Persistent symptoms following concussion can be debilitating for patients and challenging for clinicians; however, evidence-based approaches to symptom management are emerging. The presentation of postconcussion syndrome can be variable among patients. Given this variability, a thorough history and physical examination are necessary to tailor an individualized treatment approach. Pharmacologic interventions can be considered when prolonged symptoms are negatively affecting quality of life. This article reviews evidence available to guide such treatment decisions.
Key points
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Persistent symptoms following concussion can be challenging for clinicians, given variable presentations among patients.
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A thorough history and physical examination are key to developing a treatment approach.
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Pharmacologic treatments can be considered when symptoms are negatively affecting quality of life.
Introduction
Concussion awareness, particularly in sports, has significantly increased over the past decade, and the body of literature regarding diagnostic criteria, evaluation, management, risk factors, prognosis, and long-term effects has grown exponentially. Recommendations for acute concussion management emphasize physical and cognitive rest balanced with supervised graded exertion until symptoms resolve before return to play. Although this approach is effective in most patients with concussion, it is estimated that the incidence of postconcussion syndrome (PCS) can range from 1.4% to 29.3% among different populations evaluated using inconsistent diagnostic criteria.
Persistent symptoms following concussion can be debilitating for patients and challenging for clinicians, given the limited data available on the management of prolonged recovery from concussion. PCS refers to the collection of symptoms across several clinical domains that occur after concussion. Symptoms may include headache, nausea, dizziness, impaired balance, blurred vision, confusion, memory impairment, mental “fogginess,” and fatigue, in varying combinations. Although evidence-based approaches are emerging, issues related to the diagnostic criteria continue to complicate the literature and clinical identification. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition , and International Classification of Diseases, 10th Revision , both provide criteria for the diagnosis of PCS; however, Rose and colleagues were able to demonstrate ongoing variability among practitioners by using an electronic survey. Another challenge to developing strict diagnostic criteria is that symptoms seen following PCS also have been reported in a variety of other diagnoses, such as uninjured controls, patients with general trauma, personal injury claimants, soldiers with combat stress, patients suffering from depression/anxiety, and patients with chronic pain.
Introduction
Concussion awareness, particularly in sports, has significantly increased over the past decade, and the body of literature regarding diagnostic criteria, evaluation, management, risk factors, prognosis, and long-term effects has grown exponentially. Recommendations for acute concussion management emphasize physical and cognitive rest balanced with supervised graded exertion until symptoms resolve before return to play. Although this approach is effective in most patients with concussion, it is estimated that the incidence of postconcussion syndrome (PCS) can range from 1.4% to 29.3% among different populations evaluated using inconsistent diagnostic criteria.
Persistent symptoms following concussion can be debilitating for patients and challenging for clinicians, given the limited data available on the management of prolonged recovery from concussion. PCS refers to the collection of symptoms across several clinical domains that occur after concussion. Symptoms may include headache, nausea, dizziness, impaired balance, blurred vision, confusion, memory impairment, mental “fogginess,” and fatigue, in varying combinations. Although evidence-based approaches are emerging, issues related to the diagnostic criteria continue to complicate the literature and clinical identification. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition , and International Classification of Diseases, 10th Revision , both provide criteria for the diagnosis of PCS; however, Rose and colleagues were able to demonstrate ongoing variability among practitioners by using an electronic survey. Another challenge to developing strict diagnostic criteria is that symptoms seen following PCS also have been reported in a variety of other diagnoses, such as uninjured controls, patients with general trauma, personal injury claimants, soldiers with combat stress, patients suffering from depression/anxiety, and patients with chronic pain.
Pathophysiology
Concussion is a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces. Following impact, the brain experiences a complex cascade of ionic, metabolic, and physiologic events, well described by Giza and Hovda. Indiscriminate release of excitatory amino acids, coupled with a massive efflux of potassium, induces a brief period of hyperglycolysis. This is in response to ATP-powered sodium-potassium pumps operating at maximum capacity in attempts to restore neuronal membrane potential. The hypermetabolic state occurs in the setting of diminished cerebral blood flow causing a cellular “energy crisis,” as the supply of glucose cannot meet the demand. What follows is a period of depressed metabolism secondary to persistent calcium influx causing mitochondrial dysfunction and impaired oxidative metabolism. ATP consumption and production become unbalanced, thus worsening the energy crisis. In the later stages of the cascade, the balance between glucose metabolism and cerebral blood flow is restored, but delayed cell death, chronic alterations in neurotransmission, and axonal disconnection occur. The metabolic derangement and the postconcussion “energy crisis” are considered chiefly responsible for the compromised synaptic plasticity and subsequent cognitive deficits. Clinical signs and symptoms of concussion, such as impaired coordination, attention, memory, and cognition are manifestations of underlying neuronal dysfunction, likely due to the processes described.
Using animal models, Rathbone and colleagues described the potential role systemic inflammation may have regarding symptoms of PCS. These models have demonstrated activation of immune and nonimmune cells and increases in inflammatory mediators (ie, cytokines) following brain injury. Microglia, which become activated after injury, appear to be an important component of the long-term inflammatory response. Once activated, they release immune factors, such as reactive oxygen species, prostaglandins, and excitotoxins. The role of inflammation in headache, irritability, anxiety and depression, personality changes, apathy, sleep disturbance, fatigue, and reduced tolerance to stress has been described via literature review in animal and human subjects with no history of head injury. These symptoms are commonly reported in PCS and it may be postulated that PCS following concussion represents a “persistent, low-grade, chronically smoldering neuroinflammatory response.”
Risk factors for prolonged recovery
It has been stated that recovery from concussion occurs within a relatively short time frame, with more than 90% of injured athletes returning to play within 7 to 14 days after injury. However, recent work by Henry and colleagues evaluated 66 subjects (64% male, ages 14–23 years) and found that although the greatest rate of symptom improvement occurred in the first 2 weeks after injury, recovery time across all symptoms, neurocognitive and vestibular-ocular outcomes happened by 21 to 28 days after injury.
Literature regarding specific risk factors for the development of PCS is conflicting. This is likely due to the varied nature of postconcussive symptoms and the subjectivity of symptom reporting. Variables, such as genetics, mental health history, life stressors, medical problems, chronic pain, depression, personality factors, and other psychosocial and environmental factors, may play an influential role. The presence of premorbid psychiatric illnesses, such as anxiety, depression, and compulsive, histrionic, and narcissistic personality disorders or those with a family history of mood disorder have been found to have higher incidence of PCS. Negative perceptions of concussion and “all or nothing” personality types were found to be correlated with prolonged recoveries. Patients with histories of premorbid learning disorders or attention deficits may experience exacerbation of baseline symptoms after concussion. Additionally, practitioners may experience difficulty interpreting results of neuropsychological testing if no baseline testing was performed, due to questions about which abnormalities are new or were preexisting. Signs and symptoms immediately following impact and their association with recovery patterns have been described by several studies. Most recently, Lau and colleagues followed 107 high school football players from time of impact to return to play so as to determine which on-field signs and symptoms were predictive of a protracted (>21 days) versus rapid (<7 days) recovery. On-field signs and symptoms included confusion, loss of consciousness, posttraumatic amnesia, retrograde amnesia, imbalance, dizziness, visual problems, personality changes, fatigue, sensitivity to light/noise, numbness, and vomiting. Dizziness was found to have the strongest correlation with a protracted recovery, whereas the remaining signs and symptoms were not predictive of prolonged recoveries. In the days after concussion, fogginess, memory impairment, anxiety, and noise sensitivity also have been identified as risk factors for persistent postconcussion symptoms.
There are conflicting data regarding the association between female gender and increased risk of developing PCS. Dick and colleagues and McCauley and colleagues identified female gender as a risk factor for development of PCS compared with male counterparts. Farace and colleagues also found that women had poorer outcomes across 85% of variables used in a meta-analysis of 20 clinical outcomes. In another study of female and male soccer players, female athletes reported more symptoms and neurocognitive impairment compared with their male counterparts. However, outcome studies suggest that differences reported between genders may be limited, as women may be more inclined to report symptoms than men.
There may be a relationship between the number of previously sustained concussions and the development of PCS. Evidence exists that athletes who have sustained previous concussions experience prolonged recovery patterns in comparison with their counterparts who have not had previous concussions. Additionally, 2 studies reported findings of poor executive function and information processing speed in high school and college athletes with 2 or more previous concussions. However, alternative studies have shown no relationship, and this continues to be an area of uncertainty.
Finally, genetic influences on outcomes following concussion have been studied. The APOE gene (located on chromosome 9 at position q13.2) produces apolipoprotein E (ApoE), which assists with lipid transport in the brain, maintains neural integrity, and assists with recovery after brain injury. After injury, production of ApoE increases with ApoE-epsilon 4 (allele of ApoE) inhibiting neurite outgrowth. ApoE-epsilon 4 has been identified as a risk factor for Alzheimer disease and is associated with worse functional and cognitive outcomes after severe traumatic brain injury. Based on current research, the presence of ApoE-epsilon 4 does not appear to prognosticate a worse outcome following concussion ; however, preliminary research is suggesting that individuals with the APOE promoter G-219T-TT genotype may be predisposed to concussion. Currently, no genetic screening test is available for routine use in the clinical setting.
Effects of multiple concussions
In general, the prognosis is good for full recovery after sustaining a single concussion and many individuals will have spontaneous symptom resolution without further sequelae; however, evidence is suggesting that there may be long-term consequences in individuals who sustain multiple concussions. Athletes who have sustained multiple concussions may be at risk for sustaining additional concussions during the recovery period and the second injury may be the result of a relatively mild impact. The most concerning, albeit rare, consequence of repeated head injury during the acute phase is the second impact syndrome (SIS). Initially described in 1973, SIS occurs when a second concussive impact is sustained before symptoms of the initial impact have fully resolved, causing rapid and catastrophic brain swelling that is severely disabling and typically fatal.
Chronic effects of multiple concussions in younger individuals continue to be a subject of debate. In studies of high school/collegiate athletes with histories of multiple concussions, no neuropsychological deficits were demonstrated 6 months after concussion ; however, other studies have shown lower baseline testing; neuropsychological deficits in memory, planning, and visuo-perceptual tasks; and increased vulnerability to repeated concussions in athletes who have sustained multiple concussions.
Studies performed using older, former athletes who have sustained multiple concussions describe relationships between number of concussions sustained and findings of impaired neurocognitive performance in episodic memory and response inhibition, neuroelectrophysiological alterations, higher than average rates of depression, and increasing risk of mild cognitive impairment (a condition that converts to Alzheimer disease at a rate of 10%–20% annually).
Differences seen in younger versus older athletes who have sustained multiple concussions may be explained by the concept of “physiologic reserve.” Through recruitment of brain networks and/or alternative cognitive strategies, the brain is able to compensate for damage. Throughout a person’s life, cognitive reserve is reduced due to damage from environmental, developmental, and genetic sources. This combined with accumulating brain damaging experiences and waning health as a result of aging leads to a decline in cognitive function. Younger athletes are likely able to rely on their cognitive reserve after multiple concussions, but this may not be the case over time.
The long-term effects of repetitive subconcussive hits are less clear, as they are usually asymptomatic. Although conventional imaging studies (computed tomography, MRI) are negative for most concussions, in cases in which athletes sustain multiple hits to the head (ie, boxers), the presence of age-inappropriate volume loss, cavum septum pellucidum, and subcortical and periventricular white matter disease has been demonstrated compared with controls. Cavum septum pellucidum has been speculated to be a marker of chronic brain trauma.
There is no consensus regarding the decision of when to forgo high-contact sports/activities when multiple concussions have been sustained. It has been suggested that removal should be considered when the time between concussions is decreasing, symptoms are becoming more severe and prolonged with each subsequent injury, or when concussions are occurring with less and less force.
Evaluation
The evaluation of a patient with suspected PCS should always start with a thorough history. Components that should be assessed include mood and affect, structure and quality of thought, sleep, somatic symptoms (headache profile, vision, dizziness, balance, nausea/emesis), musculoskeletal pain (particularly cervical/trapezius pain associated with headaches), prescribed medication history (before and after injury), premorbid risk factors (particularly anxiety/depression, migraines, history of concussions, learning disabilities), family history of psychiatric/neurologic illness, substance abuse history, and history of self-injurious behavior or ideation. It has also been recommended that the use of standardized symptom assessment scales be used. Differential diagnoses should remain broad, as signs and symptoms of PCS can be seen with a variety of other diagnoses.
Physical examination should consist of a thorough neurologic examination of cognition, cranial nerve function, strength, sensation, reflexes, cerebellar function, and gait and balance. Cerebellar examination should include evaluations for appendicular ataxia, truncal ataxia, and eye movement abnormalities. Tests for appendicular ataxia include finger-nose-finger test, heel shin test, and rapid alternating movements. The examiner is looking for signs of dysrhythmia, dysmetria, or dysdiadochokinesia. The Romberg test and tandem gait evaluate for truncal ataxia, with loss of balance (usually toward the side of the lesion) considered positive. Finally, abnormalities of eye movements can be observed, including ocular dysmetria (saccades overshoot or undershoot their targets), nystagmus, and impairment of vestibule-ocular reflex (VOR) suppression. VOR testing consists of 2 parts: patient fixates on a static object while performing rapid horizontal/vertical head movements followed by fixation on a static object while rotating entire trunk. The patient should be able to maintain gaze on static object during dynamic movement without nystagmus. Examination of the cervical spine and neck musculature is indicated in complaints of neck pain and headaches, and whiplash syndrome should be considered.
Computed tomography is the imaging modality of choice in the acute care setting following possible concussive injury, and is abnormal in fewer than 10% of cases with 0.1% to 1% requiring surgical intervention. Conventional MRI is often considered when symptoms are prolonged; however, the utility of MRI in concussion is debated. A normal MRI does not exclude concussion, as it is not sensitive enough to identify structural injury to axons consistently or detect ongoing metabolic abnormalities. Imaging modalities such as functional MRI, single-photon emission computed tomography, magnetic resonance spectroscopy, or magnetoencephalogram may be more appropriate for concussion, as they provide a better understanding of brain function rather than structure alone; however, they are not routinely used in clinical evaluation currently and their utility in identifying appropriate clinical interventions remains to be investigated.
Finally, there is evidence that neuropsychological testing is useful in the evaluation of concussion, particularly for acute management decisions on the sideline and tracking recovery in the acute phase. Although questions remain regarding which battery of tests to administer, in what form and at what time points, neuropsychological testing can be considered in the evaluation of the patient with persistent symptoms, particularly those with cognitive complaints.
General treatment principles
As symptom presentations vary, treatment approaches should be tailored to the individual. Patient education and reassurance should be a primary intervention. Miller and Mittenberg found that a single psychoeducational session is a key factor in preventing or shortening PCS. In the acute phase, a reasonable amount of cognitive and physical rest is recommended; however, it has been demonstrated that prolonged rest can be detrimental to recovery and should not be extended past the first few weeks following injury. As patients begin their gradual return to activity, academic and work accommodations may be needed.
Meehan described conditions in which pharmacologic intervention can be considered: when symptoms last longer than expected recovery time, quality of life is affected, and the clinician is knowledgeable in the management of brain injury. On initiation of medication management, physicians and patients need to set clear treatment goals, and close follow-up should be arranged. Polypharmacy should be avoided and medications should be started at low doses, given an appropriate amount of time to assess effectiveness and monitor for side effects with slow upward titration. If possible, medications that target more than one symptom and have favorable side-effect profiles should be used.
In the following sections, symptoms are divided into 4 classes for simplicity: sleep, somatic (posttraumatic headaches, vestibular-vision dysfunction), mood, and cognitive. However, it should be recognized that there can be considerable overlap in symptom presentations that change over time, as explored by Kontos and colleagues using factor analysis of symptom reporting on the Post Concussion Symptom Scale before and after injury (up to 7 days).
Sleep
Sleep disturbance is a common complaint following all severities of traumatic brain injuries (TBIs). Up to 70% of patients with TBI report sleep-wake cycle disruption (difficulty falling asleep or staying asleep), 33% report fatigue, and 10% report insomnia/excessive daytime sleepiness. Many factors can contribute to sleep disturbance, including the injury itself, medication side effects, pain, preexisting sleep disorders, and environmental stimuli. Poor sleep can exacerbate symptoms of cognitive function, fatigue, irritability, and difficulty concentrating, leading to significant morbidity, poor quality of life, and prolonged recovery. In 443 concussed patients with sleep-wake disturbances (SWD), Chaput and colleagues found the patients were more likely to suffer from concomitant headaches, depressive symptoms, and irritability.
Conservative management begins with emphasis on sleep hygiene, including regular bedtime and rise time, avoiding stimulants and heavy exercise late in the day, limiting technology use before bed, avoiding spending time in bed awake, and improving sleep consolidation (ie, the ability to maintain sleep with minimal interruption). Returning to daytime physical and mental activities also may be helpful in restoring sleep architecture. Assessment for underlying psychiatric disorders should be performed, as anxiety and depression have been associated with greater daytime sleepiness, poorer sleep quality, and more naps in TBI versus controls. In addition, any pain complaints should be evaluated and treated. If sleep disturbance is related to anxiety or other underlying psychiatric condition, referral to a behavioral health specialist for assistance with implementation of sleep hygiene and relaxation techniques can be considered.
Limited evidence exists regarding medication management of sleep disorders of TBI, and treatment strategies are adopted often from insomnia literature. Trazodone, a selective serotonin reuptake inhibitor (SSRI), has been used most commonly despite limited research regarding its efficacy. It has a favorable side-effect profile with anxiolytic and hypnotic properties. Side effects can include dry mouth, dizziness, nausea, priapism, and headache.
Melatonin, an endogenous hormone produced by the pineal gland, also has a safe side-effect profile and may potentially be neuroprotective. Although the exact mechanism of action is unclear, it is hypothesized to play a role in the regulation of circadian rhythm, reduction in core temperature, and via direct action on brain structures responsible for sleep.
In a study of blast-related concussions in Iraq/Afghanistan veterans, prazosin, an alpha-1 antagonist, in combination with sleep hygiene counseling, compared with counseling alone demonstrated improvements in sleep, headaches, and cognition. This was felt to be secondary to prazosin’s ability to decrease sleep latency and nocturnal arousals.
Amitriptyline, a tricyclic antidepressant, can be considered in patients complaining of SWD in addition to posttraumatic headache and mood disorder and may be a desirable choice to avoid polypharmacy in patients with this multitude of symptoms. However, its use in concussion has not been well-studied and caution must be used in patients with cardiovascular disease, in geriatric patients, and in women of childbearing age.
Although benzodiazepines are effective in inducing sleep and reducing anxiety, they have been shown to be potentially detrimental to neurorecovery and should be used with caution. Nonbenzodiazepine hypnotics, including zolpidem, can be considered; however, potential side effects in TBI are unknown and these medications should be used in low doses to reduce the risk of adverse effects. Somnambulation and cognitive impairment have been described.
Headache
Posttraumatic headache (PTH) is the most commonly reported symptom after concussion. Prevalence of PTH has been found to range from 30% to 90%, with 18% to 22% lasting more than 1 year. PTH is typically classified as a secondary headache disorder and is diagnosed based on its close temporal relationship to injury (onset within 7 days). The most commonly reported headache types are migraine/probable migraine, tension, and cervicogenic when classified using The International Classification of Headache Disorders (ICHD)-2 diagnostic criteria. Other variables related to trauma may complicate the diagnosis, such as medication overuse, emotional distress, myofascial pain, occipital neuralgia, cervical referred pain, and vascular etiologies. Whiplash injury occurs as a result of excessive neck extension-flexion secondary to acceleration-deceleration forces, and myofascial pain is a predominant feature. Myofascial injury may lead to tension-type headaches. Additionally, neuralgic headache pain may result from injuries to the occipital nerves or facet joints. Previous history of primary headache disorder and female gender have been described as risk factors for development of PTH.
History should include headache location, pain characteristics, frequency, duration, severity, associated symptoms (such as nausea, vomiting, photo/phonosensitivity), and any aggravating/alleviating factors. Of note, headache characteristics may change from headache to headache or as time from initial injury passes. Patients also may present with characteristics of more than one subtype of headache. Migraine typically presents as a unilateral, moderate to severe, throbbing headache that worsens with activity and is accompanied by nausea, vomiting, and photophobia and/or phonophobia. Tension-type headache is characterized by mild to moderate bilateral pain that is viselike in nature, does not worsen with activity, and has no systemic systems, such as nausea, vomiting, or light and/or sound sensitivity.
Initial management should include education regarding proper sleep hygiene, exercise, and dietary considerations. Common headache triggers include irregular eating schedules, dehydration, too much or too little sleep, and reduced physical activity. Should there be a relationship between cognitive exertion and headache, interventions such as rest breaks during the day and school/work accommodations may be helpful.
Biologically based interventions include a variety of biofeedback mechanisms, physical therapy, manual therapy, immobilization devices, ice, and injections. Using systematic review, Wantabe and colleagues found a single class II study in which manual spine therapy was found to be superior to treatment with cold packs alone in patients with PTH after concussion. However, treatment effect was not sustained past 8 weeks. Three class III studies provided evidence for utilization of cognitive and/or behavioral therapy, biofeedback, and relaxation techniques for treatment of PTH; however, Tatrow and colleagues found no statistically significant differences between types of treatments. In a case series by Hect, 8 of 10 patients with mixed TBI severity experienced complete relief of occipital neuralgia pain following 5% bupivacaine blocks. Finally, for treatment of whiplash injury, active therapy versus immobilization in a cervical collar demonstrated a lower percentage of patients with headaches in the therapy group. Freund and Schwartz also found patients who received onabotulinum toxin A for whiplash injury fared significantly better at 2 and 4 weeks than patients who received saline injections.
Pharmacologic treatment approach to PTH is twofold: acute or abortive therapy used on an as-needed basis and preventive therapy or prophylaxis used on a daily basis when attack frequency is high or patients fail to respond adequately to acute therapy interventions. Nonspecific acute therapies, such as aspirin, acetaminophen, paracetamol, and nonsteroidal anti-inflammatory drugs, are generally less effective than more specific acute therapies; however, they may be helpful if used early when pain is mild and symptoms are developing slowly. Potential side effects include gastritis, gastrointestinal bleeding, increased bleeding time, and peptic ulcer disease. Frequent use of these medications may contribute to rebound headaches and it is recommended that their use be limited to no more than 3 times per week. Specific acute therapies for migrainous symptoms include triptans, ergotamines, and dihydroergotamine (DHE), which are primarily serotonin 1B/D agonists. With the development of triptans, ergots are being used less frequently due to poor absorption and nausea when taken orally. Triptans possess vasoconstrictive properties and are contraindicated in patients with vascular disease. Finally, DHE is available in a nasal form, which has inconsistent absorption, or an injectable form, which is inconvenient to use. Use of opioids for treatment of PTH is not recommended given the relative ineffectiveness for migraine phenotypes, risk of dependency and overuse, and sedating effects that may impair cognitive function.
Preventive treatment may be considered when use of abortive medications fails to control frequency or intensity of attacks, pain is disabling, and there is concern for medication overuse. Preventive treatments have been shown to decrease headache frequency, severity, and duration and may improve the response to acute therapies. The only medications that have been approved by the Food and Drug Administration for use in migraine are propranolol, timolol, valproic acid, and topiramate. Amitriptyline and topiramate have been found to be effective in treatment of tension-type headache in patients without concussion. SSRIs and selective norepinephrine reuptake inhibitors are also used but less commonly. Patients also may find herbal, vitamin, and mineral supplements helpful. Supplementation with magnesium, vitamin B2, alpha lipoic acid, and coenzyme q10 have been found to be effective in randomized double-blinded studies; however, their use has not been studied specifically for treatment of PTH. The mechanism of action of preventive therapies is unknown; however, hypotheses include inhibition of cortical spreading depression, inhibition of glutamate dependent mechanisms, and modulation of serotonergic, dopaminergic, and adrenergic pathways and receptors. Beta blockers decrease vascular dilation, and prevent platelet adhesion and aggregation while reducing the central activity of catecholamines. Anticonvulsants facilitate neuronal inhibition via GABA potentiation while reducing neuronal hyperexcitability, and tricyclic antidepressants (TCAs) alter central monamines, specifically serotonin.
Vestibular/Vision Dysfunction
Together, the vestibular, oculomotor, and somatosensory systems consist of highly specialized neural networks with direct, indirect, and reciprocal projections to the spinal cord, autonomic nervous system, brainstem nuclei, cerebellum, thalamus, basal ganglia, and cerebral cortex. Through special sensory organs located within the vestibulum of the inner ear, skin, muscles, joints, and brainstem, they interact to regulate gait, maintain balance and postural control, and coordinate eye movements. The VOR regulates gaze stabilization during head acceleration and the vestibulo-spinal reflex coordinates head, neck, and trunk positioning during dynamic body movements. Dysfunction within these components may adversely affect subsystems, leading to complex symptoms and impairments. Dizziness has been correlated with other PCS symptoms, particularly headache and anxiety.
Dizziness and postural instability have been reported in up to 80% in the days to weeks following concussion. Causes have been found to be both central and peripheral in nature and include posttraumatic benign paroxysmal positional vertigo, labyrinth concussion, perilymphatic fistula, endolymphatic hydrops, otolith disorders, and central vestibulopathy; 46% of patients have been found to have dysfunction related to more than one mechanism.
Patients will often complain of diplopia or blurry vision, convergence deficiencies with difficulty reading (such as losing their spot or skipping words), eye strain, motion sensitivity, or difficulty walking on uneven surfaces, headache, and anxiety in crowded places. The physical examination should involve testing of visual acuity and visual fields, pupillary function, extraocular movements, convergence, and vergence. Often symptoms of dizziness, headache, and blurred vision will be elicited, and it is important to document which tests provoke symptoms. Mucha and colleagues conducted a cross-sectional study for validity using the Vestibular-Ocular Motor Screen (VOMS), a brief clinical screening tool used to assess vestibular/ocular motor impairments and symptoms of sports-related concussions. The VOMS demonstrated internal consistency as well as sensitivity in identifying patients (n = 64) with concussions based on correlations with the Post Concussion Symptom Scale. Patients were tested between 0.5 and 9.5 days after concussion, and although the role of VOMS testing in PCS is unclear, it may be a useful tool for diagnosis of vestibular/oculomotor impairments.
Vestibular therapy and repositioning techniques are the cornerstones of treatment and have been demonstrated to be helpful after concussion. Principles of vestibular rehabilitation include recalibration of depth and spatial perception under static and dynamic conditions by reestablishing efficient integration of the vestibular, visual, and somatosensory subsystems. Treatment programs should be designed to improve function of the VOR, cervico-ocular reflex, depth perception, somatosensory retraining, dynamic gait, and aerobic training.
Vision therapy programs for oculomotor dysfunction (OD) following concussion are also supported in the literature. In a study of 160 patients with TBI, 90% demonstrated improvement of OD after completing vision therapy. Vision therapy programs consist of exercises to improve function with fixation, pursuit, predictable and unpredictable saccade, mergence, and accommodation.
Finally, should symptoms limit participation in therapies or significantly affect quality of life, a trial of vestibular suppressants (ie, meclizine) for peripheral causes or anxiolytics (ie, clonazepam) for central causes can be considered. Use of vestibular suppressants following concussion has not been studied, and efficacy is unknown. Additionally, use of vestibular suppressants may limit the brain’s ability to compensate for centrally driven vestibular disorders.
Emotional
Although most concussion symptoms will improve with education, reassurance, healthy coping strategies, and the support of family and friends, persistent symptoms may be secondary to an interaction of pathophysiological and psychological etiologies. Prolonged cognitive, sleep, and somatic symptoms may result in patients becoming frustrated or anxious. Patients also may feel increasingly isolated as a result of treatment (physical and cognitive rest) that imposes limitations on activities such as school, work, and athletics. Emotional symptoms may contribute to the expression or persistence of PCS. Perceptions of physical symptoms may be exacerbated, and if emotional symptoms are left untreated, they can mimic neurocognitive symptoms of concussion. History of preexisting psychiatric disorders should be established, as premorbid depression and anxiety are known risk factors for the development of PCS.
Cognitive behavioral therapy (CBT) is recommended as an overall first-line treatment for anxiety and depressive reactions. CBT aims to improve self-esteem, problem-solving skills, and psychosocial functioning following TBI and decreases depressive, anxiety, or anger symptoms. Behavioral interventions also may reduce the frequency of problematic behaviors or cognitive distortions resulting from injury that may prolong recovery.
If emotional symptoms are persistent despite conservative interventions, pharmacologic treatment should be considered. SSRIs are often used as a first-line pharmacologic intervention in this population, and agents with no antimuscarinic effects are preferred, as this can impair cognitive function. Sertraline, citalopram, or escitalopram have been shown to be effective for treating depressive symptoms, self-reported postconcussive symptoms, and cognition. Paroxetine has been found to be as effective as citalopram at treating emotional symptoms in concussion; however, it does possess antimuscarinic properties and should be used with caution. Fluoxetine also has been considered and is generally well tolerated; however, it has the potential for drug-drug interactions given its significant cytochrome P450 inhibition. With TCAs, although considered effective for other symptoms of PCS, such as posttraumatic headaches and sleep dysfunction, evidence for efficacy in TBI-related depression is lacking. All psychotropic medications should be used with caution in the adolescent population, as they can increase risk of suicidality. Parental consent and close monitoring are warranted.
Cognitive
It has been reported that 40% to 60% of patients with TBI experience cognitive impairment at 1 to 3 months after injury. Symptoms may include impaired memory, concentration, processing speed, and mental “fogginess,” which may lead to declining academic or work performance. Patients also may report worsening somatic symptoms with cognitive exertion. Underlying factors such as emotional symptoms, sleep disturbance, chronic pain, or medication side effects should be evaluated. Neuropsychological testing can be helpful in assessing cognitive deficits in a quantitative manner.
Although most cognitive symptoms resolve over time, in those with significantly protracted recovery, cognitive rehabilitation may be helpful to develop compensatory strategies for cognitive deficits. For example, use of memory logs, to-do lists, and digital alarms set with reminders may help with memory and organization. Portable mobile electronic devices contain most of these features in a compact form and use should be encouraged. Cicerone and colleagues and Rohling and colleagues have established efficacy of cognitive rehabilitation in both civilian and military populations. Referral to speech therapies may be appropriate for individuals who experience adverse effects on work or school performance due to cognitive difficulties.
Evidence supporting the use of neurostimulants for treatment of cognitive deficits after TBI is emerging. This is based on the understanding of the biological effects of neurotransmitters on the regulation of cognitive activity; however, there are no randomized controlled studies and this has been identified as an area of needed study.
Dopamine, a neurotransmitter involved in the transmission of signals linked to executive function, arousal, and memory, has been targeted for its neurorecovery potential. Dopaminergic agonists are frequently used to address cognitive impairment following TBI. In a study of concussed adolescent athletes, use of amantadine was associated with improvements in verbal memory and reaction time on computerized neurocognitive testing, as well as improvements in reported symptoms. Giacino and colleagues found amantadine accelerated the pace of functional recovery in 184 vegetative or minimally conscious patients during active treatment 4 to 16 weeks after injury compared with placebo. Amantadine increases the concentration of dopamine in the synaptic cleft through both presynaptic and postsynaptic actions. Additionally, it acts as an antagonist at N-methyl-D-aspartate (glutamate) receptors and may be neuroprotective. This medication is generally well tolerated and common side effects include gastrointestinal complaints (diarrhea, constipation, nausea), orthostatic hypotension, and increased irritability. Livedo reticularis, a lacelike purplish discoloration of the skin, may be observed and can become permanent. Use with caution in those with a previous history of compulsive behaviors, as amantadine can worsen these.
Medications used in the treatment of attention-deficit disorder and attention-deficit/hyperactivity disorder that target both dopamine and norepinephrine through presynaptic and postsynaptic mechanisms have also been considered in the treatment of cognitive impairment following TBI. Randomized studies using methylphenidate in moderate to severe TBI showed improvement of attention deficits and processing speed. However, no randomized-placebo controls exist. Side effects of these medications include elevated heart rate and blood pressure in higher doses and should be used with caution, if at all, in people with cardiac abnormalities (arrhythmias, recent myocardial infarction, structural abnormalities, cardiomyopathy, severe cardiac disease). Additionally, patients with history of motor tics/Tourette syndrome may experience tic worsening. Finally, cholinergic agents, such as donepezil, a long-acting acetylcholinesterase inhibitor, has been shown to improve short-term and long-term memory in patients with TBI.
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