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Staying in the game: a pilot study examining the efficacy of protective headgear in an animal model of mild traumatic brain injury (mTBI)
Abstract
Primary Objective: Rugby is one of the few contact sports that do not mandate protective headgear, possibly because studies have shown poor efficacy for protection related to concussion pathology with existing headguards.
Research Design: Following innovative material technology utilization to produce headgear believed to have protective capabilities, this study examined the effects of a soft-shell headgear constructed from a novel viscoelastic material, on both behaviour and serum biomarkers after high and average impact force mild traumatic brain injuries (mTBI).
Methods and Procedures: Seventy-five male Sprague Dawley rats were divided into five groups: control, average - 37G impact, with and without headgear, and high - 106G impact, with and without headgear. Rats were sacrificed at 3 or 48 hours and serum samples were analyzed for levels of TNF-α, NEF-L, and GFAP. Animals sacrificed at 48 hours also underwent testing for balance and motor coordination, and exploratory/locomotor behaviour.
Main Outcomes and Results: The novel headgear offered significant protection against mTBI symptomology and biomarkers in the group that experienced an average impact force, but only moderated protection for the animals in the high impact group.
Conclusions: This innovative headgear may prevent some of the negative sequel associated with concussion pathology.
... Based on these equations, a mouse λ = of 13.8 and a rat λ = 11 are validated in the literature (Namjoshi et al., 2014;Viano et al., 2009). The majority of studies assessed did not use a scaling factor of this nature, with only seven studies using impact velocities in the range of those seen in human impacts Candy, Ma, McMahon, Farrell, & Mychasiuk, 2017;Hamberger et al., 2009;Salberg, Yamakawa, Christensen, Kolb, & Mychasiuk, 2017;Tagge et al., 2018;Viano et al., 2009;Yamakawa, Lengkeek, Salberg, Spanswick, & Mychasiuk, 2017). This should be a focus of further studies to ensure that the forces administered to animals are accurate representations of those encountered on the playing field. ...
... As a measure of astroglial activation in human mTBI, GFAP has been shown to be a sensitive and specific marker of injury (Papa et al., 2016). GFAP was commonly assessed in the animal studies of this review, and demonstrated utility in detecting injury either via mRNA expression (Yu, Wergedal, Rundle, & Mohan, 2014), protein levels in the brain (Fehily et al., 2019;Viano et al., 2012), or in serum (Candy et al., 2017). Production of inflammatory cytokines is also linked with glial cell activation following injury, and was commonly assessed in these studies. ...
... While these traits spontaneously resolve, in some individuals balance and motor dysfunction has also been associated with CTE symptomology (Tharmaratnam et al., 2018). In the studies assessed in this review, balance and motor deficits were found in the shortterm post-TBI phase, with rodents in the mTBI groups more likely to have difficulty on beam walking and rotarod tasks than their shaminjured controls (Candy et al., 2017;Liu et al., 2017). Human balance and motor analysis, often assessed with field tests such as the sports concussion assessment tool, has identified deficits in postural stability up to 72 hr post-mTBI (McCrory et al., 2017). ...
Sports‐related head trauma has emerged as an important public health issue, as mild traumatic brain injuries (mTBIs) may result in neurodegenerative disorders such as chronic traumatic encephalopathy (CTE). Research into mTBI and CTE pathophysiology are difficult to undertake in athletes, with observational trials and post‐mortem analysis the current mainstays. Thus, animal models play an important role in the study of mTBI, however, traditional animal models have focused on acute, severe injuries rather than the more typical mTBI's seen in sport injuries. Recently, a number of animal models have been developed that are both appropriately scaled and biomechanically relevant to the forces sustained by athletes. This review aimed to examine the literature for variables included in these animal models, and the resulting neurotrauma as evidenced by pathology and behavioral deficits. A systematic search of the literature was performed in multiple electronic databases. The inclusion criteria required mimicry of athlete mTBI conditions: freedom of head movement, lack of surgical alteration of the skull, and application of direct contact force. Studies were analyzed for variables including apparatus design features (impact force, change in animal head velocity, and kinetic energy transfer to the head), demonstrated pathology (phosphorylated tau, TDP‐43 aggregation, diffuse axonal injury, gliosis, cytokine inflammation response, and genetic integrity), and behavioral changes. These studies suggested that appropriate animal models can assist in understanding the pathological and functional outcomes of athlete mTBI, and could be used as a platform for future studies of diagnostic/prognostic markers and in the development of treatment interventions.
... Increased attention on the negative effects of sports concussions and recent advances in technology have resulted in a number of innovative theoretical approaches being developed in order to analyse impacts in a sports context [22,23]. Approaches have to include laboratory simulations, human tests, and tests with animals [22][23][24][25]. Whyte et al. (2019) provided a comprehensive review of impact testing for sports headgear and highlighted the need for experimental validation in all theoretical approaches [23]. ...
... Whyte et al. (2019) provided a comprehensive review of impact testing for sports headgear and highlighted the need for experimental validation in all theoretical approaches [23]. In accordance with these research innovations, our research approach is focussed on the potential of soft-shell headgear to reduce peak linear accelerations [24,25]. ...
The purpose of this study was to examine the potential of soft-shelled rugby headgear to reduce linear impact accelerations. A hybrid III head form instrumented with a 3-axis accelerometer was used to assess headgear performance on a drop test rig. Six headgear units were examined in this study: Canterbury Clothing Company (CCC) Ventilator, Kukri, 2nd Skull, N-Pro, and two Gamebreaker headgear units of different sizes (headgears 1-6, respectively). Drop heights were 238, 300, 610, and 912 mm with 5 orientations at each height (forehead, front boss, rear, rear boss, and side). Impact severity was quantified using peak linear acceleration (PLA) and head injury criterion (HIC). All headgear was tested in comparison to a no headgear condition (for all heights). Compared to the no headgear condition, all headgear significantly reduced PLA and HIC at 238 mm (16.2-45.3% PLA and 29.2-62.7% HIC reduction; P < 0.0005, ηp2 = 0.987-0.991). Headgear impact attenuation lowered significantly as the drop height increased (32.4-5.6% PLA and 50.9-11.7% HIC reduction at 912 mm). There were no significant differences in PLA or HIC reduction between headgear units 1-3. Post hoc testing indicated that headgear units 4-6 significantly outperformed headgear units 1-3 and additionally headgear units 5 and 6 significantly outperformed headgear 4 (P < 0.05). The lowest reduction PLA and HIC was for impacts rear orientation for headgear units 1-4 (3.3 ± 3.6%-11 ± 5.8%). In contrast, headgear units 5 and 6 significantly outperformed all other headgear in this orientation (P < 0.0005, ηp2 = 0.982-0.990). Side impacts showed the greatest reduction in PLA and HIC for all headgear. All headgear units tested demonstrated some degree of reduction in PLA and HIC from a linear impact; however, units 4-6 performed significantly better than headgear units 1-3.
... In this context, McIntosh & Patton (2015a have argued that commercially available headgear is at best fulfilling a secondary injury risk management objective, preventing superficial head injury. Furthermore, the headguard provides some protection against linear impacts to the head (Beckwith, Chu, & Greenwald, 2007;Candy, Ma, McMahon, Farrell, & Mychasiuk, 2017). Some headguard models provide protection against neck injuries (Beckwith et al., 2007;McIntosh & Patton, 2015b). ...
... There are almost no randomised control trials (for an exception see Haglund & Erkisson, 1993), no longitudinal research designs (except from Loosemore et al., 2015b) and no direct measurement of injuries to the head, except from a study on rats (Candy et al., 2017). In most cases, no reference is made to other sport-related research on protective headgear and head injuries, such as for example, rugby, taekwondo, soccer, ice hockey (with the exception of Bartsch et al. (2012a) and McIntosh and Patton (2015b)). ...
In 2013, the International Boxing Association (AIBA) prohibited the use of headguards for elite male Olympic boxing competitions. Could the removal of the headguard from elite male boxing competitions potentially cause increased injury risk for boxers? The aim of the literature review is to analyse current knowledge about the use of protective headgear and injury prevention in boxing, in order to determine if there are increased injury risks associated with headguard use. Peer-reviewed studies (language: English, Norwegian, Swedish, Danish and Dutch) published from 1980 and onwards were considered. Five academic databases and grey literature sources were searched, and articles were assessed for methodological quality. Only studies that included boxers as the study population with headguards as a factor were considered. A total of 39 articles were included in the review. The analysis of the reviewed literature indicates that headguards protect well against lacerations and skull fractures, while less is known about the protective effects against concussion and other traumatic brain injuries. Most of the analysed studies however use indirect evidence, obtained through self-report or observational techniques with relatively small non-representative samples. There are almost no randomised control trials, longitudinal research designs or samples from recreational boxing. Therefore, AIBA’s decision to remove the headguard has to be seen with caution and injury rates among (male) boxers should be continuously evaluated.
... Lab studies, particularly more recent studies involving more recently developed technology, reported generally more promising findings, but these have yet to be generalised to the field [11,24,46]. Although not looked at specifically in this paper, animal studies have found headgear offered significant protection from moderate mTBI symptoms in animal models [63]. ...
Objectives
To review the rate of soft-shell headgear use in rugby union, consumer knowledge of the protection potential of soft-shell headgear, incidence of concussion reported in rugby headgear studies, and the capacity of soft-shell headgear to reduce acceleration impact forces.
Design
A systematic search was conducted in July and August 2021 using the databases SPORT Discus, PubMed, MEDLINE, CINAHL (EBSCO), Scopus, and Science Direct. The review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The protocol for this systematic review was registered on PROSPERO (registration number: CRD42021239595).
Outcome measures
Rates of headgear use, reports of estimated protection of headgear against head injury, incidence of concussion and magnitude of impact collisions with vs. without headgear, impact attenuation of headgear in lab studies.
Results
Eighteen studies were identified as eligible: qualitative (N = 4), field (N = 7), and lab (N = 7). Qualitative studies showed low rates of headgear use and varying understanding of the protection afforded by headgear. Field studies showed negligible association of headgear use with reduced impact magnitude in headgear vs. non-headgear cohorts. Lab studies showed increased energy attenuation for thicker headgear material, poorer performance of headgear after repetitive impacts and increased drop heights, and promising recent results with headgear composed of viscoelastic polymers.
Conclusions
Rates of adoption of soft-shell headgear remain low in rugby and any association between its use and reduction in acceleration impact forces remains unclear. Lab results indicating improved impact attenuation need to be validated in the field. Further headgear-related research is needed with youth and female rugby players.
... Neither site displayed differences at 3 months. This limited response could be due to sampling time and marker kinetics, as previous studies have seen robust increase in the first 24 hours following injury and a decreased to baseline by 48 hours [79]. An additional limiting factor may be the lack of severity of impact in our model, as the majority of brain injury literature examining TNF has done so in moderate or severe injuries using rodent brain or human CSF [80,81]. ...
The cumulative effect of mild traumatic brain injuries (mTBI) can result in chronic neurological damage, however the molecular mechanisms underpinning this detriment require further investigation. A closed head weight drop model that replicates the biomechanics and head acceleration forces of human mTBI was used to provide an exploration of the acute and chronic outcomes following single and repeated impacts. Adult male C57BL/6J mice were randomly assigned into one of four impact groups (control; one, five and 15 impacts) which were delivered over 23 days. Outcomes were assessed 48 hours and 3 months following the final mTBI. Hippocampal spatial learning and memory assessment revealed impaired performance in the 15-impact group compared with control in the acute phase that persisted at chronic measurement. mRNA analyses were performed on brain tissue samples of the cortex and hippocampus using quantitative RT-PCR. Eight genes were assessed, namely MAPT, GFAP, AIF1, GRIA1, CCL11, TARDBP, TNF, and NEFL, with expression changes observed based on location and follow-up duration. The cortex and hippocampus showed vulnerability to insult, displaying upregulation of key excitotoxicity and inflammation genes. Serum samples showed no difference between groups for proteins phosphorylated tau and GFAP. These data suggest that the cumulative effect of the impacts was sufficient to induce mTBI pathophysiology and clinical features. The genes investigated in this study provide opportunity for further investigation of mTBI-related neuropathology and may provide targets in the development of therapies that help mitigate the effects of mTBI.
... Indeed, testing of the N-Pro foam on a rodent model of mTBI has shown that it can prevent impact-associated behavioural and blood biomarker changes. 25 While it is evident that there is much still to be learnt about mTBI and how repeated impacts can have long-term pathological sequelae, the known linear relationship between impact force and injury provides one rationale by which injury can be minimised. Nothing can provide 100% protection against sports-related head injuries but the development of a head guard with such excellent impact attenuation properties provides great hope, at least, for development of equipment that could reduce head-injury risk in a hugely popular game. ...
Objectives
In the aim to develop a usable and wearable head guard for rugby that could reduce impact energy and lessen the likelihood of concussive and subconcussive injury during play, a combination of viscoelastic materials was employed to develop a guard with similar dimensions to those currently used in international rugby.
Methods
The head guard was tested for impact energy reduction following linear acceleration, using drop tests, as required by World Rugby. The head guard was also subjected to pendulum tests, allowing acceleration to be simultaneously measured on two headforms, as well as repeated impacts to mimic ageing and repeated use. Impact following rotational acceleration was determined at two impact locations and at three impact velocities.
Results
The viscoelastic head guard (N-Pro) was shown to reduce linear impacts by up to 75% in comparison to the use of a commercially available rugby head guard and repeated impacts did not impair the attenuation of impact energy. Rotational impact energy was also reduced by an average of 34% across three speeds and two sites of impact test sites, in comparison to tested bare headforms.
Conclusions
This heralds a new generation of soft-shelled headgear that could help reduce two primary risk factors in sports-induced mild traumatic brain injury: linear and rotational impacts to the head.
Background
The neuroinflammatory response following traumatic brain injury (TBI) is known to be a key secondary injury factor that can drive ongoing neuronal injury. Despite this, treatments that have targeted aspects of the inflammatory pathway have not shown significant efficacy in clinical trials. Main bodyWe suggest that this may be because classical inflammation only represents part of the story, with activation of neurogenic inflammation potentially one of the key initiating inflammatory events following TBI. Indeed, evidence suggests that the transient receptor potential cation channels (TRP channels), TRPV1 and TRPA1, are polymodal receptors that are activated by a variety of stimuli associated with TBI, including mechanical shear stress, leading to the release of neuropeptides such as substance P (SP). SP augments many aspects of the classical inflammatory response via activation of microglia and astrocytes, degranulation of mast cells, and promoting leukocyte migration. Furthermore, SP may initiate the earliest changes seen in blood-brain barrier (BBB) permeability, namely the increased transcellular transport of plasma proteins via activation of caveolae. This is in line with reports that alterations in transcellular transport are seen first following TBI, prior to decreases in expression of tight-junction proteins such as claudin-5 and occludin. Indeed, the receptor for SP, the tachykinin NK1 receptor, is found in caveolae and its activation following TBI may allow influx of albumin and other plasma proteins which directly augment the inflammatory response by activating astrocytes and microglia. Conclusions
As such, the neurogenic inflammatory response can exacerbate classical inflammation via a positive feedback loop, with classical inflammatory mediators such as bradykinin and prostaglandins then further stimulating TRP receptors. Accordingly, complete inhibition of neuroinflammation following TBI may require the inhibition of both classical and neurogenic inflammatory pathways.
Head Computed Tomography (CT) imaging is still a commonly obtained diagnostic test for patients with minor head injury despite availability of clinical decision rules to guide imaging use and recommendations to reduce radiation exposure resulting from unnecessary imaging. This prospective multi-center observational study of 251 patients with suspected mild to moderate traumatic brain injury (TBI) evaluated three serum biomarkers' (Glial Fibrillary Acidic Protein [GFAP], Ubiquitin C-Terminal Hydrolase-L1 [UCH-L1] and S100B measured within 6-hours of injury) ability to differentiate CT negative and CT positive findings. Of the 251 patients, 60.2% were male and 225 (89.6%) had a presenting Glasgow Coma Scale score of 15. A positive head CT (intracranial injury), was found in 36 (14.3%). UCH-L1 was 100% sensitive and 39% specific at a cutoff value > 40 pg/ml. To retain 100% sensitivity, GFAP was 0% specific (cutoff value 0 pg/ml) and S100B had a specificity of only 2% (cutoff value 30 pg/ml). All three biomarkers had similar values for areas under the receiver operator characteristic curve; 0.79 (95% CI; 0.70 to 0.88) for GFAP, 0.80 (0.71 to 0.89) for UCH-L1, and 0.75 (0.65 to 0.85) for S100B. Neither GFAP nor UCH-L1 curve values differed significantly from S100B (p=0.21 and p=0.77 respectively). In our patient cohort, UCH-L1 outperformed GFAP and S100B when the goal was to reduce CT use without sacrificing sensitivity. UCH-L1 values < 40 pg/ml could potentially have aided in eliminating 83 of the 215 negative CT scans. These results require replication in other studies before the test is used in actual clinical practice.
Concussion and mild traumatic brain injury (mTBI) research has made minimal progress diagnosing who will suffer from lingering symptomology or generating effective treatment strategies. Research demonstrates that dietary intake affects many biological systems including brain and neurological health. This study determined if exposure to a high fat diet (HFD) or caloric restriction (CR) altered post-concussion susceptibility or resiliency using a rodent model of pediatric concussion. Rats were maintained on HFD, CR, or standard diet (STD) throughout life (including the prenatal period and weaning). At postnatal day 30, male and female rats experienced a concussion or a sham injury which was followed by 17 days of testing. Prefrontal cortex and hippocampus tissue was collected for molecular profiling. Gene expression changes in BDNF, CREB, DNMT1, FGF-2, IGF1, LEP, PGC-1α, SIRT1, Tau, and TERT were analyzed with respect to injury and diet. Analysis of telomere length (TL) using peripheral skin cells and brain tissue found that TL in skin significantly correlated with TL in brain tissue and TL was affected by dietary intake and injury status. With respect to mTBI outcomes, diet was correlated with recovery as animals on the HFD often displayed poorer performance than animals on the CR diet. Molecular analysis demonstrated that diet induced epigenetic changes that can be associated with differences in individual predisposition and resiliency to post-concussion syndrome.
Background: Direct impacts with the head (linear acceleration or pressure) and inertial loading of the head (rotational acceleration or strain) have been postulated as the 2 major mechanisms of head-related injuries such as concussion. Although data are accumulating for soccer and American football, there are no published data for nonhelmeted collision sports such as rugby union.
Purpose: To quantify head impacts via instrumented mouthguard acceleration analyses for rugby union players over a season of matches.
Study Design: Descriptive epidemiology study.
Methods: Data on impact magnitude and frequency were collected with molded instrumented mouthguards worn by 38 premier amateur senior rugby players participating in the 2013 domestic season of matches.
Results: A total of 20,687 impacts >10g (range, 10.0-164.9g) were recorded over the duration of the study. The mean ± SD number of impacts per player over the duration of the season of matches was 564 ± 618, resulting in a mean ± SD of 95 ± 133 impacts to the head per player, per match over the duration of the season of matches. The impact magnitudes for linear accelerations were skewed to the lower values (Sp = 3.7 ± 0.02; P < .001), with a mean linear acceleration of 22.2 ± 16.2g. Rotational accelerations were also skewed to the lower values (Sp = 2.0 ± 0.02; P < .001), with a mean rotational acceleration of 3902.9 ± 3948.8 rad/s2.
Conclusion: The acceleration magnitudes and number of head impacts in amateur rugby union players over a season of matches, measured via instrumented mouthguard accelerations, were higher than for most sports previously reported. Mean linear acceleration measured over a season of matches was similar to the mean linear accelerations previously reported for youth, high school, and collegiate American football players but lower than that for female youth soccer players. Mean rotational acceleration measured over a season of matches was similar to mean rotational accelerations for youth, high school, and collegiate American football players but less than those for female youth soccer players, concussed American collegiate players, collegiate American football players, and professional American football players.
Concussions and subconcussive impacts sustained in American football have been associated with short- and long-term neurologic impairment, but differences in head impact outcomes across playing positions are not well understood. The American Medical Society for Sports Medicine has identified playing position as a key risk factor for concussion in football and one for which additional research is needed. This study examined variation in head impact outcomes across primary football playing positions in a group of 730 NCAA Division I Football Championship Series athletes, using a self-report questionnaire. Although there were no significant differences between position groups in the number of diagnosed concussions during the 2012 football season, there were significant differences between groups in undiagnosed concussions (p=0.008) and "dings" (p<0.001); offensive linemen reported significantly higher numbers than most other positions. Significant differences were found between position groups in the frequencies of several post-impact symptoms including dizziness (p<0.001), headache (p<0.001), and seeing stars (p<0.001) during the 2012 football season, with offensive linemen reporting significantly more symptoms compared to most other groups. There were also positional differences in frequency of returning to play while symptomatic (p<0.001) and frequency of participating in full contact practice (p<0.001). Offensive linemen reported having returned to play while experiencing symptoms more frequently and participating in more full-contact practices than other groups. These findings suggest that offensive linemen, a position group that experiences frequent but low-magnitude head impacts, develop more post-impact symptoms than other playing positions, but do not report these symptoms as a concussion.
Diagnosis of mild TBI is hampered by the lack of imaging or biochemical measurements for identifying or quantifying mild TBI in a clinical setting. We have previously shown increased biomarker levels of protein reflecting axonal (neurofilament light protein and tau) and glial (GFAP and S-100B) damage in cerebrospinal fluid (CSF) after a boxing bout. The aims of this study were to find other biomarkers of mild TBI, which may help clinicians diagnose and monitor mild TBI, and to calculate the role of APOE ε4 allele genotype which has been associated with poor outcome after TBI.
Thirty amateur boxers with a minimum of 45 bouts and 25 non-boxing matched controls were included in a prospective cohort study. CSF and blood were collected at one occasion between 1 and 6 days after a bout, and after a rest period for at least 14 days (follow up). The controls were tested once. CSF levels of neurofilament heavy (pNFH), amyloid precursor proteins (sAPPα and sAPPβ), ApoE and ApoA1 were analyzed. In blood, plasma levels of Aβ42 and ApoE genotype were analyzed.
CSF levels of pNFH were significantly increased between 1 and 6 days after boxing as compared with controls (p<0.001). The concentrations decreased at follow up but were still significantly increased compared to controls (p = 0.018). CSF pNFH concentrations correlated with NFL (r = 0.57 after bout and 0.64 at follow up, p<0.001). No significant change was found in the other biomarkers, as compared to controls. Boxers carrying the APOE ε4 allele had similar biomarker concentrations as non-carriers.
Subconcussive repetitive trauma in amateur boxing causes a mild TBI that may be diagnosed by CSF analysis of pNFH, even without unconsciousness or concussion symptoms. Possession of the APOE ε4 allele was not found to influence biomarker levels after acute TBI.
Neuropathology after traumatic brain injury (TBI) is the result of both the immediate impact injury and secondary injury mechanisms. Unresolved post-traumatic glial activation is a secondary injury mechanism that contributes to a chronic state of neuroinflammation in both animal models of TBI and human head injury patients. We recently demonstrated, using in vitro models, that p38α MAPK signaling in microglia is a key event in promoting cytokine production in response to diverse disease-relevant stressors and subsequent inflammatory neuronal dysfunction. From these findings, we hypothesized that the p38α signaling pathway in microglia could be contributing to the secondary neuropathologic sequelae after a diffuse TBI. Mice where microglia were p38α-deficient (p38α KO) were protected against TBI-induced motor deficits and synaptic protein loss. In wild-type (WT) mice, diffuse TBI produced microglia morphological activation that lasted for at least 7 d; however, p38α KO mice failed to activate this response. Unexpectedly, we found that the peak of the early, acute phase cytokine and chemokine levels was increased in injured p38α KO mice compared with injured WT mice. The increased cytokine levels in the p38α KO mice could not be accounted for by more infiltration of macrophages or neutrophils, or increased astrogliosis. By 7 d after injury, the cytokine and chemokine levels remained elevated in injured WT mice but not in p38α KO mice. Together, these data suggest that p38α balances the inflammatory response by acutely attenuating the early proinflammatory cytokine surge while perpetuating the chronic microglia activation after TBI.
Unlabelled:
PURPOSE OF THE STATEMENT: ▸ To provide an evidence-based, best practises summary to assist physicians with the evaluation and management of sports concussion. ▸ To establish the level of evidence, knowledge gaps and areas requiring additional research.
Importance of an amssm statement:
▸ Sports medicine physicians are frequently involved in the care of patients with sports concussion. ▸ Sports medicine physicians are specifically trained to provide care along the continuum of sports concussion from the acute injury to return-to-play (RTP) decisions. ▸ The care of athletes with sports concussion is ideally performed by healthcare professionals with specific training and experience in the assessment and management of concussion. Competence should be determined by training and experience, not dictated by specialty. ▸ While this statement is directed towards sports medicine physicians, it may also assist other physicians and healthcare professionals in the care of patients with sports concussion.
Definition:
▸ Concussion is defined as a traumatically induced transient disturbance of brain function and involves a complex pathophysiological process. Concussion is a subset of mild traumatic brain injury (MTBI) which is generally self-limited and at the less-severe end of the brain injury spectrum.
Pathophysiology:
▸ Animal and human studies support the concept of postconcussive vulnerability, showing that a second blow before the brain has recovered results in worsening metabolic changes within the cell. ▸ Experimental evidence suggests the concussed brain is less responsive to usual neural activation and when premature cognitive or physical activity occurs before complete recovery the brain may be vulnerable to prolonged dysfunction.
Incidence:
▸ It is estimated that as many as 3.8 million concussions occur in the USA per year during competitive sports and recreational activities; however, as many as 50% of the concussions may go unreported. ▸ Concussions occur in all sports with the highest incidence in football, hockey, rugby, soccer and basketball. RISK FACTORS FOR SPORT-RELATED CONCUSSION: ▸ A history of concussion is associated with a higher risk of sustaining another concussion. ▸ A greater number, severity and duration of symptoms after a concussion are predictors of a prolonged recovery. ▸ In sports with similar playing rules, the reported incidence of concussion is higher in female athletes than in male athletes. ▸ Certain sports, positions and individual playing styles have a greater risk of concussion. ▸ Youth athletes may have a more prolonged recovery and are more susceptible to a concussion accompanied by a catastrophic injury. ▸ Preinjury mood disorders, learning disorders, attention-deficit disorders (ADD/ADHD) and migraine headaches complicate diagnosis and management of a concussion.
Diagnosis of concussion:
▸ Concussion remains a clinical diagnosis ideally made by a healthcare provider familiar with the athlete and knowledgeable in the recognition and evaluation of concussion. ▸ Graded symptom checklists provide an objective tool for assessing a variety of symptoms related to concussions, while also tracking the severity of those symptoms over serial evaluations. ▸ Standardised assessment tools provide a helpful structure for the evaluation of concussion, although limited validation of these assessment tools is available.
Sideline evaluation and management:
▸ Any athlete suspected of having a concussion should be stopped from playing and assessed by a licenced healthcare provider trained in the evaluation and management of concussions. ▸ Recognition and initial assessment of a concussion should be guided by a symptoms checklist, cognitive evaluation (including orientation, past and immediate memory, new learning and concentration), balance tests and further neurological physical examination. ▸ While standardised sideline tests are a useful framework for examination, the sensitivity, specificity, validity and reliability of these tests among different age groups, cultural groups and settings is largely undefined. Their practical usefulness with or without an individual baseline test is also largely unknown. ▸ Balance disturbance is a specific indicator of a concussion, but not very sensitive. Balance testing on the sideline may be substantially different than baseline tests because of differences in shoe/cleat-type or surface, use of ankle tape or braces, or the presence of other lower extremity injury. ▸ Imaging is reserved for athletes where intracerebral bleeding is suspected. ▸ There is no same day RTP for an athlete diagnosed with a concussion. ▸ Athletes suspected or diagnosed with a concussion should be monitored for deteriorating physical or mental status.
Neuropsychological testing:
▸ Neuropsychological (NP) tests are an objective measure of brain-behaviour relationships and are more sensitive for subtle cognitive impairment than clinical exam. ▸ Most concussions can be managed appropriately without the use of NP testing. ▸ Computerised neuropsychological (CNP) testing should be interpreted by healthcare professionals trained and familiar with the type of test and the individual test limitations, including a knowledgeable assessment of the reliable change index, baseline variability and false-positive and false-negative rates. ▸ Paper and pencil NP tests can be more comprehensive, test different domains and assess for other conditions which may masquerade as or complicate assessment of concussion. ▸ NP testing should be used only as part of a comprehensive concussion management strategy and should not be used in isolation. ▸ The ideal timing, frequency and type of NP testing have not been determined. ▸ In some cases, properly administered and interpreted NP testing provides an added value to assess cognitive function and recovery in the management of sports concussions. ▸ It is unknown if use of NP testing in the management of sports concussion helps prevent recurrent concussion, catastrophic injury or long-term complications. ▸ Comprehensive NP evaluation is helpful in the post-concussion management of athletes with persistent symptoms or complicated courses.
Return to class:
▸ Students will require cognitive rest and may require academic accommodations such as reduced workload and extended time for tests while recovering from a concussion.
Return to play:
▸ Concussion symptoms should be resolved before returning to exercise. ▸ A RTP progression involves a gradual, step-wise increase in physical demands, sports-specific activities and the risk for contact. ▸ If symptoms occur with activity, the progression should be halted and restarted at the preceding symptom-free step. ▸ RTP after concussion should occur only with medical clearance from a licenced healthcare provider trained in the evaluation and management of concussions. SHORT-TERM RISKS OF PREMATURE RTP: ▸ The primary concern with early RTP is decreased reaction time leading to an increased risk of a repeat concussion or other injury and prolongation of symptoms. LONG-TERM EFFECTS: ▸ There is an increasing concern that head impact exposure and recurrent concussions contribute to long-term neurological sequelae. ▸ Some studies have suggested an association between prior concussions and chronic cognitive dysfunction. Large-scale epidemiological studies are needed to more clearly define risk factors and causation of any long-term neurological impairment.
Disqualification from sport:
▸ There are no evidence-based guidelines for disqualifying/retiring an athlete from a sport after a concussion. Each case should be carefully deliberated and an individualised approach to determining disqualification taken.
Education:
▸ Greater efforts are needed to educate involved parties, including athletes, parents, coaches, officials, school administrators and healthcare providers to improve concussion recognition, management and prevention. ▸ Physicians should be prepared to provide counselling regarding potential long-term consequences of a concussion and recurrent concussions.
Prevention:
▸ Primary prevention of some injuries may be possible with modification and enforcement of the rules and fair play. ▸ Helmets, both hard (football, lacrosse and hockey) and soft (soccer, rugby) are best suited to prevent impact injuries (fracture, bleeding, laceration, etc.) but have not been shown to reduce the incidence and severity of concussions. ▸ There is no current evidence that mouth guards can reduce the severity of or prevent concussions. ▸ Secondary prevention may be possible by appropriate RTP management.
Legislation:
▸ Legislative efforts provide a uniform standard for scholastic and non-scholastic sports organisations regarding concussion safety and management.
Future directions:
▸ Additional research is needed to validate current assessment tools, delineate the role of NP testing and improve identification of those at risk of prolonged post-concussive symptoms or other long-term complications. ▸ Evolving technologies for the diagnosis of concussion, such as newer neuroimaging techniques or biological markers, may provide new insights into the evaluation and management of sports concussion.
Mild traumatic brain injury (mTBI) results from a transfer of mechanical energy into the brain from traumatic events such as rapid acceleration/deceleration, a direct impact to the head, or an explosive blast. Transfer of energy into the brain can cause structural, physiological and/or functional changes in the brain that may yield neurological, cognitive and behavioral symptoms that can be long-lasting. As mild TBI can cause these symptoms in the absence of positive neuroimaging findings, its diagnosis can be subjective and often is based on self-reported neurological symptoms. Furthermore, proper diagnosis can be influenced by the motivation to conceal or embellish signs and/or an inability of the subject to notice subtle dysfunctions or alterations of consciousness. Therefore, appropriate diagnosis of mTBI would benefit from objective indicators of injury. Concussion and mTBI are often used interchangeably with concussion being primarily used in sport medicine, whereas mTBI is used in reference to traumatic injury. This review provides a critical assessment of the status of current biomarkers for the diagnosis of human mTBI. We review the status of biomarkers that have been tested in TBI patients with injuries classified as mild, and introduce a new concept for the discovery of biomarkers (termed symptophenotypes) to predict common and unique symptoms of concussion. Finally, we discuss the need for biomarker/biomarker signatures that can detect mTBI in the context of polytrauma, and to assess the consequences of repeat injury on the development of secondary injury syndrome, prolongation of post-concussion symptoms, and chronic traumatic encephalopathy.
Glial fibrillary acidic protein (GFAP) is the main astrocytic intermediate filament (IF). GFAP splice isoforms show differential expression patterns in the human brain. GFAPδ is preferentially expressed by neurogenic astrocytes in the subventricular zone (SVZ), whereas GFAP(+1) is found in a subset of astrocytes throughout the brain. In addition, the expression of these isoforms in human brain material of epilepsy, Alzheimer and glioma patients has been reported. Here, for the first time, we present a comprehensive study of GFAP isoform expression in both wild-type and Alzheimer Disease (AD) mouse models. In cortex, cerebellum, and striatum of wild-type mice, transcripts for Gfap-α, Gfap-β, Gfap-γ, Gfap-δ, Gfap-κ, and a newly identified isoform Gfap-ζ, were detected. Their relative expression levels were similar in all regions studied. GFAPα showed a widespread expression whilst GFAPδ distribution was prominent in the SVZ, rostral migratory stream (RMS), neurogenic astrocytes of the subgranular zone (SGZ), and subpial astrocytes. In contrast to the human SVZ, we could not establish an unambiguous GFAPδ localization in proliferating cells of the mouse SVZ. In APPswePS1dE9 and 3xTgAD mice, plaque-associated reactive astrocytes had increased transcript levels of all detectable GFAP isoforms and low levels of a new GFAP isoform, Gfap-ΔEx7. Reactive astrocytes in AD mice showed enhanced GFAPα and GFAPδ immunolabeling, less frequently increased vimentin and nestin, but no GFAPκ or GFAP(+1) staining. In conclusion, GFAPδ protein is present in SVZ, RMS, and neurogenic astrocytes of the SGZ, but also outside neurogenic niches. Furthermore, differential GFAP isoform expression is not linked with aging or reactive gliosis. This evidence points to the conclusion that differential regulation of GFAP isoforms is not involved in the reorganization of the IF network in reactive gliosis or in neurogenesis in the mouse brain.
The biomarkers glial fibrillary acid protein (GFAP) and S100B are increasingly used as prognostic tools in severe traumatic brain injury (TBI). Data for mild TBI are scarce. This study aims to analyze the predictive value of GFAP and S100B for outcome in mild TBI and the relation with imaging.
In 94 patients biomarkers were determined directly after admission. Collected data included injury severity, patient characteristics, admission CT, and MRI 3 months postinjury. Six months postinjury outcome was determined with Glasgow Outcome Scale Extended (GOSE) and return to work (RTW).
Mean GFAP was 0.25 μg/L (SD 1.08) and S100B 0.54 μg/L (SD 1.18). In 63% GFAP was not discernible. GFAP was increased in patients with an abnormal CT (1.20 μg/L, SD 2.65) compared to normal CT (0.05 μg/L, SD 0.17, p < 0.05). Also in patients with axonal injury on MRI GFAP was higher (0.65 μg/L, SD 0.91 vs 0.07 μg/L, SD 0.2, p < 0.05). GFAP was increased in patients with incomplete RTW compared to complete RTW (0.69 μg/L, SD 2.11 vs 0.12 μg/L, SD 0.38, p < 0.05). S100B was not related to outcome or imaging studies. In multivariate analysis GFAP was not predictive for outcome determined by GOSE and RTW.
A relation between GFAP with imaging studies and outcome (determined by RTW) was found in contrast to S100B. As the positive predictive value of GFAP is limited in this category of TBI patients, this biomarker is not suitable for prediction of individual patient outcome.
More than 1.6 million sport-related concussions occur every year in the United States, affecting greater than 5% of all high school athletes who participate in contact sports. As more females participate in sports, understanding possible differences in concussion symptoms between sexes becomes more important.
To compare symptoms, symptom resolution time, and time to return to sport between males and females with sport-related concussions.
Descriptive epidemiology study.
Data were collected from 100 high schools via High School RIO (Reporting Information Online).
Athletes from participating schools who sustained concussions while involved in interscholastic sports practice or competition in 9 sports (boys' football, soccer, basketball, wrestling, and baseball and girls' soccer, volleyball, basketball, and softball) during the 2005-2006 and 2006-2007 school years. A total of 812 sport concussions were reported (610 males, 202 females).
Reported symptoms, symptom resolution time, and return-to-play time.
No difference was found between the number of symptoms reported (P = .30). However, a difference was seen in the types of symptoms reported. In year 1, males reported amnesia (exact P = .03) and confusion/disorientation (exact P = .04) more frequently than did females. In year 2, males reported more amnesia (exact P = .002) and confusion/disorientation (exact P = .002) than did females, whereas females reported more drowsiness (exact P = .02) and sensitivity to noise (exact P = .002) than did males. No differences were observed for symptom resolution time (P = .40) or return-to-play time (P = .43) between sexes.
The types of symptoms reported differed between sexes after sport-related concussion, but symptom resolution time and return-to-play timelines were similar.
Traumatic brain injury is a significant disease affecting 1.4 to 2 million patients every year in the USA. Currently, there are no FDA-approved therapeutic remedies to treat TBI despite the fact that there have been over 200 clinical drug trials, all which have failed. These drugs used the traditional single drug-to-target approach of drug discovery and development. An alternative based upon the advances in genomics, proteomics, bioinformatic tools, and systems biology software has enabled us to use a Systems Biology-based approach to drug discovery and development for TBI. It focuses on disease-relevant converging pathways as potential therapeutic intervention points and is accompanied by downstream biomarkers that allow for the tracking of drug targeting and appears to correlate with disease mitigation. When realized, one is able to envision that a companion diagnostic will be codeveloped along the therapeutic compound. This "theranostic" approach is perfectly positioned to align with the emerging trend toward "personalized medicine".
Little is known about the molecular events following severe traumatic brain injury (TBI) in humans and to date there are no efficient therapies for the treatment of patients. In this study, the first of its kind in human tissue, a total of 21 post mortem trauma brain samples were analyzed. The inflammatory response within the brain tissue was explored by measuring the expression of various inflammatory cytokines at the mRNA and protein levels. These mediators were interleukin (IL)-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and granulocyte-macrophage colony-stimulating factor (GM-CSF). This study shows for the first time in human brain tissue that 1) pro-inflammatory mediator protein levels are significantly increased in situ following acute brain injury while anti-inflammatory cytokines protein levels remain unchanged; 2) the cerebral inflammatory response begins within minutes of acute TBI, much earlier than previously thought; 3) IL-6, IL-8, TNF-alpha, and IL-1beta mRNA levels are significantly increased following injury; 4) the rise in cytokine protein level coincides with increased levels of their mRNAs suggesting that traumatic injury elicits an immediate cerebral inflammatory response. Altogether these data confirm and extend previous observations on the release of cytokines in the cerebrospinal fluid of severe TBI patients. Finally, this study highlights the need to characterize the cell source of cytokines and elucidate their mode of action.
In a model of closed head injury (CHI) in the rat we have shown the activation of phospholipase A2 and the production of eicosanoids after injury: at 15 min, mainly 5-hydroxyeicosatetraenoic acid (5-HETE), and at 24 h, mainly prostaglandin E2. The present study was designed to test whether CHI can also trigger the production of cytokines in the brain. CHI was induced in ether-anesthesized rats by a weight-drop device falling over the exposed skull covering the left hemisphere, 1-2 mm lateral to the midline in the midcoronal plane. In the posttraumatic period (1-24 h), the rats were decapitated, cortical tissue from the injured zone of the contused and contralateral hemispheres was removed and sonicated, and cytokine activity was assessed. Whereas no tumor necrosis factor alpha (TNF alpha) activity was found in normal brain tissue, it was detectable in the contused hemisphere (approximately of 72 +/- 50 pg/mg protein) as early as 1 h post-CHI. TNF alpha levels increased at 2 h, peaked at 4 h, (approximately of 609 +/- 540 pg/mg protein), and declined thereafter. At parallel intervals, only low levels of TNF alpha were detected in the contralateral hemisphere. In normal brain, interleukin-6 (IL-6) was nondetectable. Following CHI, high levels of IL-6 were present, although their accumulation lagged behind that of TNF alpha by 2-4 h, peaking at 8 h (62 +/- 31 ng/mg protein). We suggest that the rapid production of TNF alpha and IL-6 following CHI is a local inflammatory response of brain tissue to primary insult.
A profound inflammatory response is initiated immediately following traumatic brain injury (TBI) and is characterized by the release of several cytokines with pro- and anti-inflammatory functions. In order to elucidate which cytokines are released in the human brain in response to injury as well as in the peripheral compartment, IL-1, IL-6, IL-8, IL-10, TNF-alpha and TGF-beta were monitored in CSF and serum of severely brain-injured patients. Furthermore, we investigated the possible modulation of systemic reactions by IL-6 and the ability of IL-6 and IL-8 to promote the synthesis of nerve growth factor.
This study examined the time course of the blood-brain barrier (BBB) opening and correlated this with brain edema formation after a lateral controlled cortical impact (CCI) brain injury in rats. Quantitative measurement of Evans blue (EB) extravasation using fluorescence was employed at 2, 4, 6 h and 1, 2, 3, 4 and 7 days after injury. Brain edema was measured by specific gravity of the tissue at corresponding time points. Two prominent EB extravasations were observed at 4-6 h and 3-day after injury in the injury-site cortex and the ipsilateral hippocampus. Brain edema became progressively more severe over time and peaked at 24 h after injury and began to decline after day 3. These results suggest that there is a biphasic opening of the BBB after CCI brain injury and the second opening of the BBB does not contribute to a further increase in edema formation.
Traumatic brain injury (TBI) increases susceptibility to Alzheimer's disease (AD), but it is not known how TBI contributes to the onset or progression of this common late life dementia. To address this question, we studied neuropathological and behavioral consequences of single versus repetitive mild TBI (mTBI) in transgenic (Tg) mice (Tg2576) that express mutant human Abeta precursor protein, and we demonstrate elevated brain Abeta levels and increased Abeta deposition. Nine-month-old Tg2576 and wild-type mice were subjected to single (n = 15) or repetitive (n = 39) mTBI or sham treatment (n = 37). At 2 d and 9 and 16 weeks after treatment, we assessed brain Abeta deposits and levels in addition to brain and urine isoprostanes generated by lipid peroxidation in these mice. A subset of mice also was studied behaviorally at 16 weeks after injury. Repetitive but not single mTBI increased Abeta deposition as well as levels of Abeta and isoprostanes only in Tg mice, and repetitive mTBI alone induced cognitive impairments but no motor deficits in these mice. This is the first experimental evidence linking TBI to mechanisms of AD by showing that repetitive TBI accelerates brain Abeta accumulation and oxidative stress, which we suggest could work synergistically to promote the onset or drive the progression of AD. Additional insights into the role of TBI in mechanisms of AD pathobiology could lead to strategies for reducing the risk of AD associated with previous episodes of brain trauma and for preventing progressive brain amyloidosis in AD patients.
To examine the attitudes of players and coaches to the use of protective headgear, particularly with respect to the prevention of concussion.
A questionnaire designed to assess attitudes to headgear was administered to 63 players from four different Canadian teams, each representing a different level of play (high school, university, community club, national). In addition, coaches from all four levels were questioned about team policies and their personal opinions about the use of headgear to prevent concussion.
Although the players tended to believe that the headgear could prevent concussion (62%), the coaches were less convinced (33%). Despite the players' belief that headgear offers protection against concussion, only a minority reported wearing headgear (27%) and few (24%) felt that its use should be made mandatory. Common reasons for not wearing headgear were "its use is not mandatory", "it is uncomfortable", and "it costs too much".
Although most players in the study believe that rugby headgear may prevent concussion, only a minority reported wearing it. Coaches tended to be less convinced than the players that rugby headgear can prevent concussion.
Females comprise an increasing percentage of the athlete population across all age groups, and analysis of recent literature reveals that they sustain more concussions in collegiate sports. Results of human and animal studies indicate that females may have poorer outcomes after traumatic brain injury; however, no return-to-play guideline takes sex or other individual differences into account. In the present study the authors evaluated the influence of patient sex on objective neurocognitive performance and subjective reporting of symptoms following sports-related concussion.
According to preseason baseline neurocognitive computerized testing in 2340 male and female high school and collegiate athletes, individuals who sustained sports-related concussions (155 persons) were reevaluated using an alternate form of the cognitive test. Sex differences in the magnitude of cognitive change from baseline levels and the subjective experience of symptoms were analyzed. To account for the possible protective effects of helmets, comparisons were performed among females, males with helmets, and males without helmets; none of the female athletes wore helmets. Female athletes had significantly greater declines in simple and complex reaction times relative to preseason baseline levels, and they reported more postconcussion symptoms compared with males. As a group, females were cognitively impaired approximately 1.7 times more frequently than males following concussions. Furthermore, females experienced more objective and subjective adverse effects from concussion even after adjusting for the use of helmets by some groups of male athletes (for example, in football).
Return-to-play decisions and concussion management must be objective and made on an individual basis, including consideration of factors such as patient sex rather than relying on a one-size-fits-all guideline.
Impacts causing concussion in professional football were simulated in laboratory tests to determine collision mechanics. This study focuses on the biomechanics of concussion in the struck player.
Twenty-five helmet impacts were reconstructed using Hybrid III dummies. Head impact velocity, direction, and helmet kinematics-matched game video. Translational and rotational accelerations were measured in both players' heads; 6-axis upper neck responses were measured in all striking and five struck players. Head kinematics and biomechanics were determined for concussed players. Head displacement, rotation, and neck loads were determined because finite element analysis showed maximum strains occurring in the midbrain after the high impact forces. A model was developed of the helmet impact to study the influence of neck strength and other parameters on head responses.
The impact response of the concussed player's head includes peak accelerations of 94 +/- 28 g and 6432 +/- 1813 r/s2, and velocity changes of 7.2 +/- 1.8 m/s and 34.8 +/- 15.2 r/s. Near the end of impact (10 ms), head movement is only 20.2 +/- 6.8 mm and 6.9 +/- 2.5 degrees. After impact, there is rapid head displacement involving a fourfold increase to 87.6 +/- 21.2 mm and 29.9 +/- 9.5 degrees with neck tension and bending at 20 ms. Impacts to the front of the helmet, the source of the majority of National Football League concussions, cause rotation primarily around the z axis (superior-inferior axis) because the force is forward of the neck centerline. This twists the head to the right or left an average of 17.6 +/- 12.7 degrees, causing a moment of 17.7 +/- 3.3 Nm and neck tension of 1704 +/- 432 N at 20 ms. The head injury criterion correlates with concussion risk and is proportional to deltaV(4)/d(1.5) for half-sine acceleration. Stronger necks reduce head acceleration, deltaV, and displacement. Even relatively small reductions in deltaV have a large effect on head injury criterion that may reduce concussion risks because changes in deltaV change head injury criterion through the 4th power.
This study addresses head responses causing concussion in National Football League players. Although efforts are underway to reduce impact acceleration through helmet padding, further study is needed of head kinematics after impact and their contribution to concussion, including rapid head displacement, z-axis rotation, and neck tension up to the time of maximum strain in the midbrain. Neck strength influences head deltaV and head injury criterion and may help explain different concussion risks in professional and youth athletes, women, and children.
Glial fibrillary acidic protein (GFAP), Ubiquitin Carboxyl-Terminal Hydrolase-L1 (UCH-L1), and S100B have been shown to be predictive of patients with brain injury. Kinetics of these biomarkers in injured humans have not been extensively examined. This prospective multi-center study included patients with mild to moderate traumatic brain injury. Blood samples obtained at enrollment and every 6 hours up to 24 hours post-injury were assayed for GFAP, UCH-L1, and S100B. Random effects models examined changes in the biomarkers' level over time. 167 patients were enrolled; mean age was 46.0 ± 17.8, 61.1% were male, 143 (85.6%) had a Glasgow Coma Scale score 15, and 33 (19.8%) had a positive head CT. Baseline median biomarker concentrations for all three were higher among CT positive patients (p<0.0001) but GFAP was the only biomarker that significantly increased over time among CT positive patients relative to CT negative patients (log transformed values 0.037; 95% CI 0.02, 0.05, p<0.001) indicating a 3.7% per hour rise in GFAP concentration per hour. There was no significant increase in either UCH-L1 or S100B in CT positive patients (p=0.15 and p=0.47 respectively). GFAP concentrations increased 3.7% per hour among CT positive patients whereas neither UCH-L1 nor S100B increased when compared to CT negative patients. The kinetics and temporal profile of GFAP suggest it may be a more robust biomarker to detect patients with positive CT findings; particularly at later post-injury times. Further study is needed to determine if GFAP is a useful test to follow throughout a patient's clinical course.
Given questions about "lower thresholds" for concussion, as well as possible effects of repetitive concussion and chronic traumatic encephalopathy (CTE), and associated controversy, there is increasing interest in "subconcussive" blows and their potential significance.
A formative review with critical examination of the developing literature on subconcussive blows in athletes with an emphasis on clinical outcomes.
Studies of biomechanical, performance and/or symptom-based, and neuroimaging data were identified via PubMed search and critically reviewed. Five studies of symptom reporting/performance and 4 studies of neuroimaging were included.
The relation between biomechanical parameters and diagnosed concussion is not straightforward (ie, it is not the case that greater and more force leads to more severe injury or cognitive/behavioral sequelae). Neuropsychological studies of subconcussive blows within a single athletic season have failed to demonstrate any strong and consistent relations between number and severity of subconcussive events and cognitive change. Recent studies using neuroimaging have demonstrated a potential cumulative effect of subconcussive blows, at least in a subset of individuals.
Human studies of the neurological/neuropsychological impact of subconcussive blows are currently quite limited. Subconcussive blows, in the short-term, have not been shown to cause significant clinical effects. To date, findings suggest that any effect of subconcussive blows is likely to be small or nonexistent, perhaps evident in a subset of individuals on select measures, and maybe even beneficial in some cases. Longer-term prospective studies are needed to determine if there is a cumulative dose effect.
Apart from therapeutic discovery, the study of mild traumatic brain injury (mTBI) has been focused on two challenges: why do a majority of individuals recover with little concern, while a considerable proportion suffer with persistent and often debilitating symptomology; and, how do mild injuries significantly increase risk for an early-onset neurodegeneration? Owing to a lack of observable damage following mTBI, this study was designed to determine if there were changes in neuronal morphology, synaptic connectivity, and epigenetic patterning that could contribute to the manifestation of persistent neurological dysfunction. Prefrontal cortex tissue from male and female rats was used for Golgi-Cox analysis along with the profiling of changes in gene expression (BDNF, DNMT1, FGF2, IGF1, Nogo-A, OXYR, and TERT) and telomere length, following a single mTBI or sham injury in the juvenile period. Golgi-Cox analysis of dendritic branch order, dendritic length, and spine density demonstrate that an early mTBI increases complexity of pyramidal neurons in the mPFC. Furthermore, there are also substantial changes in the expression levels of the 7 genes of interest and telomere length following a single mild injury in this brain region. The results from the neuroanatomical measures and changes in gene expression indicate that the mTBI disrupts normal pruning processes that are typically underway at this point in development. In addition, there are significant interactions between the social environment and epigenetic processes that work in concert to perpetuate neurological dysfunction.
Copyright © 2014. Published by Elsevier Ltd.
Epilepsy is a heterogeneous and chronic neurological condition of undefined etiology in the majority of cases. Similarly, the pathogenesis of the unprovoked seizures that lead to epilepsy is not known. We are interested in the factors that modify inherent seizure susceptibility, with a particular focus on those occurring during the prenatal and early postnatal periods. Female Sprague-Dawley rats were bred in-house or transported during pregnancy at one of two gestational days (G9 or G16). The effects of transport stress, maternal behavior, and offspring sex were then examined in terms of how they were related to provoked seizure susceptibility to kainic acid (KA) or a model of febrile convulsions (FCs) on postnatal day 14 (P14). We also examined the pattern of neuronal activation in the hippocampus and amygdala as indicated by the density of FosB protein immunoreactivity (FosB-ir). Results demonstrated only a small and inconsistent effect of transport alone, suggesting that the groups differed slightly prior to experimental manipulations. However, the influence of maternal behaviors such as licking and grooming (LG), arched back nursing (ABN), and dam-off time (DO) exerted a much stronger effect on the offspring. Dams designated as high LG gave birth to smaller litters, had pups that weighed less, had greater seizure susceptibility and severity, and had more FosB-ir neurons predominantly in the ventral hippocampus and the medial subnucleus of the amygdala (MeA). We also found a sex-dependent effect such that P14 males were smaller than their female littermates and had a greater seizure susceptibility and severity. Taken together, these results suggest an impact of prenatal and postnatal factors, as well as sex, on seizure susceptibility in young animals.
Traumatic brain injury (TBI) has long been recognized to be a risk factor for dementia. This association has, however, only recently gained widespread attention through the increased awareness of 'chronic traumatic encephalopathy' (CTE) in athletes exposed to repetitive head injury. Originally termed 'dementia pugilistica' and linked to a career in boxing, descriptions of the neuropathological features of CTE include brain atrophy, cavum septum pellucidum, and amyloid-β, tau and TDP-43 pathologies, many of which might contribute to clinical syndromes of cognitive impairment. Similar chronic pathologies are also commonly found years after just a single moderate to severe TBI. However, little consensus currently exists on specific features of these post-TBI syndromes that might permit their confident clinical and/or pathological diagnosis. Moreover, the mechanisms contributing to neurodegeneration following TBI largely remain unknown. Here, we review the current literature and controversies in the study of chronic neuropathological changes after TBI.
Traumatic brain injury (TBI) is a leading cause of mortality and morbidity both in civilian life and on the battlefield worldwide. Survivors of TBI frequently experience long-term disabling changes in cognition, sensorimotor function and personality. Over the past three decades, animal models have been developed to replicate the various aspects of human TBI, to better understand the underlying pathophysiology and to explore potential treatments. Nevertheless, promising neuroprotective drugs that were identified as being effective in animal TBI models have all failed in Phase II or Phase III clinical trials. This failure in clinical translation of preclinical studies highlights a compelling need to revisit the current status of animal models of TBI and therapeutic strategies.
Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disease thought to be caused, at least in part, by repetitive brain trauma, including concussive and subconcussive injuries. It is thought to result in executive dysfunction, memory impairment, depression and suicidality, apathy, poor impulse control, and eventually dementia. Beyond repetitive brain trauma, the risk factors for CTE remain unknown. CTE is neuropathologically characterized by aggregation and accumulation of hyperphosphorylated tau and TDP-43. Recent postmortem findings indicate that CTE may affect a broader population than was initially conceptualized, particularly contact sport athletes and those with a history of military combat. Given the large population that could potentially be affected, CTE may represent an important issue in public health. Although there has been greater public awareness brought to the condition in recent years, there are still many research questions that remain. Thus far, CTE can only be diagnosed post-mortem. Current research efforts are focused on the creation of clinical diagnostic criteria, finding objective biomarkers for CTE, and understanding the additional risk factors and underlying mechanism that causes the disease. This review examines research to date and suggests future directions worthy of exploration.
Tumor necrosis factor (TNF) is a cytokine which mediates protein wasting in pathological states by promoting the catabolism of visceral tissues and skeletal muscle. The role that TNF plays in nitrogen wasting following head injury was studied by measuring TNF in the serum of 21 patients with severe head injury. Parallel measurements of TNF and urinary nitrogen excretion were performed on days 1, 3 and 5 after head injury. TNF values after head injury ranged from 65 pg/ml to 7500 pg/ml, with a mean of 1147 pg/ml, compared to control values of serum TNF of less than 38 pg/ml. The mean daily urinary nitrogen loss was 13 g/day with a range of 2.8 to 27.6 g/day, and the mean nitrogen balance was −5.8 g with a range of +4.6 to −19.1 g. While both serum TNF levels and nitrogen loss were increased after head injury, the elevation of TNF did not correlate strongly with nitrogen wasting.
Previous concussion biomechanics research has relied heavily on the animal model or laboratory reconstruction of concussive injuries captured on video footage. Real-time data collection involves a novel approach to better understanding the medical issues related to sport concussion. Recent studies suggest that a concussive injury threshold is elusive and may, in fact, be irrelevant when predicting the clinical outcome.
The rising awareness of the long-term health problems associated with concussions re-emphasizes the need for understanding the mechanical etiology of concussions. This article reviews past studies defining the common mechanisms for mild traumatic brain injury and summarizes efforts to convert the external input to the head (force, acceleration, and velocity) into estimates of motions and deformations of the brain that occur during mild traumatic brain injury. Studies of how these mechanical conditions contribute to the cellular mechanisms of damage in mild traumatic brain injury are reviewed. Finally, future directions for improving understanding concussion biomechanics are discussed.
Since the 1920s, it has been known that the repetitive brain trauma associated with boxing may produce a progressive neurological deterioration, originally termed dementia pugilistica, and more recently, chronic traumatic encephalopathy (CTE). We review 48 cases of neuropathologically verified CTE recorded in the literature and document the detailed findings of CTE in 3 profession althletes, 1 football player and 2 boxers. Clinically, CTE is associated with memory disturbances, behavioral and personality changes, parkinsonism, and speech and gait abnormalities. Neuropathologically, CTE is characterized by atrophy of the cerebral hemispheres, medial temporal lobe, thalamus, mammillary bodies, and brainstem, with ventricular dilatation and a fenestrated cavum septum pellucidum. Microscopically, there are extensive tau-immunoreactive neurofibrillary tangles, astrocytic tangles, and spindle-shaped and threadlike neurites throughout the brain. The neurofibrillary degeneration of CTE is distinguished from other tauopathies by preferential involvement of the superficial cortical layers, irregular patchy distribution in the frontal and temporal cortices, propensity for sulcal depths, prominent perivascular, periventricular, and subpial distribution, and marked accumulation of tau-immunoreactive astrocytes. Deposition of beta-amyloid, most commonly as diffuse plaques, occurs in fewer than half the cases. Chronic traumatic encephalopathy is a neuropathologically distinct slowly progressive tauopathy with a clear environmental etiology.
A concussion model was developed to study injury mechanisms, functional effects, treatment, and recovery. Concussions in National Football League football involve high-impact velocity (7.4-11.2 m/s) and rapid change in head velocity (DeltaV) (5.4-9.0 m/s). Current animal models do not simulate these head impact conditions.
One hundred eight adult male Wistar rats weighing 280 to 350 g were used in ballistic impacts simulating 3 collision severities causing National Football League-type concussion. Pneumatic pressure accelerated a 50 g impactor to velocities of 7.4, 9.3, and 11.2 m/s at the left side of the helmet-protected head. A thin layer of padding on the helmet controlled head acceleration, which was measured on the opposite side of the head, in line with the impact. Peak head acceleration, DeltaV, impact duration, and energy transfer were determined. Fifty-four animals were exposed to single impact, with 18 each having 1, 4, or 10 days of survival. Similar tests were conducted on another 54 animals, which received 3 impacts at 6-hour intervals. An additional 72 animals were tested with a 100g impactor to study more serious brain injuries. Brains were perfused, and surface injuries were identified.
The 50 g impactor matches concussion conditions scaled to the rat. Impact velocity and head DeltaV were within 1% and 3% of targets on average. Head acceleration reached 450 g to 1750 g without skull fracture. The test is repeatable and robust. Gross pathology was observed in 11%, 28%, and 33% of animals in the 7.4-, 9.3-, and 11.2-m/s single impacts, respectively. At 7.4 m/s, a single diameter area of less than 0.5 mm of fine petechial hemorrhage occurred on the brain surface in the parenchyma and meninges nearest the point of impact. At higher velocities, there were larger areas of bleeding, sometimes with subdural hemorrhage. When the 50 g impactor tests were examined by logistic regression, greater energy transfer increased the probability of injury (odds ratio, 5.83; P = 0.01), as did 3 repeat impacts (odds ratio, 4.72; P = 0.002). The number of survival days decreased the probability of observing injury (odds ratio, 0.25 and 0.11 for 4 and 10 days, respectively, compared with 1 day). The 100g impactor produced more severe brain injuries.
A concussion model was developed to simulate the high velocity of impact and rapid head DeltaV of concussions in National Football League players. The new procedure can be used to evaluate immediate and latent effects of concussion and more severe injury with greater impact mass.
To determine if there is evidence that equipment use reduces sport concussion risk and/or severity.
12 electronic databases were searched using a combination of Medical Subject Headings and text words to identify relevant articles. Review
Specific inclusion and exclusion criteria were used to select studies for review. Data extracted included design, study population, exposure/outcome measures and results. The quality of evidence was assessed based on epidemiologic criteria regarding internal and external validity (ie, strength of design, sample size/power calculation, selection bias, misclassification bias, control of potential confounding and effect modification).
In total, 51 studies were selected for review. A comparison between studies was difficult due to the variability in research designs, definition of concussion, mouthguard/helmet/headgear/face shield types, measurements used to assess exposure and outcomes, and variety of sports assessed. The majority of studies were observational, with 23 analytical epidemiologic designs related to the subject area. Selection bias was a concern in the reviewed studies, as was the lack of measurement and control for potentially confounding variables.
There is evidence that helmet use reduces head injury risk in skiing, snowboarding and bicycling, but the effect on concussion risk is inconclusive. No strong evidence exists for the use of mouthguards or face shields to reduce concussion risk. Evidence is provided to suggest that full facial protection in ice hockey may reduce concussion severity, as measured by time loss from competition.
Mild traumatic brain injury accounts for 1% to 2% of emergency department visits in the United States. Up to 15% of these patients will have an acute intracranial lesion identified on head computed tomography; less than 1% of mild traumatic brain injuries will require neurosurgical intervention. Clinical research over the past decade has focused on identifying the subgroup of patients with mild traumatic brain injury with acute traumatic lesions on computed tomography and specifically those at risk for harboring a potentially catastrophic lesion. This research has been used to generate evidence-based guidelines to assist in clinical decision making. There is no evidence to support the use of plain film radiographs in the evaluation of patients with mild traumatic brain injury. The utility of brain-specific biomarkers is rapidly evolving, and a growing body of evidence supports their potential role in determining the need for neuroimaging. Clinical predictors for identifying patients with abnormal computed tomography have been established and, if used, may have a significant positive impact on traumatic brain injury-related morbidity and healthcare utilization in the United States. Patients with negative computed tomography are at almost no risk of deteriorating; however, they should be counseled regarding postconcussive symptoms and should be given appropriate written instructions and referrals at discharge.
Concussion is a serious problem in many contact sports, including rugby union football. The study's primary aim was to measure the efficacy of padded headgear in reducing the rates of head injury or concussion.
A cluster randomized controlled trial with three arms was conducted with rugby union football teams as the unit of randomization. Teams consisted of males participating in under 13-, 15-, 18-, and 20-yr age group competitions. The interventions were "standard" and "modified" padded headgear. Headgear wearing and injury were measured for each study team at each game over two seasons.
Eighty-two teams participated in year 1 and 87 in year 2. A total of 1493 participants (10,040 player hours) were in the control group, 1128 participants (8170 player hours) were assigned to the standard headgear group, and 1474 participants (10,650 player hours) were assigned to the modified headgear group. The compliance rates were low in all groups, but 46% of participants wore standard headgear. An intention-to-treat analysis showed no differences in the rates of head injury or concussion between controls and headgear arms. Incidence rate ratios for standard headgear wearers referenced to controls were 0.95 and 1.02 for game and missed game injuries. Analyses of injury rates based on observed wearing patterns also showed no significant differences. Incidence rate ratios for standard headgear wearers referenced to nonwearers were 1.11 and 1.10 for game and missed game injuries.
Padded headgear does not reduce the rate of head injury or concussion. The low compliance rates are a limitation. Although individuals may choose to wear padded headgear, the routine or mandatory use of protective headgear cannot be recommended.
Traumatic brain injury triggers a cascade of events resulting in delayed edema, necrosis and impaired function. Harmful mediators are accumulating in the brain after injury and recently, the role of cytokines in the pathophysiology of brain injury has been suggested. We have developed an experimental model for closed head injury (CHI), in which edema, blood-brain-barrier disruption, motor and memory dysfunctions have been demonstrated. In this study, spatial and temporal induction of IL-1, IL-6 and TNF-alpha gene mRNA transcription and of TNF-alpha and IL-6 activity in rat brain after CHI are shown. Dexanabinol, HU-211, is a synthetic cannabinoid devoid of cannabimimetic effects; it exhibits pharmacological properties of N-methyl-D-aspartate (NMDA)-receptor antagonist and is an effective cerebroprotectant. We report here that HU-211 is a novel inhibitor of TNF-alpha production at a post-transcriptional stage. HU-211, pentoxyfilline and TNF-binding protein improved the outcome of CHI. We suggest that TNF-alpha is a primary mediator of neurotoxicity after CHI, as inhibition of TNF-alpha is associated with better clinical recovery. TNF-alpha modulating agents, if given within the early time window post-injury, may improve the final neurological outcome in victims of brain trauma.
Tumor necrosis factor-alpha (TNF alpha) is a pleiotropic cytokine involved in inflammatory cascades associated with CNS injury. To examine the role of TNF alpha in the acute pathophysiology of traumatic brain injury (TBI), we studied its expression, localization and modulation in a clinically relevant rat model of non-penetrating head trauma. TNF alpha levels increased significantly in the injured cortex at 1 and 4, but not at 12, 24 or 72 h after severe lateral fluid-percussion trauma (2.6-2.7 atm). TNF alpha was not elevated after mild injury. At 1 and 4 h after severe TBI, marked increases of TNF alpha were localized immunocytochemically to neurons of the injured cerebral cortex. A small population of astrocytes, ventricular cells and microvessels, also showed positive TNF alpha staining, but this expression was not injury-dependent. Macrophages that were present in a hemorrhagic zone along the external capsule, corpus callosum and alveus hippocampus at 4 h after TBI did not express TNF alpha. Intracerebroventricular administration of a selective TNF alpha antagonist--soluble TNF alpha receptor fusion protein (sTNFR:Fc) (37.5 microg)--at 15 min before and 1 h after TBI, improved performance in a series of standardized motor tasks after injury. In contrast, intravenous administration of sTNFR:Fc (0.2, 1 or 5 mg/kg) at 15 min after trauma did not improve motor outcome. Collectively, this evidence suggests that enhanced early neuronal expression of TNF alpha after TBI contributes to subsequent neurological dysfunction.
Controlling the extent of inflammatory responses following brain injury may be beneficial since posttraumatic intracranial inflammation has been associated with adverse outcome. In order to elucidate the potential role of anti-inflammatory mediators, the production of interleukin-10 (IL-10) was monitored in paired cerebrospinal fluid (CSF) and serum of 28 patients with severe traumatic brain injury (TBI) and compared to control samples. The pattern of IL-10 was analyzed with respect to the patterns of IL-6, tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1 (TGF-beta1) in both fluids during a time period of up to 22 days. In parallel, the function/dysfunction of the blood-brain barrier (BBB) was monitored using the CSF-/serum-albumin quotient (Q(A)) and compared to intrathecal cytokine levels. Mean IL-10 concentration in CSF was elevated in 26 out of 28 TBI patients (range: 1.3-41.7 pg/ml) compared to controls (cut-off: 1.06 pg/ml), whereas only seven patients had elevated mean IL-10 concentration in serum (range: 5.4-23 pg/ml; cut-off: 5.14 pg/ml). The time course of IL-10 was similar in both fluids, showing a peak during the first days and a second, lower rise in the second week. Intrathecal IL-10 synthesis is hypothesized since CSF-IL-10 levels exceeded serum-IL-10 levels in most of the patients, IL-10-index (CSF/serum-IL-10/QA) was elevated in 23 individuals, and elevation of CSF-IL-10 showed to be independent from severe BBB dysfunction. Neither CSF nor serum IL-10 values correlated with the dysfunction of the BBB. IL-10, IL-6 and TGF-beta1 showed similar patterns in CSF over time, whereas rises of TNF-alpha corresponded to declines of IL-10 levels. Our results suggest that IL-10 is predominantly induced intrathecally after severe TBI where it may downregulate inflammatory events following traumatic brain damage.
To determine whether protective headgear reduced the incidence of concussion in a pilot study of under 15 rugby union.
Sixteen under 15 rugby union teams were recruited from three interschool competitions in metropolitan Sydney and the adjacent country region. A prospective study was undertaken over a single competitive season. The study had two arms: a headgear arm and a control arm. Headgear wearing rates and injury data were reported to the investigators and verified using spot checks.
A total of 294 players participated in the study. There were 1179 player exposures with headgear and 357 without headgear. In the study time frame, there were nine incidences of concussion; seven of the players involved wore headgear and two did not. There was no significant difference between concussion rates between the two study arms.
Although there is some controversy about the desirability of wearing protective headgear in football, this pilot study strongly suggests that current headgear does not provide significant protection against concussion in rugby union at a junior level.
Traumatic brain injury (TBI) elicits a complex sequence of putative autodestructive and neuroprotective cellular cascades. It is hypothesized that the genomic responses of cells in the injured brain serve as the basis for these cascades. Traditional methods for analyzing differential gene expression following brain trauma demonstrate that immediate early genes, cytokines, transcription factors, and neurotrophic factors can all participate in the brain's active and directed response to injury, and may do so concurrently. It is this complexity and multiplicity of interrelated molecular mechanisms that has demanded new methods for comprehensive and parallel evaluation of putative as well as novel gene targets. Recent advances in DNA microarray technology have enabled the simultaneous evaluation of thousands of genes and the subsequent generation of massive amounts of biological data relevant to CNS injury. This emerging technology can serve to further current knowledge regarding recognized molecular cascades as well as to identify novel molecular mechanisms that occur throughout the post-traumatic period. The elucidation of the complex alterations in gene expression underlying the pathological sequelae following TBI is of central importance in the design of future therapeutic agents.
Individuals sustaining mild traumatic brain injuries often report a constellation of physical, cognitive, and emotional/behavioral symptoms referred to as post concussion symptoms (PCS). The most commonly reported post concussion symptoms are headache, dizziness, decreased concentration, memory problems, irritability, fatigue, visual disturbances, sensitivity to noise, judgment problems, depression, and anxiety. Although these PCS often resolve within one month, in some individuals PCS can persist from months to years following injury and may even be permanent and cause disability. When this cluster of PCS is persistent in nature, it is often called the post concussion syndrome or persistent PCS. Both physiological and psychological etiologies have been suggested as causes for persistent post concussion symptoms and this has led to much controversy and debate in the literature. Most investigators now believe that a variety of pre-morbid, injury-related, and post-morbid neuropathological and psychological factors contribute to the development and continuation of these symptoms in those sustaining mild traumatic brain injury (MTBI).
Neurofilament light chain is a component of the axonal cytoskeleton. The concentration of the neurofilament light chain in cerebrospinal fluid may reflect axonal damage or the extent of white matter damage. In this study we describe a sensitive immunoassay for the detection of neurofilament light chain in cerebrospinal fluid using commercially available materials. The detection limit of the assay was 5 ng/l and the assay was linear up to 390 ng/l. Mean recovery was 91.5% and inter-assay and intra-assay coefficients of variation were below 18%. Strongly increased levels of neurofilament light chain were observed in patients with cerebrovascular accidents, subarachnoid hemorrhage and severe traumatic brain injury, suggesting the occurrence of axonal damage in these conditions.
Our purpose was to determine whether sex differences exist with respect to post-concussion symptoms and neurocognitive function in concussed collegiate athletes.
A prospective dependent-sample cohort design was used to compare baseline and post-concussion neuropsychological test scores and endorsed symptoms as functions of serial post-concussion assessment with respect to time and sex. The Immediate Post-concussion Assessment and Cognitive Testing (ImPACT) battery was administered to a multicenter analysis group of 79 concussed athletes. This computerized neuropsychological test was given to the athletes during the preseason and, on average, 2 and 8 days postinjury.
Multivariate analyses revealed no significant between-group differences on baseline test performance with respect to sex on any of the ImPACT composite scores or on the total symptom score. Multivariate analyses of post-concussion data revealed a significant main effect of time on ImPACT scores, but no main effect of sex was identified, and no time-by-sex interaction existed. Post hoc analysis revealed that concussed female athletes performed significantly worse than concussed male athletes on visual memory tasks (P = 0.001), and analysis of endorsed post-concussion symptoms revealed that concussed men were significantly more likely than concussed women to report post-concussion symptoms of vomiting (P = 0.001) and sadness (P = 0.017). Athletes' scores were examined individually using the reliable-change methodology. At 2 days post-injury, 58% of concussed athletes had one or more reliable incidents of performance decline or increases in symptom reporting. At 8 days post-concussion, 30% of concussed athletes were still showing one or more reliable change from preseason values.
College athletes exhibit differences on visual memory composite scores and symptoms post-concussion as a function of sex. These data support the importance of evaluating neuropsychological status and post-concussion symptoms in concussed athletes. In addition, these data illustrate the importance of analyzing an individual athlete's recovery pattern, because individual differences in recovery trajectories may be overshadowed by global norm-group comparisons.
To determine the relationship between recorded head accelerations and impact locations and acute clinical outcome of symptomatology, neuropsychological, and postural stability tests after cerebral concussion in Division I collegiate football players.
A prospective field study was used in which accelerometers were embedded in the football helmets of 88 collegiate football players. Linear and rotational accelerations of all head impacts sustained over the course of 2004 to 2006 National Collegiate Athletic Association football seasons were collected in real-time. Change scores were calculated on clinical measures from the players' preseason baseline to postinjury (within 48 h) and regressed against the recorded linear and rotational accelerations of the head at the time of the concussion.
Thirteen concussions were recorded ranging in impact magnitudes of 60.51 to 168.71 g. Linear regression showed no significant relationships between impact magnitude (linear or rotational acceleration) or impact location and change scores for symptom severity, postural stability, or neurocognitive function (P > 0.05).
Our findings suggest that football players are concussed by impacts to the head that occur at a wide range of magnitudes and that clinical measures of acute symptom severity, postural stability, and neuropsychological function all appear to be largely independent of impact magnitude and location. Because of the varying magnitudes and locations of impacts resulting in concussion as well as other factors such as the frequency of subconcussive impacts and number of previous concussions, it may be difficult to establish a threshold for concussive injury that can be applied to all football players.
Traumatic brain injury (TBI) can be caused by accidents and often leads to permanent health issues or even death. Brain injury criteria are used for assessing the probability of TBI, if a certain mechanical load is applied. The currently used injury criteria in the automotive industry are based on global head kinematics. New methods, based on finite element modeling, use brain injury criteria at lower scale levels, e.g., tissue-based injury criteria. However, most current computational head models lack the anatomical details of the cerebrum. To investigate the influence of the morphologic heterogeneities of the cerebral cortex, a numerical model of a representative part of the cerebral cortex with a detailed geometry has been developed. Several different geometries containing gyri and sulci have been developed for this model. Also, a homogeneous geometry has been made to analyze the relative importance of the heterogeneities. The loading conditions are based on a computational head model simulation. The results of this model indicate that the heterogeneities have an influence on the equivalent stress. The maximum equivalent stress in the heterogeneous models is increased by a factor of about 1.3-1.9 with respect to the homogeneous model, whereas the mean equivalent stress is increased by at most 10%. This implies that tissue-based injury criteria may not be accurately applied to most computational head models used nowadays, which do not account for sulci and gyri.
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