Traumatic brain injury (TBI) is a common condition that is often complicated by neuropsychiatric sequelae that can have major impacts on function and quality of life. An alteration in the sense of smell is recognised as a relatively common complication of TBI, however in clinical practice this complication may not be sought or adequately characterized. We conducted a systematic review of studies concerned with olfactory functioning following TBI. Our predetermined criteria led to the identification of 25 studies published in English which we examined in detail. We have tabulated the data from these studies in 8 separate tables, beginning with Table 1 which highlights each study’s key findings, and we provide a summary/synthesis of the findings in the accompanying results and discussion sections. Despite widely differing methodologies, the studies attest to a high frequency of post-TBI olfactory dysfunction and indicate that its presence can serve as a potential marker of additional structural or functional morbidities.

Many professional sports have introduced sideline video review to help recognise concussions. The reliability and validity of identifying clinical and observable signs of concussion using video analysis has not been extensively explored. This study examined the reliability and validity of clinical signs of concussion using video analysis in the National Rugby League (NRL). All 201 professional NRL matches from the 2014 season were reviewed to document six signs of possible concussion (unresponsiveness, slow to get up, clutching/shaking head, gait ataxia, vacant stare, and seizure). A total of 127,062 tackles were reviewed. Getting up slowly was the most common observable sign (2240 times in the season, 1.8% of all tackles) but only 223 times where it appeared to be a possible concussion (0.2% of all tackles and 10.0% of the times it occurred). Additionally, clutching/shaking the head occurred 361 times (on 212 occasions this sign appeared to be due to a possible concussion), gait ataxia was observed 102 times, a vacant stare was noted 98 times, unresponsiveness 52 times, and a possible seizure 4 times. On 383 occasions, one or more of the observable signs were identified and deemed associated with a possible concussion. There were 175 incidences in which a player appeared to demonstrate two or more concussion signs, and 54 incidences where a player appeared to demonstrate three or more concussion signs. A total of 60 diagnosed concussions occurred, and the concussion interchange rule was activated 167 times. Intra-rater reliability (κ = 0.65–1.00) was moderate to perfect for all six video signs; however, the inter-rater reliability was not as strong (κ = 0.22–0.76). Most of the signs had relatively low sensitivity (0.18–0.75), but high specificity (0.85–1.00). Using video replay, observable signs of concussion appear to be sensitive to concussion diagnoses when reviewing known injuries among professional rugby league players. When reviewing an entire season, however, certain signs occur very commonly and did not identify concussion. Thus, the implementation of video review in the NRL is challenging, but can provide a useful addition to sideline concussion identification and removal from play decisions.

The purpose of this study was to examine cortical thickness and subcortical volumes in professional rugby players with an extensive history of concussions compared to control subjects. Participants included 24 active and former professional rugby league players [Age M(SD) = 33.3(6.3); Range = 21-44] with an extensive history of concussion and 18 age- and education-matched controls with no history of neurotrauma or participation in contact sports. Participants underwent T1-weighted imaging and completed a neuropsychological battery, including two tests of memory. Whole brain cortical thickness analysis and structural volume analysis was performed using FreeSurfer version 6.0. Professional rugby league players reported greater alcohol consumption (p < .001) and had significantly worse delayed recall of a visually complex design (p = .04). They did not differ from controls on other clinical outcome measures. There were no differences in cortical thickness between the groups. Professional players had smaller whole brain (p = .003), bilateral hippocampi (ps = .03), and left amygdala volumes (p = .01) compared to healthy controls. Within the players group, there were significant associations between greater alcohol use and smaller bilateral hippocampi and left amygdala volumes. There were no associations between structural volumes and history of concussions or memory performance. The literature examining cortical thickness in athletes with a history of multiple concussions is mixed. We did not observe differences in cortical thickness in professional rugby league players compared to controls. However, smaller subcortical volumes were found in players that were, in part, associated with greater alcohol consumption.