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Secondary prevention of harm from sport-related concussion is contingent on immediate removal from play post-injury. To-date, educational efforts to reduce the prevalent risk behavior of continued play while symptomatic have been largely ineffective. Social norms theory may hold promise as a foundation for more effective concussion education aimed at increasing concussion reporting. The primary objective of this study was to assess whether perceived team concussion reporting norms would be less supportive of an individual's safe concussion symptom reporting behavior than objective team norms. Participants were 328 male and female US collegiate athletes. Written surveys were completed in person during the spring of 2014. Among both male and female athletes, team concussion reporting norms were significantly misperceived, with athletes tending to think that they themselves have safer attitudes about concussion reporting than their teammates. Perceived norms were associated with symptom reporting intention, independent of the team's objective reporting norm. A social norms approach to concussion education, in which misperceived group norms are corrected and shifted in the direction of safety, is an important avenue for program development and evaluation research aimed at the secondary prevention of harm from concussion. Implications for the design of this type of educational programming are discussed., (© The Author 2015. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Background: Communication between coaches and athletes about concussion safety can reinforce or undermine a sport culture in which concussion under-reporting is often endemic., Method: This study tested a model in which self-reported coach communication about concussion safety was predicted by factors including concussion knowledge, attitudes and beliefs, sex of the coach, and sex of the team coached. Participants were 997 coaches of contact and collision sports teams competing in National Collegiate Athletic Association Division I, II, or III., Results: Concussion attitudes and beliefs were the strongest predictors of communication, and the small effect of knowledge on communication was transmitted nearly entirely through its effect on attitudes and beliefs. Much of the variability in communication was attributable to the sex of the coach and the sex of the team coached., Conclusions: These results serve as a starting point for the design of coach-targeted interventions that encourage communication about health and safety with athletes.

Concussion from sport is increasingly recognized as a public health priority. In response, all states and the District of Columbia have enacted youth concussion legislation. This paper first examines key developments in concussion-related policy and legislation and then uses the findings from recent scientific studies to highlight the need to incorporate evolving scientific evidence into concussion legislation in order to better protect youth and adolescent athletes. Next, the paper discusses the framework of empirical health law research and why it should be applied in the case of concussion legislation. Finally, this paper argues that empirical health law research should be considered in any decision about whether legislation can help improve the health and safety of young players, a particularly vulnerable population whose unique needs have not yet been adequately addressed.

Chronic traumatic encephalopathy is a progressive tauopathy that occurs as a consequence of repetitive mild traumatic brain injury. We analysed post-mortem brains obtained from a cohort of 85 subjects with histories of repetitive mild traumatic brain injury and found evidence of chronic traumatic encephalopathy in 68 subjects: all males, ranging in age from 17 to 98 years (mean 59.5 years), including 64 athletes, 21 military veterans (86% of whom were also athletes) and one individual who engaged in self-injurious head banging behaviour. Eighteen age- and gender-matched individuals without a history of repetitive mild traumatic brain injury served as control subjects. In chronic traumatic encephalopathy, the spectrum of hyperphosphorylated tau pathology ranged in severity from focal perivascular epicentres of neurofibrillary tangles in the frontal neocortex to severe tauopathy affecting widespread brain regions, including the medial temporal lobe, thereby allowing a progressive staging of pathology from stages I-IV. Multifocal axonal varicosities and axonal loss were found in deep cortex and subcortical white matter at all stages of chronic traumatic encephalopathy. TAR DNA-binding protein 43 immunoreactive inclusions and neurites were also found in 85% of cases, ranging from focal pathology in stages I-III to widespread inclusions and neurites in stage IV. Symptoms in stage I chronic traumatic encephalopathy included headache and loss of attention and concentration. Additional symptoms in stage II included depression, explosivity and short-term memory loss. In stage III, executive dysfunction and cognitive impairment were found, and in stage IV, dementia, word-finding difficulty and aggression were characteristic. Data on athletic exposure were available for 34 American football players; the stage of chronic traumatic encephalopathy correlated with increased duration of football play, survival after football and age at death. Chronic traumatic encephalopathy was the sole diagnosis in 43 cases (63%); eight were also diagnosed with motor neuron disease (12%), seven with Alzheimer's disease (11%), 11 with Lewy body disease (16%) and four with frontotemporal lobar degeneration (6%). There is an ordered and predictable progression of hyperphosphorylated tau abnormalities through the nervous system in chronic traumatic encephalopathy that occurs in conjunction with widespread axonal disruption and loss. The frequent association of chronic traumatic encephalopathy with other neurodegenerative disorders suggests that repetitive brain trauma and hyperphosphorylated tau protein deposition promote the accumulation of other abnormally aggregated proteins including TAR DNA-binding protein 43, amyloid beta protein and alpha-synuclein.

The synthetic N3im-methyl analogue of thyrotropin releasing hormone (methyl-TRH) was administered intravenously to 15 euthyroid men, ages 36-62, in graded doses from 6.25 mug to 500 mug in order to establish the range of response of prolactin (PRL), TSH, T3 and T4 to various doses of methyl-TRH. There was a dose-related rise in serum TSH, PRL, T3, and T4 which gave a nearly linear relationship when the integrated area of response was used as an index of response to the various doses of methyl-TRH. All 15 men had a clear elevation in TSH, PRL, T3 and T4 following the lowest dose of methyl-TRH TESTED (6.25 mug). There was considerable variability in the response to methyl-TRH among the individuals. One hundred mug of methyl-TRH gave a maximum TSH response; a 25 mug dose elicited a maximum PRL response.

The N3im-methyl analogue of thyrotropin releasing hormone (methyl-TRH) was compared with ordinary TRH as a prolactin (PRL) releaser in 32 euthyroid volunteers (20 male and 12 female, ages 17-66 years). The mean PRL response to 100 mug of methyl-TRH was greater (P less than 0.025) than the PRL response to 500 mug of TRH at 10 min and at all sampling times from 30 to 240 min after administration of the releasing factors. The mean peak PRL (at 10 min), maximum deltaPRL, and integrated PRL response area were greater (P less than 0.025) after administration of methyl-TRH than after TRH. The PRL response to methyl-TRH was greater (P less than 0.005) for the 12 women than for the 20 men in this study. The mean baseline PRL was correlated with the peak PRL (r=0.74, P less than 0.01) and the maximum deltaPRL (r=0.58, P less than 0.01) after methyl-TRH. Following administration of methyl-TRH, the peak PRL was correlated with the peak TSH (r=0.43, P less than 0.05), the maximum deltaPRL was correlated with the maximum deltaTSH (r=0.43, P less than 0.05), and integrated PRL response area was correlated with the integrated TSH response area (r=0.44, P less than 0.05). Similar correlations between PRL and TSH responses were seen after giving TRH. Age was inversely correlated with baseline PRL (r=-0.55, P less than 0.01), with maximum deltaPRL (r=-0.64, P less than 0.01), and with the PRL response area (r=0.48, P less than 0.01) after administration of methyl-TRH or TRH. Methyl-TRH did not significantly alter serum levels of growth hormone (16 subjects) and luteinizing hormone and follicle stimulating hormone (14 subjects). The results of this study indicate that methyl-TRH is a more potent prolactin releaser than TRH. Like TRH, methyl-TRH has specificity in its effects on the pituitary, releasing only TSH and PRL in normal man.

The N3im-methyl analogue of thyrotropin release hormone (methyl-TRH) was compared with TRH as a thyrotropin releaser in 30 euthyroid volunteers (ages 19-61 years). The mean TSH response to 100 mug of methyl-TRH was greater (P less than 0.005) than the TSH response to 500 mug of TRH from 10 min to 240 min after giving the releasing factors. The mean peak TSH (at 30 min), maximum deltaTSH, and integrated TSH response area were greater (P less than 0.005) after administration of methyl-TRH than after TRH. The TSH response to methyl-TRH was significantly greater (P less than 0.05) for the 11 females than for the 19 males in this study. The mean baseline TSH was correlated with the maximum deltaTSH (r = 0.72, P less than 0.01) after methyl-TRH stimulation. The mean serum T3 concentration after methyl-TRH was significantly elevated at 60 min, peaked at 210 min and remained significantly elevated at 240 min. The peak serum T3, maximum T3 and T3 response area were significantly greater (P less than 0.005) after giving methyl-TRH than after TRH. The methyl-TRH induced T3 response area was 1.4 times the TRH induced T3 response area. The serum T4 concentration after methyl-TRH was elevated at 90 min (P less than 0.005), reached a peak at 210 min, and at 240 min was still 1.25 times the mean baseline T4. The peak serum T4, maximum deltaT4 and T4 response area after methyl-TRH were significantly greater than after TRH. The methyl-TRH induced T4 response area was 1.4 times the TRH induced T4 response area. The data indicate that methyl-TRH is a more potent thyrotropin releaser than TRH. Since N3im-methyl-histidine has been found in the brain, the possibility that this methyl analogue of TRH is a physiologic thyrotropin releaser should be evaluated.

The plasma clearance rate (PCR) and plasma half-disappearance time (t1/2) of TRH was compared to the PCR and t1/2 of pyroglutamyl-N3im-methyl-histidyl prolineamide (methyl-TRH), a more potent analog of TRH in normal subjects. The PCR for TRH was 1500 +/- 329 (SD) ml/min, which was significantly greater than the PCR of methyl-TRH (783 +/- 96 ml/min). The t1/2 of TRH was 6.2 min compared to a t1/2 of 11.5 min for methyl-TRH. The slower clearance of methyl-TRH is probably due to the increased resistance to degradation by serum enzymes of methyl-TRH compared to TRH.