How Can Neurologists Diagnose and Manage Sport-Related Concussion?

RIVIERA BEACH, FL—If a neurologist is at a sporting event during which a player sustains a head injury, audience members or officials may look to him or her for guidance, according to an overview delivered at the 44th Annual Meeting of the Southern Clinical Neurological Society. Understanding how to diagnose and manage concussion may be a vital skill for neurologists, regardless of specialty.

What Is Concussion?

Steven C. Kosa, MD

Loss of consciousness previously was considered necessary for a diagnosis of concussion. Later, it was taken as a marker of serious injury. Neither of these principles is accepted any longer. Data indicate that at least 90% of concussions are not associated with loss of consciousness, and studies have not shown that loss of consciousness portends a worse prognosis or protracted recovery from the injury, said Dr. Kosa.

The pathophysiology of concussion is not certain. The current proposal is that concussion entails disruption of neuronal cell membranes resulting from disruption of normal ion channels (eg, calcium, potassium, and sodium), leading to a loss of normal neuronal homeostasis. This situation can cause a cascade of events, including mitochondrial dysfunction that causes neuronal energy failure, loss of normal glucose metabolism, activation of NMDA receptors from increased levels of glutamate, production of lactic acid, and generation of free radicals, all of which damage the neurons and supporting cells. Most cells survive the concussive injury, but can be functionally compromised. Severe injuries can lead to neuronal cell death.

What Are the Possible Sequelae of Concussion?

Concussion increases the risk of second impact syndrome, which can occur if the patient sustains another injury at between 24 hours and 10 days after a concussion. Research on second impact syndrome is limited, but the syndrome is understood to entail rapid and massive brain edema that leads to brain herniation and likely death or severe disability. The syndrome occurs within minutes of the second impact and is thought to be enabled by the period of vulnerability that follows an initial concussion. The syndrome occurs mostly in young patients, but has been described in boxers. For this reason, neurologists should be especially cautious when deciding whether to let a child with concussion return to play, said Dr. Kosa. The Centers for Disease Control and Prevention (CDC) estimate that second impact syndrome causes four to six deaths in patients under age 18 annually.

Concussion may be accompanied by traumatic brain injury (TBI). In 2010, the CDC reported 2.5 million hospital encounters related to TBI. Among these encounters, 87% of patients were treated in the emergency department and released, 11% were hospitalized and discharged, and 2% died. The highest incidence of TBI is in young children, and causes include sports accidents, bicycle accidents, skateboard accidents, vehicular accidents, and falls. The CDC estimates that between 3.2 million and 5.3 million people in the United States have permanent TBI-related disability, which results in great economic, physical, and emotional burdens.

Patients with repeated mild TBI may be at risk of chronic traumatic encephalopathy (CTE). This disorder has been described in football players, veterans, and boxers. Symptoms develop later in the patient’s life, and four stages have been described. The first stage includes headaches, inattention, and poor concentration. Stage two consists of significant mood disturbance with depression, along with explosive bouts of anger and short-term memory impairment. The third stage includes further cognitive or memory impairment that manifests as prominent executive dysfunction, where reasoning and organization or planning are most affected. In stage four, the patient has dementia; the cognitive and memory impairment has progressed to the point where the patient depends on others for activities of daily living.

McKee et al observed that CTE was associated with cerebral atrophy, mammillary body atrophy, dilation of the lateral ventricles, fenestrations of the septum pellucidum, and tau deposition. Researchers and clinicians, however, have not arrived at a consensus about the pathologic and clinical criteria for CTE. Furthermore, Cantu et al stated that it is not yet possible to determine the causality or risk factors of CTE with certainty. The hypothesis that repeated concussion or subconcussive impacts leads to the development of CTE has not been scientifically proven to date, they added.

What Should Be Done on the Field?

If a player at a sporting event sustains a head injury, he or she should be removed from play immediately and not allowed to return to the game. If he or she has not directly observed the injury, the neurologist should get information about it from witnesses. The neurologist should perform a focused physical examination, searching for evidence of decreased level of consciousness, confusion, focal weakness or incoordination, visual disturbance, cervical spine injury, or facial fractures. The Sport Concussion Assessment Tool (SCAT) can assist the clinician in concussion evaluation and treatment in a standardized and methodical way to determine whether and when a player can safely return to play.

A patient with an abnormal examination may need to be transferred to the local emergency department for further testing. CT imaging should not be performed automatically, because it may expose the patient to radiation unnecessarily. Two sets of criteria offer guidance about CT imaging. The New Orleans criteria state that a patient should undergo CT if he or she has a headache, has vomited, is older than 60, had been using alcohol or other drugs, had a seizure, has visible trauma above the clavicle, or has a short-term memory deficit. The Canadian CT Head Rule lists similar criteria, including a Glasgow Coma Scale score at two hours of less than 15, any sign of a basal skull fracture, and amnesia for events that took place 30 minutes before the injury.

Anticoagulants increase the risk of immediate or delayed hemorrhage after head injury. If a patient has intracranial hemorrhage on CT and has been using anticoagulants, the clinician should rapidly reverse the anticoagulant effect with the appropriate agent. A repeat head CT 24 hours later should be considered in those thought to be at high risk for intracranial hemorrhage and whose initial CT imaging is negative for bleed. “Err on the side of admitting these patients, at least for observation,” said Dr. Kosa. Before the patient is discharged from the emergency room, he or she should receive education about postconcussion symptoms that should prompt another visit to the emergency department. Educational materials are available on the CDC’s website.

When Can a Patient Return to Play?

The consensus statement on concussion in sport adopted at the Third International Conference on Concussion in Sport includes guidelines for graduated return to play. At first, the patient should undergo symptom-limited physical and cognitive rest until he or she recovers. Next, the patient may start light aerobic exercise such as walking, swimming, or cycling. The goal is to increase heart rate, but the patient should reduce activity if symptoms occur. Then, the patient may engage in sport-specific exercise. If recovery proceeds well, the patient may begin noncontact training drills and, later, full contact practice. Only when the patient has full confidence and coaching or training staff has assessed his or her functional skills can the athlete return to play.

What Concussion Research Is Under Way?

Investigations currently under way aim to improve understanding of concussion, as well as to aid diagnosis and treatment. Researchers are looking for a reliable biomarker of concussion that can be detected with an easy, cost-effective, and preferably noninvasive test. Saliva, tears, urine, blood, and CSF are among the candidate samples being studied. CSF is the most reliable fluid to test because of its proximity to the brain and its low susceptibility to extracerebral confounders, but it is the most invasive option. Groups are examining potential serum biomarkers such as S100b, neuron-specific enolase, myelin basic protein, glial fibrillary acidic protein, and cleaved tau.

In addition, McKee and colleagues are working to define clear pathologic criteria defining the various stages of CTE. They also are seeking a way of distinguishing CTE from Alzheimer’s disease, amyotrophic lateral sclerosis, and other neurodegenerative diseases in postmortem brain tissue. The group’s ultimate goal is to identify features that may assist in the diagnosis of CTE in living people using advanced neuroimaging.

—Erik Greb

Suggested Reading

Giza CC, Kutcher JS, Ashwal S, et al. Summary of evidence-based guideline update: evaluation and management of concussion in sports: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2013;80(24):2250-2257.

McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on concussion in sport--the 3rd International Conference on concussion in sport, held in Zurich, November 2008. J Clin Neurosci. 2009;16(6):755-763.

Omalu BI, Hamilton RL, Kamboh MI, et al. Chronic traumatic encephalopathy (CTE) in a National Football League Player: Case report and emerging medicolegal practice questions. J Forensic Nurs. 2010;6(1):40-46.