Postconcussion Syndrome

Debate in the literature exists over which symptoms of postconcussion syndrome are due to organic causes and which have a psychological basis. Researchers have hypothesized that early postconcussion syndrome symptoms are more likely to be organic, whereas PCS symptoms that persist beyond 3 months have a nonorganic, psychological basis. While recent research has shown that psychological factors may be present early, other studies using imaging techniques such as magnetic resonance imaging (MRI), single-photon emission computed tomography (SPECT), and magnetoencephalography (MEG) have demonstrated the presence of organic brain injury in patients with persistent PCS at greater than 1 year after injury.

Neuropsychological assessments have pointed toward an organic basis for some of the symptoms of postconcussion syndrome. Patients with PCS have been found to have cognitive deficits in memory, attention, and learning when compared with controls. A prospective study found impaired eye movements in patients with PCS, as compared to controls, that were both persistent and independent of factors such as depression or intellectual ability.[7] Findings from neuropsychological evaluations demonstrate that symptom severity is not necessarily dependent on neurologic status immediately following injury. However, in other series, the length of LOC or posttraumatic amnesia may be correlated with the probability of developing PCS.

Some studies have found certain characteristics such as female sex, noise sensitivity, and anxiety predict development of symptoms.[8] Another study found a simple test in the ED of immediate and delayed memory for 5 words and a VAS for acute headache provided an 80% sensitivity and 76% specificity for the development of PCS.[9] In addition, another study found that higher educational levels, along with mild symptoms and no extracranial symptoms predicted a low likelihood of significant dysfunction from PCS.

More than 1 million instances of minor head injury occur in the United States each year. The overall incidence rate of minor head injury for persons not hospitalized, with data compiled by the National Hospital Ambulatory Medical Care Survey, was 503 per 100,000 population or 1,367,101 visits per year to hospital EDs in the United States.[10]  Depending on the definitions used and population examined, approximately 50% of patients with minor head injury have symptoms of postconcussion syndrome at 1 month and 15% have symptoms at 1 year. The number of patients who sustain minor head injury and do not present for medical care is unknown; therefore, the number of patients with PCS is likely significantly underdiagnosed.

Morbidity is mainly due to the persistence of symptoms, which make it difficult for patients to resume premorbid functions. Between 14 and 29% of children with mild traumatic brain injury will continue to have postconcussion symptoms at 3 months.[11, 12]

Fifty percent of those who experience minor head injury are aged 15-34 years. However, postconcussion syndrome has no predilection for any specific age group.[1, 13]

Approximately 500,000 children a year visit the ED for traumatic brain injuries (TBIs). TBIs are largest cause of ED visits for adolescents. Eighty to ninety percent of these are mild (mTBIs), or concussions, and are not life-threatening, but even a mild TBI can have ongoing effects. Young children are more susceptible to concussion than adults not only because they are more likely to be active and involved in sports but also because their brains are not yet fully developed and therefore are more vulnerable to injury.[14]

According to the University of Pittsburgh's Brain Trauma Research Center, more than 300,000 sports-related concussions occur annually in the United States, and the likelihood of suffering a concussion while playing a contact sport is estimated to be as high as 19% per year of play. More than 62,000 concussions are sustained each year in high school contact sports, and among college football players, 34% have had one concussion and 20% have had multiple concussions. Estimates show that between 4 and 20% of college and high school football players will sustain a brain injury over the course of one season. The risk of concussion in football players is 3 to 6 times higher in players who have had a previous concussion.[15]

A study conducted by McGill University found that 60% of college soccer players reported symptoms of a concussion at least once during the season and that concussion rates in soccer players were comparable to those of football players. Athletes who suffered a concussion were found to be 4 to 6 times more likely to suffer a second concussion.[16]

True prognosis is difficult to define given that many patients with minor symptoms may not enter the health care system and those that participate in research appear to have more significant symptoms at baseline. In addition, a wide heterogeneity exists in patients enrolled in studies.

Most patients recover fully in less than 3 months, although some small studies suggest persistence of minor cognitive defects for asymptomatic minor traumatic brain injury patients.[17]

Approximately 15% of patients complain of problems more than 12 months after injury. This group is likely to experience persistent and intrusive symptoms that may be refractory to treatment and impose a lifelong disability.

At least one study found the persistence of dizziness as a symptom seemed to portend a longer and more significant symptom complex.[18] Other studies found the depression, pain, and symptom invalidity were correlated with longer and worse symptoms.[19] Another found patients with early clinical symptoms, such as headache, dizziness, and intracranial lesions were more likely to have persistent PCS.

PCS is commonly associated with multiple concussions, but in one series, 23.1% of patients experienced PCS after only 1 concussion (average was 3.3 concussions). Median duration of symptoms in this series was 7 months.[20]

Hiploylee et al found that time to recovery often depended on the number of initial symptoms reported, with each symptom reducing recovery rate by about 20%. They also found that PCS may be permanent if recovery hasn't occurred withiin 3 years. Those who did not recover were more likely to be noncompliant regarding the recommendation to not return to play.[21]

Most patients present shortly after a minor head injury (MHI). Often, patients return after a previous evaluation in the emergency department (ED) because of persistent postconcussion symptoms.[6] Findings may include the following:

• Headache - This is the most common symptom of PCS. The specific type is variable. One study found a prevalence of persistent posttraumatic headache in 15.3% of patients with minor head injury compared to 2.2% of matched minor injury ED controls.[22]

• Cranial nerve symptoms and signs - Dizziness (the second most common symptom), vertigo, nausea, tinnitus, blurry vision, hearing loss, diplopia, diminished sense of taste and smell, light and noise sensitivity

• Psychological and neurovegetative problems - Anxiety, irritability, depression, sleep disturbance, change in appetite, decreased libido, fatigue, personality change

• Cognitive impairment - Memory impairment, diminished concentration and attention, delayed information processing and reaction time

Tator and Davis performed a retrospective cohort study of 138 patients who had sports-related postconcussion syndrome (PCS) based on three or more postconcussion symptoms lasting 1 month or longer. The patients averaged 3.4 concussions, ranging from 1 to more than 12. Over 80% of the PCS patients had at least one previous concussion, and only 19.6% had no previous concussion. In 21% of patients, the authors identified a history of a previous psychiatric condition, attention-deficit disorder or attention-deficit/hyperactive disorder, learning disability, or previous migraine headaches.[23]

In general, the findings at physical examination are normal. The patient may exhibit subtle neurologic findings, but objective focal motor deficits should raise a concern about an undiagnosed intracranial bleed. Other findings may include the following:

• Depressed affect

• Decreased ability to smell and taste

• Neurasthenia or hyperesthesia (nondermatomal distribution)

• Cognitive deficits

  • Neuropsychological testing has revealed that deficits can persist 6 months or longer when other symptoms are present.

  • These deficits include difficulties with vocabulary, short-term and intermediate-term memory, attention, cognitive flexibility, information processing, object recall, drawing, and mathematics.

  • Patients without other subjective symptoms usually perform normally on these tests.

  • However, testing also has revealed that these deficits resolve when other somatic and neurologic symptoms do not.

Risk factors for the development of postconcussion syndrome include nonsporting mechanisms, loss of consciousness, amnesia for the event, female sex, and abnormal neurobehavioral testing results after the incident.

• A common perception is that patients who develop PCS from head injury are those who perceive a source of blame for the injury and desire to pursue litigation. However, a single study evaluating this did not demonstrate a correlation between blame and litigation. In fact, PCS symptoms persisted after settlement.

• Some authors have concluded that persons with a history of depressive and anxiety disorders, certain premorbid personality types, or poor coping skills may be predisposed to PCS, but the data are conflicting.

• Neck pain after a head injury has not been correlated with the development of PCS.

• Although the numbers of patients tend to be relatively small, more recent studies suggest that PCS is more likely to develop in patients presenting with nausea, headache, and dizziness.

• One study found an inverse association between number of years of education and development of PCS in adult patients.[24]

• Patients with premorbid physical problems have also been found to have a higher incidence of PCS after minor head injury.

• One study found that perception of the illness itself may have an effect on the development of PCS. Patients who believed that their symptoms had serious negative consequences on their lives were at increased risk of developing PCS.[25]

No specific laboratory studies are needed, unless concomitant illness is suspected or unless the diagnosis is unclear and believed to be of toxic or metabolic origin. While some newer studies have searched for evidence of specific proteins or biomarkers as predictive of PCS, there is no definitive correlations as of yet.

Neurological examination and CT scan findings are frequently normal in patients with postconcussion syndrome; however, this does not confirm the absence of damage to the brain. Imaging modalities such as MRI, SPECT, and MEG have been shown to be more sensitive than CT at detecting brain injuries associated with PCS. These modalities have demonstrated an association between basal ganglia hypoperfusion and headaches, temporal lobe abnormalities and memory deficits, parietal lobe abnormalities and attention problems, and frontal lobe abnormalities and problems with executive function in patients with PCS. Interestingly, these imaging modalities have not born out associations between posttraumatic brain abnormalities and psychiatric symptoms in PCS.

It has been hypothesized that axonal injury at the time of trauma could underlie PCS. Shear strain on the neurons that leads to diffuse axonal injury can occur without CT abnormalities. However, a recent study of a biomarker for axonal injury, serum cleaved tau (C-tau), showed no correlation between C-tau levels at the time of injury and the later development of PCS.[26] Studies looking at serum levels of S-100B, a protein found most commonly in astrocytes, in patients with minor head injury have found conflicting results regarding a correlation between initial levels of the protein and development of PCS.[27]

In a study by Ramos-Zuniga et al, neuropsychological and spectroscopy testing confirmed the diagnosis of postconcussion syndrome in patients with mild head injury (MHI). According to the authors, spectroscopy revealed neurometabolite disturbances in 54% of cases, particularly N-acetylaspartate (Naa) and the Naa/lactate ratio in the frontal lobe. In addition, the authors noted that 55% of patients experienced physical disturbances such as headache and postural vertigo.[28]

CT scanning is used to determine the presence of intracranial abnormalities and skull fractures. In young patients with no loss of consciousness and a normal neurologic examination, CT scanning is of very low yield and is unlikely to be positive. Patients with PCS usually do not present immediately after the trauma.

If a CT scan has already been obtained, the utility of a repeat scan is minimal in the absence of focal neurologic signs or unless the patient is at risk for delayed hemorrhage (eg, an elderly patient on warfarin.)

If a CT scan has not been obtained and if the patient had a loss of consciousness and a GCS of 15, the likelihood of finding an operable lesion is extremely limited. Unfortunately, these patients with symptoms and a normal examination may still harbor an injury that requires intervention. In general, a single head CT scan is still a reasonable, fast, and effective screening test in the significantly symptomatic patient, although it should be balanced by the risks of radiation, especially in children.

MRI, SPECT, and positron emission tomography (PET) scans are more sensitive than CT scans in detecting abnormalities associated with minor head injury and PCS.[28, 29, 30, 31, 32, 33]

An MRI obtained in the acute period has little clinical significance. If one is obtained, it should be obtained on an outpatient basis in conjunction with follow-up. Although traumatic lesions may be depicted on MRIs in patients with minor head injury and a normal nonenhanced CT scan, they rarely influence the acute clinical course.

Principal component analysis of diffusion tensor images (DTI) has been found to identify white matter injury patterns on DTI that correlate with clinically relevant symptoms in mild traumatic brain injury.[32]

An MRI, SPECT, or PET scan obtained 4-24 months after injury may reveal a variety of abnormalities, though this rarely influences treatment or outcome.

In a study of cerebral blood flow (CBF) measured by MRI in pediatric patients (8-18 yr) 40 days after mild traumatic brain injury, global CBF was higher in the symptomatic group and lower in the asymptomatic group compared with controls.[34]

Neuropsychological testing rarely is performed in the acute setting, although it may have some value in predicting the development of symptoms. A series of standardized tests and questionnaires are used to measure attention, language, memory, emotional functioning, and other neurobehavioral parameters.

The Rivermead Postconcussion Symptoms Questionnaire is used to quantify postconcussion syndrome symptoms.

Neuropsychological assessments may be used. These include the Wechsler Adult Intelligence Scale and specific subtests (digit span and vocabulary), Trail Making Test, complex figure drawings (eg, Rey Osterreith), copy trials and memory trials, category tests, controlled oral word association (Hopkins Verbal Learning Test), Wisconsin Card Sorting Test, and the Paced Auditory Serial Addition Task.

The objective personality measure, Minnesota Multiphasic Personality Inventory, Second Edition (MMPI2), may be used.

The Hospital Anxiety and Depression Scale, Impact of Even Scale, Galveston Orientation and Amnesia Test, and assessments of posttraumatic amnesia are used together as prognostic screening instruments for predicting PCS persistence.

In an exploratory factor and confirmatory factor analysis of a 19-item Postconcussion Symptom Scale broken up into 3 factors (neurocognitive, somatic, emotional), patients seen more than 14 days after the concussion injury had worse factor 3 (emotional) scores than those seen less than 14 days after injury. Females and patients with anxiety disorders had significantly worse (higher) scores on all 3 factors.[35]

Sport Concussion Assessment Tool version 3 (SCAT-3) is one of the most widely researched concussion assessment tools in athletes. The presence and frequency of posttraumatic headache are associated with the SCAT-3 symptom severity score, which is an important predictor of post-concussion recovery.[36, 37, 38, 39, 40]

No specific care is required in the ED. Patients with the symptom constellation consistent with postconcussion syndrome (PCS) require thorough physical and neurological examinations. A CT scan should be obtained if significant concern about intracranial hemorrhage exists, although this injury is rare in the patient presenting late with nonfocal findings at examination.[41]

• Supportive care may include the use of nonnarcotic analgesics and antiemetics. However, there does not appear to be any medications at discharge that can prevent or hasten the resolution of PCS. Several drugs are under investigation, but none have proven to be clinically useful yet.

• Several studies have shown that providing patients with an explanation of symptoms as well as expectations may decrease the severity and duration of postconcussive symptoms.

• Although rare, patients may be admitted if symptoms are severe, the majority can be discharged. Several studies have revealed that patients admitted acutely after a minor head injury (MHI) may have a lower incidence of PCS and its attendant social and psychological morbidity. This finding, however, may be due to active interventions at follow-up.

• Prompt follow-up care and reassurance may hasten resolution of symptoms. Patients should be referred to a primary care doctor, neurologist, or psychiatrist depending on their symptoms.

• Follow-up and patient education on what to expect after minor head injuries is useful, as many patients will have symptoms for weeks after discharge.[42]

Rarely is consultation warranted in the ED once the diagnosis is made. Outpatient referral is the cornerstone of treatment. One study suggests that findings of early neuropsychological assessment may determine the prognosis; however, this assessment rarely is performed in the ED.

Outpatient care is the cornerstone of treatment of patients with postconcussion syndrome and involves multidisciplinary teams that provide testing and treatment, including cognitive rehabilitation, psychotherapy, stress management, vocational counseling, and symptomatic treatment with medications.

• No treatments have been proven effective, though neurotherapy or quantitative EEG biofeedback is a modality that has been shown in recent studies to improve symptoms of PCS. More controlled studies are needed at this point.

• A neurologist, physical medicine specialist, primary care physician, or psychologist specializing in these disorders usually coordinates treatment.

The goals of pharmacotherapy are to provide supportive care to reduce morbidity and prevent complications. Supportive care may include the use of nonnarcotic analgesics and antiemetics.

Class Summary

Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet, and aids physical therapy regimens. Many analgesics have sedating properties that benefit patients who experience pain.

Acetaminophen (Acephen, Tylenol, CetafenFeverall Childrens, Ofirmev, Valorin)

Acetaminophen is the drug of choice for pain in patients with documented hypersensitivity to aspirin or NSAIDs, who have upper GI disease, or who are taking oral anticoagulants.

Class Summary

Antiemetics are useful in the treatment of nausea associated with postconcussive syndrome.

Metoclopramide (Metozolv ODT, Reglan)

Metoclopramide blocks dopamine receptors in the chemoreceptor trigger zone of the central nervous system.

Ondansetron (Zofran, Zofran ODT, Zuplenz)

Ondansetron is a selective 5-HT3-receptor antagonist that blocks serotonin both peripherally and centrally. It prevents the nausea and vomiting.

Prochlorperazine (Compazine, Compro)

Prochlorperazine may relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine receptors through its anticholinergic effects and depressing the reticular activating system.