Recent studies have shown that the detrimental effects of sports concussions on cognitive and motor function may persist up to a few years post-injury. The present study sought to investigate the effects of having sustained a sports concussion more than 30 years prior to testing on cognitive and motor functions. Nineteen healthy former athletes, in late adulthood (mean age = 60.79; SD = 5.16), who sustained their last sport-related concussion in early adulthood (mean age = 26.05; SD = 9.21) were compared with 21 healthy former athletes with no history of concussion (mean age = 58.89; SD = 9.07). Neuropsychological tests sensitive to age-related changes in cognition were administered. An auditory oddball paradigm was used to evoke P3a and P3b brain responses. Four TMS paradigms were employed to assess motor cortex excitability: (i) resting motor threshold; (ii) paired-pulse intracortical inhibition and intracortical facilitation; (iii) input/output curve and (iv) cortical silent period (CSP). A rapid alternating movement task was also used to characterize motor system dysfunctions. Relative to controls, former athletes with a history of concussion had: (i) lower performance on neuropsychological tests of episodic memory and response inhibition; (ii) significantly delayed and attenuated P3a/P3b components; (iii) significantly prolonged CSP and (iv) significantly reduced movement velocity (bradykinesia). The finding that the P3, the CSP as well as neuropsychological and motor indices were altered more than three decades post-concussion provides evidence for the chronicity of cognitive and motor system changes consecutive to sports concussion.

OBJECTIVE. Using transcranial magnetic stimulation paradigms, this study investigated motor cortex integrity as a function of an athlete's prior history

Primary objective: This event-related potentials study investigated the long-term effects associated with a history of one or multiple concussions on the N2pc and P3 components using a visual search oddball paradigm. Methods and procedure: A total of 47 university football players were assigned to three experimental groups based on prior concussion history: Athletes with a history of one concussion (single-concussion group); Athletes with two or more concussions (multi-concussion group); non-concussed athletic controls. The average post-concussion period was 31 months for athletes in the multi-concussion group and 59 months for the single-concussion group. Results: This study found significantly suppressed P3 amplitude in the multi-concussed athletes group compared to the single-concussion and non-concussed athletes even when using the time since the latest concussion as a covariate. Conclusion: This finding suggests that the multi-concussed athletes group showed long-lasting P3 amplitude suppression when compared with single-concussion or non-concussed athletes despite equivalent neuropsychological test scores and post-concussion symptoms self-reports. This pattern of results is important because it shows that ‘old’ concussions do not cause general or ubiquitous electrophysiological suppression. The specificity of the long-term effects of previous concussions to the P3, along with an intact N2pc response, suggests that further work may allow one to pinpoint the cognitive system that is specifically affected by multiple concussions.

In this review the authors discuss persistent and cumulative alterations in both cognitive and motor function after sports concussions detected with some of the newest, most sophisticated brain investigation techniques. Ranging from subclinical neurophysiological alterations in young concussed athletes to quantifiable cognitive and motor function declines in former athletes in late adulthood with concussions sustained decades earlier, this review is also intended to provide new insights into the neuropathophysiology of sports concussion.

Background: Retired athletes with a history of sports concussions experience cognitive and motor declines with aging, and the risk of severe neurodegenerative conditions is magnified in this population. The present study investigated the effects of aging on motor system metabolism and function in former university-level athletes who sustained their last concussion several decades prior to testing. Methods: To test the hypothesis that age and remote concussions induce functional as well as metabolic alterations of the motor system, we used proton magnetic resonance spectroscopy to detect metabolic abnormalities in the primary motor cortex and the serial reaction time task (SRTT) to evaluate motor learning. Results: Our results indicate that motor learning is significantly reduced in former concussed athletes relative to controls. In addition, glutamate/H₂O ratio in M1 was disproportionately reduced in concussed athletes with advancing age and was found to strongly correlate with motor learning impairments. Conclusion: Findings from this study provide evidence that the acquisition of a repeated motor sequence is compromised in the aging concussed brain and that its physiological underpinnings could implicate disproportionate reductions of M1 glutamate concentrations with advancing age.

Sleep disturbances are widely prevalent following a traumatic brain injury (TBI) and have the potential to contribute to numerous post-traumatic physiological, psychological, and cognitive difficulties developing chronically, including chronic pain. An important pathophysiological mechanism involved in the recovery of TBI is neuroinflammation, which leads to many downstream consequences. While neuroinflammation is a process that can be both beneficial and detrimental to individuals’ recovery after sustaining a TBI, recent evidence suggests that neuroinflammation may worsen outcomes in traumatically injured patients, as well as exacerbate the deleterious consequences of sleep disturbances. Additionally, a bidirectional relationship between neuroinflammation and sleep has been described, where neuroinflammation plays a role in sleep regulation and, in turn, poor sleep promotes neuroinflammation. Given the complexity of this interplay, this review aims to clarify the role of neuroinflammation in the relationship between sleep and TBI, with an emphasis on long-term outcomes such as pain, mood disorders, cognitive dysfunctions, and elevated risk of Alzheimer’s disease and dementia. In addition, some management strategies and novel treatment targeting sleep and neuroinflammation will be discussed in order to establish an effective approach to mitigate long-term outcomes after TBI.