In April 2013, the NCAA Sport Science Institute hosted a Concussion Task Force comprised of concussion experts (scientists, physicians, clinicians) whose charge was to study concussion in college sports and to develop a consensus, when possible, on concussion definition, epidemiology, pathophysiology, management and long-term ramifications. When a consensus was not possible, the NCAA Concussion Task Force members made recommendations for further study that could provide a pathway for consensus. This article will summarize some key points of this task force.
The consensus definition from the 4th International Conference on Concussion in Sport (Zurich 2012) is that concussion is a brain injury and is defined as a complex pathophysiological process affecting the brain, induced by biomechanical forces. These guidelines further describe common features that incorporate clinical, pathologic and biomechanical injury constructs that may be utilized in defining the nature of a concussive head injury, including:
- Direct blow to the head, face, neck or … impulsive force transmitted to the head.
- Rapid onset of short-lived impairment of neurological function that resolves spontaneously. In some cases, symptoms and signs may evolve over a number of minutes to hours.
- Functional disturbance rather than a structural injury and, as such, no abnormality is seen on standard structural neuroimaging studies.
- Grades set of clinical symptoms that may or may not involve loss of consciousness.
As noted in Table 1, there is not one uniform definition of concussion.
It is also noteworthy that concussion is sometimes used interchangeably with mild traumatic brain injury, and at other times is considered one of several possible manifestations of traumatic brain injury. Importantly, the absolute guide for mild traumatic brain injury is a Glasgow Coma Scale of 13-15 (see Table 2).
Sports Participation Definitions and Concussion Epidemiology
Concussion incidence varies among sports. The American Academy of Pediatrics provides a useful classification of sports by contact (see Table 3).
The rate of concussion in NCAA sports can be assessed in various ways. Figure 1 demonstrates the rate of competition concussion per 1,000 student-athlete exposures. It is noteworthy that the higher rates occur in contact/collision sports. All meaningfully measurable rates occur in either contact/collision or limited contact/impact sports. It is also noteworthy that women have a higher rate of concussion than men for soccer and basketball.
Another way to look at concussion is through annual estimates that include both practice and competition (see Figure 2).
Because of the large size of football teams and the higher rate of concussion relative to other sports, concussion incidence is highest in football. In assessing the available data, anticipating concussion risk can be made based on the sport; anticipating concussion risk can also be guided by impact expectation, as noted in Figure 3. For each sport, it is important to follow the institution’s concussion management plan.
Concussion is not a static event, but is rather a pathophysiological process that may evolve over minutes, hours and days. Figure 4 highlights many key components of concussion pathophysiology.
Following a biomechanical threshold impact to the brain, either directly or indirectly, the nerve cell and/or nerve axon become perturbed. The threshold impact is not known with certainty, and can vary between individuals, and even within the same individual. Threshold impact also varies based on whether the biomechanical force is linear or rotational.
Once an individual receives a traumatic impact that exceeds the nerve cell’s ability to adapt, the pathophysiological process begins. There is immediate efflux of potassium from the nerve cell, and this ionic state must be resolved through the energy-dependent sodium-potassium ATP pump. However, another traumatic brain injury consequence is reduction of cerebral blood flow. Thus, a brain energy crisis develops because of the increased need for glucose (to serve as energy for the sodium-potassium ATP pump) coupled with diminished blood flow. Calcium enters the cell following concussion, as a manifestation of both nerve cell and axonal disruption. Calcium can be toxic to the nerve cell, and leads to enzyme activation, which in turn can trigger various inflammatory responses, cytoskeletal rearrangement and programmed cell death. Neurotransmitter release is altered following concussion because excitatory neurotransmitters such as glutamate become released.
Figure 5 provides a time sequence overview for the metabolic cascade of concussion. Such temporal resolution also varies from individual to individual, and can vary within the same individual. If someone receives a concussion during the metabolic recovery phase of a prior concussion, the temporal resolution of the subsequent concussion will be further delayed.
Whereas potassium and glutamate dysfunction resolves within minutes, it may take six to ten days for calcium perturbation and cerebral blood flow to normalize. This correlates with clinical symptomatology, which is discussed next.
Clinical Manifestations of Concussion
Because the definition of concussion is not uniform and because there are no clearly defined genetic predispositions, serum/brain biomarkers, or definitive neuroimaging classifications of concussion, it is critical to be well versed in clinical manifestations of concussion. Unlike many other medical conditions (e.g. breast cancer, myocardial infarction) in which there are numerous identified predispositions, biomarkers, and imaging criteria, concussion remains largely defined by its clinical presentation, which can be varied, subtle and easily overlooked. Concussion results from a brain pathophysiological process, but the brain location (or locations), and the extent of brain perturbation can vary considerably from concussion to concussion. Thus, concussion manifestations can range from mild visual obscurations (e.g. “seeing stars”) to profound amnesia, incoordination and even loss of consciousness. There are no clear prognostic factors for the many varied concussion manifestations. Table 4 lists signs and symptoms of concussion, as included in the American Medical Society of Sports Medicine Position Stand (AMSSM, 2012).
As noted in Table 4, concussion symptoms and signs are varied. Also, many symptoms are non-specific (e.g., headache, difficulty concentrating), and need to be placed in the proper context. A student-athlete may have difficulty concentrating and complain of headache after a night of alcohol drinking and sleep deprivation, but that does not mean he or she is suffering with a concussion. However, if the student-athlete develops such symptoms following a traumatic head impact, either directly or indirectly, then concussion is highly probable.
Any athlete who is suspected of suffering with concussion must be evaluated immediately, either on the field, sideline, or in a quiet locker room. Many tools exist to aid in the diagnosis of concussion, and it is best to include a combination of symptoms checklist, cognitive testing and balance testing, all within a clinical context. The SCAT2 and SCAT3 combine these variables into one test. Sensitivity and specificity of various sideline tests, as noted in AMSSM 2012, are shown in Table 5. There is universal consensus, and NCAA policy, that any athlete who is diagnosed with a concussion must not return to play or practice that day, and must be cleared by a health care professional (team physician or his or her designee) before returning to play or practice.
The diagnosis of concussion is influenced by:
- Medical Team Awareness. When there exists a comprehensive program in which all medical team members and athletes are well versed in concussion management, there is a high internal consistency and reliability in diagnosing concussion. Conversely, when the medical team and athletes have not rehearsed concussion management, the internal consistency and reliability for concussion diagnosis diminish considerably.
- Athlete Self-Report. Unfortunately, even well-educated athletes have a high rate of not reporting concussion symptoms. Indeed, studies reveal that 40 to50 percent of athletes will not report concussion symptoms, especially if they have had a prior concussion. Reasons vary, and range from a sense of invincibility to fear of losing one’s playing position.
- Over-Reliance on Computerized Testing. Concussion diagnosis must be clinical, and cannot be made by computerized testing. Such tests may help make a clinical decision, but are not valid indicators of a diagnosis as a stand-alone tool.
Detailed concussion management guidelines are provided in the NCAA Sports Medicine Handbook. The cornerstone of concussion management is immediate rest, followed by a gradual resumption of activities. Because of the brain energy crisis following concussion, physical activities must be resumed in a gradual, step-wise manner (see Table 6).
In general, it is recommended that each rehabilitation stage take 24 hours before progressing to the next stage and such progression should be individualized. If symptoms return upon progression of exercise, then the athlete should return to the previous stage until he or she is asymptomatic. Most athletes are without symptoms after one week and a minority have symptoms after one month.
There is considerable controversy with regard to long-term implications of concussion. On one end of the spectrum, some claim that repeated concussions cause a neuro-degenerative brain disease called chronic traumatic encephalopathy or CTE. On the other end of the spectrum, some claim that there are no significant long-term sequelae of concussion. The murky evidence lies somewhere in between.
Post-Concussion Syndrome: Post-concussive syndrome refers to prolonged concussion symptoms following concussion. It is not truly a ‘syndrome’ because there is no core of consistent symptoms and there is no clear correlation with type or severity of concussion, biomarkers, or genetic/personality predisposition. Symptoms include neurologic (e.g. dizziness, light sensitivity), cognitive (memory, attention deficits) and emotional (depression, anxiety). Post-concussive syndrome is best considered a neuropsychiatric disorder, and it is important to recognize that it has no bearing on the extent of, or expected recovery from, concussion. Post-concussive syndrome is best managed in a multi-disciplinary manner that includes gradual increase in physical and cognitive activity. Management is distinctly different from acute concussion management and individuals should not simply be relegated to prolonged rest, which may perpetuate the symptomatology.
Chronic Neurobehavioral Impairment: Cognitive and executive dysfunction have been described following multiple concussions. However, only 2 Class I studies exist, and this is for jockeys and rugby players. There are 7 Class II studies that include boxers, NFL players and soccer players, which demonstrate long-term cognitive impairment. Two studies show an association with apoE4 genotype, suggesting a genetic predisposition, and one study shows an association with a prior history of learning disability. There is one Class III study of NFL players. There is some correlation with magnitude of exposure and chronic neurobehavioral impairment in professional athletes, but the relationship between exposure and chronic neurobehavioral impairment in amateur athletes is uncertain. This may be from a combination of underpowered studies and possible brain adaptations that are different in younger individuals.
Depression: Depression has also been reported as a possible long-term manifestation of repeated concussion. Two Class II studies of retired NFL players note an increased rate of depression in a dose-response manner, and one Class III study of retired NFL players notes a higher depression rate than the general population. There are also studies that show no clear relationship between depression and prior concussion. Of note: about 21 percent of college student-athletes report depression at baseline.
Chronic Traumatic Encephalopathy (CTE): CTE is a progressive neuro-degenerative disease whose pathologic hallmark is abnormal tau deposition, with clinical manifestations of mood disorder, neuromuscular incoordination, dementia, and death. There are not agreed-upon pathological and clinical criteria for CTE, although it seems clear that CTE is a distinct clinical entity from Alzheimer’s disease. In a 2012 publication of CTE case series (Brain), CTE is described as a “progressive tauopathy that occurs as a consequence of repetitive mild traumatic brain injury.” However, in the Zurich 2012 consensus paper, it is noted that “… it is not possible to determine the causality or risk factors [of CTE] with any certainty. As such, the speculation that repeated concussion or subconcussive impacts cause CTE remains unproven.” What makes the CTE debate even more confusing is that one of the co-authors of the paper in Brain also served as a co-author of the Zurich guidelines! The universal consensus in the NCAA Concussion Task Force was that we need to better understand CTE with regard to genetic predispositions and biomarkers. No task force member noted a clear cause-and-effect relationship between concussion and CTE.
We have much work ahead of us. 2012 was the first year in which there was universal consensus that athletes with a diagnosis of concussion should not return to play on the same day. That is progress. On the other hand, we continue to interchange concussion with mild traumatic brain injury, which many consider a misnomer. How is a brain injury mild? We don’t use such terminology with other conditions. For example, we do not say: “You have mild breast cancer.” Clearly, we need to define concussion with regard to biomechanics (single and cumulative hits to the head as measured by rapidly evolving sensors), serum biomarkers, imaging biomarkers and genetic predispositions. We need to combine such evidence with clinical skill and diagnostic tools. Together, we can make this happen.
Last Updated: Jul 11, 2013