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

/pdf/american-medical-society-for-sports-medicine-position-ohfiva9at3.pdf

American Medical Society for Sports Medicine position statement: concussion in sport

Objective: To review the underlying pathophysiologic processes of concussive brain injury and relate these neurometabolic changes to clinical sports-related issues such as injury to the developing brain, overuse injury, and repeated concussion. Data Sources: Over 100 articles from both basic science and clinical medical literature selected for relevance to concussive brain injury, postinjury pathophysiology, and recovery of function. Data Synthesis: The primary elements of the pathophysiologic cascade following concussive brain injury include abrupt neuronal depolarization, release of excitatory neurotransmitters, ionic shifts, changes in glucose metabolism, altered cerebral blood flow, and impaired axonal function. These alterations can be correlated with periods of postconcussion vulnerability and with neurobehavioral abnormalities. While the time course of these changes is well understood in experimental animal models, it is only beginning to be characterized following human concussion. Conclusions/Recommendations: Following concussion, cerebral pathophysiology can be adversely affected for days in animals and weeks in humans. Significant changes in cerebral glucose metabolism can exist even in head-injured patients with normal Glasgow Coma Scores, underscoring the need for indepth clinical assessment in an effort to uncover neurocognitive correlates of altered cerebral physiology. Improved guidelines for clinical management of concussion may be formulated as the functional significance and duration of these postinjury neurometabolic derangements are better delineated.

/pdf/the-new-neurometabolic-cascade-of-concussion-2j9x87tmr6.pdf

The new neurometabolic cascade of concussion

The molecular pathophysiology of concussive brain injury.

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

The pathophysiology of traumatic brain injury at a glance

Aim or objective The aim of this study is to consolidate studies of physiological measures following sport-related concussion (SRC) to determine if a time course of postinjury altered neurobiology can be outlined. This biological time course was considered with respect to clinically relevant outcomes such as vulnerability to repeat injury and safe timing of return to physical contact risk. Design Systematic review. Data sources PubMed, CINAHL, Cochrane Central, PsychINFO. Eligibility criteria for selecting studies Studies were included if they reported original research on physiological or neurobiological changes after SRC. Excluded were cases series  Results A total of 5834 articles were identified, of which 80 were included for full-text data extraction and review. Relatively few longitudinal studies exist that follow both physiological dysfunction and clinical measures to recovery. Summary/conclusions Modalities of measuring physiological change after SRC were categorised into the following: functional MRI, diffusion tensor imaging, magnetic resonance spectroscopy, cerebral blood flow, electrophysiology, heart rate, exercise, fluid biomarkers and transcranial magnetic stimulation. Due to differences in modalities, time course, study design and outcomes, it is not possible to define a single ‘physiological time window’ for SRC recovery. Multiple studies suggest physiological dysfunction may outlast current clinical measures of recovery, supporting a buffer zone of gradually increasing activity before full contact risk. Future studies need to use generalisable populations, longitudinal designs following to physiological and clinical recovery and careful correlation of neurobiological modalities with clinical measures.

https://bjsm.bmj.com/content/bjsports/51/12/935.full.pdf

What is the physiological time to recovery after concussion? A systematic review.

Among the enormous population of head-injured children and young adults are a growing subpopulation who experience repeat traumatic brain injury (RTBI). The most common cause of RTBI in this age group is sports-related concussions, and athletes who have experienced a head injury are at greater risk for subsequent TBI, with consequent long-term cognitive dysfunction. While several animal models have been proposed to study RTBI, they have been shown to either produce injuries too severe, were conducted in adults, involved craniotomy, or failed to show behavioral deficits. A closed head injury model for postnatal day 35 rats was established, and single and repeat TBI (1-day interval) were examined histologically for axonal injury and behaviorally by the novel object recognition (NOR) task. The results from the current study demonstrate that an experimental closed head injury in the rodent with low mortality rates and absence of gross pathology can produce measurable cognitive deficits in a juvenile age group. The introduction of a second injury 24 h after the first impact resulted in increased axonal injury, astrocytic reactivity and increased memory impairment in the NOR task. The histological evidence demonstrates the potential usefulness of this RTBI model for studying the impact and time course of RTBI as it relates to the pediatric and young adult population. This study marks the first critical step in experimentally addressing the consequences of concussions and the cumulative effects of RTBI in the developing brain.

/pdf/repeat-traumatic-brain-injury-in-the-juvenile-rat-is-41qhz0rrvm.pdf

Repeat Traumatic Brain Injury in the Juvenile Rat Is Associated with Increased Axonal Injury and Cognitive Impairments

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Repeat Traumatic Brain Injury in the Juvenile Rat Is Associated with Increased Axonal Injury and Cognitive Impairments