How Can Neurologists Diagnose and Manage Sport-Related Concussion?

Current guidelines can direct treatment, and investigators are searching for reliable biomarkers to improve diagnosis.

Neurology Reviews. 2017 March;25(3):1,42-45

March 7, 2017|Neurology

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?

Concussion is a direct blow to the head, neck, face, or body with an impulsive force transmitted to the head, said Steven C. Kosa, MD, neurologist at Meritas Health in North Kansas City, Missouri. If the concussion is mild, it results in a rapid, short-lived impairment of neurologic function that resolves spontaneously within seven to 10 days. Otherwise, neurologic function improves slowly and sequentially over time. Standard imaging such as CT and MRI typically appears normal, especially in mild brain injuries. When torsional forces are applied to the brain, the resulting injuries are thought to be particularly serious. A small percentage of patients with concussion have postconcussive symptoms, which can be disabling. These symptoms include headaches, dizziness or imbalance, cognitive or memory problems, and mood disturbance.

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.