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Abstract Since the original descriptions of postconcussive pathophysiology, there has been a significant increase in interest and ongoing research to study the biological underpinnings of concussion. The initial ionic flux and glutamate release result in significant energy demands and a period of metabolic crisis for the injured brain. These physiological perturbations can now be linked to clinical characteristics of concussion, including migrainous symptoms, vulnerability to repeat injury, and cognitive impairment. Furthermore, advanced neuroimaging now allows a research window to monitor postconcussion pathophysiology in humans noninvasively. There is also increasing concern about the risk for chronic or even progressive neurobehavioral impairment after concussion/mild traumatic brain injury. Critical studies are underway to better link the acute pathobiology of concussion with potential mechanisms of chronic cell death, dysfunction, and neurodegeneration. This “new and improved” article summarizes in a translational fashion and updates what is known about the acute neurometabolic changes after concussive brain injury. Furthermore, new connections are proposed between this neurobiology and early clinical symptoms as well as to cellular processes that may underlie long-term impairment.

For over two decades, the Concussion in Sport Group has held meetings and developed five international statements on concussion in sport. This 6th statement summarises the processes and outcomes of the 6th International Conference on Concussion in Sport held in Amsterdam on 27–30 October 2022 and should be read in conjunction with the (1) methodology paper that outlines the consensus process in detail and (2) 10 systematic reviews that informed the conference outcomes. Over 3½ years, author groups conducted systematic reviews of predetermined priority topics relevant to concussion in sport. The format of the conference, expert panel meetings and workshops to revise or develop new clinical assessment tools, as described in the methodology paper, evolved from previous consensus meetings with several new components. Apart from this consensus statement, the conference process yielded revised tools including the Concussion Recognition Tool-6 (CRT6) and Sport Concussion Assessment Tool-6 (SCAT6, Child SCAT6), as well as a new tool, the Sport Concussion Office Assessment Tool-6 (SCOAT6, Child SCOAT6). This consensus process also integrated new features including a focus on the para athlete, the athlete’s perspective, concussion-specific medical ethics and matters related to both athlete retirement and the potential long-term effects of SRC, including neurodegenerative disease. This statement summarises evidence-informed principles of concussion prevention, assessment and management, and emphasises those areas requiring more research.

Correspondence to Dr Paul McCrory, The Florey Institute of Neuroscience and Mental Health, Heidelberg 3084, Victoria, Australia; paulmccrory@icloud.com Preamble The 2017 Concussion in Sport Group (CISG) consensus statement is designed to build on the principles outlined in the previous statements1–4 and to develop further conceptual understanding of sport-related concussion (SRC) using an expert consensus-based approach. First and foremost, this document is intended to guide clinical practice; however, the authors feel that it can also help form the agenda for future research relevant to SRC by identifying knowledge gaps. At present, there is no perfect diagnostic test or marker that clinicians can rely on for an immediate diagnosis of SRC in the sporting environment. Because of this evolving process, it is not possible to rule out SRC when an injury event occurs associated with a transient neurological symptom. [...]tests include the SCAT5, which incorporates the Maddocks' questions6 7 and the Standardised Assessment of Concussion (SAC).8–10 It is worth noting that standard orientation questions (eg, time, place, person) are unreliable in the sporting situation when compared with memory assessment.7 11 It is recognised, however, that abbreviated testing paradigms are designed for rapid SRC screening on the sidelines and are not meant to replace a comprehensive neurological evaluation; nor should they be used as a standalone tool for the ongoing management of SRC.

Traumatic brain injury (TBI) is defined as an impact, penetration or rapid movement of the brain within the skull that results in altered mental state. TBI occurs more than any other disease, including breast cancer, AIDS, Parkinson’s disease and multiple sclerosis, and affects all age groups and both genders. In the US and Europe, the magnitude of this epidemic has drawn national attention owing to the publicity received by injured athletes and military personnel. This increased public awareness has uncovered a number of unanswered questions concerning TBI, and we are increasingly aware of the lack of treatment options for a crisis that affects millions. Although each case of TBI is unique and affected individuals display different degrees of injury, different regional patterns of injury and different recovery profiles, this review and accompanying poster aim to illustrate some of the common underlying neurochemical and metabolic responses to TBI. Recognition of these recurrent features could allow elucidation of potential therapeutic targets for early intervention.

Chronic traumatic encephalopathy (CTE) is an acquired primary tauopathy with a variety of cognitive, behavioral, and motor symptoms linked to cumulative brain damage sustained from single, episodic, or repetitive traumatic brain injury (TBI). No definitive clinical diagnosis for this condition exists. In this work, we used [F-18]FDDNP PET to detect brain patterns of neuropathology distribution in retired professional American football players with suspected CTE ( n = 14) and compared results with those of cognitively intact controls ( n = 28) and patients with Alzheimer’s dementia (AD) ( n = 24), a disease that has been cognitively associated with CTE. [F-18]FDDNP PET imaging results in the retired players suggested the presence of neuropathological patterns consistent with models of concussion wherein brainstem white matter tracts undergo early axonal damage and cumulative axonal injuries along subcortical, limbic, and cortical brain circuitries supporting mood, emotions, and behavior. This deposition pattern is distinctively different from the progressive pattern of neuropathology [paired helical filament (PHF)-tau and amyloid-β] in AD, which typically begins in the medial temporal lobe progressing along the cortical default mode network, with no or minimal involvement of subcortical structures. This particular [F-18]FDDNP PET imaging pattern in cases of suspected CTE also is primarily consistent with PHF-tau distribution observed at autopsy in subjects with a history of mild TBI and autopsy-confirmed diagnosis of CTE. Significance Mild traumatic brain injuries are frequent events in the general population and are associated with a severe neurodegenerative disease, chronic traumatic encephalopathy (CTE). This disease is characterized by abnormal accumulation of protein aggregates, primarily tau proteins, which accumulate in brain areas responsible for mood, fear, stress, and cognition. There is no definitive clinical diagnosis of CTE at the present time, and this new work shows how a tau-sensitive brain imaging agent, [F-18]FDDNP, may be able to detect the disease in living people with varying degrees of symptoms. Early detection would facilitate the most effective management strategies and provide a baseline to measure the effectiveness of treatments.

This article presents the Child Sport Concussion Assessment Tool 5th Edition (Child SCAT5). The Sport Concussion Assessment Tool was introduced in 2004, following the 2nd International Conference on Concussion in Sport in Prague, Czech Republic. Following the 4th International Consensus Conference, held in Zurich, Switzerland, in 2012, the SCAT 3rd edition (Child SCAT3) was developed for children aged between 5 and12 years. Research to date was reviewed and synthesised for the 5th International Consensus Conference on Concussion in Sport in Berlin, Germany, leading to the current revision of the test, the Child SCAT5. This article describes the development of the Child SCAT5.

Soccer participation in the United States (U.S.) has increased over time, and injuries as well as interest to prevent injuries has become more common. This study described Emergency Department (ED) visits related to concussions, intracranial injuries (ICI), and all-other injuries attributed to soccer play; described healthcare cost and length of hospital stay of soccer-related injuries; and determined independent predictors of concussions, ICI, and all-other soccer injuries leading to ED visits. The study examined soccer-related weighted discharge data from the Nationwide Emergency Department Sample, Healthcare Cost and Utilization Project, Agency for Healthcare Research and Quality. Weighted tabular analysis of univariate and bivariate analyses and weighted and adjusted logistic regression models were conducted. A total of 480,580 of U.S. ED visits related to soccer injuries were available for analysis between 2010 to 2013. Generally, 98% of soccer-related ED visits resulted in routine (treat-and-release) visits. However, the odds of transfer to a short-term hospital following ED evaluation and treatment was more than 37-fold higher for soccer-injured youth and adults diagnosed with ICI when compared to all-other soccer injuries; additionally, these patients showed 28-fold higher odds of being admitted for inpatient care at the ED-affiliated hospital. For concussion, soccer-injured patients with concussion showed nearly 1.5-fold higher odds of being transferred to a short-term hospital than did those with any other soccer injury. Soccer-related ED visits cost more than 700 million in U.S. dollars from 2010 to 2013. Notable differences were noted between concussions, ICI, and all-other soccer injuries presenting to U.S. ED. Albeit underestimated given that this study excludes other forms of health care and treatment for injuries, such as outpatient clinics, over the counter medications and treatment, and rehabilitation, healthcare cost associated with soccer-related injuries presenting to ED is high, and remarkably costly in those with an ICI diagnosis.

Neuroimaging has expanded our understanding of pediatric brain disorders in which white matter organization and connectivity are crucial to functioning. Paralleling the known pathobiology of many neurodevelopmental disorders, traumatic brain injury (TBI) in childhood can alter trajectories of brain development. Specifically, diffusion tensor imaging (DTI) studies in TBI have demonstrated white matter (WM) abnormalities that suggest microstructural disruptions that may underlie atypical neurodevelopment. The neurocognitive correlates of these previous findings will be explored in this study. Indicators of WM organization were collected in 44 pediatric patients with moderate/severe TBI and 76 controls over two post-injury time points: T1 (8-20 weeks) and T2 (54-96 weeks). Our previous work identified two TBI subgroups based on information processing differences: one with slower interhemispheric transfer times (IHTT) of visual information than controls and another with comparable IHTT. We extend this prior work by evaluating neurocognitive trajectories associated with divergent WM structure post-injury in slow and normal IHTT TBI subgroups. At T1, both TBI subgroups performed significantly worse than controls on a norm-referenced working memory index (WMI), but only the Normal IHTT TBI subgroup significantly improved over the 12-month follow-up period ( = 0.014) to match controls ( = 0.119). In contrast, the Slow IHTT TBI subgroup did not show any recovery in working memory performance over time and performed more poorly than the control group ( < 0.001) at T2. Improvement in one of the two WMI subtests was associated with DTI indicators of WM disorganization in CC tracts to the precentral, postcentral, frontal, and parietal cortices. IHTT and WM mean diffusivity predicted 79% of the variance in cognitive recovery from T1 to T2 when also accounting for other known predictors of TBI recovery. In the year following TBI, some pediatric patients experienced persisting working memory disturbance while others exhibited recovery; stratification was based on an event-related potential marker. More or less improvement in neurocognition was also associated with the degree of WM disorganization. IHTT, measured post-acutely after TBI, and progression of WM disorganization over time predicted neurocognitive trajectories at the chronic timeframe - potentially representing a prognostic biomarker.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of nigrostriatal dopaminergic neurons and the accumulation of alpha-synuclein. Both traumatic brain injury (TBI) and pesticides are risk factors for PD, but whether TBI causes nigrostriatal dopaminergic cell loss in experimental models and whether it acts synergistically with pesticides is unknown. We have examined the acute and long-term effects of TBI and exposure to low doses of the pesticide paraquat, separately and in combination, on nigrostriatal dopaminergic neurons in adult male rats. In an acute study, rats received moderate TBI by lateral fluid percussion (LFP) injury, were injected with saline or paraquat (10 mg/kg IP) 3 and 6 days after LFP, were sacrificed 5 days later, and their brains processed for immunohistochemistry. TBI alone increased microglial activation in the substantia nigra, and caused a 15% loss of dopaminergic neurons ipsilaterally. Paraquat increased the TBI effect, causing a 30% bilateral loss of dopaminergic neurons, reduced striatal tyrosine hydroxylase (TH) immunoreactivity more than TBI alone, and induced alpha-synuclein accumulation in the substantia nigra pars compacta. In a long-term study, rats received moderate LFP, were injected with saline or paraquat at 21 and 22 weeks post-injury, and were sacrificed 4 weeks later. At 26 weeks post injury, TBI alone induced a 30% bilateral loss of dopaminergic neurons that was not exacerbated by paraquat. These data suggest that TBI is sufficient to induce a progressive degeneration of nigrostriatal dopaminergic neurons. Furthermore, TBI and pesticide exposure, when occurring within a defined time frame, could combine to increase the PD risk.

Traumatic brain injury (TBI) in children, while the brain is in a state of rapid change and development, can adversely impact their development, their extended environment, and their families. The extant literature has identified several physiological, genetic, and environmental variables that predict outcomes after pediatric TBI; nonetheless, the individual course of recovery and later development of a given child is uniquely shaped by injury-related factors (e.g., nature and extent of the injury itself, the developmental status of the child) as well as a number of personal and family variables (e.g., pre-injury cognitive, genetic, and psychological status of the child, family functioning and resources, coping style). Further, the effects of a brain injury during development may or may not become evident immediately after injury depending on a number of factors. Instead, observing trajectories of development over time may allow for a better understanding of the long-term consequences in many functional domains that interest researchers, clinicians, and families. The current article reviews the chronic aspects of medical/health, cognitive/academic, emotional/behavioral, and family/social outcomes after pediatric TBI, with the goal of providing monitoring and treatment strategies for affected children and their families, as well as serving as a resource for researchers designing studies to better understand this heterogeneous population.