“Put Me Back In, Coach!” Concussion and Return to Play

Abstract

Concussion is a mild traumatic brain injury (TBI) sustained as a result of blunt force or acceleration/deceleration injury to the head.^1,2 Approximately 1.4–3.8 million concussions occur each year in the United States, making the understanding of concussion pathophysiology and how it can impact one’s gross function an essential part of a physician’s toolbelt.^3,4 It is important to recognize that the biochemical changes of concussion that result in functional cognitive deficits and compromised synaptic plasticity are greatest at three days and still active more than 15 days post-injury.^6,7 Therefore, prompt diagnosis of concussion and subsequent proper treatment can help promote adequate healing and prevent synergistic effects of second-impact syndrome. Recognition of the common signs and symptoms of concussion combined with pertinent physical examination findings, concussion assessment tools aid with proper identification and triage of patients. Consensus guidelines have delineated return to play protocol and treatment regimen for these patients and athletes. The goal of treatment for concussion is important to limit long-term deleterious effects that can result from single or multiple injuries to the brain.

Introduction

Concussion is a mild traumatic brain injury (TBI) sustained as a result of blunt force or acceleration/deceleration injury to the head.^1,2 In 2012, the International Conference of Concussion in Sport determined concussion as “A brain injury defined by a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces resulting in neurologic impairment reflected by functional disturbances.” Resolution of concussions follows a sequential course, though duration is largely dependent on severity. The Center for Disease Control (CDC) approximates 1.4–3.8 million concussions per year in the United States.^3,4 However, due to debate about precise definition of concussion and underreporting of incidence, epidemiologic estimations have limited strength.⁵

Pathophysiology of Concussion

Concussive brain injury results in transient neuronal dysfunction in the absence of gross anatomic lesion on imaging. It is a functional disturbance. A complex cascade of neurochemical and neurometabolic events ensues within the brain secondary to acceleration/deceleration forces after impact.⁶ The axonal and neuronal membrane stretch causes dysregulation of ion channels and membrane instability. Thus, excitatory neurotransmitters, most notably glutamate, are dispersed. Glutamate binds to a N-methyl-d-aspartate receptor on the cell membrane, resulting in calcium influx to the cell and ultimately disrupting mitochondrial energy production. This disruption results in the build-up of reactive oxygen species (ROS) which hinder the cell’s ability to re-establish proper ion balance, minimizing effective oxygen-dependent energy production within the cell. In other words, the initial traumatic injury causes depressed brain energy metabolism, resulting in a so-called “energy crisis” which results in functional cognitive deficits and compromised synaptic plasticity.⁶ This neurologic dysfunction occurs within the first 30 minutes to four hours of injury. The biochemical changes after concussion are greatest at three days and still active at more than 15 days post-injury.⁷ Timing of the cascade of events reveals an ongoing process of injury that is imperative to understand for proper evaluation and treatment.

Initial Concussion Assessment

The most vital component of concussion care is prompt recognition of the concussion itself.¹ Ninety percent of the time concussion occurs without loss of consciousness (LOC), making it more difficult to recognize.^8,9 Team personnel should immediately remove any athlete from play that is suspected of a concussion in order to minimize risk of further injury.¹⁰ A more severe head injury is indicated by LOC greater than 30 minutes, post-traumatic amnesia greater than 24 hours, or Glasgow coma score (GSC) of 12 or less.¹ Current recommendations denote that players diagnosed with concussion should not return to play the same day; previous guidelines recommended this only if the individual was under 18 years.¹¹

A recently published literature review from March 2016 reevaluated the physical examination findings most relevant for concussion assessment. The essential examine points should include cranial nerves, manual muscle testing, deep tendon reflexes, inspection of head and neck for trauma/tenderness and cervical range of motion, Spurling maneuver, a static or dynamic balance assessment, screening ocular assessment, and mental status examination which includes orientation, recall, concentration, mood, affect, insight, and judgment.¹² Simple questions of orientation are not adequate to rule out a concussion.¹³ Common early concussion symptoms include headache, dizziness, lack of awareness of surroundings, nausea, and vomiting.⁹ Headache tends to be the most common symptom. Additional signs of concussion may include: vacant stare, delayed verbal expression, poor concentration, disorientation, slurred speech, imbalance/incoordination, mood lability, anxiety, fatigue, memory impairments, irritability, and anxiety.¹⁴

The Sports Concussion Assessment Tool (SCAT3) is an expert consensus standardized concussion assessment utilized worldwide. It combines aspects from previous concussion tools into eight components. In 2013, the SCAT2 was revised to the SCAT 3 to further incorporate ideas/recommendations discussed at the 2012 CISG (Concussion in Sport Group). Changes were made to the assessment of amnesia, disorientation, vacant looks, GSC, and Maddocks questions along with increasing emphasis on symptom severity.^15,16 The SCAT3 added the Balance Error Scoring System (BESS) to improve detection of balance deficits. Still, testing paradigms are not fully inclusive and should not replace comprehensive neurologic examination.¹⁷ Baseline neurocognitive testing for comparison is debatable; the ImPACT study of 2009 demonstrates athletic trainers have been shown to base return to play more on symptoms versus previous functional status.¹⁸

Neuroimaging is not necessary for all concussion patients. However, if there is question of the diagnosis or neurologic deterioration, immediate neuroimaging is indicated. The initial test of choice is a non-contrast head CT to assess for intracranial bleeding or fracture.

Treatment and Management

Physician evaluation should occur within a few days of the injury if not done so initially. The cornerstone of concussion management is physical and cognitive rest until symptom resolution.¹¹ Activities that should be limited include scholastic activity, video games, computer usage, text messaging, television screen time, etc. Once an athlete is asymptomatic, graduated return to play (RTP) protocol can be initiated. Pharmacologic treatment is aimed at prolonged symptoms or those symptoms that are affecting quality of life. Headaches should be monitored for regression and treated if not improving within several days or persisting beyond one to two weeks; topiramate or amitriptyline are first line medications for treatment.²¹

Return to Play Protocol

The current published data evaluating the effect of rest following a sports-related concussion is sparse. There is good evidence to indicate benefit from rest 24–48 hours post-concussive injury. However, data on required rest beyond that time period is limited. The current recommendation is a graduated RTP protocol as noted in Table 1 with a goal of limiting symptom exacerbation.

Table 1.

From Zurich 2012 conference CONSENSUS STATEMENT: McCrory, Paul, et al. “Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012.

GRADUATED RETURN TO PLAY PROTOCOL
Rehabilitation Stage	Functional exercise at each stage of rehabilitation	Objective of each stage
1. No activity	Symptom limited physical and cognitive rest	Recovery
2. Light aerobic exercise	Walking, swimming, or stationary cycling keeping intensity <70% maximum permitted heart rate. No resistance training	Increase HR
3. Sport-specific exercise	Skating drills in ice hockey, running drills in soccer. No head impact activities	Add movement
4. Non-contact training drills	Progression to more complex training drills, e.g. passing drills in football and ice hockey. May start progressive resistance training	Exercise, coordination, and cognitive load
5. Full-contact practice	Following medical clearance participate in normal training exercise	Restore confidence and assess functional skills by coaching staff
6. Return to play	Normal game play

The graduated RTP follows a stepwise approach. The typical consensus is that each step takes at least 24 hours and if no symptom exacerbation, the player may move on to the next step the following day. At any time if post-concussive symptoms arise, the patient needs to drop back to the level at which the symptoms subside. From there, the player may proceed from that level after 24 hours of rest. While this protocol serves as guideline, clinical judgement of patient’s status and situation should be considered and return to play schedule modified as necessary.

Recovery/Prognosis

The majority (80–90%) of concussions resolve in a short (7–10 day) period, although the recovery time frame may be longer in children and adolescents.¹⁹ However, as stated above, the biochemical changes may not be resolved at the time of functional symptom resolution.

Prolonged Concussion

Persistent concussion symptoms (>3 months) have been noted in approximately 15% of concussion patients.⁶ Post-concussive syndrome (PCS) is defined by at least three concussive symptoms lasting a minimum of three months with specific criteria defined in DSM-IV. If symptoms persist, further evaluation to rule out co-existent pathologies should be considered.²⁰ Evaluation by a multidisciplinary team can be initiated based on symptoms and may incorporate neuropsychological testing for concentration deficits, vestibular therapy for balance/dizziness issues, and potential imaging to exclude structural pathology. Pharmacologic treatment is another consideration for persistent post-concussive symptoms. Amitriptyline has been studied specifically for persistent posttraumatic headaches and is an ideal first line treatment.²¹ With ongoing cognitive deficits, methylphenidate and amantadine have been shown to be beneficial in treating deficits in attention and processing speed. Of note, Amantadine may have N-methyl-d-aspartate antagonist effects and thereby be effective in halting the direct metabolic disturbances induced by concussion injury.²¹ After thorough evaluation, graded exercise program would be recommended at a level that does not exacerbate symptoms to improve mood and aid in cognitive recovery.^20,22

Second Impact Syndrome/Chronic Traumatic Encephalopathy

Second impact syndrome results from a person sustaining a second brain injury prior to biochemical resolution of their previous concussion. Evidence demonstrates that “concussed” brain cells maintain a state of vulnerability for a time after injury due to metabolic energy perturbations. This heightened vulnerability to even minor trauma can cause these brain cells disproportionate damage if such head insult occurs, resulting in irreversible damage and even cell death.⁶ This cell death can result in impairment of the brain’s vascular autoregulation leading to engorgement and increased intracranial pressure with potential for herniation. Clinically, severe symptoms may be manifested as rapid (within seconds to minutes) decompensation in the form of collapse, pupil dilation, loss of eye tracking, respiratory failure, and semi-comatose state.¹⁴ When this occurs, mortality rates are between 50%–100%. Injury in this vulnerable period may also contribute to morbidity. Multiple studies have shown that the metabolic effects of two concussions can be additive and the degree of clinical severity depends on which phase of metabolic recovery the brain is in at the time of the second concussion.⁶

Chronic Traumatic Encephalopathy (CTE) is derived from multiple concussions and/or subconcussive blows resulting in a neurodegenerative process that clinically features motor deficits, progressive dementia, and difficulty with depression/emotional instability which begins several years after the end of exposure to repeated head blows.²³ Currently, the definitive diagnosis relies on post-mortem examination. This syndrome has been most widely studied in football players and boxers and is another consequence of repeated concussion.

Conclusion

A concussion is a form of mild traumatic brain injury sustained from traumatic biomechanical forces. These forces initiate a complex cascade of neurochemical and neurometabolic events, leading to “energy crisis” within the brain which results in functional cognitive deficits and compromised synaptic plasticity. Due to the serious pathology underlying concussion, prompt recognition is an imperative part of management. Currently, rest is the initial treatment for concussion. Though there is lack of scientific evidence for duration of rest to resolve concussion, graduated return to play protocol is the recommended standard to avoid further complications of brain injury. The majority of patients recover from concussion within 7–10 days. Prolonged symptoms (>3 months) may require additional investigation and treatment by a multidisciplinary team. Serious consequences of improper management or lack of recognition of concussion can reflect the additive nature of multiple head injuries as noted in post-concussive syndrome, second impact syndrome, and chronic traumatic encephalopathy.

Biography

Christopher J. Wolf, DO, is Associate Professor of Clinical PM&R, and Katie Fast, MD, is a Resident, both in Department of Physical Medicine and Rehabilitation, University of Missouri Health Care.

Contact: wolfch@health.missouri.edu