Concussion Management and Prevention


January 1, 2024


January 31, 2026


Katherine Hale, PharmD, BCPS, MFA
Freelance Medical Writer
Tri-Cities, Washington


Dr. Hale has no actual or potential conflicts of interest in relation to this activity.

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To update pharmacists regarding current concepts in concussion evaluation, management, and prevention.


After completing this activity, the participant should be able to:

  1. Review risk factors, clinical presentation, assessment, and diagnosis of concussion.
  2. Understand the pathophysiology of concussion.
  3. Identify potential medication interventions for the management of concussion-related symptoms.
  4. Recognize the role of the pharmacist in concussion management and prevention.

ABSTRACT: More than 2 million emergency department visits each year are attributed to traumatic brain injury, with more than half of these identified as mild traumatic brain injury, or concussion. Up to 1.9 million sports-related concussions are estimated to occur annually in children aged 18 years or younger, with many never evaluated by a healthcare provider. A concussion results from an alteration in brain function due to an external force, such as a blow or rapid acceleration/deceleration, to the head. Symptoms are multifactorial and affect cognitive, physical, emotional, and sleep-related domains. Nonpharmacologic methods are an essential first step in managing concussion. Currently, there are no FDA-approved medications specifically for concussion management.

Concussion is a term that is frequently used synonymously with mild traumatic brain injury (mTBI). Many definitions of mTBI exist; most share specific commonalities. mTBI occurs when the head is injured by an external force that results in alteration of brain function. That external force may be a blow to the head (head striking an object or an object striking the head), or it may be an event that causes rapid acceleration/deceleration of the brain.1,2 This injury results in one or more of the following: 1) transient confusion, disorientation, or impaired consciousness; memory loss of events before/after injury; loss of consciousness for not more than 30 minutes; and 2) observed signs of neurologic or neuropsychologic dysfunction (headache, confusion, disorientation, dizziness).1,3,4 Concussion is often due to a contact injury such as a fall or to playing sports, but other mechanisms, such as whiplash from a car accident, have been proposed.5-7 The term concussion is used to describe the symptoms that occur because of mTBI.5,8,9 A concussion has been defined as an alteration in mental status and change in brain function, during which loss of consciousness may or may not occur, that is due to trauma caused by an external force to the head or body.8-12 The Glasgow Coma Scale (GCS) is used to assess brain activity and defines consciousness levels based on verbal and motor responses and eye opening.13 Severity of TBI based on GCS scoring ranges from mild (GCS 13-15) to moderate (GCS 9-12) to severe (GCS 3-8).2,13

In 2013 the CDC reported 2.8 million TBI-related emergency department (ED) visits (approximately 2.5 million, ED only), hospitalizations (approximately 282,000), and deaths (about 56,000).14 Concussion contributes to 30% of all injury-related deaths.7 Of these individuals, mTBI occurs in 75% or more.1 In a 2003 report to Congress on mTBI in the United States, the yearly national burden of mTBI was $17 billion, although current estimates may be higher.1 In 2020, an estimated 214,110 TBI-related hospitalizations were reported, and in 2021 there were just over 69,000 TBI-related deaths. Per day, that is 190 deaths and 586 hospitalizations due to TBI. Unfortunately, these estimates do not include TBI diagnosed in primary or urgent-care practices or those in the ED, nor do they include untreated TBI.15 Data collection for mTBI can be challenging due to current reporting structures, lack of standardized definitions of mTBI and mTBI impairments and disabilities, and lack of data collection regarding untreated mTBI.1

Those most likely to sustain a TBI are children aged 0 to 4 years, adolescents aged 15 to 19 years, and adults aged 65 years and older, with adults aged 75 years and older having the highest rates of hospitalization and death.7 Each year, half a million or more visits to the ED for TBI are in children aged 0 to 14 years. Rates of TBI are higher in males compared with females for all age groups.7

In children aged 18 years or younger, an estimated 1.1 million to 1.9 million sports and recreation-related concussions (SRRCs) occur each year. Many of these children are not seen by a healthcare provider. For those who were evaluated by a healthcare provider, most were seen on an outpatient basis (377,978 visits).16

Falls, motor vehicle accidents, and SRRCs are leading causes of TBI each year, with falls most prominent (35.2% overall).7,16 It should be noted that fall rates are highest for individuals aged 0 to 4 years (50.2%) and those aged 75 years or older (60.7%).7 From 2010 to 2016, there were 283,000 ED visits in the U.S. for SRRCs, of which 45% were due to contact sports. Football, basketball, and soccer have the highest rates of SRR-TBI ED visits. Notably, contact sport-related TBI visits to the ED decreased by 32% from 2012 to 2018. This was mostly due to a decline in football-related SRR-TBI ED visits as a result of implementation of contact limitations and less participation in tackle football. For noncontact sports, ED visits also declined by about 23%.17


A neurometabolic cascade occurs in response to a concussion.18,19 Neuronal dysfunction occurs due to axonal stretching. Abrupt release of excitatory neurotransmitters, namely glutamate, leads to ionic flux (potassium efflux, calcium, and sodium influx), which triggers voltage- or ligand-gated ion channels. This creates a “spreading depression-like” state and may account for postconcussion impairments. An energy crisis results due to a significant increase in glucose metabolism, which is the result of ATP-requiring ion pumps working overtime.18,19 With normal or reduced cerebral blood flow, this increase in energy need leads to a mismatch between energy supply and demand. A period of intracellular calcium flux occurs, and sequestration of calcium into mitochondria causes mitochondrial dysfunction, worsening the cellular energy crisis. Oxidative stress occurs due to damaging free radicals that are produced when the intracellular redox state is altered in response to mitochondrial dysfunction. Calcium flux may also lead to the collapse of neurofilament side-arms of neurons and glia, compromising axonal structural integrity.18,19

Additional research has linked the neurometabolic cascade with the long-term sequelae of concussion.19 For example, ionic flux may be associated with migraine headache. Axonal injury may be connected to impaired cognition and slowed processing and reaction times. The energy crisis may increase vulnerability to second injury.19


Signs and symptoms of concussion affect multiple domains—physical, cognitive, emotional, and sleep-related. Physical symptoms may include headache, dizziness, fatigue, vision changes, neck pain, nausea, and/or vomiting. Symptoms affecting cognition may include confusion, amnesia, slurred speech, or slow to answer questions. Individuals may be more emotional (irritable, sad, nervous) or have changes in sleep (increase, decrease, or trouble staying asleep).2,12,20 Loss of consciousness (up to 30 or fewer minutes) may or may not have occurred with the injury, as well as amnesia to the event itself. Patients may present with coordination difficulties, with impaired balance and gait.2,9,20,21 A summary of signs and symptoms of concussion is presented in TABLE 1.2,12


Currently no validated tests or laboratory criteria are available to assist in the diagnosis of concussion. Diagnosis is based on clinician assessment and patient presentation.9,11,20 This makes it challenging for primary care providers due to the potential for confounding factors, as patient evaluation may occur many days, or even weeks, post injury.

In diagnosing concussion, it is important to first establish the mechanism by which injury occurred and rule out conditions that may mimic or confound concussion presentation.11,13,20 Potential confounders include alcohol or illicit drug use, neurotologic disorders (vertigo, nystagmus, Meniere's disease), acute changes in mental health (posttraumatic stress, anxiety, depression), severe acute/ chronic pain, hypoglycemia, or changes in pulmonary function.9,11,13

While no standardized tests or laboratory measurements are currently available, symptom check-lists have been developed. Using more than one checklist or assessment tool increases sensitivity and specificity, but the optimal combination of tools has not yet been elucidated. Use of multidimensional tools is recommended.20 While not mandatory, obtaining a preseason or preparticipation assessment for athletes is recommended.5,11,12 The Concussion in Sport Group developed the Sports Concussion Assessment Tool (SCAT) for adolescents/adults (aged 13 years and older) and for children (aged younger than 13 years) to assess sport-related concussion on the sidelines. Currently in their sixth iteration, the SCAT6 and Child SCAT6 guide the healthcare provider through a thorough sideline assessment of players.22 Other standardized assessment tools evaluating concussion include the Standardized Assessment of Concussion, Post-Concussion Symptom Scale, and Acute Concussion Evaluation.23 The Health and Behavior Inventory, Post-Concussion Symptom Inventory, and Acute Concussion Evaluation may also be used for children.24

Algorithms for concussion evaluation begin with assessment of the cervical spine to rule out spinal injury and determine the presence or absence of emergent medical issues. Severity of the injury must also be assessed. If the individual was unconscious for more than 30 minutes or other indications for imaging exist, a higher level of care should be sought. Individuals should then be evaluated for mental status changes, and a neurologic assessment should be performed. Symptoms, cognition, and postural stability should be evaluated. A “yes” to any of these components of the algorithm may be used to establish a concussion diagnosis, and additional assessment tools should be completed to establish a baseline to guide further management.2,20,25

Neuroimaging is not recommended unless a concern for more severe TBI is present. To determine a need for urgent imaging post concussion, providers may use the Canadian Head CT Rule or the New Orleans Criteria (ages 16-64 years) or the PECARN Rule (ages 5-18 years).11,20,26-30 There is an increased risk of intracranial bleed for anticoagulated individuals and adults aged 65 years or older; therefore, CT scan and/or hospital admission for observation is recommended.11 If neuroimaging is used, a CT scan is preferred over an MRI.20


Initial and long-term management post concussion is multifactorial and involves a plan for education, rest, transition back to work or school, return to activity or play, and an assessment of risk of prolonged recovery.11,12,20 For sports-related concussions, clinical symptoms typically resolve in 2 weeks for 80% to 90% of older athletes and adults. For younger athletes or adults aged 40 years or older, the time frame may be longer, with recovery taking up to 4 weeks.9,31,32


Before going home, individuals and family members should receive education regarding what a concussion is, symptom management, recovery expectations, and plan of care moving forward.11,20


The first step to managing a concussion, rest should be both physical and cognitive in nature, and at least 24 to 48 hours are recommended to start.5,9,11,20

Transition Back to School or Work

Limited data exist regarding specific recommendations for return to school or work and should be guided by symptom resolution. Generally, when individuals are able to tolerate visual or auditory stimulation for 30 to 45 minutes at a time, a return to work or school may be attempted with accommodations.12,20,33 In student athletes, a time frame of 6 to 10 days has been reported.34,35

School accommodations include slow reintegration with rest breaks, reduction in assignments, distraction-free work areas, and no standardized test administration. Continued monitoring for 2 to 3 months post concussion is recommended, with adjustments made where needed.20

Transition Back to Activity and Return to Play

After the initial cognitive and physical rest period, individuals should begin incorporating activities in progressive steps, with each step given a minimum of 24 hours.20 Activities of daily living and noncontact aerobic exercise are implemented first, with a gradual increase in activity level and intensity depending on symptoms. If symptoms return or worsen, the individual should stop activities and return to the rest period until symptom resolution.9,11,12,20 Until clinically recovered, no individual should resume any activity that may increase the risk of repeat concussion, such as collision sports (football, soccer, hockey).9,11,12 For the athlete, a return-to-play protocol must be followed, outlining progression in physical activity based on physical demands and contact risk. This protocol is supervised by a healthcare provider.12

Assessment of Prolonged Recovery Risk

For some individuals, neurologic symptoms may persist, or symptoms immediately following the injury are more severe. Others may have continued symptoms of headache, fatigue, and/or fogginess. These symptom-based factors may prolong recovery and may require management by a concussion specialist. Factors that may increase risk of prolonged recovery include history of previous concussion, age, concurrent health conditions, and high-risk sport and/or aggressive play style.9,12,20

Pharmacologic management is based on presenting symptoms, with the goal of preventing masking of concussion symptoms or exacerbating symptoms. It should also be noted that there are no FDA-approved pharmacotherapies for general management of concussion or specific concussion symptoms.


In the initial 24 to 48 hours post concussion, headache is a commonly reported symptom in up to 90% of individuals.2 Headache often develops within 7 days of concussion, with resolution occurring within 3 months. However, headache symptoms may persist in some people.2 Nonpharmacologic and pharmacologic management methods are recommended. First, it is important to determine the type of headache that is experienced, with the three most common headache types tension-type headaches (may In the initial 24 to 48 hours post concussion, headache is a commonly reported symptom in up to 90% of individuals.2 Headache often develops within 7 days of concussion, with resolution occurring within 3 months. However, headache symptoms may persist in some people.2 Nonpharmacologic and pharmacologic management methods are recommended. First, it is important to determine the type of headache that is experienced, with the three most common headache types tension-type headaches (may contain cervicogenic component), migraine headaches, and a mix of both.2,20 Assessment of headache type includes a review of pain intensity and characterization; duration; affect on activities of daily living; location; and the presence or absence of phonophobia or photophobia, nausea, malaise, or palpable muscle tenderness or contraction.2 Nonpharmacologic methods to manage headache are summarized in TABLE 2.

In the period immediately after concussion injury, acetaminophen may be used because it does not increase the risk of intracranial bleed. As symptoms improve and bleed risk decreases, prescription or OTC nonsteroidal anti-inflammatory drugs (NSAIDs) may be used. NSAIDs are recommended for use in tension-type postconcussion headaches. Oral options include ibuprofen and naproxen. Ketorolac may be administered intramuscularly as a single dose of 30 mg or 60 mg.2,20 Common adverse effects of NSAIDs include stomach upset and dizziness. Cautious use of NSAIDs is recommended for patients on anticoagulants or who have a history of gastrointestinal ulcer or abdominal complications, or if there is a history of ischemic cardiovascular events or high risk of such events.2 To prevent rebound headaches, acetaminophen or NSAIDs should be used no longer than 15 days or 12 days per month, respectively.2

Abortive migraine therapies include serotonin (5-hydroxytryptamine) receptor agonists, or triptans.2 If an alternative to oral triptan administration is needed, intranasal formulations (sumatriptan and zolmitriptan) and a subcutaneous injection (sumatriptan) are available.36-38 Side effects include dizziness, somnolence, nausea, vertigo, hypertension, and injection-site reactions. Cautious use is recommended in patients with cardiac event history or who are currently taking multiple serotonergic agents (due to risk of serotonin syndrome). Triptans should be used for no longer than 12 days per month due to risk of rebound headache.2,36-38

Oral combination formulations such as butalbital/caffeine in combination with either acetaminophen or aspirin are considered third-line therapies due to risk of dependence and/or rebound headache. For patients in whom triptan use is contraindicated, these formulations may be considered.

Prophylactic medications for headache may be considered if patients experience disability despite aggressive treatment, to decrease frequency of acute attacks or if headaches affect activities of daily living. Prophylactic medications may include anticonvulsants such as topiramate or gabapentin, beta-blockers such as propranolol, prazosin (an alpha-blocker), or tricyclic antidepressants (TCAs) such as amitriptyline or nortriptyline.2,39 Many preventive headache therapies have side effects that may affect cognition; therefore, reviewing side-effect profiles prior to medication initiation is important. (Further review of prophylactic headache therapies is outside of the scope of this article.)

Dizziness and/or Changes in Equilibrium

Referrals to physical therapy, ear/nose/throat specialists, psychiatry, psychology, or neurology may benefit most patients with ongoing dizziness and disequilibrium post concussion.2 Ophthalmology or optometry should be considered for visual dysfunction concerns. A review of complete medication history, including OTC, prescription, or recreational drug use, may also identify potential causes of dizziness or changes to equilibrium. If indicated, short courses of OTC meclizine or dimenhydrinate may be used; scopolamine is a 72-hour prescription-only patch formulation.2

Sleep Disturbances

To manage sleep disturbances, nonpharmacologic approaches should be attempted first, with a focus on improving and maintaining good sleep hygiene (TABLE 3).40 Goals include maintaining a regular sleep schedule with a normal circadian rhythm, allowing for sufficient sleep, and avoiding daytime naps, when possible. Cognitive behavioral therapy (CBT) may also provide benefit.11

Medication management of sleep disorders should be short-term only to assist in regulation of the sleep schedule. TCAs, antidepressants, trazodone, and melatonin may provide some benefit. Benzodiazepines should be avoided.2,8,9,11 Nonbenzodiazepine hypnotic medications should also be avoided due to potential cognitive side effects. The alpha-blocker prazosin may be used for patients with a history of posttraumatic stress disorder and nightmares. It should be noted that TCAs and mirtazapine have the potential to lower the seizure threshold and should be avoided in patients in whom risk of seizure is a concern.2 Side effects of these agents include sedation, headache, somnolence, dry mouth, and anticholinergic side effects. Mirtazapine may cause weight gain.2

Neuropsychiatric Symptoms

Depression, anxiety, irritability, and emotional lability may also occur post concussion due to the imbalances of norepinephrine, serotonin, and dopamine that may occur with concussive injury.41 While there is a paucity of literature evaluating medication management post TBI, selective serotonin reuptake inhibitors (SSRIs) are currently considered first line for symptom management. Alternatives such as serotonin-norepinephrine reuptake inhibitors (SNRIs), TCAs, trazodone, and mirtazapine may also be used. Benzodiazepines should be avoided.39,41,42 Bupropion should also be avoided due to its seizure threshold–lowering potential.41 The recommended treatment duration is 6 months, then reevaluate ongoing needs.11,41,42

Of the SSRIs, the most studied appear to be sertraline and citalopram. However, studies are conflicting regarding their effectiveness in management of depression post TBI. Many studies are small, with fewer than 100 participants, often fewer than 50 participants, and are open-label or nonrandomized.43-47

For example, conflicting evidence exists regarding the effectiveness of sertraline in reducing depression symptoms post concussion.44,45 A small, nonrandomized, single-blind, placebo run-in trial evaluated 15 patients diagnosed with major depression 3 to 24 months post mTBI treated with sertraline titrating from 25 mg to 200 mg over 8 weeks, as tolerated. By Week 8, it was found that 87% (n = 13) achieved a response based on a reduction in the Hamilton Rating Scale for Depression (HAM-D) by 50% or more. Remission was achieved in 67% (n = 10). There were two nonresponders and no response to placebo.44 Alternatively, a double-blind, randomized, controlled trial evaluated the efficacy of sertraline compared with placebo for major depressive disorder within 1 year of TBI injury in 62 participants (46.8% mild TBI, 21% moderate TBI, and 32.2% severe TBI). No statistically significant difference in response between sertraline and placebo was found; however, both treatment groups demonstrated a significant improvement in depression from baseline to 12 weeks (P <.001).45 Additional studies evaluating sertraline versus placebo also report improvement in depression symptoms for both sertraline and placebo groups, with no statistically significant difference between groups.43 Nonpharmacologic management is strongly recommended, with a focus on concussion education (prognosis, treatment plan, and expectations of injury), CBT, and psychotherapy.11

Cognitive Impairment

Ongoing cognitive symptoms, such as fogginess, memory problems, confusion, and difficulty with concentration and attention, have been reported following a concussion, with an incidence of 10% to 33%.42 Frequently, improvements in headache, sleep, and psychologic symptoms also improve cognitive symptoms.39

A functional cognitive assessment is recommended for patients with cognitive symptoms persisting for 30 to 90 days.2 Nonpharmacologic methods for managing cognitive symptoms include goal setting that is specific to patient needs, identifying and implementing adaptive strategies, and the use of cognitive rehabilitation. Cognitive rehabilitation may include various members of the patient-care team, such as occupational, physical, and speech therapies, and vocational rehabilitation.2

Limited data are available regarding pharmacotherapeutic options for cognitive symptoms post concussion. Methylphenidate and amantadine appear to have the most studies evaluating their use; however, results are mixed regarding their effect on cognitive symptoms post concussion.39,42,48,49 Most studies evaluating the effect of methylphenidate on cognitive symptoms after brain injury are of small size and primarily include adult patients with moderate or severe TBI, rather than mTBI or concussion, or do not specify severity of brain injury.39,42,48,49

Methylphenidate increases the release of norepinephrine and dopamine into the extraneuronal space by blocking the reuptake into the presynaptic neuron. Methylphenidate may also lower seizure threshold.42,50 The direct mechanism of action of amantadine is not known. It may affect dopamine neurons directly and indirectly, and amantadine has been found to have weak, noncompetitive N-methyl-D-aspartate antagonist effects.42,51 The role of methylphenidate and amantadine in concussion symptom management and the mechanism by which effects are exerted have not been fully elucidated.41.42


A myriad of strategies to prevent concussion and sport-related concussion may be employed. Education regarding prevention and management of concussion is most prominent, with many programs available for the general public, coaches, and healthcare providers. For example, the CDC created the Heads Up campaign, which provides useful trainings, tools, and resources for healthcare providers.52 For the elderly and those with impairments to mobility, education on fall risk and prevention may be provided. Additional resources are summarized in TABLE 4.52,53

Additional preventive strategies include use of protective gear, such as helmets, mouthguards, and pads in certain sports. While head and dental injuries have decreased with the use of protective gear, the effect in concussion reduction is not yet known.20,54 Age limits may be placed on specific types of body contact. For example, body checking is not recommended in youth ice hockey for those aged younger than 15 years.55 Monitoring injury patterns and making changes to rules in sports may also help reduce sport-related concussions. The Zackery Lystedt Law was enacted in 2009 in Washington State requiring concussion education for coaches, athletes, and parents and mandates removal of athletes from activity following suspected concussion until required clearance by a licensed clinician allows for return to play.56 Return to Play laws have now been enacted in all 50 states.57,58


Regardless of practice setting, pharmacists are well poised to assist with education and management of concussion. Pharmacists may develop or participate in community-based education regarding concussion prevention, sports-related concussion and guidelines, and fall risk prevention. Community pharmacists can guide patients and caregivers away from OTC products that may affect cognition or worsen concussion symptoms and assist them in identifying nonpharmacologic methods for management. Pharmacists in hospital and ambulatory care settings may assist with concussion management protocols and making pharmacotherapy recommendations for concussion-related sequelae. Medication regimen reviews may be performed to identify medications and OTC products that may affect cognition and to suggest alternative options, where applicable.


Concussion, or mild TBI, may affect individuals of all ages and is a significant burden on the healthcare system. Symptoms often improve with time, rest, and a return to work/school and return to play management plan. Currently there are no FDA-approved medications specific to management of concussion, and a paucity of data exists regarding symptom-specific options. Further research is needed.

The content contained in this article is for informational purposes only. The content is not intended to be a substitute for professional advice. Reliance on any information provided in this article is solely at your own risk.


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