to site content Skip directly to search An official website of the United States government Here's how you know Official websites use .gov A .gov website belongs to an official government organization in the United States. Secure .gov websites use HTTPS A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites. May 16, 2024 About Repeated Head Impacts Key Points Repeated head impacts may or may not lead to concussion symptoms. Collisions while playing sports is one way a person may experience repeated head impacts. Chronic traumatic encephalopathy (CTE) is a brain disease that affects how the brain works. Overview There is growing concern about the long-term effects on the brain of people who experience multiple or repeated head impacts. Repeated head impacts include not only head impacts that lead to a mild TBI or concussion, but also head impacts that do not cause the person to feel symptoms after a hit to the head. Collisions while playing sports is one way a person may experience repeated head impacts. A CDC study found that youth tackle football athletes ages 6 to 14 sustained 15 times more head impacts than flag football athletes during a practice or game and sustained 23 times more high-magnitude head impacts (hard head impacts). Chronic Traumatic Encephalopathy (CTE) Chronic traumatic encephalopathy (CTE) is a brain disease that affects how the brain works. It is linked to a build-up of abnormal proteins that damage brain tissue and cause brain cells to undergo cell death. 1 2 Research suggests CTE is associated with long-term exposure to repeated hits to the head (head impacts). There is no strong evidence that shows that getting one or more concussions (or other mild traumatic brain injuries) or occasional hits to the head leads to CTE. 3 4 More research is needed to better understand: Potential

indicates that the brain damage in CTE is caused by the cumulative impact of all collisions involving a player's head, which confirms what was generally known Chronic traumatic encephalopathy (CTE) is a type of brain damage that has been found in 345 of 376 deceased former National Football League (NFL) players, according to a 2023 report by the Boston University CTE Center, which has led the effort to diagnose CTE cases. In comparison, a 2018 BU study of the general population found one CTE case in 164 autopsies, and the one person with CTE had played Chronic traumatic encephalopathy (CTE) is a type of brain damage that has been found in 345 of 376 deceased former National Football League (NFL) players, according to a 2023 report by the Boston University CTE Center, which has led the effort to diagnose CTE cases. In comparison, a 2018 BU study of the general population found one CTE case in 164 autopsies, and the one person with CTE had played college football. The NFL acknowledged a link between playing American football and being diagnosed with CTE in 2016, after denying such a link for over a decade and arguing that players' symptoms had other causes. While much attention in the NFL has focused on limiting or treating concussions, the latest medical research indicates that the brain damage in CTE is caused by the cumulative impact of all collisions involving a player's head, which confirms what was generally known nearly a century ago but was then largely forgotten. The NFL has implemented rule changes to reduce collisions to the head and has sought to improve football helmet design. Critics respond that significant head trauma is inevitable for bigger, faster players in tackle football and that helmets are of limited use in preventing a player's brain from crashing into their skull, which is the cause of the brain damage that leads to CTE. As more parents (including some NFL players) decide not to let their children play football, it remains to be seen whether football will eventually face a significant decline in popularity like boxing, which fell from prominence as the brain damage suffered by ex-boxers drew more public attention. As of 2023 football is the most-watched sport in the U.S. by a substantial margin while basketball is the most-played sport.

Background Sport-related concussions (SRCs) are known to have short-term effects on cognitive processes, which can result in diverse clinical presentations. The long-term effects of SRC and repeated exposure to head impacts that do not result in SRC on specific cognitive health outcomes remain unclear. Objectives To synthesize and appraise the evidence base regarding cognitive health in living retired athletes with a history of head-impact exposure or SRC. Data Sources A systematic search of the EMBASE, PsycINFO, MEDLINE/PubMed, CINAHL, Cochrane Central Register of Controlled Trials, and Web of Science databases was conducted from inception to April 2018 using common key words and medical subject headings related to 3 components: (1) the participant (eg, retired athlete), (2) the primary outcome measure (eg, cognitive test used), and (3) the secondary outcome measure (eg, history of sport concussion). Study Selection Cross-sectional studies of living retired male or female athletes in which at least 1 cognitive test was used as an outcome measure were included. Two reviewers independently screened studies. Data Extraction Data extraction was performed using Strengthening the Reporting of Observational Studies in Epidemiology guidelines. Methodologic quality was assessed independently by 2 reviewers using the Downs and Black tool. Data Synthesis The search yielded 46 cross-sectional observational studies that were included in a qualitative synthesis. Most included studies (80%