Postconcussion (postconcussive) syndrome (PCS), a sequela of minor head injury (MHI), has been a much-debated topic. Understanding of this condition has been hindered by conflicting findings regarding symptom duration, an absence of objective neurologic findings, inconsistencies in presentation, poorly defined etiology, and significant methodologic problems in the literature. Depending on the definition employed and the population examined, 29-90% of patients experience postconcussion symptoms shortly after the traumatic insult.[1, 2, 3, 4]
The terms MHI and concussion are generally used interchangeably in the medical literature; however, it should be noted that the traditional definition of concussion precludes findings of intracranial hemorrhage (ICH) on computed tomography (CT), whereas the definition of MHI does not (though it does preclude the presence of a skull fracture). The term mild traumatic brain injury (TBI) is sometimes used as well.
An MHI typically indicates a blow to the head with a brief period of loss of consciousness (LOC) or posttraumatic amnesia or disorientation. At presentation, the Glasgow Coma Scale (GCS) score ranges from 13 to 15. However, the literature has suggested (and many clinicians concur) that there is a significantly lesser chance of intracranial injury on CT with a GCS score of 14 or 15 than with a GCS score of 13.
Although no universally accepted definition of PCS exists, most of the literature defines the syndrome as the development of at least three of the following symptoms:
There has been some disagreement in the literature with regard to the timing and duration of symptoms in PCS. Some authors define the syndrome as involving symptoms of at least 3 months' duration, whereas others define it as involving symptoms appearing within the first week. In this article, PCS is loosely defined as the occurrence and persistence of symptoms within several weeks after the initial insult. To define persistent PCS (PPCS), most authors cite a symptom duration of more than 1 month, whereas others cite 6 months or 1 year. Generally, however, the term PPCS applies to ongoing chronic symptoms that continue past their expected resolution.
In a study of patients aged 5 years to younger than 18 years who presented with acute head injury in pediatric emergency departments (EDs), 801 of the 2584 patients (31%) experienced PPCS or acute concussion followed by ongoing somatic, cognitive, and psychological or behavioral symptoms.[5]
The ICD-10 criteria for PCS include a history of TBI and the presence of three or more of the following eight symptoms:
In the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), published by the American Psychiatric Association (APA), PCS is given a diagnosis of either major or mild neurocognitive disorder (NCD) due to TBI.[4] The DSM-5 criteria for neurocognitive disorder due to TBI include the following:
Findings may include headache, cranial nerve signs and symptoms (eg, dizziness, vertigo, and nausea), psychological and neurovegetative problems (eg, anxiety, depression, or sleep disturbance), and cognitive impairment (eg, memory loss and decreased ability to concentrate).[6]
Imaging modalities such as magnetic resonance imaging (MRI), single-photon emission computed tomography (SPECT), and magnetoencephalography (MEG) have been shown to be more sensitive than CT at detecting brain injuries associated with PCS.
Patients who have a symptom constellation consistent with PCS require thorough physical and neurologic examinations. A CT scan should be obtained if significant concern about ICH exists.
There has been some debate as to which symptoms of PCS are due to organic causes and which have a psychological basis. It has been hypothesized that early PCS symptoms are more likely to be organic, whereas PCS symptoms that persist beyond 3 months have a nonorganic, psychological basis. Although it is known that psychological factors may be present early, studies using imaging techniques such as MRI, SPECT, and MEG have demonstrated the presence of organic brain injury in patients with persistent PCS at more than 1 year after injury.
Neuropsychological assessments have pointed toward an organic basis for some of the symptoms of PCS. Patients with PCS have been found to have cognitive deficits in memory, attention, and learning when compared with controls. A prospective study found that patients with PCS, compared with control subjects, had impaired eye movements that were both persistent and independent of factors such as depression or intellectual ability.[7]
Findings from neuropsychological evaluations have demonstrate that symptom severity is not necessarily dependent on neurologic status immediately following injury. In other series, however, the duration of LOC or posttraumatic amnesia may be correlated with the probability of developing PCS.
Some studies have found the certain patient characteristics (eg, female sex, noise sensitivity, and anxiety) can predict development of symptoms.[8] One study found that a simple test in the ED of immediate and delayed memory for five words, along with a Visual Analogue Scale (VAS) for acute headache, provided an 80% sensitivity and 76% specificity for the development of PCS.[9] Another study found that higher educational levels, along with mild symptoms and the absence of any extracranial symptoms, predicted a low likelihood of significant dysfunction from PCS.
Risk factors for the development of PCS include nonsporting mechanisms, LOC, 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 any correlation between blame and litigation. In fact, PCS symptoms persisted after settlement.
Some authors have suggested that persons with a history of depressive and anxiety disorders,[10] 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, there is some evidence to suggest that PCS is more likely to develop in patients presenting with nausea, headache, and dizziness.
One study found an inverse association between the number of years of education and development of PCS in adult patients.[11]
Patients with premorbid physical problems have also been found to have a higher incidence of PCS after MHI.
One study found that perception of the illness itself may have an effect on the development of PCS.[12] Patients who believed that their symptoms had serious negative consequences on their lives were at increased risk for developing PCS.
More than 2 million instances of TBI occur in the United States each year. In a descriptive study that examined ED visits for mild TBI (mTBI) in the United States between 2006 and 2012, Cancelliere et al found that the annual frequency of such visits rose from 569.4 per 100,000 to 807.9 over this period.[13] Depending on the definitions employed and the population examined, approximately 50% of patients with MHI have PCS symptoms at 1 month, and 15% have symptoms at 1 year. The number of patients who sustain MHI but do not present for medical care is unknown; therefore, it is likely that PCS is 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 mTBI will continue to have postconcussion symptoms at 3 months.[14, 15]
Approximately 50% of those who sustain MHIs are in the age range of 15-34 years; however, PCS has not been shown to have a predilection for any specific age group.[1, 16]
More than 800,000 children a year visit an ED for head injuries each year in the United States; the vast majority of these are MHIs.[17] TBIs are largest cause of ED visits for adolescents. Although 80-90% of these are mTBIs, or concussions, and are not life-threatening, even an mTBI 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.
It has been estimated that more than 300,000 sports-related concussions occur annually in the United States and that the likelihood of sustaining a concussion while playing a contact sport may be as high as 19% per year of play.[18] Participants in high school contact sports sustain more than 62,000 concussions annually; in college football, 34% of players have had one concussion and 20% have had more than one. Over the course of a single season, 4-20% of college and high school football players will sustain a brain injury. The risk of concussion in football players is three to six times higher in players who have had a previous concussion.
In a study from McGill University, concussion rates in soccer players were found to be comparable to those in football players.[19] Approximately 60% of college soccer players experienced concussion symptoms at least once during the playing season. Once an athlete sustained a concussion, he or she was four to six times more likely to sustain a second one.
An accurate prognosis has been difficult to achieve, given that many patients with minor symptoms may not enter the healthcare system and that those who 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, though some small studies have suggested persistence of minor cognitive defects can persist in asymptomatic mTBI patients.[20]
Approximately 15% of patients report still having problems more than 12 months after injury. This group is likely to experience persistent and intrusive symptoms that may be refractory to treatment and may impose a lifelong disability.
At least one study found that the persistence of dizziness as a symptom seemed to portend a longer and more significant symptom complex.[21] Other studies found that depression, pain, and symptom invalidity were correlated with longer and worse symptoms.[22] Some evidence suggests that patients with early clinical symptoms (eg, headache, dizziness, and intracranial lesions) are more likely to have PPCS.
PCS is commonly associated with multiple concussions, but in one series (N = 221; average number of concussions, 3.3, median symptom duration, 7 mo), 23.1% of patients experienced PCS after only one concussion.[23]
Hiploylee et al found that the time to recovery often depended on the number of initial symptoms reported, with each symptom reducing the recovery rate by about 20%.[24] They also found that PCS may be permanent if recovery does not occur within 3 years. Those who did not recover were more likely to be noncompliant regarding the recommendation to refrain from returning to play.
A meta-analysis (six studies) by Wyrwa et al evaluated 13 prognostic prediction models (PPMs) for predicting postconcussion recovery in pediatric patients.[25] All of the studies defined outcomes differently, and none of them specifically addressed the clinical utility of the models. The risk of bias was high for all six studies. The PPM with the best evidentiary support was the Predicting and Preventing Postconcussive Problems in Pediatrics (5P) score, which the authors suggested could be considered for clinical application; the other PPMs would require external validation.
Most patients with postconcussion (postconcussive) syndrome (PCS) 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:
Tator and Davis performed a retrospective cohort study of 138 patients who were diagnosed with sports-related PCS on the basis of three or more postconcussion symptoms lasting 1 month or longer.[27] The patients averaged 3.4 concussions, with some having no more than one and others having more than 12. More than 80% of the PCS patients had had at least one previous concussion; only 19.6% had not. In 21% of patients, the authors identified a history of a previous psychiatric condition, attention-deficit/hyperactive disorder (ADHD), learning disability, or previous migraine headaches.
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 undiagnosed intracranial hemorrhage (ICH). Other findings may include the following:
Neuropsychological testing has revealed that cognitive deficits can persist for 6 months or longer when other symptoms are present. However, testing also has revealed that these deficits can resolve when other somatic and neurologic symptoms do not. Patients without other subjective symptoms usually perform normally on tests for cognitive deficits.
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. Efforts have been made to search for evidence of specific proteins or biomarkers as predictive of postconcussion (postconcussive) syndrome (PCS), but definitive correlations remain to be established.
Neurologic examination findings and computed tomography (CT) scans findings are frequently normal in patients with PCS; however, this does not confirm the absence of damage to the brain.
CT 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 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 unless focal neurologic signs are present or 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 small. 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 a significantly symptomatic patient, though the decision to obtain it should be weighed against the risks of radiation, especially in children.
Magnetic resonance imaging (MRI), single-photon emission computed tomography (SPECT), positron emission tomography (PET),and magnetoencephalography (MEG) have been shown to be more sensitive than CT at detecting brain injuries associated with PCS.[28, 29, 30, 31, 32, 33] These modalities have demonstrated associations 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 PCS. However, they have not confirmed 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, in a study focusing on a biomarker for axonal injury, serum cleaved tau (C-tau), no correlation was established between C-tau levels at the time of injury and the later development of PCS.[34] Studies looking at serum levels of S-100B, a protein found most commonly in astrocytes, in patients with minor head injury (MHI) have yielded conflicting results regarding a correlation between initial levels of the protein and development of PCS.[35]
In a study by Ramos-Zúñiga et al, neuropsychological and spectroscopy testing confirmed the diagnosis of PCS in patients with MHI.[28] Spectroscopy revealed neurometabolite disturbances in 54% of cases, particularly N-acetylaspartate (Naa) and the Naa-to-lactate ratio in the frontal lobe. In addition, the authors noted that 55% of patients experienced physical disturbances such as headache and postural vertigo.
MRI obtained in the acute period has little clinical significance. If ordered, it should be obtained on an outpatient basis in conjunction with follow-up. Although traumatic lesions may be depicted on MRI in a patient with MHI and a normal nonenhanced CT scan, this rarely influences 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 (TBI).[32] A study by Berto et al found such analysis to be prognostic of persistent PCS in college athletes.[36]
MRI, SPECT, or PET obtained 4-24 months after injury may reveal a variety of abnormalities, though such findings rarely influence treatment or outcome.
In a study of cerebral blood flow (CBF) measured by means of MRI in pediatric patients (8-18 y) 40 days after mild TBI (mTBI), global CBF was higher in the symptomatic group and lower in the asymptomatic group as compared with control subjects.[37]
Neuropsychological testing is rarely performed in the acute setting, although it may have some value in predicting the development of symptoms. Various 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 PCS symptoms.
Neuropsychological assessments that may be used include the Wechsler Adult Intelligence Scale and specific subtests (digit span and vocabulary), the Trail Making Test, complex figure drawings (eg, Rey Osterreith), copy trials and memory trials, category tests, controlled oral word association (the Hopkins Verbal Learning Test), the 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, the Impact of Event Scale, the Galveston Orientation and Amnesia Test, and assessments of posttraumatic amnesia are used together as prognostic screening instruments for predicting PCS persistence.
In a study by Joyce et al, the 19-item Postconcussion Symptom Scale was broken up into three discrete factors: (1) neurocognitive, (2) somatic, and (3) emotional.[38] 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 three factors.
The Sport Concussion Assessment Tool (SCAT), published in its sixth version (SCAT6) in 2023,[39] is one of the most widely researched concussion assessment tools in athletes. The presence and frequency of posttraumatic headache are associated with the SCAT symptom severity score, which is an important predictor of postconcussion recovery.[40, 41]
No specific care is required in the emergency department (ED). Patients with the symptom constellation consistent with postconcussion syndrome (PCS) require thorough physical and neurologic examinations. Computed tomography (CT) should be obtained if significant concern about intracranial hemorrhage exists, though this injury is rare in patients who present late with nonfocal findings at examination.[42]
Supportive care may include the use of nonnarcotic analgesics and antiemetics. At present, however, there appear to be no medications given at discharge that can prevent or hasten the resolution of PCS. Several drugs are under investigation, but none have been prove to be clinically useful.
Providing patients with an explanation of symptoms as well as expectations may decrease the severity and duration of postconcussion symptoms.
Patients may be admitted if symptoms are severe, though this is rare; the majority of patients can be discharged home. 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 may, however, 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 physician, neurologist, or psychiatrist, depending on their symptoms.
Follow-up and patient education on what to expect after minor head injuries is useful, given that many patients will have symptoms for weeks after discharge.[43]
Outpatient care is the cornerstone of treatment of patients with PCS and involves multidisciplinary teams that provide testing and treatment, including cognitive rehabilitation, psychotherapy, stress management, vocational counseling, and symptomatic pharmacologic therapy.
No treatments have been proved to be effective. Some evidence exists to suggest that neurotherapy or quantitative electroemcephalographic (EEG) biofeedback may improve symptoms of PCS. Additional data from controlled studies are needed.
Treatment is usually coordinated by a neurologist, a physical medicine specialist, a primary care physician, or a psychologist specializing in these disorders.
A study (N = 26) by Rausa et al assessed the feasibility of a multimodal intervention called Concussion Essentials (CE) for managing persistent psotconcussion symptoms in children and adolescents (age range, 6-18 y).[44] The intervention comprised education, physiotherapy, and psychology modules, which were employed for up to 8 weeks or until symptoms improved. CE participants (n =13) were matched to a cohort that received usual care (n = 13). All of the patients in the CE group reported symptomatic improvement, compared with approximately half of the usual care group.
Once the diagnosis is made, consultation in the ED is only rarely warranted. Outpatient referral is the cornerstone of treatment. It has been suggested that findings from early neuropsychological assessment may determine the prognosis; however, such assessment is rarely performed in the ED.
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.
Clinical Context: 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.
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.
Clinical Context: Metoclopramide blocks dopamine receptors in the chemoreceptor trigger zone of the central nervous system.
Clinical Context: Ondansetron is a selective 5-HT3-receptor antagonist that blocks serotonin both peripherally and centrally. It prevents the nausea and vomiting.
Clinical Context: Prochlorperazine may relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine receptors through its anticholinergic effects and depressing the reticular activating system.
Antiemetics are useful in the treatment of nausea associated with postconcussive syndrome.