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11 Articles in Volume 14, Issue #4
Recognizing and Treating Concussions Related to Sports Injuries
CDC Initiative: Concussion in Sports and Play
Pain Management After ACL Surgery
Risk Assessment in the Digital Age: Developing Meaningful Screening Tools for Opioid Prescribers
Testosterone Replacement: Essential in Pain Management
Why Is There Hydromorphone In My Patient’s Urine?
Benzodiazepines in Pain Practice: Necessary But Troubling
Commentary: Risk Assessment in the Digital Age
Zohydro Debate: Drug Hysteria or True Concern
Benefit of Long-acting Versus Short-acting Opioids?
Epidural Steroid Injections, Coping Skills, Medical Marijuana

Recognizing and Treating Concussions Related to Sports Injuries

Efforts by the Centers for Disease Control and Prevention (CDC), state and local governments, and advocacy groups around the country have drawn attention to the risk of traumatic brain injuries (TBIs) in sports.

The stories are heartbreaking. The young athlete who sustains a concussion while competing and needs intensive rehabilitation for cognitive, balance, sleep, and emotional symptoms—occasionally with long-term disability and pain. A concerted effort by the CDC, state and local governments, and advocacy groups around the country have drawn attention to the risk for traumatic brain injuries (TBIs) in sports. Early recognition, screening, and treatment have helped prevent more serious injuries in thousands of children.

Despite these efforts, however, TBIs remain an all too frequent occurrence. In the United States, between 1.7 and 3.8 million TBIs occur each year,1 with over 240,000 of these injuries occurring due to sports and recreational activities.2 Between 2001 to 2009, the number of sports-related TBIs seen in emergency departments (EDs) increased 62%, from 153,375 to 248,418; the highest rates are among males between 10 and 19 years of age, with 70% (173,285) of the TBIs occurring in this population.2 TBI was cited as a contributing factor in approximately 30% of all injury-related deaths—accounting for 52,000 deaths per year (see sidebar).

Concussion, referred to as commotion cerebris in European nations, is a subset of TBI that is defined as “a complex pathophysiological process affecting the brain, induced by biomechanical forces.”3 Typically, it is caused by a direct impact to the head but can occur as a result of any ‘impulsive’ force transmitted to the head.

Neurologic impairments such as headache, cognitive impairment, emotional symptoms, and behavioral changes rapidly occur and usually are short lived, but less frequently may evolve over a period of hours.3 Concussion is thought to be a functional disturbance and, thus, the results of imaging studies such as computed tomography (CT) scans usually are normal because these tests evaluate brain structure rather than function.3

Studies of the common symptoms that occur after a sport-related concussion (SRC) demonstrate that there is a natural grouping of symptoms, with 4 symptom clusters reported: sleep disturbance, headache, cognitive deficits (slow reaction time, feeling in a fog), and neuropsychiatric features (emotional aspects, irritability).4,5 These symptoms account for the great majority of morbidity after a SRC and provide clinicians with opportunities for intervention.

This article will focus on non-pharmacologic therapy of pain after a SRC, which is strongly recommended as the backbone of recovery, as well as several pharmacological interventions for symptom alleviation, which are not supported by strong evidence. These pharmacologic therapies should be used cautiously, with close consideration of individual risks and benefits by clinicians with experience managing patients with SRC.

Non-Pharmacologic Therapy

It is widely accepted that the most important intervention in the management of SRC involves physical and cognitive rest until the acute symptoms have resolved. The majority of concussions (80%-90%) resolve in a short period (7-10 days), although the recovery timeframe may be longer in children and adolescents.3

Athletes who have suffered previous concussions are at a significantly higher risk for incurring a repeat concussion,6 especially in the acute post-concussive period. There may be a risk for “second-impact syndrome,” diffuse cerebral swelling with catastrophic deterioration, postulated to occur after repeated concussions, and particularly in adolescent males.7,8 Thus, concussed athletes should be removed from physical activities that may expose them to further risk for impact to the head.

Cognitive rest involves abstaining from activities requiring concentration and attention, such as schoolwork and video games. Due to a dearth of published literature assessing the appropriate duration of rest during recovery from SRC, current guidelines are largely based on consensus opinion employing a cautious approach, in which the patient gradually increases their levels of activity and eventually returns to sports. Typically, the initial period of rest after concussion should last at least 24 to 48 hours or until the resolution of acute symptoms.

Following this initial period of rest, athletes should follow a stepwise graduated return to play protocol. A 2012 consensus statement from the international Concussion in Sport Group (CISG) suggested the following steps in the graduated return to play protocol: 1) no activity, 2) light aerobic exercise, 3) sports-specific exercise, 4) non-contact training drills, 5) full-contact practice, and 6) return to play.3 It generally is recommended that athletes spend at least 24 hours in each step (overall, approximately 1 week); if post-concussion symptoms occur at any of the steps, the patient should be returned to the last asymptomatic step and attempt to advance again after another 24 hours of rest (Table 1). Absolutely no athlete should be allowed to return to play on the day of injury.

According to CISG, symptoms persist beyond 10 days in 10% to 15% of patients with concussions. They recommend that in cases of concussion where recover is greater than 10 days, the athlete should be managed in a multidisciplinary setting by clinicians with experience in sports-related concussion, with consideration of other possible pathologies.

Pharmacologic Therapy

Generally, pharmacologic therapy plays 2 roles in the aftermath of a SRC. According to the CISG, these include the alleviation of specific symptoms (headache, sleep, anxiety) and the modification of the pathophysiologic process underlying concussion to reduce the duration of post-concussion symptoms.3 Because there have been few clinical trials of medications that modify the underlying pathophysiologic process, the remainder of this article will focus on symptom alleviation.

Unfortunately, there is still a lack of published evidence delineating the role of pharmacologic agents for SRCs.9 Thus, pharmacologic agents must only be employed by clinicians with experience in the management of concussion, specifically SRC. In addition, medications are not without risk; Meehan suggests that they only should be used if the athlete’s symptoms persist longer than the typical recovery period (>3 weeks, perhaps longer for athletes who have experienced multiple prior concussions), and if the benefits of pharmacologic treatment outweigh the potential risks related to nontreatment.4 Additionally, athletes must be symptom-free and typically off all medications before they can return to play because there is a safety concern that pharmacologic therapy may mask the symptoms of lingering pathophysiology after concussion.


Headache is the most common symptom experienced after SRC, and TBIs in general. Any headache that develops within 1 week of a SRC is defined as a post-traumatic headache (PTH).10 As with any other type of headache, it is important to determine its characteristics, because PTH may have various etiologies, including vascular, neuropathic, musculoskeletal, and iatrogenic factors. A review of headaches after TBI found that 33.6% of PTHs fell into the tension-type group, with bilateral, non-throbbing headache of mild to moderate intensity, whereas 28.6% had migraine-type headaches, with sensitivity to light or noise.10

Abortive Therapy

Traditional therapies have been used for these types of headaches in the post-concussion period. The traditional migraine-specific abortive medications used for treatment of acute migraines and migrainous headaches—for example, dihydroergotamine (DHE-45) and triptans—may be used to treat acute headaches.11 A reformulated diclofenac potassium preparation (Cambia), with very rapid absorption kinetics, also is FDA approved for mild to moderate migraine.

Migraine-specific abortive therapy centers on the triptan family of compounds. These agents primarily decrease neural activity in trigeminovascular afferent nerves that are sending signals from dural nerve endings to the trigeminal nucleus caudalis in the brainstem. They also have vasoconstrictive properties on blood vessels in this system, but the main effect is on neural firing. Triptans act specifically on serotonin (5HT)-1B and 1D receptors. They should be used for migraines that are moderate to severe in intensity and are disabling.

Triptans can be used in conjunction with antiemetics (metoclopramide [Reglan, others], ondansetron [Zofran, others], promethazine [Phenergan, others], etc), and perhaps anti-inflammatory compounds. Although they are indicated for moderate to severe migraines, early intervention in the migraine process is always desirable. Some of the triptans are available in faster delivery systems such as injectable and nasal spray formulations.11

There also are a number of non-FDA approved agents that are used to treat migraines, including anticonvulsants, beta blockers, antidepressants, calcium channel blockers, and non-steroidal anti-inflammatory drugs (NSAIDs).9,12

Preventive Therapy

When TBI migraines become disabling and occur more frequently than 3 times per week despite successful treatment with triptans or other migraine-specific therapies, suppressive or prophylactic therapy is in order. Only 4 medications are FDA-approved for this indication: topiramate (Topamax, others), valproate sodium (Depakote, others), propranolol (Inderal LA, others), and onabotulinumtoxin A (Botox).11 Topamax, recently approved for use in adolescents, is the first agent approved to prevent migraine in this age group.13

Tension-type Headache

Simple analgesics and NSAIDs commonly are used for acute exacerbations of tension-type headaches after concussion, whereas antidepressants and muscle relaxants are commonly used for prophylaxis.10

Another subtype of headache more specific to concussion is “cognitive-fatigue headache,” which occurs in the context of cognitive exertion post-concussion. Cognitive exertion may trigger these headaches, and treating the underlying cognitive symptoms with psychostimulants may be more effective than primary treatment of the headache itself.

Medication Overuse Headache

One important consideration for athletes presenting with persistent headache after concussion is the possibility of medication overuse headache, which is frequent among patients presenting to headache clinics.14 An accurate history of medication use typically reveals a history of chronic daily (or near-daily) analgesic use, with little to no relief of headache symptoms. Treatment for this type of headache is withdrawal of the analgesic, and relief occurs after a brief period of increased headache.14

We strongly recommend against the use of opioids in PTH. DeVries et al found that almost half of adolescents who presented to outpatient providers for non-traumatic headache received an opioid prescription, despite guidelines against this practice.15 Opioid use has adverse cognitive/physiological effects, the potential for abuse and dependence, and may predispose to medication overuse headache. The study found that adolescents who had been given opioids also were more likely to have an ED visit for headache during the follow-up period than those not receiving opioids (28% versus 14%, P<0.01).15

Sleep Disturbances

As noted, sleep disturbances are a common occurrence after a TBI. The first line of treatment should include proper sleep hygiene.16 This should be attempted prior to initiation of pharmacologic therapy.17 Most poor sleep is at least partially due to a non-adherence to a regimen for good sleep hygiene—using the bed only for sleeping, not “trying” to sleep, avoiding coffee, alcohol, and nicotine, going to bed at the same time every night, and avoiding sources of stimuli in bed, such as televisions, computers, and mobile phones—which is especially important among adolescents and young adult athletes.

Along with the adoption of sound sleep hygiene practices, melatonin and the melatonin agonist ramelteon (Rozerem) may be useful as first-line pharmacologic therapy. Melatonin, a hormone endogenously synthesized and secreted by the pineal gland, is crucial to the maintenance of the circadian rhythm. In normal light-dark cycles, melatonin is released into the blood during the night, and levels become undetectable by daytime. It is hypothesized that melatonin serves as a signal for darkness, which helps organize behavior and physiologic processes that lead to the initiation of sleep.18 Melatonin and melatonin agonists have been shown to be safe and efficacious in the treatment of insomnia.19,20

A close second-line treatment for insomnia, according to Meehan, is trazodone, a non-habit-forming, non-tricyclic antidepressant with mildly sedating properties.4,21 Benzodiazepine sedative-hypnotics, although logical at first-glance, may be inappropriate for multiple reasons. They have been shown to be addictive, alter psychomotor ability, cause sedation, impair memory, and disrupt balance (vertigo).22 Although non-benzodiazepine sedative-hypnotics, such as zolpidem (Ambien, others), zaleplon (Sonata, others), and eszopiclone (Lunesta), may have a lower risk of addiction, they may be undesirable due to various amnestic, motor, and cognitive side-effects that may exacerbate post-concussive symptoms.22 The remaining classes of sedatives, tricyclic antidepressants, and antihistamines, may be undesirable because they both possess anticholinergic effects detrimental to attention and memory as well as the potential for blurry vision and constipation.

Thus, we recommend the adoption of good sleep hygiene as the mainstay of therapy for sleep disturbance after a SRC, followed by melatonin and trazodone as pharmacologic interventions.

Cognitive Deficits

Athletes often present with quantifiable deficits on neurocognitive testing after concussion. Cognitive deficits also may contribute to cognitive-fatigue headache, in addition to contributing to independent morbidity. Both methylphenidate (Ritalin, Concerta, others), a psychostimulant used to treat attention deficit hyperactivity disorder, and amantadine, an agent used to manage Parkinson’s disease, have been found to have efficacy in improving cognitive deficits after TBI.

Two small, randomized, placebo-controlled trials have shown methylphenidate to result in improvements on speed of information processing, attention, and motor performance compared with placebo.23,24 These studies have not been replicated in children, however. Williams et al found that there was no significant difference in cognitive outcome in pediatric patients taking methylphenidate versus placebo.25 Methylphenidate must be used cautiously because there is concern related to an increased risk for seizures. Amantadine, a dopaminergic agent, has been shown to improve cognitive function in pediatric patients.26

Other agents, such as cholinesterase inhibitors (eg, donepezil [Aricept, others], rivastigmine [Exelon, others]), selective serotonin reuptake inhibitor (SSRI) antidepressants, selective norepinephrine reuptake inhibitors, and other dopaminergic agonists have not been as well-studied in SRCs.

For athletes who suffer from persistent neurocognitive deficits associated with significant negative effects on quality of life, we recommend cautious use of methylphenidate and/or amantadine. There is too little evidence to recommend the other agents.

Neuropsychiatric Disturbances

Depression and emotional disturbances are frequent occurrences after mild TBI, and may be due to a combination of factors, including changes in brain neurochemistry in addition to a significant adjustment to post-concussion restrictions on activity. Meehan recommends that SSRIs and tricyclic antidepressants should be used to treat depression related to TBIs.4 In particular, sertraline (Zoloft, others) has been well studied in the treatment of depression, and also may have cognitive benefits.4 Significant improvements of psychomotor speed, memory, and cognition were observed in patients treated with sertraline after TBI versus those given placebo, although this was not a sports-specific population.27 Amitriptyline may be less efficacious in the treatment of depression after TBI, but it may have a role in the treatment of depression with sleep disturbances and headache.

Depression after SRCs usually resolves spontaneously in a short period of time. We recommend that depression of long duration after SRC be managed primarily by providers with experience in depression management. If necessary, sertraline may be a safe and efficacious treatment for depression after SRC, until follow-up with such a provider can be arranged.


The mainstay of therapy after SRC is a non-pharmacologic regimen involving a graduated recovery protocol, with frequent reassessment to watch for post-concussion symptoms before advancement to the next step. Headache is the most common symptom after concussion, and an approach similar to that for primary headache should be applied, with surveillance for medication overuse headaches. Opiate use in headache is problematic and strongly discouraged.

Various pharmacologic therapies for SRCs may be translated from the general TBI literature for sleep disturbances, cognitive deficits, and neuropsychiatric disturbances. However, the evidence behind the majority of these pharmacologic therapies is lacking, and they should be used on an individual basis, with consideration of risks versus benefits, by clinicians with experience treating concussion. Non-pharmacologic therapy with physical and behavioral rest, as recommended by CISG2 should be attempted prior to the initiation of pharmacologic therapy.

Last updated on: April 14, 2015

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