Post-concussion syndrome, also known as postconcussive syndrome or PCS, is a set of symptoms that a person may experience for weeks, months, or occasionally years after a concussion–a mild form of traumatic brain injury (abbreviated TBI). PCS may also occur in moderate and severe cases of traumatic brain injury. Symptoms of PCS, which is the most common entity to be diagnosed in people who have suffered TBI, may occur in 38–80% of mild head injuries. A diagnosis may be made when symptoms resulting from concussion last for more than three months after the injury, or it may be made starting within a week or ten days of trauma. In late, persistent, or prolonged PCS (PPCS), symptoms last for over six months, or by other standards, three.
The condition can cause a variety of symptoms: physical, such as headache; cognitive, such as difficulty concentrating; and emotional and behavioral, such as irritability. As many of the symptoms in PCS are common to, or exacerbated by, other disorders, there is a risk of misdiagnosis. Though there is no treatment for PCS itself, symptoms can be treated; medications and physical and behavioral therapy may be used, and patients can be educated about symptoms and their usual prognosis. The majority of PCS cases disappear after a period of time.
It is not known what causes PCS symptoms to occur and persist, or why some people who suffer a mild traumatic brain injury (MTBI) develop PCS while others do not. The nature of the syndrome and the diagnosis itself have been the subject of intense debate since the 19th century. However, certain risk factors have been identified; for example, preexisting medical or psychological conditions, expectations of disability, and older age all increase the chances that someone will suffer PPCS. Physiological and psychological factors present before, during, and after the injury are all thought to be involved in the development of PCS.
The acronym PCS may also be used to mean post-concussion symptoms. Symptoms can appear immediately, or weeks to months after the initial injury. Their severity lessens progressively over time. The nature of the symptoms tends to change over time: they are most commonly of a physical nature following the injury, but tend to become predominantly psychological later. Signs and symptoms such as noise sensitivity, problems with concentration and memory, irritability, depression, anxiety, fatigue, and poor judgment may be called 'late symptoms' because they generally do not occur immediately after the injury, but rather days or weeks after. Nausea and drowsiness commonly occur early after concussion but usually do not last, while headache and dizziness occur immediately after the injury and are long lasting.
Dizziness, the second most common symptom, occurs in about half of people with PCS and is still present in up to a quarter of them a year after the injury. Older people are at especially high risk for dizziness.
About 10% of people with PCS develop sensitivity to light or noise, about 5% experience a decreased sense of taste or smell, and about 14% have blurred vision. People may also have double vision or ringing in the ears, also called tinnitus. Loss of hearing occurs in 20% of cases. PCS may cause insomnia, fatigue, sleepiness, or other problems with sleep. Other physical symptoms include nausea and vomiting.
No definition of PCS is accepted by all health professionals, and doubt exists about the validity of the diagnosis. One reason for this is that symptoms of PCS also occur in people who have no history of head injury, but who have other medical and psychological complaints. In one study, 80% of healthy, uninjured people reported having three or more symptoms similar to those found after concussion. In another study, 64% of people with TBI met the criteria set out by the ICD-10 for post-concussion syndrome, but so did 40% of people that had injuries not to the head; 11% of those with brain injuries and 7% of those with other injuries met the DSM-IV criteria for post-concussion syndrome (see diagnosis, below). Having depression, post-traumatic stress disorder, or chronic pain virtually guarantees that a person will report symptoms resembling those of PCS. One study found that while people with chronic pain without TBI do report many symptoms similar to those of post-concussion syndrome, they report fewer symptoms related to memory, slowed thinking, and sensitivity to noise and light than people with MTBI do.
In a syndrome, a set of symptoms is consistently present, and symptoms are linked such that the presence of one symptom suggests that of others. Because PCS symptoms are so varied and many can be associated with a large number of other conditions, doubt exists about whether the term "syndrome" is appropriate for the constellation of symptoms found after concussion. The fact that the persistence of one symptom is not necessarily linked to that of another has similarly led to doubt about whether "syndrome" is the appropriate term.
A longstanding controversy surrounding PCS concerns the nature of its etiology – that is, the cause behind it – and the degree to which psychological factors and organic factors involving brain dysfunction are responsible. The debate has been referred to as 'psychogenesis versus physiogenesis' (psychogenesis referring to a psychological origin for the condition, physiogenesis to a physical one).
It is possible that some post-concussion symptoms are due to physical causes while others are psychological. One hypothesis holds that physiological factors are responsible for early symptoms that occur after mild head trauma, whereas symptoms that occur later are due to psychological factors.
While the cause of symptoms occurring shortly after head trauma is likely to be physiological, it is less clear whether PPCS has an organic basis, and nonorganic factors are likely to be involved in symptoms that last longer than three months. PPCS may be caused by physiological, psychological, or psychosocial factors, chronic pain, or an interaction of some or all of these. The majority of experts believe that PPCS results from a mix of factors, including preexisting psychological factors, and those directly relating to the physical injury.
Studies using positron emission tomography have linked PCS to a reduction in glucose use by the brain, and changes in cerebral blood flow have been found to exist for as long as three years after a concussion in studies using single photon emission computed tomography (SPECT). At least one study with functional magnetic resonance imaging (fMRI) has shown differences in brain function during tasks involving memory after MTBI, and fMRI has shown changes in the brains of athletes within a week of a concussion. Not all people with PPCS have abnormalities on imaging, however, and abnormalities found in studies such as fMRI, PET, and SPECT could result from other comorbid conditions such as depression, chronic pain, and post-traumatic stress disorder (PTSD). Electroencephalograms, while usually normal in people with PCS, have occasionally been used to detect changes in brain function following mild head injury. Electrophysiological measures of brain function of people with PPCS show abnormal evoked potentials and event-related potentials compared to controls, supporting the hypothesis that PPCS has an organic basis.
Proponents of the view that PCS has a physical or organic basis point to findings that people with post-concussive symptoms have deficits on standardized tests of cognitive function as an indication that brain dysfunction is a factor in PCS. Studies have shown that people with PPCS score lower than controls on neuropsychological tests that measure attention, verbal learning, reasoning, and information processing. But although decreased scores on cognitive tests point to brain dysfunction, they cannot diagnose brain damage. Recovery as measured by scores on cognitive tests frequently do not correlate with resolution of symptoms; people may still report subjective symptoms after their cognitive function has returned to normal. Another study found that although children with PPCS had poorer scores on tests of cognitive functioning after the injury, they also had poorer behavioral adjustment before the injury than children with no persistent symptoms; these findings support the idea that PCS may result from a combination of factors such as brain dysfunction resulting from head injury and preexisting psychological or social problems. Different symptoms may be predicted by different factors; for example, one study found that cognitive and physical symptoms were not predicted by the manner in which parents and family members coped with the injury and adjusted to its effects, but psychological and behavioral symptoms were.
| Headache |
|Sleep problems |
|Problems tolerating |
anxiety, or depression
|Changes in |
The International Statistical Classification of Diseases and Related Health Problems (ICD-10) and the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders have set out criteria for PCS and postconcussional disorder (PCD), respectively.
The ICD-10 established a set of diagnostic criteria for PCS in 1992. In order to meet these criteria, a patient must have had a head injury with loss of consciousness and develop at least three of the eight symptoms marked with a check mark in the table at right under "ICD-10" within four weeks. About 38% of people who suffer a head injury with symptoms of concussion and no radiological evidence of brain lesions meet these criteria. In addition to these symptoms, people that meet the ICD-10 criteria for PCS may fear that they will have permanent brain damage, which may worsen the original symptoms. Preoccupation with the injury may be accompanied by the assumption of a "sick role" and hypochondriasis. The criteria focus on subjective symptoms and mention that neuropsychological evidence of significant impairment are not present. With their focus on psychological factors, the ICD-10 criteria support the idea that the cause of PCS is functional. Like the ICD-10, the ICD-9-CM defines PCS in terms of subjective symptoms and discusses the greater frequency of PCS in people with histories of mental disorders or a financial incentive for a diagnosis.
The DSM-IV lists criteria for diagnosis of PCD in people who suffered a head trauma with persistent post-traumatic amnesia, loss of consciousness, or post-traumatic seizures. In addition, for a diagnosis of PCD, patients must have neuropsychological impairment as well as at least three of the symptoms marked with a check mark in the table at right under "DSM-IV". These symptoms must be present for three months after the injury and must have been absent or less severe before the injury. In addition, the patient must experience social problems as a result, and must not meet criteria for another disorder that explains the symptoms better.
Neuropsychological tests exist to measure deficits in cognitive functioning that can result from PCS. The Stroop Color Test and the 2&7 Processing Speed Test (which both detect deficits in speed of mental processing) can predict the development of cognitive problems from PCS. A test called the Rivermead Postconcussion Symptoms Questionnaire, a set of questions that measure the severity of 16 different post-concussion symptoms, can be self-administered or administered by an interviewer. Other tests that can predict the development of PCS include the Hopkins Verbal Learning A test (HVLA) and the Digit Span Forward examination. The HVLA tests verbal learning and memory by presenting a series of words and assigning points based on the number recalled, and digit span measures attention efficiency by asking the examinee to repeat back digits spoken by the tester in the same order as they are presented. In addition, neuropsychological tests may be performed to detect malingering.
PCS, which shares symptoms with a variety of other conditions, is highly likely to be misdiagnosed in people with these conditions. Cognitive and affective symptoms that occur following a traumatic injury may be attributed to MTBI, but in fact be due to another factor such as post-traumatic stress disorder, which is easily misdiagnosed as PCS and vice versa. Affective disorders such as depression have some symptoms that can mimic those of PCS and lead to a wrongful diagnosis of the latter; these include problems with concentration, emotional lability, anxiety, and sleep problems. Depression, which is highly common in persistent PCS, can worsen other PCS symptoms, such as headaches and problems with concentration, memory, and sleep. PCS also shares symptoms with chronic fatigue syndrome, fibromyalgia, and exposure to certain toxins. Traumatic brain injury may cause damage to the hypothalamus or the pituitary gland, and deficiencies of pituitary hormones (hypopituitarism) can cause similar symptoms to post-concussion syndrome; in these cases, symptoms can be treated by replacing any hormone deficiencies.
In situations such as motor vehicle accidents or following a violent attack, the post-concussion syndrome may be accompanied by post-traumatic stress disorder, which is important to recognize and treat in its own right. People with PTSD, depression, and anxiety can be treated with medication and psychotherapy.
The way in which children cope with the injury after it occurs may have more of an impact than factors that existed prior to the injury. Children's mechanisms for dealing with their injuries may have an effect on the duration of symptoms, and parents that do not deal effectively with anxiety about children's post-injury functioning may be less able to help their children recover.
If another blow to the head occurs after a concussion but before its symptoms have gone away, there is a very slight risk of developing the extremely rare but deadly second-impact syndrome (SIS). In SIS, the brain rapidly swells, greatly increasing intracranial pressure. People who have repeated mild head injuries over a prolonged period, such as boxers, are at risk for dementia pugilistica, a severe, chronic disorder involving a decline in mental and physical abilities.
The existence of PCS in children is controversial. It is possible that children's brains have enough plasticity that they are not affected by long-term consequences of concussion (though such consequences are known to result from moderate and severe head trauma). On the other hand, children's brains may be more vulnerable to the injury, since they are still developing and have fewer skills that can compensate for deficits. Clinical research has found higher rates of post-concussion symptoms in children with TBI than in those with injuries to other parts of the body, and that the symptoms are more common in anxious children. Symptoms in children are similar to those in adults, but children exhibit fewer of them. Evidence from clinical studies found that high school-aged athletes had slower recoveries from concussion as measured by neuropsychological tests than college-aged ones and adults. PCS is rare in young children.
Mild brain injury-related factors that increase the risk for persisting post-concussion symptoms include an injury associated with acute headache, dizziness, or nausea; a Glasgow Coma Score of 13 or 14; post-traumatic amnesia lasting longer than an hour; and suffering another head trauma before recovering from the first. The risk is also increased in people who experience stress, have traumatic memories of the event, or expect to be disabled by the injury.